Complete Issue Critical Nursing

CriticalCareNurseF E B R U A R Y 2 0 1 5 • V O L U M E 3 5 N U M B E R 1

T h e j o u r n a l f o r h i g h a c u i t y , p r o g r e s s i v e , a n d c r i t i c a l c a r e n u r s i n g

Stroke VolumeOptimization

Therapeutic Hypothermia

Delirium

Exertional Heat Stroke

ECMO for Pediatric

Cardiac Arrest

CNE

CNE

CNE

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CriticalCareNurseT h e j o u r n a l f o r h i g h a c u i t y , p r o g r e s s i v e , a n d c r i t i c a l c a r e n u r s i n g

President TERI LYNN KISS, RN, MS, MSSW, CNML, CMSRN

President-elect KAREN MCQUILLAN, RN, MS, CNS-BC, CCRN, CNRN, FAAN

Secretary LISA RIGGS, RN, MSN, ACNS-BC, CCRN

Treasurer CHRISTINE S. SCHULMAN, RN, MS, CNS, CCRN

Directors LINDA M. BAY, RN, MSN, ACNS-BC, CCRN, PCCN

MEGAN BRUNSON, RN, MSN, CNL, CCRN-CSC

NANCY FREELAND, RN, MSN, CCRN

KAREN L. JOHNSON, RN, PhD

DEBORAH KLEIN, RN, MSN, ACNS-BC, CCRN, CHFN, FAHA

PAULA S. MCCAULEY, DNP, APRN, ACNP-BC, CNE

RIZA V. MAURICIO, RN, PhD, CCRN, CPNP-PC/AC

KATHLEEN K. PEAVY, RN, MS, CCRN, CNS-BC

MARY ZELLINGER, RN, MN, ANP, CCRN-CSC, CCNS

Chief Executive Officer DANA WOODS

Editorial OfficeAmerican Association of Critical-Care Nurses101 Columbia, Aliso Viejo, CA 92656 (800) 899-1712, (949) 362-2000Website: www.ccnonline.org e-mail: [email protected]

Publishing Manager MICHAEL MUSCATManaging Editor REBECKA WULFArt and Production Director LeROY HINTONCopy Editors BARBARA HALLIBURTON, PhD

KATIE SPILLER, MS

Book Review Editor MARY PAT AUST, RN, MS

Graphic Artist MATTHEW EDENSSenior Publishing Associate SAM MARSELLAPeer-Review Coordinator DENISE GOTTWALD

Advertising Sales OfficeSLACK Incorporated6900 Grove Road, Thorofare, NJ 08086(800) 257-8290, (856) 848-1000

National Account Manager KATHY HUNTLEYRecruitment Manager MONIQUE McLAUGHLIN Administrator ASHLEY SEIGFRIED

Editor JoAnn Grif Alspach, RN, MSN, EdD

THOMAS AHRENS, RN, PhD, CCRN, CS

Clinical Specialist/Research Scientist, Nursing DepartmentBarnes-Jewish Hospital, St Louis, Missouri

SUSAN D. BELL, RN, MS, CNRN, CNP

Nurse Practitioner, NeurosurgeryOhio State University Medical Center, Columbus, Ohio

SUZETTE CARDIN, RN, DNSc, CNAA

Adjunct Assistant Professor, Graduate Nursing Administration Program UCLA School of Nursing, Los Angeles, California

BONNIE M. JENNINGS, RN, PhD, FAAN

Professor, Nell Hodgson Woodruff School of NursingEmory University, Atlanta, Georgia

SUSAN G. TREVITHICK, RN, MS, CNA

Clinical Support Manager, Specialty Care CenterSalt Lake City Veterans Administration Medical Center, Utah

GLENNA TRAIGER, RN, MSN, CCRN

Clinical Nurse Specialist, Pulmonary Arterial Hypertension Program Greater LA VA Medical Center, Los Angeles, California

Editorial Board

Contributing EditorsAdvanced PracticeANDREA M. KLINE-TILFORD, CPNP-AC/PC, CCRN, FCCM

Bariatric CareBRENDA K. HIXON VERMILLION, RN, DNP, ACNS-BC,

ANP-BC, CCRN

Basic and Advanced Life SupportPRISCILLA K. GAZARIAN, RN, PhD

Cardiovascular SurgeryKRISTINE CHAISSON, RN, BSN, MS, CCRN

Certification Test PrepCAROL RAUEN

Cochrane Review SummaryDAPHNE STANNARD, RN, PhD, CCRN, CCNS

Complementary TherapiesDEBRA KRAMLICH, RN, MSN, CCRN

Critical Care AppsCLAIRE CURRAN, RN, MSN, CCRN

Cultural DiversityMAJELLA S. VENTURANZA, RN, MA, CCRN

ECGs and PacemakersJANE N. MILLER, RN, DNP, CCRN, CCNS

Emergency DepartmentDOROTHY DUNCAN, RN, DNP, ACNP-BC, CCRN, CEN

End-of-Life CareKATHLEEN OUIMET PERRIN, RN, PhD, CCRN

Evidence-Based PracticeMARCIA BELCHER, RN, MSN, BBA, CCRN-CSC, CCNS

Family-Centered CarePATRICIA BROWN, DNP, APN, CNS, CCRN

Gastrointestinal DisordersROSEMARY K. LEE, DNP, ARNP, ACNP-BC, CCNS, CCRN

Geriatric CareSONYA R. HARDIN, RN, PhD, CCRN, ACNS-BC, NP-C

Healthy Work EnvironmentsVIRGINIA C. HALL, BSN, CCRN

Heart FailureKAREN L. COOPER, RN, MSN, CCRN, CNS

Management/AdministrationMARIA CHRISTABELLE CASTRO, RN, MSHA, CCRN, NE-BC

Military Critical Care Nursing: Air ForceBENJAMIN SCHULTZE, RN, ACNP-BC, MEd, MSN

Military Critical Care Nursing: ArmyLINDA A. VALDIRI, COL, ANC, USA, RN, MS, CCNS

Military Critical Care Nursing: NavyCARL GOFORTH, RN, MSN, CCRN

Neonatal CareRACHEL A. JOSEPH, PhD, CCRN

Neurology/NeurosurgeryGLENN CARLSON, MSN, ACNP-BC, CCRN

NutritionCOLLEEN O’LEARY-KELLEY, RN, PhD, CNE

Pain ManagementDIANE GLOWACKI, RN, MSN, CNS, CNRN-CMC

Patient Education and Discharge PlanningFLORENCE M. SIMMONS, RN, MSN, CCRN

Patient SafetyELIZABETH MATTOX, RN, MSN, ARNP

Patient TransportMELISSA RACH, RN, BSN, CCRN, CMC

Pediatric CareJODI E. MULLEN, RN-BC, MS, CCRN, CCNS

PharmacologyKELLY THOMPSON-BRAZILL, RN, MSN, ACNP, CCRN-CSC, FCCM

Postanesthesia RecoveryTITO D. TUBOG, RN-BC, CRNA, APRN, CCRN-CSC-CMC, CEN

PreceptingLIZ ROGAN, RN, EdD-c, CNE

Progressive CareMARGARET M. ECKLUND, RN, MS, CCRN, ACNP-BC

Pulmonary CareDEBRA SIELA, RN, PhD, ACNS-BC, CCNS, CCRN, CNE, RRT

Quality Improvement ReportsJULIE M. STAUSMIRE, RN, MSN, ACNS-BC

Rural SettingsCHARLENE A. WINTERS, PhD, APRN, ACNS-BC

SimulationKATE MOORE, RN, DNP, CCRN, CEN, AGACNP-BC, AGPCNP-BC

Staff DevelopmentLESLIE SWADENER-CULPEPPER, APRN-CNS, MSN,

CCRN, CCNS

Tele-ICUPAT JUAREZ, APN, CCRN, CCNS

ToxicologyDANA BARTLETT, RN, MSN, MA, CSPI

TraumaMICHAEL W. DAY, RN, MSN, CCRN

www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 1

CriticalCareNurseT h e j o u r n a l f o r h i g h a c u i t y , p r o g r e s s i v e , a n d c r i t i c a l c a r e n u r s i n g

F E B R U A R Y 2 0 1 5 • V O L U M E 3 5 N U M B E R 1

Stroke Volume Optimization:

The New Hemodynamic Algorithm

CNE

Alexander Johnson and Thomas Ahrens

Page 11

CRITICAL CARE NURSE (ISSN 0279-5442, eISSN 1940-8250) is published bimonthly (February, April, June, August, October, December) by theAmerican Association of Critical-Care Nurses (AACN), 101 Columbia, Aliso Viejo, CA 92656. Telephone: (949) 362-2000. Fax: (949) 362-2049.E-mail: [email protected]. Copyright 2015 by AACN. All rights reserved. CRITICAL CARE NURSE is an official publication of AACN. No part of thispublication may be reproduced or transmitted in any form or by any means, electronic or mechanical, in cluding photocopying, recording orby any information storage retrieval system without permission of AACN. For all permission requests, please contact the Copyright ClearanceCenter, Customer Service, 222 Rosewood Drive, Danvers, MA 01923. (978) 750-8400. The statements and opinions contained herein aresolely those of individual contributors and not of the editor or AACN. The editor and AACN assume that articles emanating from a particularinstitution are submitted with the approval of the requisite authority, including all matters pertaining to human studies and patient privacyrequirements. Advertisements in this journal are not a warranty, endorsement, or approval of the products by the editor or AACN, who dis-claim all responsibility for any injury to persons or property resulting from any ideas or products referred to in articles or advertisements.Individual subscriptions (print and online): US, $39; outside of US, US$60. Student rates: US, $25; outside of US, $38. Institutional rates (printand online): US, $412; outside of US, US$504. Institutional rates (print only): US, $294; outside of US, US$387. Institutional rates (online only):US, $276; outside of US, US$276. Single copies and back issues: US, $40; outside of US, US$50. Fax requests to CCN Back Issues at (949) 362-2049 or write to CCN, 101 Columbia, Aliso Viejo, CA 92656, or phone (800) 899-1712; (949) 362-2050, ext 532. Prices on single copies orbulk reprints of articles are available on request from AACN at (949) 362-2050, ext 532.

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2 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org

CCN FAST FACTSUse of a Nursing Checklist to Facilitate

Implementation of TherapeuticHypothermia After Cardiac Arrest

Page 38

Nonpharmacological Interventions toPrevent Delirium: An Evidence-Based

Systematic ReviewPage 50

Cover illustration by Kimberly Martens

OnlineNOWAbstracts of articles available exclusively

online at www.ccnonline.org

Page 10

Methods Used by Critical CareNurses to Verify Feeding TubePlacement in Clinical Practice

Annette M. Bourgault, Janie Heath, Vallire Hooper, Mary Lou Sole, and Elizabeth G. NeSmith

Page e1

FEATURESUse of a Nursing Checklist to

Facilitate Implementation of Therapeutic Hypothermia After

Cardiac ArrestKathleen Ryan Avery, Molly O’Brien, Carol Daddio Pierce,

and Priscilla K. Gazarian

Page 29

Nonpharmacological Interventionsto Prevent Delirium: An Evidence-

Based Systematic ReviewRyan M. Rivosecchi, Pamela L. Smithburger, Susan Svec,

Shauna Campbell, and Sandra L. Kane-Gill

Page 39

MILITARY CRITICAL CARE NURSING: NAVY

Exertional Heat Stroke in Navy andMarine Personnel: A Hot Topic

Carl W. Goforth and Josh B. Kazman

Page 52

PEDIATRIC CAREExtracorporeal Membrane Oxygenation

for Pediatric Cardiac ArrestJennie Ryan

0

EDITORIALImproving Cardiac Arrest ResuscitationOutcomes: A Valentine Worth Sending

JoAnn Grif Alspach, Editor

Page 6

CERTIFICATION TEST PREPCelebrate and Be Proud!

Carol Rauen, Kirtley Ceballos, and Steve Risch

Page 71

ASK THE EXPERTSComparing Blood Pressure Measures:

Does One Measurement Equal Another?Barbara McLean

Page 75

IN OUR UNITImplementation of Early Exercise and

Progressive Mobility: Steps to SuccessMelody R. Campbell, Julie Fisher,

Lyndsey Anderson, and Erin Kreppel

Page 82

COLUMNS

DEPARTMENTS

ALSO IN THIS ISSUE

CNE

CNE


ContributorsPage 5

CorrectionsPage 9

Book ReviewsPage 89

Education DirectoryPage 91

I Am a Critical Care NursePage 92

Venous cannula

Rightatrium

Leftatrium

Rightventricle

Leftventricle

Aortic cannula

Aorta

Superior venacava

Page 60

Normalsystole

Normaldiastole

Constantmean

Overestimatedsystole

UnderestimateddiastoleComparing normal

with underdamped

Page 75 Page 89

pharmacy and therapeutics at the University of

Pittsburgh School of Pharmacy.

Coauthor of Exertional Heat Stroke in Navy

and Marine Personnel, Josh Kazman is a

research associate with the Consortium for

Health and Military Performance at Uniformed

Services University of the Health Sciences.

Elizabeth G. NeSmith, coauthor of Methods

Used to Verify Feeding Tube Placement, is an

associate professor and chair of the Depart-

ment of Physiological and Technological

Nursing at Georgia Regents University, College

of Nursing, in Augusta.

Molly O’Brien, coauthor of Implementation

of Therapeutic Hypothermia After Cardiac

Arrest, is the research coordinator in the car-

diac ICU at Shapiro Cardiovascular Center at

Brigham and Women’s Hospital.

Coauthor of Use of a Nursing Checklist to

Facilitate Implementation of Therapeutic

Hypothermia After Cardiac Arrest, Carol

Daddio Pierce is the clinical educator in the

medical ICU at Brigham and Women’s Hospital.

Ryan M. Rivosecchi, coauthor of Nonphar-

macological Interventions to Prevent Delirium,

is a pharmacy resident in critical care at the

University of Pittsburgh Medical Center, Pres-

byterian Hospital.

Author of Extracorporeal Membrane Oxygena-

tion for Pediatric Cardiac Arrest, Jennie Ryan

in a nurse practitioner in the ICU at Nemours

Cardiac Center, Wilmington, Delaware.

Coauthor of Nonpharmacological Inter-

ventions to Prevent Delirium, Pamela L.

Smithburger is an assistant professor of

pharmacy and therapeutics, University of

Pittsburgh School of Pharmacy.

Mary Lou Sole, coauthor of Methods Used to

Verify Feeding Tube Placement, is the Orlando

Health Distinguished Professor at University of

Central Florida, College of Nursing.

Coauthor of Nonpharmacological Interventions to

Prevent Delirium, Susan Svec is the clinical director of

the medical ICU, University of Pittsburgh Medical Cen-

ter, Presbyterian Hospital.CCN

Coauthor of Stroke Volume

Optimization, Thomas Ahrens

is a research scientist, Barnes-

Jewish Hospital, St Louis, Missouri.

Kathleen Ryan Avery, coauthor of

Implementation of Therapeutic

Hypothermia After Cardiac Arrest, is

the clinical educator for the cardiac ICU

at Brigham and Women’s Hospital,

Boston, Massachusetts.

Coauthor of Methods Used to Verify

Feeding Tube Placement, Annette M.

Bourgault is an assistant professor at

Georgia Regents University, College of

Nursing, in Augusta.

Shauna Campbell, coauthor of Non-

pharmacological Interventions to Prevent

Delirium, is the nursing director of the

medical ICU at the University of Pittsburgh

Medical Center, Presbyterian Hospital.

Priscilla K. Gazarian, coauthor of

Implementation of Therapeutic Hypother-

mia After Cardiac Arrest, is the nursing

program director for resuscitative clinical

practice at Brigham and Women’s Hospital.

Coauthor of Exertional Heat Stroke in

Navy and Marine Personnel, Carl Goforth

is the clinical subject matter expert for the

Marine Corps Combat Development

Command located in Quantico, Virginia.

Janie Heath, coauthor of Methods to

Verify Feeding Tube Placement, is dean of

the College of Nursing at University of

Kentucky in Lexington.

Coauthor of Methods Used to Verify

Feeding Tube Placement, Vallire Hooper

is the manager of nursing research at Mis-

sion Hospital in Asheville, North Carolina.

Coauthor of Stroke Volume Optimiza-

tion, Alexander Johnson is a clinical nurse

specialist, Central DuPage Hospital–North-

western Medicine, Winfield, Illinois.

Sandra L. Kane-Gill, coauthor of Non-

pharmacological Interventions to Prevent

Delirium, is an associate professor of

Contributors

KANE-GILL

AHRENS KAZMAN

AVERY

BOURGAULT

GAZARIAN

GOFORTH

HEATH

HOOPER

JOHNSON SVEC

SOLE

SMITHBURGER

RIVOSECCHI

PIERCE

NeSMITH

RYAN


Improving Cardiac Arrest ResuscitationOutcomes: A Valentine Worth Sending

Survival Rates Remain DishearteningEach year nearly 568 500 sudden cardiac

arrests occur in the United States. Of these,

approximately 359400 (63%) are out-of-hospital

cardiac arrests (OHCAs) and 209 000 (37%)

are in-hospital cardiac arrests.1 Of the nearly

360 000 cardiac arrests that happen outside

hospitals, 88% occur in the home.3 If effective

cardiopulmonary resuscitation (CPR) can be

delivered immediately after cardiac arrest, the

victim’s probability of survival is doubled or

tripled.3 However, despite decades of research,

the instruction of millions of laypersons and

professional heath care providers, countless

public service announcements, and national

programs provided by organizations such as the

AHA and American Red Cross, only 32%3 to 40%

of OHCAs are responded to with bystander CPR.1

Among all OHCA victims, only 8%3 to 9.5%

survive to hospital discharge.4

A few distinctions between out-of-hospital

and in-hospital patient populations are worth

noting. An OHCA can be defined as “cessation

of cardiac mechanical activity that occurs out-

side of the hospital setting and is confirmed by

the absence of signs of circulation.”5 Although

it may develop from a variety of noncardiac

etiologies such as trauma or drug overdose, a

substantial majority of OHCAs is attributable

to cardiac causes.5

An in-hospital cardiac arrest occurs in a

hospital and typically includes resuscitation

efforts such as defibrillation, chest compressions,

or both.6 As admission to a hospital becomes

Editorial

In the United States, February 14 is Valentine’s

Day, when expressions of love are sent to

those we care about most. The American

Heart Association’s (AHA’s) designation of

February as American Heart Month reminds

us that we could extend those sentiments

beyond a single day by demonstrating how to

protect our loved ones from cardiac disease,

still ranked as the nation’s number 1 cause of

death.1 In recognition of the burden that heart

disease represents in our patient populations,

this issue of Critical Care Nurse is devoted to

the topic of cardiac arrest, a challenging condi-

tion that teeters its victims between life and

death. One of the particularly vexing and long-

standing attributes of this disorder is our lim-

ited success in prevailing against its potentially

ominous outcomes.

Definition of Cardiac Arrest Cardiac arrest is defined as the abrupt loss

of cardiac function in someone who may or

may not have a diagnosis of heart disease. It

arises instantaneously, often without preceding

symptoms,2 making it virtually impossible to

anticipate and challenging to correctly recog-

nize, manage, and reverse before irreversible

and fatal consequences ensue. Although it

may arise from a number of distinct etiologies,

most cases of cardiac arrest are associated with

development of a cardiac arrhythmia, typically

ventricular fibrillation.1

JoAnn Grif Alspach

©2015 American Association of Critical-Care Nursesdoi: http://dx.doi.org/10.4037/ccn2015167


more selective based on need for services, in-hospital

patients who experience cardiac arrest are likely to be

sicker and have more clinically significant comorbidities

compared to their neighbors living at home. As a result,

despite the greater availability of health care profession-

als to provide CPR, in-patient cardiac arrest victims may

have more clinically advanced systemic disorders that

could limit their ability to benefit from CPR.

During the 1990s, reports of survival to discharge

rates following in-hospital cardiac arrest and CPR ranged

from 7% to 26%.7,8 In the United States, the most recent

in-hospital cardiac arrest statistics from the Resuscitation

Outcomes Consortium Cardiac Epistry and Get With The

Guidelines-Resuscitation data show an overall survival rate

to hospital discharge for adult victims of cardiac arrest of

23.9%.4 For patients in the United Kingdom, the

National Cardiac Arrest Audit found an overall survival

to hospital discharge rate of 18.4%.9 As in the United

States, higher rates of survival to hospital discharge are

found in patients with shockable rhythms (ventricular

fibrillation or pulseless ventricular tachycardia) compared

to those with nonshockable rhythms (asystole or pulse-

less electrical activity).9

For patients over 70 years, the chance of survival to

hospital discharge following in-hospital CPR ranges at a

lower plateau between 11.6% and 18.7%, with declining

survival associated with increasing age.10 Although some

improvements in cardiac arrest survival can be noted,

the body of research in this area suggests that significant

improvements have not yet been realized. Until those

advances can be identified to influence clinical practice,

critical care nurses might consider making their contribu-

tions by pursuing alternative efforts that represent poten-

tial inroads toward improving cardiac arrest outcomes.

Critical Care Nurses Can Contribute toImproved Outcomes

Recent research suggests that 2 of the inroads that

may lead to better cardiac arrest resuscitation outcomes

include doing more and doing less than we are currently

doing in managing this condition.

Doing MoreThe Doing More strategy recognizes that 92% of the

360 000 Americans who suffer an OHCA each year will

die, that a majority of those deaths might have been

avoided if timely and effective interventions known

to improve survival from cardiac arrest had been

provided, and that one of those timely and effective

interventions is provision of bystander CPR. As a recent

AHA Science Advisory explained,11 OHCA survival

rates have increased in communities where bystander

CPR participation was expanded. These are especially

important initiatives in poor, non–English-speaking,

Black, and Latino neighborhoods, where few know

how to provide bystander CPR. Instructional and

recruitment programs to inform, involve, and teach

CPR to residents of these neighborhoods could launch

lifesaving efforts with immediate impact.

Doing LessAs in many aspects of life, doing less at times yields

more. Two approaches to doing less with resuscitation

for cardiac arrest suggested by recent literature include

focusing on immediate and effective provision of Basic

Life Support (BLS) rather than delaying or interrupt-

ing that to provide Advanced Life Support (ALS) and

teaching laypersons to perform chest compressions-only

CPR rather than standard CPR that includes intermit-

tent breaths.

An intriguing study reported by Sanghavi and

colleagues12 at Harvard University used a nationally

representative sample of Medicare beneficiaries from

nonrural areas of the United States that included 1643

patients managed with BLS and 31 292 managed with

ALS. The researchers concluded that OHCA patients

had higher survival at discharge (BLS 13.1% vs ALS

9.2%, 95% CI, 2.3-5.7), higher survival at 90 days (BLS

8.0% vs 5.4% for ALS; 95% CI, 1.2-4.0), and lower rates

of poor neurological functioning (BLS 21.8% vs ALS

44.8%; 95% CI, 18.6-27.4) when they received only BLS

rather than ALS from emergency medical services.

These results need to be interpreted with caution (the

ALS was provided by emergency medical services staff

rather than hospital physicians or nurses, the timing

of initiation of either form of resuscitation is not

included in data, data rely on billing record rather than

clinical documentation of measures provided, and ALS

is usually preceded by BLS, so it is not clear how those

influences were distinguished to capture measurement

of ALS alone, some patients require the medications,

equipment, and therapies reserved for ALS) to ensure


that the methodology and analysis are sufficiently vetted

and not found wanting. Despite that customary admo-

nition, the results are thought-provoking and worthy

of further consideration and repeat testing.

A second avenue of Doing Less involves the use of

compression-only CPR in place of traditional CPR

procedures that include intermittent use of mouth-to-

mouth breaths. Since the AHA updated its CPR guide-

lines in 2005 to recommend use of chest-compression

CPR by untrained rescuers as well as in dispatcher-

assisted CPR in an effort to expand the quality and

provision of bystander CPR, a number of reports13,14

have heralded support for compression-only CPR

(hands-only) as an effective form of CPR with survival

outcomes comparable to those of conventional CPR.

Additional studies15 have noted better neurological

outcomes at 1 month with hands-only CPR compared

to conventional CPR when hands-only CPR is com-

bined with public-access automated external defib-

rillators. More recently, a meta-analysis of studies

including more than 92 000 adult patients with OHCAs

further supported the efficacy of hands-only CPR in

producing survival rates comparable to those achieved

with conventional CPR for patients whose arrest was

of cardiac etiology.16

Because nearly 90% of cardiac arrests occur within

the home, most of us will encounter victims who are

family members, close friends, or neighbors, as stated

by the AHA mantra: “The life you save with CPR is

mostly likely to be someone you love.”3 For those of us

already thoroughly trained and certified to provide

lifesaving resuscitation, our ability to respond to that

emergency is automatic, immediate, and competent.

In addition, critical care nurses could join with colleagues

in home health, school and community health, and

numerous other surrounding organizations to instruct

and empower residents in our neighborhoods, schools,

communities, places of worship or recreation, towns

or cities to serve their own loved ones as bystander-CPR

providers. Sending them a text, e-mail, tweet, card, or

brochure that reads “If you love someone, learn how

to save their life” and invites them to see the brief video

of how easily and quickly they can learn hands-only

CPR17 can represent the best valentine’s gift they ever

received. Critical care nurses can do that. We know

you can.

Join the ConversationIf you can suggest other strategies for improving

patient outcomes following cardiac arrest, please send

them to us at [email protected] so Critical Care Nurse can

share these with our readers. CCN

JoAnn Grif Alspach, RN, MSN, EdD

Editor, Critical Care Nurse

References1. Go AS, Mozaffarian D, Roger VL, et al; for the American Heart Associa-

tion Statistics Committee and Stroke Statistics Subcommittee. Executivesummary: heart disease and stroke statistics—2014 update: a reportfrom the American Heart Association. Circulation. 2014;129:399-410.

2. American Heart Association. Cardiac Arrest. http://www.heart.org/HEARTORG/Conditions/More/CardiacArrest/About-Cardiac-Arrest_UCM_307905_Article.jsp. Accessed December 2, 2014.

3. American Heart Association. CPR Statistics. Last updated September 3,2014. http://www.heart.org/HEARTORG/CPRAndECC/WhatisCPR/CPRFactsandStats/CPR-Statistics_UCM_307542_Article.jsp. AccessedDecember 2, 2014.

4. American Heart Association. Cardiac Arrest Statistics. Last updated Sep-tember 11, 2014. http://www.heart.org/HEARTORG/General/Cardiac-Arrest-Statistics_UCM_448311_Article.jsp. Accessed December 2, 2014.

5. McNally B, Robb R, Mehta M, et al; Centers for Disease Control andPrevention. Out-of-hospital cardiac arrest surveillance—Cardiac ArrestRegistry to Enhance Survival (CARES), United States, October 1, 2005-December 31, 2010. MMWR Surveill Summ. 2011;60(8):1-19.

6. Morrison LJ, Neumar RW, Zimmerman JL, et al; for the American HeartAssociation Emergency Cardiovascular Care Committee, Council onCardiopulmonary, Critical Care, Perioperative and Resuscitation,Council on Cardiovascular Nursing, Council on Clinical Cardiology,and Council on Peripheral Vascular Disease. Strategies for improvingsurvival after in-hospital cardiac arrest in the United States: 2013 con-sensus recommendations: a consensus statement from the AmericanHeart Association. Circulation. 2013;127:1538-1563.

7. Ebell MH, Becker LA, Barry HC, et al. Survival after in-hospital cardiopul-monary resuscitation: a meta-analysis. J Gen Intern Med. 1998;13:805-816.

8. Tresch D, Heudebert G, Kutty K, et al. Cardiopulmonary resuscitationin elderly patients hospitalized in the 1990s: a favorable outcome. J AmGeriatr Soc. 1994;42:137-141.

9. Nolan JP, Soar J, Smith GB, et al. National Cardiac Arrest Audit. Incidenceand outcome of in-hospital cardiac arrest in the United Kingdom NationalCardiac Arrest Audit. Resuscitation. 2014;85(8):987-992.

10. van Gijn MS, Frijns D, van de Glind EM, C van Munster B, HamakerME. The chance of survival and the functional outcome after in-hospitalcardiopulmonary resuscitation in older people: a systematic review. AgeAgeing. 2014;43(4):456-463.

11. Sasson C, Meischke H, Abella BS, et al; for the American Heart Associa-tion Council on Quality of Care and Outcomes Research, EmergencyCardiovascular Care Committee, Council on Cardiopulmonary, CriticalCare, Perioperative and Resuscitation, Council on Clinical Cardiology,and Council on Cardiovascular Surgery and Anesthesia. Increasing car-diopulmonary resuscitation provision in communities with lowbystander cardiopulmonary resuscitation rates: a science advisory fromthe American Heart Association for healthcare providers, policymakers,public health departments, and community leaders. Circulation.2013;127:1342-1350.

12. Sanghavi P, Jena AB, Newhouse JP, Zaslavsky AM. Outcomes after out-of-hospital cardiac arrest treated by basic vs advanced life support. JAMAIntern Med. In press. http://archinte.jamanetwork.com /journal.aspx.Accessed December 2, 2014.

13. Bohm K, Rosenqvist M, Herlitz J, Hollenberg J, Svensson L. Survivalis similar after standard treatment and chest compression only inout-of-hospital bystander cardiopulmonary resuscitation. Circulation.2007;116(25):2908-2912.


14. Iwami T, Kawamura T, Hiraide A, et al. Effectiveness of bystander-initi-ated cardiac-only resuscitation for patients with out-of-hospital cardiacarrest. Circulation. 2007;116(25):2900-2907.

15. Iwami T, Kitamura T, Kawamura T, et al. Chest-compression-only car-diopulmonary resuscitation for out-of-hospital cardiac arrest withpublic-access defibrillation. Circulation 2012;126:2844-2851. http://circ.ahajournals.org/content/126/24/2844.full?sid=f1d8c729-f6cc-4041-8d91-817fde1c97a0. Accessed December 2, 2014.

16. Yao L, Wang P, Zhou L, et al. Compression-only cardiopulmonary resus-citation vs standard cardiopulmonary resuscitation: an updated meta-analysis of observational studies. Am J Emerg Med. 2014;32(6):517-523.

17. American Heart Association. Two Steps to Staying Alive With Hands-Only CPR. http://www.heart.org/HEARTORG/CPRAndECC/HandsOnlyCPR/Hands-Only-CPR_UCM_440559_SubHomePage.jsp.Accessed December 2, 2014.

Corrections

In the December article by Chaisson et al, “Improving Patients’ Readiness forCoronary Artery Bypass Graft Surgery”(Crit Care Nurse. 2014;34[6]:29-38),the e-mail address listed for the cor-responding author (Kristine Chaisson)was invalid. The correct e-mail [email protected].

©2015 American Association of Critical-Care Nurses doi:http://dx.doi.org/10.4037/ccn2015359

TemporalScanner™

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OnlineNOW

Methods Used by Critical Care Nurese to Verify FeedingTube Placement in Clinical Practice

ANNETTE M. BOURGAULT, RN, PhD, CNL

JANIE HEATH, PhD, APRN-BC

VALLIRE HOOPER, RN, PhD, CPAN

MARY LOU SOLE, RN, PhD, CCNS

ELIZABETH G. NeSMITH, PhD, APRN-BC

BACKGROUND The American Association of Critical-Care Nurses practice alert on verification of feeding tube placement makes

evidence-based practice recommendations to guide nursing management of adult patients with blindly inserted feeding tubes.

Many bedside verification methods do not allow detection of improper positioning of a feeding tube within the gastrointestinal

tract, thereby increasing aspiration risk.

OBJECTIVES To determine how the expected practices from the American Association of Critical-Care Nurses practice alert were

implemented by critical care nurses.

METHODS This study was part of a larger national, online survey that was completed by 370 critical care nurses. Descriptive

statistics were used to analyze the data.

RESULTS Seventy-eight percent of nurses used a variety of methods to verify initial placement of feeding tubes, although 14% were

unaware that tube position should be confirmed every 4 hours. Despite the inaccuracy of auscultation methods, only 12% of

nurses avoided this practice all of the time.

CONCLUSIONS Implementation of expected clinical practices from this guideline varied. Nurses are encouraged to implement

expected practices from this evidence-based, peer reviewed practice alert to minimize risk for patient harm. (Critical Care Nurse.

2015;35[1]:e1-e7)

©2015 American Association of Critical-Care Nurses http://dx.doi.org/10.4037/ccn2015984

Critical Care Nurse offers an online publication process that provides current, relevant and useful information about the bedsidecare of critically and acutely ill patients in the most timely and efficient manner possible. The abstracts below represent full-textarticles available exclusively on the Critical Care Nurse website, www.ccnonline.org. These OnlineNOW articles are fully peerreviewed, edited, formatted, and citable. Reprints of the full-text articles are available by calling (800) 899-1712 or (949) 362-2050(ext 532) or by e-mailing [email protected].

Do you have a QR scanner app on youriPhone or Android? Scan this QR code withyour phone to access this article instantly.

Nurses commonly experience scenarios where hemodynamic monitoring is focused

on hypovolemia (see case study) in clinical practice. In this article, we provide

an overview of the use of stroke volume (the amount of blood ejected from the left

ventricle with each beat) for hemodynamic management of critically ill patients.

We also discuss the limitations of conventional assessment parameters, methods

of measuring stroke volume, hemodynamic variables that influence stroke volume, the stroke volume

optimization (SVO) replacement algorithm, supporting literature, and nursing considerations.

Much of the supporting literature (mostly studies in perioperative patients) on stroke volume as a

primary hemodynamic monitoring parameter focuses on the treatment of hypovolemia, as in the case

Stroke Volume Optimization: The NewHemodynamic AlgorithmALEXANDER JOHNSON, RN, MSN, ACNP-BC, CCNS, CCRN

THOMAS AHRENS, RN, PhD

This article has been designated for CNE credit. A closed-book, multiple-choice examination follows this article,which tests your knowledge of the following objectives:

1. Discuss the use of stroke volume optimization in a hypovolemic patient2. Define corrected flow time, peak velocity, stroke distance, and stroke index3. State various methods used to obtain blood flow measurement

©2015 American Association of Critical-Care Nurses doi: http://dx.doi.org/10.4037/ccn2015427

CNE Continuing Nursing Education

Cover


Critical care practices have evolved to rely more on physical assessments for monitoring cardiac output

and evaluating fluid volume status because these assessments are less invasive and more convenient to

use than is a pulmonary artery catheter. Despite this trend, level of consciousness, central venous pressure,

urine output, heart rate, and blood pressure remain assessments that are slow to be changed, potentially

misleading, and often manifested as late indications of decreased cardiac output. The hemodynamic

optimization strategy called stroke volume optimization might provide a proactive guide for clinicians to

optimize a patient’s status before late indications of a worsening condition occur. The evidence supporting

use of the stroke volume optimization algorithm to treat hypovolemia is increasing. Many of the cardiac

output monitor technologies today measure stroke volume, as well as the parameters that comprise stroke

volume: preload, afterload, and contractility. (Critical Care Nurse. 2015;35[1]:11-28)

study. In the following section, we review the clinical

importance of hypovolemia that may go undetected

(occult hypovolemia) when conventional assessment

techniques are used.

Importance of Occult HypovolemiaTo illustrate the nature of subclinical or occult

hypovolemia and to test the sensitivity of gastrointestinal

tonometry for detecting such hypovolemia, Hamilton-

Davies et al1 conducted a study on 6 healthy volunteers

in the critical care unit at University College of London

Hospitals, London, England. Each of the volunteers had

a mean of 25% (21%-31%) of their overall blood volume

removed during a 1-hour period, and the volunteers’

response was measured. Variables such as heart rate,

blood pressure, serum levels of lactate, and stroke volume

were measured every 30 minutes throughout the study.

After 90 minutes, decreases in gut intramucosal pH were

observed, as well as marked decreases in stroke volume,

by a mean of 16.5 mL (P < .01). Despite this compromised

flow, no clinically significant or consistent postinterven-

tional changes were noted in serum levels of lactate,

arterial blood pressure, heart rate, or arterial blood gases

according to serial measurements obtained throughout

the study period. Retransfusion was started after 90 min-

utes. The results of this study1 may provide insight into

the reliability of routinely used measurements such as

heart rate and systolic blood pressure as volume deple-

tion progressed in these volunteers.

Hypovolemia (defined as inadequate left ventricular

filling volumes)2 affects the cardiovascular system in a

characteristic sequence of events as the hypovolemia

worsens3-6 (Table 1). First, stroke volume decreases

Alexander Johnson is a clinical nurse specialist, Central DuPage Hospital, Cadence Health System–Northwestern Medicine, Winfield, Illinois.

Thomas Ahrens is a research scientist, Barnes-Jewish Hospital, St Louis, Missouri.

Corresponding author: Alexander Johnson, 4007 Schillinger Dr, Naperville, IL 60564 (e-mail: [email protected]).

To purchase electronic or print reprints, contact the American Association of Critical-Care Nurses, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].

Authors


Acritical care nurse cares for a patient who had

a 3-vessel coronary artery bypass graft approx-

imately 30 minutes earlier. No indications of

bleeding are present, and both cardiac output and urine

output are within the reference limits. However, the

patient’s systolic arterial blood pressure has decreased

to 77 mm Hg 3 times in the past 20 minutes. Because

the decrease seems to respond to fluid administration,

the nurse begins administering a fourth bottle of 5%

albumin via the rapid infuser in accordance with the sur-

geon’s standing orders. Even though the patient’s central

venous pressure has remained at 3-4 mm Hg since the

patient arrived from surgery, the nurse notes that the

stroke volume has remained between 75 and 80 mL

since the second bottle of albumin. On the basis of the

patient’s hemodynamic profile and this recent

sequence of events, the nurse calls the surgeon to inquire

about an order to administer a vasoactive agent. In

this case, decreased stroke volume response to fluid

suggests adequate volume expansion even though low

central venous pressure values suggest hypovolemia.

CASE STUDY

Blood loss, %

Heart rate, beats per minute

Blood pressure, mm Hg

Pulse pressure

Respiratory rate, breaths per minute

Mental status

Class 4

> 40%

> 140

Decreased

Decreased

> 35

Confused, lethargic

Class 3

30%-40%

> 120

Decreased

Decreased

30-40

Anxious, confused

Class 2

15%-30%

> 100

Normal

Decreased

20-30

Mildly anxious

Class 1

< 15%

< 100

Normal

Normal or increased

14-20

Slightly anxious

Table 1 Classes of shock by Advanced Trauma Life Support (ATLS) designationa

a Reprinted from American College of Surgeons,5 with permission.

because of decreased overall circulating volume (class 1).

Next, heart rate increases and vasoconstriction occurs to

maintain blood pressure and cardiac output (the volume

of blood pumped by the heart per minute)7 (class 2). A

surge of endogenous catecholamines helps shunt blood

from the periphery and splanchnic circulation to the brain

and great vessels to preserve vital organs. Once compen-

satory mechanisms are exhausted, cellular respiration

begins to change from aerobic metabolism to anaerobic

metabolism, and tissue oxygenation is threatened. Oxy-

gen extraction rates increase, and mixed venous oxygen

saturation (Sv̄O2) and central venous oxygen saturation

(ScvO2) decrease because of decreased cardiac output,

compromised blood flow, and decreased oxygen deliv-

ery to tissues (class 3).2,7 Finally, urine output, level of

consciousness, and blood pressure decrease (class 4).3-5

Each event may take minutes to hours. Despite this known

sequence, aggressive intervention often is not implemented

until hypotension occurs.8,9 Traditionally, clinicians are

trained to monitor for early indications of decompensa-

tion, and the first hemodynamic monitoring parameter

to decrease in hypovolemia is stroke volume.1-5

Hypovolemia frequently occurs in patients during

surgery and in the critical care unit because of bleeding,

hypoalbuminemia, capillary leak and interstitial edema,

diarrhea, vomiting, and insensible water loss. If the hypo-

volemia is left untreated (or undertreated), circulatory

hypoxia may develop because of the decreased blood flow

and hypoperfusion. Compensatory diversion of blood

flow centrally, away from the peripheral and splanchnic

circulation, often masks hypoperfusion.2

If not recognized and treated promptly, decreased

circulating volume (particularly at the microvascular level)

leads to diminished oxygen delivery, depletion of intra-

cellular energy reserves, acidosis, anaerobic glycolysis,

and lactate accumulation. Hypovolemia can also lead to

ischemic gastrointestinal complications, including nau-

sea, vomiting, and intolerance of oral intake. Therefore,

diligent monitoring, via accurate assessment of cardiac

output and stroke volume, for hypovolemia is important

for monitoring blood flow.

Limitations of Conventional AssessmentsCurrent conventional assessments such as heart rate,

blood pressure, urine output, central venous pressure

(CVP), and level of consciousness often lack precision as

indicators of changes in a patient’s status. Although the

values obtained in these assessments somewhat correlate

with hemodynamic variables, the values are slow to

change and the changes are often late indications of a

patient’s worsening condition.3-5 Several studies10-17 suggest

that using physical assessment to evaluate cardiac output

may yield inaccurate findings. More recent data18-20 sug-

gest that the predictive power of blood lactate levels for

mortality and morbidity are independent of blood pres-

sure and common physiological triage variables (eg,

heart rate, blood pressure, mental status, capillary refill).

Despite these limitations, assessments such as blood

pressure are still considered a standard of care, and cur-

rent practice mandates use of the assessments. However,

blood pressure itself is a composite of so many factors2-5

(Figure 1) that it is of limited value as an early sign of

hemodynamic derangements such as hypovolemia.

Compensatory mechanisms such as vasoconstriction

and tachycardia influence the cardiovascular system to

keep blood pressure normal,2 making the correlation

between blood pressure and blood flow slow to change

as circulating volume decreases.1-5 The terms compensated

shock and cryptic shock are now being used to define

patient scenarios that meet clinical criteria for shock in


Figure 1 A, Complexity of blood pressure (BP): interrela-tionship of variables comprising BP. BP is the cardiacoutput (CO) multiplied by systemic vascular resistance(SVR). CO is the product of heart rate (HR) and strokevolume (SV). SV is influenced by preload, afterload, contractility, and rhythm. SVR is calculated by dividingthe difference between mean arterial pressure (MAP) and central venous pressure (CVP) by the CO and thenmultiplying by 80. (Derivation of content as described inAlspach.2) B, CO and SVR coexist in a balanced “seesaw”-type relationship. In general, when one decreases, the otherincreases (and vice versa) to maintain normal blood pressure.

BP = CO x SVR

A

B

HR x SV

MAP – CVP x 80

• Preload• Afterload• Contractility• Rhythm

CO

CO SVR

the presence of normal blood pressures.18 Blood pressure

measurements are more useful for conditions that involve

treatment of hypertension rather than treatment of

hypovolemia or shock.21,22 International guidelines such

as the Seventh Report of the Joint National Committee on

Prevention, Detection, Evaluation, and Treatment of High

Blood Pressure22 help guide care providers in the man-

agement of hypertension according to a systematic and

stepwise approach. However, currently no such guidelines

exist for the management of hypotension.

Reconsidering Fluid Replacement End Points

In an article published in 1996, Connors et al23 sug-

gested that use of a pulmonary artery catheter (PAC) was

associated with an increased likelihood of patient death.

Since then, use of PACs has generally decreased. Although

values obtained via a PAC were once considered the gold

standard for bedside hemodynamic monitoring,24,25 the

precision of a PAC for assessing preload status via filling

pressures is limited. As early as 1971, Forrester et al26

pointed out the inaccuracies of CVP monitoring. In a more

recent systematic review of CVP as a predictor of cardiac

output and fluid responsiveness, Marik et al27 concluded

that CVP should

not be used as a

basis for clinical

decisions on fluid

management. In

fact, Marik et al27

noted that the

only published study28 suggesting CVP could be an accurate

indication of preload was done in horses. Even though

guidelines such as those of the Surviving Sepsis Campaign29

recommend using CVP to monitor preload, no study of

CVP or pulmonary artery occlusive pressure (PAOP) has

shown that these pressures consistently correlate with

blood flow or volume status.30 Early and aggressive use

of fluid replacement to preestablished end points such

as ScvO2 is more likely than the measurement of CVP

itself to provide patients benefit.31,32 The limitations of

CVP are further pointed out in the landmark study on

septic shock by Rivers et al33 published in 2001. These

investigators randomized 263 patients with septic shock

to receive either treatment according to a protocol on

fluid replacement known as early goal-directed therapy

or conventional care (control group). The patients treated

according to the protocol had a 17% reduction in mortality,

even though CVP was used as part of the basis for treat-

ment in both the interventional and the control group.33

PAOP is also an inaccurate predictor of fluid respon-

siveness in critically ill patients, further indicating that

blood pressures do not correlate with blood flow param-

eters such as cardiac output and stroke volume.34,35 This

lack of correlation occurs because many factors can

alter the pressure-volume relationship within the heart.

For example, conditions that increase PAOP but not

preload include, but are not limited to, positive-pressure

mechanical ventilation, positive end-expiratory pressure,

and decreased ventricular compliance. Conditions that

alter cardiac compliance include aging, obesity, diabetes,

myocardial ischemia, and sepsis.36 The challenge encoun-

tered with interpreting PAOP is further illustrated in

Figure 2; the 3 hearts in the drawing have different cardio -

myopathies and various left ventricular end-diastolic vol-

umes (LVEDVs), but each heart has the same PAOP. As a

result, the baseline Frank-Starling pressure-volume

curves for the 3 hearts differ vastly (Figure 3). When

LVEDV increases in normal hearts, pressure increases in

a characteristic curvilinear relationship. However, in con-

ditions such as left ventricular hypertrophy, decreased

wall compliance increases intracardiac pressure without

a concomitant increase in volume. Measurements based

on blood flow, such as stroke volume, help clinicians

avoid incorrect assumptions based on pressure-volume

curves.36 Ultimately, blood flow is more reliable and pre-

cise than are blood pressures, and blood flow can decrease

before blood pressures decrease.1,3,5,18

CVP and PAOP were never intended to be used alone;

both are filling pressures meant to guide the optimiza-

tion of stroke volume.27,32 The fundamental reason to

administer a fluid bolus to a patient is to increase stroke

volume.27,35,37 Although stroke volume monitoring is not

considered a standard of care, as is conventional moni-

toring of vital signs, plotting or documenting stroke

volume in response to a fluid challenge may be the clos-

est clinicians can come to using the Frank-Starling curve

in routine bedside practice. Stroke volume is more likely

to indicate hypovolemia before other monitoring param-

eters do because the former is not influenced by most

compensatory mechanisms.1-5 Treatments that include

giving fluids and medications such as drugs that improve

contractility (inotropes) are often administered with the

goal of improving stroke volume. Specifically targeting


Ultimately, blood flow is more reliableand precise than blood pressures, andblood flow can decrease before bloodpressures decrease.

stroke volume for hemodynamic management is termed

SVO. Indications for use of SVO include age, heart failure,

low urine output, bleeding, monitoring of fluid boluses

and vasoactive infusions, cardiac conditions, and risk for

hypoperfusion or organ dysfunction. Awareness of con-

traindications is just as important: for example, esophageal

Doppler monitoring is contraindicated in patients with

esophageal strictures or varices.

Stroke Volume As the Newest CardiacVital SignAssessing for Adequate Perfusion

Using mean arterial pressure to evaluate a patient for

adequate perfusion to the vital organs is a controversial

but important idea for bedside clinicians to consider.38,39

As oxygen supply decreases or oxygen demand increases,

tissue hypoxia can develop. However, exactly when the

hypoxia occurs in an individual patient is unclear. ScvO2

can be a helpful global indicator; however, monitoring

microcirculatory perfusion at the end-organ level is not

readily available yet.40 When compromised perfusion

progresses to the point of eventual acidosis, organ dam-

age most likely is occurring, even when blood pressures

are normal.1

The complexity of these changes defies overreliance

on parameters such as blood pressure. Ongoing fluid

replacement decisions should be based on stroke volume,

variations in pulse pressure, cardiac output derived by

using a minimally invasive method, and passive leg-raising

maneuvers supported by integrated assessment to more


Figure 2 Challenges associated with interpreting pulmonary artery occlusion pressure (PAOP). Left ventricular end-diastolicvolume (LVEDV) can be independent of PAOP. A, PAOP is 22 mm Hg. Normal left ventricle has very high LVEDV. B, PAOP is22 mm Hg. Dilated right ventricle creates increased juxtacardiac pressure; LVEDV is normal. C, PAOP is 22 mm Hg. Left ventric-ular hypertrophy with noncompliant myocardium creates decreased space within the left ventricle; LVEDV is low. Use of PAOPalone to reflect LVEDV may not be accurate.Based on data from Marik et al27 and Turner.36

Illustration courtesy of Lisa Merry, RN, Merry Studio, Bloomington, Illinois.

B CA

Figure 3 Fluid replacement to optimize stroke volume(SV) vs cardiac filling pressures as primary end point.Information in blue is displayed when filling pressuresform the basis for routine bedside preload monitoring.Patient-specific differences in myocardial compliance and filling capacity markedly limit ability to estimate end-diastolic volume and thus, SV, on the basis of cardiac fill-ing pressures. Note also the widening of the Doppleraortic pulse waveform (systolic flow time, or FTc) as pre-load increases. SV measurements (in red) are the primarytarget for fluid in SV optimization. Blood-flow-based tech-nology allows clinicians to estimate SV more directlyalong this pressure-volume curve. This approach helpseliminate “guesstimation” of blood flow based on cardiacfilling pressures.

Stro

ke v

olum

e, m

L

25

Fluid bolus administered

Pulmonary arteryocclusive pressure

50

SV 100 mL

SV 75 mL

SV 40 mL

500 mL 1000 mL 1500 mL4 mm Hg➔➔

12 mm Hg 18 mm Hg

75

100

120

precisely determine the response to the replacement

efforts.32,35,41,42 Methods of actually measuring blood flow

by more direct methods are becoming increasingly

available. These methods can provide true blood-flow

measurements, such as stroke volume, stroke distance,

variation in stroke volume, and systolic flow time.

Methods of Measuring Stroke VolumeTraditionally, echocardiography has been the most

commonly used method to measure stroke volume at the

bedside. However, this method is expensive and technically

difficult and continuous or serial measurements are often

not practical in critical care. Several new technologies

enable ongoing measurement of stroke volume at the

bedside, including noninvasive Doppler imaging

(USCOM), esophageal Doppler imaging (Deltex Medical;

Figure 4), bioimpedance (SonoSite), endotracheally applied

bioimpedance (ConMed Corporation), bioreactance

(Cheetah Medical), pulse contour methods (Edwards

Lifesciences, LidCo Ltd, Pulsion Medical Systems), an

exhaled carbon dioxide method (Philips, Respironics),

and the PAC. All use various methods to calculate stroke

volume, and the results have various degrees of accuracy.

Some devices measure stroke volume directly (eg,

esophageal Doppler imaging) and may be considered

the preferred method because of the high degree of

accuracy of the results.43 Other technologies simply

divide the cardiac output by the heart rate to obtain

stroke volume (eg, PAC). Table 2 provides a more

detailed comparison.44-59

Clinical application of technology is based on

knowledge and experience in obtaining and applying

the information received. If a care provider targets the

wrong hemodynamic end points or interprets a poor

waveform as an

accurate tracing,

benefits may be

limited. These

concerns were

cited in the tech-

nology assessment report published by the Agency for

Healthcare Research and Quality60 in 2008 as some of the

most likely reasons studies have collectively suggested

no benefit for monitoring with PACs.

Disagreement may exist about which technology is best

for monitoring stroke volume because none of the tech-

nologies is appropriate for all patients in all situations.

Each technology has a unique profile of advantages and

limitations, and a patient’s situation may dictate which

technology is best at a given time. Regardless of the

technology used, the device will provide measurements

of preload, afterload, and contractility for optimizing

stroke volume.

Hemodynamic Variables That InfluenceStroke Volume

Three variables affect stroke volume: preload,

contractility, and afterload.

Measurement of Preload: Corrected Flow TimeCorrected flow time (FTc) is a measure obtained in

esophageal and noninvasive Doppler imaging via ultra-

sound technology. The FTc is an estimate of circulating

blood volume based on the amount of red blood cells


Each technology has a unique profileof advantages and limitations, and apatient’s situation may dictate whichtechnology is best at a give time.

Figure 4 Examples of minimally invasive hemodynamicmonitoring. A, Esophageal Doppler monitor: displayallows real-time measurement of preload (flow time, cor-rected, FTc), contractility (peak velocity, PV), stroke vol-ume (SV), and stroke distance (SD). B, Sagittal view ofesophageal Doppler probe in place to monitor cardiac out-put variables. Ultrasound transducer measures blood flowin the descending thoracic aorta.Images courtesy of Deltex Medical, Inc, West Sussex, England.

A

B


Description

Stroke volume estimate obtained viaultrasound probe placed at the sternalnotch or parasternally; ultrasound beamdirected at the aortic or pulmonic valve

Stroke volume estimate directly obtainedvia Doppler signal of descending aorta;typically, patient must be sedated;inserted similarly to a nasogastric tube

Bioimpedance technology via endotra-cheal tube; stroke volume obtainedfrom impedance signal from ascendingaorta; patient must be intubated

Transcutaneous electrodes placed onneck and chest; electrical impedancebetween electrodes during cardiaccycle entered into nomogram to com-pute stroke volume; for best readings,patient must have normal anatomy

Stroke volume estimated from arterialpressure waveform via methods suchas lithium infusion, pulse pressurevariation, or thermodilution; continu-ous cardiac output and beat-to-beatvariability proportional to stroke volume; changes in systemic vascularresistance and arterial pressure neces-sitate recalibration; dampening, dys-rhythmias, and ventilator triggeringalso limit accuracy

Exhaled carbon dioxide method, withFick equation; needs controlledmechanical ventilation to work; addi-tional personnel, such as respiratorytherapist, may be required; patientmust be intubated

Measures cardiac output via thermodi-lution, temperature sensed by thecatheter thermistor; stroke volumecalculated by dividing cardiac outputby heart rate; central venous accessrequired via catheterization of rightside of heart

Like bioimpedance, uses transcutaneouselectrodes; however, signal acquisitioneliminates impedance errors presentwith the first-generation technology

Randomized controlled trials regarding patient outcome

None

9 trials44-52 (2 trials hadconflicts of interest todisclose) showing reducedlength of stay, complica-tions, use of vasopres-sors, renal insufficiency, and mortality and lowerlactate levels

None

None

3 trials (each with conflictsof interest to disclose)suggesting decreasedcomplications and length of stay (LidCO),53

(FloTrac),54 and (PiCCO)55

3 trials suggesting unclearbenefit (PiCCO)56 (conflictof interest disclosed) orno benefit (FloTrac)57

and (PiCCO)58

None

Several trials,59,60 with both pro and con findings

None

Where used

Anywhere

Operating room,intensive careunit, emergencydepartment

Operating room,intensive care unit

Anywhere





Manufacturer

USCOM, Sydney, Australia

Deltex Medical, WestSussex, England

ConMed Corporation,Utica, New York

SonoSite, Bothell,Washington

FloTrac, Edwards Lifesciences, IrvineCalifornia

LidCo Ltd, Cambridge,United Kingdom

PiCCO, Pulsion Medical Systems,Munich, Germany

Philips Respironics,Andover, Massachusetts

Cheetah Medical, Portland, Oregon

Technology

External Dopplerimaging

Esophageal Doppler imaging

Endotrachealbioimpedance

Transcutaneousbioimpedance

Pulse contour

Exhaled carbondioxide method

Pulmonary arterycatheter

Bioreactance

Table 2 Technology for measuring stroke volume

that cross the ultrasound transducer beam through the

aorta during the systolic phase (Figures 4A and 4B). FTc

corresponds to the width of the pulse waveform base

and can be used to estimate preload. For example, a longer

FTc suggests that the left ventricle is pumping forward

an increased amount of blood (ie, increased preload).

The width of the pulse wave is measured in milliseconds

and represents the amount of time spent in systole com-

pared with total cardiac cycle time, and FTc is also cor-

rected for heart rate.61 The correction is based on a heart

rate of 60/min,

although the

current heart

rate is taken into

account. If a

patient’s heart

rate is 60/min, then each cardiac cycle will last 1 second,

or 1000 ms. Normal FTc is 330 to 360 ms.61,62 In other

words, for a cardiac cycle lasting 1 second, the systolic flow

period should last approximately 330 to 360 ms, provided

that adequate preload exists. An easy way to remember

the reference range is to remember that the heart is in

diastole two-thirds of the time and that normal FTc

multiplied by 3 equals 1 second, or 1000 ms62 (Figure 5).

But normal reference ranges are really just reference points,

not necessarily static physiological targets to be used for

all patients. The most important value of FTc is the degree

to which it changes in response to intravenous adminis-

tration of fluids.62 Increases in FTc in response to volume

challenge help confirm hypovolemia, which is manifested

as a narrow waveform base and a low FTc (Figure 3).

The accuracy of FTc has been questioned.63-65 However,

a complete understanding of the variable is critical before

FTc and be used effectively in clinical practice.66-68 Simply

put, FTc is suggestive of the amount of circulating volume

that passes the tip of the ultrasound probe during systole.36

Therefore, conditions such as bleeding (hypovolemia),

heart failure (low contractility), and high afterload (eg,

vasoconstriction) may contribute to low blood-flow

states and thus low FTc. These influences must be con-

sidered before FTc is accepted as a surrogate for preload

in individual patients. Several investigators66,69-72 have

suggested that FTc is as good as or better than PAOP for

indicating changes in preload. Most important, however,

improvement in stroke volume after fluid administration

is what was intended to form the basis on which preload


The most important value of correctedflow time is the degree to which itchanges in response to intraveousadministration of fluids.

Figure 5 Waveform components for stroke volume optimization (SVO): aortic pulse waveform from an esophageal Dopplerexamination. Corrected flow time (ie, the time spent in systole) corresponds to the width of the pulse waveform and is an indexof preload. Peak velocity corresponds to the height of the wave and is a measure of contractility. Stroke distance represents thearea under the curve and is used to compute stroke volume.

Peak velocity (cm/s)

Velo

city

, cm

/s

Flow time, ms

Stroke distance (cm)= area under curve

1/3 Systole 2/3 Diastole

1 Cardiac cycle

responsiveness is ultimately determined (in each of the

outcome trials studying SVO).44-52,73,74 In other words,

FTc (as well as CVP and PAOP) is best used as a decision-

making aid for optimizing stroke volume.

Measurement of Contractility: Peak VelocityPeak velocity, a measure of contractility, is indicated

by the amplitude of a Doppler waveform (Figure 5). It

indicates the acceleration of blood flow in the systolic

phase, or the speed at which a pressure wave goes from

baseline to the peak height of contraction. An overall

reference range is 50 to 120 cm/s. Peak velocity can be

age dependent; the expected range for a 20- to 30-year-

old is 90 to 120 cm/s, with gradually decreasing expected

peak velocity as a person ages. Patients more than 65

years old are expected to have a peak velocity greater

than 50 cm/s. Values less than 50 cm/s are suggestive

of poor left ventricular contractility, as in heart failure.

However, peak velocity should be evaluated with respect

to a patient’s baseline values and how those values

respond to treatments. For example, an increase in peak

velocity is expected with administration of an inotrope.

A low stroke volume can occur for 1 of 2 main rea-

sons: hypovolemia or decreased ventricular contractility.

The immediate measured availability of peak velocity

with Doppler techniques provides better information

than do the derived contractility parameters of the PAC

regarding why stroke volume may be low. For example,

if stroke volume is low but peak velocity is normal, the

problem most likely is hypovolemia.21 However, if both

stroke volume and peak velocity are low, the problem

most likely is left ventricular dysfunction.62 A patient’s

response to medications such as preload reducers, after-

load reducers, or inotropes can help differentiate the

cause of the left ventricular dysfunction (eg, fluid over-

load, high afterload, or low contractility, respectively).

Peak velocity may also help detect acute decompen-

sating systolic heart failure earlier than do other tech-

niques for monitoring cardiac output. In critical illness,

poor left ventricular contractility (low ejection fraction)

may initially lead to a compensatory increase in end-

diastolic volume, a change that implies a normal stroke

volume. The ability to monitor peak velocity allows cli-

nicians to recognize this decrease in contractility in real

time and intervene before a decrease in stroke volume

occurs. Further research is needed to better establish

SVO treatment guidelines for patients with heart failure.

Measurement of Afterload: Systemic Vascular Resistance

Systemic vascular resistance (SVR) is the resistance

that must be overcome by the ventricles to develop force

and contract, propelling blood into the arterial circulation.2

Most of the newer hemodynamic monitoring technolo-

gies (eg, esophageal Doppler imaging, bioimpedance,

pulse contour methods) have the capability to calculate

SVR. However, SVR was not a major parameter in the

algorithms used in any of the SVO trials that showed

improved outcomes in surgical patients.44-52,73,74

Evidence of lack of inclusion suggests that SVR is a

more of a secondary monitoring parameter. Elevated SVR

usually occurs in response to systemic hypertension or

as a compensatory mechanism due to decreased cardiac

output, as in shock states (Figures 1A and 1B). Therefore,

nurses must know why the SVR is elevated. If the value is

elevated in response to low cardiac output, once cardiac

output is improved with treatment (eg, fluid, inotropes),

SVR should decrease because of a decreased need for

compensatory vasoconstriction. If SVR is elevated

because of systemic hypertension, treatment may include

administration of an afterload reducer.2

When SVR decreases, the left ventricular ejection of

blood encounters lower resistance. Low afterload states

may be less problematic when blood pressure and car-

diac output are normal (Figure 1A). However, attempts

to increase low SVR generally include administration of

vasopressors.2 ScvO2 and stroke volume should also be

followed as end points to ensure that blood flow and tis-

sue oxygenation improve in response to the vasopressor21

(Figure 6). Titrating the dose of a vasopressor used to

alter ScvO2 and stroke volume allows clinicians to focus

on optimizing blood flow to both the microcirculation

and the macrocirculation. Several studies of fluid replace-

ment protocols that include use of vasopressors suggest

that optimizing ScvO231,33,75 and stroke volume47,76 improve

patients’ outcomes. However, further research is needed

to better establish how vasopressors and ScvO2 are best

used in SVO protocols.

Stroke Volume, Stroke Index, and Stroke Distance

Stroke volume is one of the primary end points for

detecting fluid responsiveness and guiding goal-directed

therapy.27,32,62 Stroke index is a standardized parameter in

which a patient’s body surface area is taken into account.


However, monitoring both stroke volume and stroke index

is generally not necessary, because they use different units

of measure to quantify the same value. Table 3 gives ref-

erence ranges for these parameters.21,77-79 However, the

ideal stroke volume value is the one that contributes to

adequate blood flow for tissue oxygenation without

increasing heart rate.

Despite the unique advantages of measuring stroke

volume, available technologies to measure this parameter

at the bedside have some limitations. Even esophageal

Doppler imaging, which provides a highly flow-directed

estimation of stroke volume, uses a calculated estimation

of aortic diameter based on the patient’s height and

weight.80 Stroke distance may be a more accurate reflec-

tion of the Doppler estimation of stroke volume. Stroke

distance is the distance a column of blood moves through

the descending thoracic aorta during each systolic phase.61

Because stroke distance is used to calculate stroke vol-

ume, the recommendation is that stroke distance be

evaluated to determine if the measurement of stroke

volume is accurate.

The SVO Algorithm: Putting It All Together

The Frank-Starling principle states that the strength

of cardiac contraction is directly related to the length of

muscle fibers at end diastole, or preload.81 Administration

of fluid on the basis of stroke volume allows clinicians to

directly apply this principle. Figure 7 displays a standard

example of an SVO fluid replacement algorithm, cited by

Schober et al,62 that is based on a synthesis of experimen-

tal SVO protocols and literature.44-52,73,74 In this type of

algorithm, determination of fluid responsiveness is used:

fluid boluses are administered as long as stroke volume

continues to improve by 10% or more. When administra-

tion of fluid boluses ceases to improve stroke volume by


Figure 6 Response of stroke volume to norepinephrine. Increasing vasopressor doses to previously established, prescribedthresholds for mean arterial pressure (MAP) and systemic vascular resistance may in turn decrease stroke volume and overallblood flow. The case example graph suggests that stroke volume is optimized at 8 μg/min of norepinephrine, even though aMAP of only 55 mm Hg is achieved at that dose. Note: patients’ responses to norepinephrine dosing may vary.

Stro

ke v

olum

e, m

L

MAP response to increasing doses of norepinephrine, mm Hg

Increasing norepinephrine dose, μg/min 2 5

75

50

25

10 15 20

65605550

Parameter

Cardiac output, L/min

Stroke volume, mL

Stroke indexb

Flow time corrected, ms

Peak velocity, cm/s

Stroke distance, cm

Cardiac indexc

Systemic vascular resistance, dyne sec cm-5

Saturation of central venous oxyhemoglobin, %

Central venous pressure, mm Hg

Stroke volume variation, %

Referencerange

4-8

50-100

25-45

330-360

30-120

10-20

2.8-4.2

900-1600

65-80

2-8

< 10-15

Table 3 Reference ranges for hemodynamic parametersa

a Based on data from Ahrens,21 Lynn-McHale Wiegand,77 Lynn-McHale Wiegand and Carlson,78 and Edwards Lifesciences.79

b Calculated as stroke volume in milliliters per heartbeat divided by bodysurface area in square meters.

c Calculated as cardiac output in liters per minute divided by body surfacearea in square meters.

10% or more, no more fluid is needed. Using this method

of fluid administration can mitigate the risk of pulmonary

edema, and bedside clinicians can be better assured that

the patient is receiving enough fluid to optimize the

macrocirculation but not more fluid than is needed.

SVR and blood pressure are usually not included in

SVO algorithms and are considered secondary monitor-

ing parameters in SVO.44-52 According to the SVO algo-

rithm, SVR and blood pressure are evaluated only after

peak velocity (contractility) and stroke volume are opti-

mized, because SVR and blood pressure are more indi-

rect reflections of cardiac output and are influenced by

other factors (see Figures 1A and 1B). Furthermore,

when blood flow and tissue oxygenation are measured

rather than assumed, doses of vasopressors can be adjusted

to optimize the end points of stroke volume (macrocir-

culation) and ScvO2 (microcirculation) rather than SVR

and blood pressure (Figure 6). Stroke volume may improve

initially with initiation and escalating doses of vasopres-

sors, but changes in afterload due to further increases in

the medication may impede stroke volume and cardiac

output.82 Surveillance of ongoing stroke volume and

cardiac output may help clinicians avoid this decrease

in stroke volume and cardiac output.

Challenges to SVO implementation may include incor-

porating new hemodynamic monitoring technology into

daily practice (eg, esophageal Doppler imaging, pulse

contour method), education of staff members, support

from physicians and leaders, and the paucity of literature

to support use in nonsurgical patients. However, potential

benefits include use of minimally invasive techniques,

allowing earlier detection of unstable hemodynamic status,

and reductions in morbidity, mortality, and length of stay.

More research is needed to determine how values

such as peak velocity and ScvO2 can be incorporated into

the SVO algorithm. The following case studies illustrate

these points and indicate how SVO can be applied in cases

involving alterations in preload, afterload, and contractility.

Case Study 1: Decreased PreloadA 59-year-old man was admitted to the surgical

intensive care unit after having a partial liver lobectomy


Figure 7 Example of an algorithm for stroke volume optimization.

Other therapies as appropriate, for example:

• High afterload state: dilators (± more fluid) if low correctedflow time, low peak velocity, and blood pressure acceptable

• Low contractility state: inotropic agents if low peak velocityand blood pressure

• Low afterload state: vasopressors if high corrected flowtime, high stroke volume, and low blood pressure

If stroke volume or correctedflow time is low

Give 200 mL of colloid or500 mL of crystalloid

Stop giving fluids;monitor stroke

volume as indicated

If stroke volume decreased > 10%

Yes (stroke volumeincreased < 10%)

No (stroke volumeincreased > 10%)

Is the heart pumping

enough blood?

after a motor vehicle accident (Table 4). On postopera-

tive day 5, he was evaluated for discharge to a general

care unit. His urine output had decreased during the

preceding 12 hours, suggestive of hypovolemia. The

hypovolemia was evidenced by low stroke volume, low

FTc, and low ScvO2 in the presence of a normal peak

velocity. After injection of a 1000-mL bolus of physiolog-

ical saline, stroke volume improved from 34 mL to 48

mL, more than a 10% (3.4 mL) improvement. So,

another bolus was given. Satisfactory response to the

bolus was manifested by normal FTc and ScvO2. Stroke

volume improved to 49 mL only with the second bolus

(<10% improvement), indicating the beginning of the

plateau along the Frank-Starling curve where increased

stretching of the ventricular myocytes does not improve

stroke volume. Thus, no further administration of fluid

was indicated.

Case Study 2: Decreased Preload Leads toDecreased Afterload

A 55-year-old woman was admitted because of sepsis

(Table 5). The patient had a dangerously reduced stroke

volume, decreased FTc, decreased ScvO2, and a normal

peak velocity, indicating hypovolemia. She was deemed

fluid responsive as indicated by an improvement in

stroke volume from 26 mL to 50 mL, a greater than 10%

(2.6 mL) improvement, after administration of a bolus of

1000 mL of physiological saline. So, another saline bolus

was indicated. However, the patient did not respond to

the second bolus, as evidenced by an improvement in

stroke volume from 50 mL to only 51 mL (<10%), suggest-

ing that the macrocirculation had been optimized. Nor-

epinephrine was started because of the reduced ScvO2

and persistent hypotension despite volume correction.

The patient responded appropriately as evidenced by the


Heart rate, beats

per minute

102

100

99

Central venousoxygen

saturation, %

49

69

70

Central venouspressure,mm Hg

3

5

6

Blood pres-sure, mean

(SD), mm Hg

100/48 (64)

94/55 (68)

100/60 (73)

Peak velocity,

cm/s

96

95

95

Flow time, corrected, ms

300

335

337

Stroke volume,

mL

34

48

49

Intervention

Administer 1000-mLbolus of physio-logical saline


Response

Table 4 Interventions used and response of 59-year-old man admitted after a motor vehicle accident

Heart rate, beats

per minute

107

105

105

106

Central venousoxygen

saturation, %

26

48

50

68

Central venouspressure,mm Hg

4

9

9

8

Blood pres-sure, mean

(SD), mm Hg

68/36 (47)

76/42 (53)

80/44 (59)

92/62 (72)

Peak velocity,

cm/s

78

76

76

72

Flow time, corrected, ms

254

341

341

344

Stroke volume,

mL

26

50

51

55

Intervention

Administer 1000-mLbolus of 0.9% normal saline


Administer norepinephrine 10 μg/min

Response

Table 5 Interventions used and response of 55-year-old woman admitted for sepsis

increase in ScvO2 to 68%, suggesting normalization of

the microcirculation.

Literature Supporting Clinical Usefulness of SVO

Before they adopt a new practice, astute clinicians

want to know that the practice is strongly supported in

the literature. Randomized controlled trials are the

highest-level research design, and the number of well-

designed randomized controlled trials is directly correlated

with the level of evidence assigned to a given practice.83-85

The findings of 11 randomized controlled trials,44-52,73,74

including 9 prospective trials,44-52 suggest that SVO results

in improved patient outcomes. Despite a thorough liter-

ature review, we were unable to find a fluid replacement

strategy supported by more research. The results of the

9 prospective trials,44-52 which included a total of about

1000 patients, consistently suggested that compared with

conventional fluid replacement, SVO fluid replacement

protocols contribute to decreases in overall hospital length

of stay (by 2 days or more), complication rates, renal

insufficiency, infection, use of vasopressors, blood lactate

levels, and time-to-tolerance of oral intake. Appropriately

implemented SVO programs that replicate these outcomes

may also be associated with decreased costs.86

Notably, the sample in all 11 trials44-52,73,74 included

perioperative patients. Although 2 of these trials44,47 also

focused on postoperative care in the critical care unit,

more research is needed to indicate the efficacy of SVO

in nonsurgical patients. However, in perioperative

patients, the strength of the supporting evidence in

favor of SVO has been substantiated by large-scale sys-

tematic literature reviews conducted by the Agency for

Healthcare Research and Quality,87 the National Health

Service,86 and third-party payers such as the Centers for

Medicare and Medicaid Services88 and Aetna.89

In 3 of these studies,86-88 the agencies recommended

SVO protocols be used for monitoring cardiac output of

patients receiving mechanical ventilation in the critical

care unit and for surgical patients who require intra -

operative fluid optimization. Esophageal Doppler imag-

ing,88 bioimpedance,90 and PACs91 are all reimbursed by

the Centers for Medicare and Medicaid Services88 on the

basis of systematic literature reviews. However,

esophageal Doppler imaging is the only technology also

supported by the Agency for Healthcare Research and

Quality.87

Similarly, the Cochrane Collaborative59 and the

Agency for Healthcare Research and Quality60 have pub-

lished technology assessments based on meta-analyses

of outcomes related to use of PACs. The analyses indi-

cated that the patients studied showed no evidence of

benefit or harm from PACs. Among the reasons cited

for the perceived lack of benefit was clinician-to-clinician

variability in management of hemodynamic data obtained

via PACs. In addition, the authors59,60 questioned the

accuracy of the interpretation of the hemodynamic

information in the studies analyzed and whether or not

patient management strategies based on hemodynamic

data were appropriate. Furthermore, none of the studies

included use of a specific protocol for PAC use. This lack

of a protocol is a key difference between PAC studies and

SVO studies. Each of the 9 randomized control trials44-52

on SVO

included a

protocol for

use of SVO.

Use of a pro-

tocol is con-

sistent with

other studies of replacement protocols that include

fluid therapy, which can be lifesaving when initiated

early in the course of treatment. Findings from a meta-

analysis of hemodynamic optimization by Poeze et al92

also suggest that replacement strategies such as SVO

improve outcomes, including patient mortality, in

high-risk surgical patients.

Nursing ConsiderationsNursing considerations associated with incorporat-

ing SVO into bedside practice include acquiring and

evaluating hemodynamic data, maintenance of skin

integrity, sedation and analgesia, and nursing research.

Acquisition and Evaluation of Hemodynamic Information

Clinical proficiency with applying or inserting the

hemodynamic monitoring device and adequate signal

acquisition are key.93 Each device has its own unique signal

acquisition technique and competency requirements.

Inappropriate application of the device may produce inac-

curate hemodynamic readings, leading to improper treat-

ment decisions.77,78 Once accurate readings are obtained,

understanding the appropriate application of “normal”


Stroke volume may improve initially with initiation and escalating doses ofvasopressors, but changes in afterloaddue to further pressor dose increases mayimpede stroke volume and cardiac output.

hemodynamic reference ranges to all patients is crucial.

Tracking trends in hemodynamic values over time is

generally more useful than is monitoring and treating

on the basis of single data points, because transient

changes in values may not be clinically importantly.

When readings are considered accurate and hypo -

volemia is identified, rapid infusion of a fluid bolus may

optimize a patient’s response. Fluid infused via a pres-

sure bag often produces a more dramatic increase in

stroke volume than does fluid administered via an intra-

venous infusion pump. A maximum rate of commonly

used intravenous pumps is 999 mL/h. Because hypo -

volemia and hypoperfusion are time-sensitive conditions,

the provider’s judgment and the patient’s condition may

determine that a more rapid infusion rate is needed.

The latest revision of the Surviving Sepsis Campaign

guidelines also suggests an increased emphasis on earlier

and more aggressive fluid replacement. For example, the

2008 guidelines94 recommended a 20 mL/kg crystalloid

fluid challenge in a 6-hour replacement bundle. In the

2012 revised guideline,29 the recommended amount of

fluid was increased (to 30 mL/kg) in a shorter time (3-hour

bundle). Clinicians must strongly consider strategies to

infuse such a volume rapidly enough, in accordance with

institutional policy as appropriate.

Maintenance of Skin IntegrityCare must be taken to avoid skin breakdown under

and around skin electrodes. With bioimpedance and

bioreactance, signals are acquired transcutaneously, and

skin care should be in accordance with the manufacturer’s

recommendations and institutional policy. Mouth ulcer-

ations are also possible with monitoring devices such as

those used for esophageal Doppler imaging93 and endo-

tracheally applied bioimpedance. Diligent oral care should

be performed as

needed while

those devices are

in place. Site care

is also important

when caring for

patients moni-

tored with intravenous pulse contour devices or PACs.

Catheter infections can be minimized by using sterile

conditions during insertion and aseptic technique during

dressing changes.77,78

Sedation and AnalgesiaSedation is sometimes required with techniques such

as the exhaled carbon dioxide method, which requires

controlled mechanical ventilation, and esophageal Doppler

imaging. These techniques may have limited accuracy

when increased respiratory rates or restlessness, respec-

tively, occur. Therefore, sedative agents or analgesics

may be administered as needed.77,78 Although not a major

focus with respect to SVO, pain cannot be overlooked;

it is not only an overall priority but can also influence

hemodynamic readings.

Nurse ResearchThe implications of patient advocacy extend beyond

routine patient care and include nurses’ participation in

designing and implementing future research on the clini-

cal usefulness of SVO in critical care. Critical care nurses

monitor and treat hypovolemia daily and have a unique

opportunity to contribute to the existing scientific body

of knowledge through participation in SVO studies in

medical critical care patients.

SummaryThe growing body of evidence supporting SVO

suggests that implementation of SVO into daily practice

should be considered.61,62,88 A new era is emerging in

which blood-flow monitoring is taking precedence over

the monitoring of blood pressures. Cardiac pressures

help provide estimates of blood volume; however, normal

cardiac pressures can be observed in a patient in shock

and provide little information about blood flow.30,95-97

Interpretation and treatment of blood pressures incor-

porate assumptions, whereas stroke volume may be

considered a more precise measure of fluid responsive-

ness and an earlier warning sign of volume depletion

than are urine output, altered mental status, CVP, heart

rate, and blood pressure.1-5 Earlier signals allow clini-

cians to anticipate rather than react to changes, improv-

ing the likelihood for maintaining a stable metabolic

state at the organ and cellular level. In addition to the

evidence supporting SVO, minimally invasive applica-

tions and improvements in accuracy also add to safety

advantages when inherent limitations of the various

methods are considered.

For years, strategies for use of SVO were not feasible

because no practical measurement method for SVO


Earlier signals such as stroke volumeallow clinicians to anticipate rather thanreact to changes, improving the likeli-hood of maintaining a stable metabolicstate at the organ and cellular level.

existed for bedside clinicians. Fortunately, technology

has improved the hemodynamic monitoring landscape.

Compared with old devices, newer technology is less inva-

sive, safe, evidence based, flow directed, cost-effective,

easier to use, and accurate. Although further research

on SVO and dynamic indices are needed to establish the

clinical efficacy of SVO in critical care units, the current

body of literature indicates that SVO is associated with

fewer complications and reduced hospital lengths of stay,

particularly in patients receiving mechanical ventilation

and in surgical patients. Until more randomized trials

on the impact of SVO protocols on the outcomes of

critical care patients are published, SVO is supported

by more evidence than is use of filling pressures for fluid

replacement in critical care units.27,32,44-52,73,74,86-88 On the

basis of our review of the current available literature, we

suggest that the SVO algorithm for fluid replacement be

considered in place of use of cardiac filling pressures for

patients in critical care, as appropriate, with attention to

outcomes. In the meantime, more research is needed to

evaluate the impact of SVO on patients other than peri-

operative patients and on nonintubated patients. CCN

AcknowledgmentsThe authors thank Terry Sears and Julie Stielstra for their contributions. Wealso thank the critical care staff, physicians, and leaders at Central DuPageHospital–Northwestern Medicine. Without their help and support, this man-uscript would have been much more difficult to complete.

Financial DisclosuresTom Ahrens has lectured for hemodynamic monitoring companies (includingDeltex Medical Inc) and is a hemodynamic monitoring consultant.

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26. Forrester JS, Diamond G, McHugh TJ, Swan HJ. Filling pressures in theright and left sides of the heart in acute myocardial infarction: a reappraisalof central-venous-pressure monitoring. N Engl J Med. 1971;285(4):190-193.

27. Marik P, Baram M, Vahid B. Does central venous pressure predict fluidresponsiveness? A systematic review of the literature and the tale ofseven mares. Chest. 2008;134(1):172-178.

28. Magdesian KG, Fielding CL, Rhodes DM, Ruby RE. Changes in centralvenous pressure and blood lactate concentration in response to acuteblood loss in horses. J Am Vet Med Assoc. 2006;229(9):1458-1462.

29. Dellinger RP, Levy MM, Rhodes A, et al; Surviving Sepsis CampaignGuidelines Committee including the Pediatric Subgroup. SurvivingSepsis Campaign: International guidelines for management of severesepsis and septic shock: 2012. Crit Care Med. 2013;41(2):580-637.

30. Ahrens T. Stroke volume optimization vs central venous pressure influid management. Crit Care Nurse. 2010;30(2):71-73.

31. Pope JV, Jones AE, Gaieski DF, Arnold RC, Trzeciak S, Shapiro NI; Emer-gency Medicine Shock Research Network (EMShockNet) Investigators.


Now that you’ve read the article, create or contribute to an online discussionabout this topic using eLetters. Just visit www.ccnonline.org and select the articleyou want to comment on. In the full-text or PDF view of the article, click“Responses” in the middle column and then “Submit a response.”

To learn more about stroke volume optimization, read “StrokeVolume Optimization Versus Central Venous Pressure in FluidManagement” by Ahrens in Critical Care Nurse, April 2010;30:71-72. Available at www.ccnonline.org.

Multicenter study of central venous oxygen saturation (ScvO2) as a pre-dictor of mortality in patients with sepsis. Ann Emerg Med. 2010;55(1):40-46.e1.

32. Marik P. Surviving sepsis: going beyond the guidelines. Ann IntensiveCare. 2011;1(17):1-6.

33. Rivers E, Nguyen B, Havstad S, et al; Early Goal-Directed Therapy Col-laborative Group. Early goal-directed therapy in the treatment of severesepsis and septic shock. N Engl J Med. 2001;345(19):1368-1377.

34. Benington S, Ferris P, Nirmalan M. Emerging trends in minimally inva-sive haemodynamic monitoring and optimization of fluid therapy. Eur JAnaesthesiol. 2009;26(11):893-905.

35. Marik P, Monnet X, Teboul JL. Hemodynamic parameters to guide fluidtherapy. Ann Intensive Care. 2011;1(1):1-9.

36. Turner MA. Doppler-based hemodynamic monitoring: a minimallyinvasive alternative. AACN Clin Issues. 2003;14(2):220-231.

37. Michard F, Teboul J. Predicting fluid responsiveness in ICU patients: acritical analysis of the evidence. Chest. 2002;121:2000-2008.

38. Dünser M, Takala J, Brunauer A, Bakker J. Re-thinking resuscitation:leaving blood pressure cosmetics behind and moving forward to permis-sive hypotension and a tissue perfusion-based approach. Crit Care. 2013;17:326. doi:10.1186/cc12727.

39. Marik P, Bellomo R. Re-thinking resuscitation goals: an alternativepoint of view! Crit Care. 2013;17:458. doi:10.1186/cc12775.

40. Knotzer H, Hasibeder W. Microcirculation function monitoring at thebedside—a view from the intensive care. Physiol Meas. 2007;28(9):R65-R86.

41. Marik P, Cavallazzi R, Vasu T, Hirani A. Dynamic changes in arterialwaveform derived variables and fluid responsiveness in mechanicallyventilated patients: a systematic review of the literature. Crit Care Med.2009;37(9):2642-2647.

42. Marik P. Techniques for assessment of intravascular volume in criticallyill patients. Intensive Care Med. 2009;24(5):329-337.

43. Dark P, Singer M. The validity of trans-esophageal Doppler ultrasonog-raphy as a measure of cardiac output in critically ill adults. Intensive CareMed. 2004;30:2060-2066.

44. Chytra I, Pradl R, Bosman R, Pelnar P, Kasal E, Zidkova A. EsophagealDoppler-guided fluid management decreases blood lactate levels inmultiple-trauma patients: a randomized controlled trial. Crit Care.2007;11(1):R24.

45. Conway DH, Mayall R, Abdul-Latif MS, Gilligan S, Tackaberry C. Ran-domized controlled trial investigating the influence of intravenous fluidtitration using esophageal Doppler monitoring during bowel surgery.Anaesthesia. 2002;57(9):845-849.

46. Gan TJ, Soppitt A, Maroof M, et al. Goal-directed intraoperative fluidadministration reduces length of hospital stay after major surgery. Anes-thesiology. 2002;97(4):820-826.

47. McKendry M, McGloin H, Saberi D, Caudwell L, Brady AR, Singer M.Randomised controlled trial assessing the impact of a nurse delivered,flow monitored protocol for optimisation of circulatory status after car-diac surgery. BMJ. 2004;329(7460):258-261.

48. Mythen MG, Webb AR. Perioperative plasma volume expansionreduces the incidence of gut mucosal hypoperfusion during cardiac sur-gery. Arch Surg. 1995;130(4):423-429.

49. Sinclair S, James S, Singer M. Intraoperative intravascular volume opti-misation and length of hospital stay after repair of proximal femoralfracture: randomised controlled trial. BMJ. 1997;315(7113):909-912.

50. Venn R, Steele A, Richardson P, Poloniecki J, Grounds M, Newman P.Randomized controlled trial to investigate influence of the fluid chal-lenge on duration of hospital stay and perioperative morbidity inpatients with hip fractures. Br J Anaesth. 2002;88(1):65-71.

51. Wakeling HG, McFall MR, Jenkins CS, et al. Intraoperative oesophagealDoppler guided fluid management shortens postoperative hospital stayafter major bowel surgery. Br J Anaesth. 2005;95(5):634-642.

52. Noblett S, Snowden C, Shenton B, Horgan A. Randomized clinical trialassessing the effect of Doppler-optimized fluid management on out-come after elective colorectal resection. Br J Surg. 2006;93(9):1069-1076.

53. Pearse R, Dawson D, Fawcett J, Rhodes A, Grounds RM, Bennett ED.Early goal-directed therapy after major surgery reduces complicationsand duration of hospital stay: a randomized, controlled trial[ISRCTN38797445]. Crit Care. 2005;9(6):R687-R693.

54. Mayer J, Boldt J, Mengistu AM, Röhm KD, Suttner S. Goal-directedintraoperative therapy based on autocalibrated arterial pressure wave-form analysis reduces hospital stay in high-risk surgical patients: a ran-domized, controlled trial. Crit Care. 2010;14(1):R18. doi:10.1186/cc8875.

55. Goepfert M, Richter H, Eulenburg C, et al. Individually optimizedhemodynamic therapy reduces complications and length of stay in theintensive care unit: a prospective, randomized controlled trial. Anesthe-siology. 2013;119(4):824-836.

56. Salzwedel C, Puig J, Carstens A, et al. Perioperative goal-directed hemo-dynamic therapy based on radial arterial pulse pressure variation andcontinuous cardiac index trending reduces postoperative complicationsafter major abdominal surgery: a multi-center, prospective, randomizedstudy. Crit Care. 2013;17(5):R191. doi:10.1186/cc12885.

57. Van der Linden PJ, Dierick A, Wilmin S, Bellens B, De Hert SG. A ran-domized controlled trial comparing an intraoperative goal-directedstrategy with routine clinical practice in patients undergoing peripheralarterial surgery. Eur J Anaesthesiol. 2010;27(9):788-793.

58. Szakmany T, Toth I, Kovacs Z, et al. Effects of volumetric vs pressure-guided fluid therapy on postoperative inflammatory response: a prospec-tive, randomized clinical trial. Intensive Care Med. 2005;31(5):656-663.

59. Rajaram SS, Desai NK, Kalra A, et al. Pulmonary artery catheters foradult patients in intensive care. Cochrane Database Syst Rev. 2013;2:CD003408. doi:10.1002/14651858.CD003408.pub3.

60. Balk E, Raman G, Chung M, et al. Evaluation of the Evidence on Benefitsand Harms of Pulmonary Artery Catheter Use in Critical Care Settings.Rockville, MD: Agency for Healthcare Research and Quality; March 28,2008. http://www.cms.gov/determinationprocess/downloads/id55TA.pdf. Accessed October 29, 2014.

61. Roche A, Miller T, Gan T. Goal-directed fluid management with trans-oesophageal Doppler. Best Pract Res Clin Anaesthesiol. 2009;23(3):327-334.

62. Schober P, Loer S, Schwarte L. Perioperative hemodynamic monitoringwith transesophageal Doppler technology. Anesth Analg. 2009;109:340-353.

63. Chew HC, Devanand A, Phua GC, Loo CM. Oesophageal Doppler ultra-sound in the assessment of haemodynamic status of patients admittedto the medical intensive care unit with septic shock. Ann Acad Med Sin-gapore. 2009;38(8):699-703.

64. Bendjelid K. Assessing fluid responsiveness with esophageal Dopplerdynamic indices: concepts and methods [comment]. Intensive Care Med.2006;32(7):1088.

65. Monnet X, Pinsky M, Teboul J. FTc is not an accurate predictor of fluidresponsiveness. Intensive Care Med. 2006;32:1090-1091.

66. Johnson A, Schweitzer D. Putting the wedge under pressure [comment].Ann Acad Med Singapore. 2010;39(10):815.

67. Singer M. The FTc is not an accurate marker of left ventricular preload:reply to the comment by Chemla and Nitenberg. Intensive Care Med.2006;32(9):1456-1457.

68. Singer M. The FTc is not an accurate marker of left ventricular preload.Intensive Care Med. 2006;32(7):1089.

69. Madan AK, UyBarreta VV, Aliabadi-Wahle S, et al. Esophageal Dopplerultrasound monitor versus pulmonary artery catheter in the hemody-namic management of critically ill surgical patients. J Trauma. 1999;46(4):607-611.

70. Seoudi H, Perkal M, Hanrahan A, Angood P. The esophageal Dopplermonitor in mechanically ventilated surgical patients: does it work[abstract]? J Trauma. 1999;47(6):1171.

71. DiCorte CJ, Latham P, Greilich PE, Cooley MV, Grayburn PA, Jessen ME.Esophageal Doppler monitor determinations of cardiac output and pre-load during cardiac operations. Ann Thoracic Surg. 2000;69(6):1782-1786.

72. Kincaid H, Fly M, Chang M. Noninvasive measurements of preloadusing esophageal Doppler are superior to pressure-based estimates incritically injured patients [abstract]. Crit Care Med. 1999;27(1):A111.

73. Mark JB, Steinbrook RA, Gugino LD, et al. Continuous noninvasivemonitoring of cardiac output with esophageal Doppler ultrasound dur-ing cardiac surgery. Anesth Analg. 1986;65(10):1013-1020.

74. Valtier B, Cholley BP, Belot JP, Coussay JE, Mateo J, Payen DM. Nonin-vasive monitoring of cardiac output in critically ill patients using trans-esophageal Doppler. Am J Respir Crit Care Med. 1998;158:77-83.

75. Micek ST, Roubinian N, Heuring T, et al. Before-after study of a stan-dardized hospital order set for the management of septic shock. CritCare Med. 2006;34(11):2707-2713.

76. Saberi D, Caudwell L, McGloin H, Singer M. Proactive circulatory man-agement in the first 4 hours postcardiac surgery: interim analysis of anurse-led, oesophageal Doppler-guided protocol [abstract]. IntensiveCare Med. 2000;26(3 suppl):S220.

77. Lynn-McHale Wiegand D, ed. AACN Procedure Manual for Critical Care.6th ed. St Louis, MO: Elsevier Saunders: 2011.

78. Lynn-McHale Wiegand D, Carlson K, eds. AACN Procedure Manual forCritical Care. 5th ed. St Louis, MO: Elsevier; 2005.

79. Edwards Lifesciences. Advanced hemodynamic monitoring. The FloTracsensor: stroke volume variation. http://www.edwards.com/products/mininvasive/Pages/strokevolumevariationwp.aspx. Accessed October30, 2014.

80. Singer M. Continuous Haemodynamic Monitoring by Oesophageal Doppler[doctoral dissertation]. London, England: University of London; April 1989.

81. Starling EH. The Linacre Lecture on the Law of the Heart. London, England:Longmans, Green & Co; 1918.


82. Ahrens T, Taylor L. Hemodynamic Waveform Analysis. St Louis, MO: WBSaunders; 1992:432, 444-447.

83. Atkins D, Best D, Briss PA, et al; GRADE Working Group. Grading quality ofevidence and strength of recommendations. BMJ. 2004;328(7454):1490-1498.

84. Guyatt G, Gutterman D, Baumann MH, et al. Grading strength of recom-mendations and quality of evidence in clinical guidelines: report from anAmerican College of Chest Physicians task force. Chest. 2006;129(1):174-181.

85. Schünemann HJ, Jaeschke R, Cook DJ, et al; ATS Documents Developmentand Implementation Committee. An official ATS statement: grading thequality of evidence and strength of recommendations in ATS guidelinesand recommendations. Am J Respir Crit Care Med. 2006;174(5):605-614.

86. Mowatt G, Houston G, Hernández R, et al. Systematic review of the clini-cal effectiveness and cost-effectiveness of oesophageal Doppler monitor-ing in critically ill and high-risk surgical patients. Health Technol Assess.2009;13(7):iii-iv, ix-xii, 1-95. doi:10.3310/hta13070.

87. Agency for Healthcare Research and Quality. Esophageal Doppler ultra-sound-based cardiac output monitoring for real-time therapeutic manage-ment of hospitalized patients: a review. http://www.cms.hhs.gov/determinationprocess/downloads/id45TA.pdf. Published January 16,2007. Accessed October 30, 2014.

88. Centers for Medicare and Medicaid Services. CMS manual system: pub100-03 Medicare national coverage determinations. http://www.cms.hhs.gov/Transmittals/Downloads/R72NCD.pdf. Published August 28,2007. Accessed October 31, 2014.

89. Aetna Health Insurance. Clinical policy bulletin: esophageal Dopplermonitoring. Publication No. 0793. http://www.aetna.com/cpb/medical/data/700_799/0793.html. Accessed October 31, 2014.

90. Centers for Medicare and Medicaid Services. CMS manual system: pub100-03 Medicare national coverage determinations. https://www.cms.gov/transmittals/downloads/R63NCD.pdf. Published December 15, 2006.Accessed October 31, 2014.

91. CMS.gov. Billing and coding guidelines. Cardiac catheterization andcoronary angiography. http://downloads.cms.gov/medicare-coverage-database/lcd_attachments/30719_6/L30719_CV006_CBG_010111.pdf. Accessed November 24, 2014.

92. Poeze M, Greve J, Ramsay G. Meta-analysis of hemodynamic optimization:relationship to methodological quality. Critical Care. 2005;9(6):R771-R779.

93. Prentice D, Sona C. Esophageal Doppler monitoring for hemodynamicassessment. Crit Care Nurs Clin North Am. 2006;18:189-193.

94. Dellinger P, Levy M, Carlet J, et al; International Surviving Sepsis Cam-paign Guidelines Committee; American Association of Critical-CareNurses; American College of Chest Physicians; American College ofEmergency Physicians; Canadian Critical Care Society; European Societyof Clinical Microbiology and Infectious Diseases; European Society ofIntensive Care Medicine; European Respiratory Society; InternationalSepsis Forum; Japanese Association for Acute Medicine; Japanese Soci-ety of Intensive Care Medicine; Society of Critical Care Medicine; Societyof Hospital Medicine; Surgical Infection Society; World Federation ofSocieties of Intensive and Critical Care Medicine. Surviving Sepsis Cam-paign: international guidelines for management of severe sepsis and sep-tic shock: 2008 [published correction appears in Crit Care Med.2008;36(4):1394-1396]. Crit Care Med. 2008;36(1):296-327.

95. Wo CC, Shoemaker WC, Appel PL, Bishop MH, Kram HB, Hardin E.Unreliability of blood pressure and heart rate to evaluate cardiac outputin emergency resuscitation and critical illness. Crit Care Med. 1993;21(2):218-223.

96. Shippy C, Appel P, Shoemaker W. Reliability of clinical monitoring to assessblood volume in critically ill patients. Crit Care Med. 1984;12:107-112.

97. Ferrer R, Artigas A, Suarez D, et al; Edusepsis Study Group. Effectivenessof treatments for severe sepsis: a prospective, multicenter, observationalstudy. Am J Respir Crit Care Med. 2009;180(9):861-866.


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CNE Test Test ID C1513: Stroke Volume Optimization: The New Hemodynamic AlgorithmLearning objectives: 1. Discuss the use of stroke volume optimization in a hypovolemic patient 2. Define corrected flow time, peak velocity, stroke distance,and stroke index 3. State various methods used to obtain blood flow measurement

Program evaluation Yes No

Objective 1 was met � �Objective 2 was met � �Objective 3 was met � �Content was relevant to my

nursing practice � �My expectations were met � �This method of CNE is effective

for this content � �The level of difficulty of this test was:

� easy � medium � difficultTo complete this program,

it took me hours/minutes.

5. Which of the following explains why clinicians prefer blood flow

monitoring versus blood pressure monitoring?

a. Compensatory mechanisms mask hypoperfusion

b. Afterload, preload, and contractility are influenced by medications

c. Blood pressure, MAP, and heart rate are late indicators of hypoperfusion

d. All of the above

6. Which of the following changes is expected in a patient who

received a 1000-mL fluid challenge that confirms hypovolemia?

a. Increase in PAOP

b. Increase in urine output

c. Increase in stroke volume, corrected flow time, and cardiac output

d. Increase in CVP and MAP

7. Volume and vasopressors are often the treatment of choice in a

patient with shock. Which of the following parameters are best used

as end points to guide therapy?

a. Stroke volume, peak velocity, and corrected flow time

b. Stroke volume, systemic vascular resistance, and central venous

oxygen saturation (ScvO2)

c. ScvO2, corrected flow time, and peak velocity

d. ScvO2 and stroke volume

8. Nursing implications in obtaining hemodynamic data include

which of the following?

a. Proficiency in application of monitoring device

b. Application of data obtained to patient population

c. Achieving optimal signal acquisition

d. All of the above

9. Mechanical ventilation with positive end-expiratory pressure can

impede blood flow and increase PAOP. How can clinicians deter-

mine proper interventions for this patient population?

a. Trend and optimize stroke volume

b. Trend cardiac filling pressures

c. Closely follow pulmonary vascularity on the chest radiograph

d. Trend blood pressure

For faster processing, takethis CNE test online at

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AACN, 101 Columbia Aliso Viejo, CA 92656.

Test ID: C1513 Form expires: February 1, 2018 Contact hours: 1.0 Pharma hours: 0.0 Fee: AACN members, $0; nonmembers, $10 Passing score: 7 correct (78%) Synergy CERP Category A Test writer: Carol Ann Brooks, BSN, RN, CCRN-K, CSC

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Test answers: Mark only one box for your answer to each question. You may photocopy this form.

1. �a �b �c �d

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6. �a �b �c �d

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4. �a �b �c �d

3. �a �b �c �d

2. �a �b �c �d

1. Which of the following hemodynamic values help determine

responsiveness to fluid replacement?

a. Stroke volume within normal values

b. Normal stroke volume with normal filling pressures

c. Adequate blood flow for tissue oxygenation without increasing

heart rate

d. Afterload and preload stabilized

2. Which of the following is the first hemodynamic parameter to

decrease in hypovolemia?

a. Pulmonary artery occlusive pressure (PAOP)

b. Central venous pressure (CVP)

c. Cardiac output

d. Stroke volume

3. After mitral valve replacement, your patient’s urine output

decreases over 3 hours. The monitor displays sinus tachycardia

with heart rate 108 beats/min, CVP 8 mm Hg, cardiac output 4

L/min, and mean arterial pressure (MAP) 80 mm Hg. The MAP

remains within normal range because of which of the following?

a. Normal cardiac output

b. No change in circulating volume

c. Compensatory mechanisms

d. MAP is an independent parameter

4. Monitoring stroke volume gives the clinician insight into which

of the following?

a. Blood flow and circulating volume

b. Cardiac filling pressures

c. Oxygenation

d. Contractility

In the United States, 359 400 people experience an out-of-hospital cardiac arrest each year, andless than 9.5% of those people survive.1 Out-of-hospital cardiac arrest continues to be associated

with high mortality, and among those patients who do survive the initial cardiac arrest, two-thirds die

as a result of neurological injury.2 Postresuscitation care is increasingly recognized as an integral component

in improving the quality of survival and neurological outcomes. Although advances have been made in

initial resuscitative efforts; anoxic neurological injury remains a major concern after return of spontaneous

circulation (ROSC).2,3 Therapeutic hypothermia improves neurological outcomes after ROSC.3

Use of a Nursing Checklist toFacilitate Implementation ofTherapeutic HypothermiaAfter Cardiac ArrestKATHLEEN RYAN AVERY, RN, MSN, CCRN

MOLLY O’BRIEN, MPH

CAROL DADDIO PIERCE, RN, MSN, CCRN

PRISCILLA K. GAZARIAN, RN, PhD


Feature

Therapeutic hypothermia has become a widely accepted intervention that is improving neurological outcomes

following return of spontaneous circulation after cardiac arrest. This intervention is highly complex but infre-

quently used, and prompt implementation of the many steps involved, especially achieving the target body

temperature, can be difficult. A checklist was introduced to guide nurses in implementing the therapeutic

hypothermia protocol during the different phases of the intervention (initiation, maintenance, rewarming, and

normothermia) in an intensive care unit. An interprofessional committee began by developing the protocol, a

template for an order set, and a shivering algorithm. At first, implementation of the protocol was inconsistent,

and a lack of clarity and urgency in managing patients during the different phases of the protocol was apparent.

The nursing checklist has provided all of the intensive care nurses with an easy-to-follow reference to facilitate

compliance with the required steps in the protocol for therapeutic hypothermia. Observations of practice and

feedback from nursing staff in all units confirm the utility of the checklist. Use of the checklist has helped reduce

the time from admission to the unit to reaching the target temperature and the time from admission to continuous

electroencephalographic monitoring in the cardiac intensive care unit. Evaluation of patients’ outcomes as related

to compliance with the protocol interventions is ongoing. (Critical Care Nurse. 2015;35[1]:29-38)


Despite recommendations from the American Heart

Association,3 the European Resuscitation Council and

the International Liaison Committee on Resuscitation4

that therapeutic hypothermia be used in comatose sur-

vivors following ROSC, challenges to implementation of

therapeutic hypothermia in clinical practice remain.

Therapeutic hypothermia is a complex but uncommon

intervention, and because of this, prompt implementation

of the many steps involved and quickly achieving the

desired temperature goal can be difficult.

BackgroundIn 2002, researchers in 2 studies5,6 reported improved

neurological outcomes and a decrease in mortality with

the use of therapeutic hypothermia after out-of-hospital

cardiac arrest. Recently published guidelines from both

the American Heart Association and the International

Liaison Committee on Resuscitation incorporated evi-

dence from research

and recommended

that clinicians imple-

ment therapeutic

hypothermia to increase the likelihood of improved

neurological outcome.3,7 Brain cells die because of several

biochemical processes resulting from cardiac arrest and

the inflammatory process following that injury. Therapeu-

tic hypothermia is believed to be effective because it reduces

cerebral metabolism, decreases cerebral blood flow, and

decreases intracranial pressure.8-10 The neuroprotective

mechanisms of therapeutic hypothermia are now widely

recognized and implemented as a standard of care.3

The American Heart Association recommended that

comatose adult patients with ROSC following out-of-

hospital cardiac arrest be cooled to 32ºC to 34ºC (90ºF-

93ºF) for 12 to 24 hours, with the strongest evidence of

survival for those patients who had pulseless ventricular

tachycardia or ventricular fibrillation rhythms.3 Less

well understood is how the timing of these therapeutic

hypothermia interventions affects patients’ outcomes. In

the 2002 studies published by Bernard et al5 and the

Hypothermia After Cardiac Arrest Study Group,6 target

temperature was reached within 8 hours after ROSC.

Although a prospective observational study11 of 986

patients did not reveal an association between the timing

of therapeutic hypothermia and neurological outcomes,

observational evidence demonstrates a 20% increase in

risk of death for every hour delay in initiating therapeu-

tic hypothermia.12 The evidence is not conclusive; how-

ever, the American Heart Association’s 2010 guidelines

recommended initiating therapeutic hypothermia as

soon as possible after ROSC.3 Our institution’s policy

states that therapeutic hypothermia should be initiated

within 6 hours of ROSC with a goal of achieving target

temperature within 4 hours of initiation of therapeutic

hypothermia. Therapeutic hypothermia has few absolute

contraindications. The ultimate decision to initiate ther-

apeutic hypothermia should be based on an assessment

of the potential risks and benefits of hypothermia in

each individual patient while considering the complete

clinical situation and comorbid conditions.9,13

Recommendations for the Use of Checklists

The implementation of institution-specific standard-

ized protocols, order sets, and a bundled care approach

have proven a successful method in combating the bar-

riers to implementation of therapeutic hypothermia14-20

and were associated with an increased efficiency in

achieving target temperature.21,22

The effectiveness of a surgical safety checklist on rates

of postoperative death and complications was documented

by Haynes et al,23 who reported a decrease in death rate

and complication rate after implementation of a check-

list. In addition to decreasing mortality and complica-

tion rates, surgical checklists have improved compliance

with safety measures, teamwork, and communication.24

Kathleen Ryan Avery is the clinical educator for the cardiac intensivecare unit and co-chair of the Therapeutic Hypothermia Committeeat Brigham and Women’s Hospital, Boston, Massachusetts.

Molly O’Brien is the research coordinator in the cardiac intensivecare unit at Shapiro Cardiovascular Center at Brigham andWomen’s Hospital.

Carol Daddio Pierce is the clinical educator in the medical intensivecare unit at Brigham and Women’s Hospital.

Priscilla K. Gazarian is the nursing program director for resuscita-tive clinical practice at Brigham and Women’s Hospital and anassociate professor of nursing at Simmons College, Boston, Massachusetts.

Corresponding author: Priscilla K. Gazarian, RN, PhD, The Center for Nursing Excel-lence, Brigham and Women’s Hospital, 1 Brigham Circle, 4th Floor, Suite 6, BostonMA 02120 (e-mail: [email protected]).

To purchase electronic or print reprints, contact the American Association of Critical-Care Nurses, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or (949)362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].

Authors

The effectiveness of a surgical safetychecklist has been documented.


Beginning in 2009, checklists have been adapted and

used to improve patients’ outcomes in other practice

situations such as in interdisciplinary rounds and

meetings, during shift handoff, and at discharge.25-29

Researchers have documented that tools such as check-

lists can increase adherence to evidence-based practice

guidelines,30 so we considered adding a checklist to our

therapeutic hypothermia bundle to support the safe,

effective, and efficient implementation of the therapeutic

hypothermia protocol.

Local ProblemAt our hospital, we have implemented therapeutic

hypothermia in 182 patients in the past 5 years. Until

2009, therapeutic hypothermia was exclusively imple-

mented in the coronary care unit (CCU). Although most

patients who are treated with therapeutic hypothermia

continue to be admitted to the CCU (73%) or the medical

intensive care unit (18%), therapeutic hypothermia is

sometimes provided in the other intensive care units

(ICUs). The number of patients receiving therapeutic

hypothermia has increased steadily each year to a total

of 59 patients in 2013 (Figure 1). Because of the low fre-

quency of therapeutic hypothermia cases and the large

number of nursing staff across different ICUs, months

can pass between case exposures, and each exposure

could be at a different phase of the protocol.

In a review of cases of therapeutic hypothermia at

our institution, we found inconsistencies in the implemen-

tation of the protocol and a lack of clarity and urgency in

managing the patients during the different phases of

the protocol (initiation, maintenance, rewarming, and

normothermia). Despite our having a standardized order

template and nursing policy for therapeutic hypothermia,

our data indicated a need for improvement in our imple-

mentation of the therapeutic hypothermia protocol.

Intended ImprovementCaring for patients after cardiac arrest in a critical

care unit is a complex, tense, and time-sensitive under-

taking. Applying an infrequently used but multifaceted

procedure such as therapeutic hypothermia under these

conditions is challenging and may diminish reliable and

consistent implementation of the intervention. Barriers

to timely implementation exist, including a delayed

decision to implement therapeutic hypothermia, lack of

protocols to guide implementation, the volume of cardiac

arrest patients treated, training, and experience of staff.31

Providing therapeutic hypothermia requires an interdis-

ciplinary collaborative approach initiated in the field by

emergency medicine services (EMS) and continued by

the emergency department, catheterization laboratory,

and the ICUs. The different phases of therapeutic

hypothermia cause physiological changes that require

intense assessment, monitoring, and intervention to

manage shifts in hemodynamics (bradycardia, hypoten-

sion, hypovolemia), electrolytes (hyper- and hypo-

glycemia, hypo- and hyperkalemia), achieving desired

temperature,

managing infec-

tion, and assessing

for evidence of

myoclonus and

seizure activity.8,9,32 Successful implementation of the

therapeutic hypothermia protocol requires collaboration

among many disciplines and is a labor-intensive task

that requires continuous monitoring, assessment, and

multitasking by the bedside nurse to rapidly initiate the

many required protocol interventions during the 4 dif-

ferent phases of therapeutic hypothermia in a 3- to 5-day

period.31-33 In addition, nurses are responsible for pro-

moting patients’ comfort and providing support to

patients’ families during the tenuous period after car-

diac arrest.33-35

Although we were decreasing the time it took to achieve

target temperature, we were not reliably achieving our

Figure 1 Number of patients who had therapeutic hypothermiaby type of intensive care unit.

Abbreviations: CCU, coronary care unit; MICU, medical intensive care unit;SICU, surgical intensive care unit. Other includes neurological, cardiac surgery,and thoracic intensive care units.

40353025201510502009 2010

CCU MICU SICU Other

2011 2012 2013

No. o

f pat

ient

s

Year

Caring for patients after cardiac arrestin a critical care unit is a complex,tense, and time-sensitive undertaking.


target temperature in fewer than 4 hours after the initia-

tion of therapeutic hypothermia (see Table). We proposed

a checklist as an intervention to improve achieving the

desired temperature goal within the recommended 4

hours and to manage the various protocol interventions

and minimize complications.

Since the release of the World Health Organization’s

surgical safety checklist study,23 checklists have gained

prominence in clinical care as visual tools for stan-

dardizing communi-

cation, especially

during high-risk

processes.24 Because

checklists have been

documented as effective tools to improve teamwork

and communication,24 we theorized that a checklist

could improve performance in reaching target tempera-

ture during therapeutic hypothermia.

Study PurposeThe purpose of our checklist was to guide ICU nurses

and the health care team in safely, effectively, and effi-

ciently implementing the therapeutic hypothermia

protocol during the different phases of the intervention

in the ICU to decrease the time required to achieve the

target temperature.

MethodsEthics

Our cardiac arrest registry was reviewed by the

Human Research Committee and was approved as

research limited to health medical records. Data from

the cardiac arrest registry were collected and managed

by using REDCap electronic data capture tools hosted

at Brigham and Women’s Hospital. REDCap (Research

Electronic Data Capture) is a secure, web-based appli-

cation designed to support data capture for research

studies.36 All patient identifiers (date of birth, medical

record number) are restricted from data reporting

within REDCap to protect the confidentiality of the data.

SettingBrigham and Women’s Hospital is a 793-bed academic

medical center with 100 adult ICU beds in 6 units and a

total of 436 critical care staff nurses.

Planning the Intervention: Improving Therapeutic Hypothermia ImplementationWith a Checklist

To achieve optimal, consistent standardized care

for patients receiving therapeutic hypothermia in our

hospital, an interprofessional committee on therapeutic

hypothermia was established in 2008 with representa-

tion from nursing, pharmacy, cardiology, neurology,

pulmonary critical care, emergency medicine, and

interventional cardiology.37 Our committee began by

developing a protocol in 2009, an order template in

2010, and a shivering algorithm in 2011. These resources

had been developed as we gained experience with the

implementation of therapeutic hypothermia and were

based on current evidence. Nurses received ongoing

education on the therapeutic hypothermia protocol via

in-service training sessions and annual competency ses-

sions. As we gained experience in caring for patients

receiving therapeutic hypothermia and as new data

were published, our hospital’s protocol for therapeutic

hypothermia underwent annual revisions.

Based on the positive feedback from the ICU nursing

staff on the 1-page shivering algorithm and building on

the success of the World Health Organization’s surgical

Time measured

Start of therapeutic hypothermia to target temperature

Admission to unit to target temperature

Admission to unit to placement of Arctic Sun

Admission to unit to continuous electroencephalographicmonitoring

After checklist (n = 61)

6:30 (4:32-9:57)

4:00 (2:00-6:56)

0:30 (0:30-1:00)

14:17 (9:15-22:42)

Goal time

< 4:00

< 3:00

—

< 18:00

Before checklist (n = 60)

7:00 (5:30-8:11)

5:47 (4:22-8:03)

1:05 (0:30-2:29)

37:27 (15:00-55:27)

Time, hours:minutes, median (interquartile range)

Table Times needed to complete therapeutic hypothermia interventions after admission to coronary care unit

Checklists have been documented aseffective tools to improve teamworkand communication.


safety checklist,23 the nursing representatives on the

Therapeutic Hypothermia Committee proposed devel-

oping a checklist on therapeutic hypothermia for inten-

sive care nurses. The goal of this checklist was to improve

the timeliness of achieving the target temperature within

the recommended 4 hours and to manage the various

interventions at all phases of the therapeutic hypother-

mia protocol while minimizing complications and main-

taining safe and high-quality patient care. Relying on a

standardized protocol improves the quality and outcomes

of an intervention such as therapeutic hypothermia.9,16-

18,20,22 Checklists have also been used as tools to increase

the quality and safety in many industries and have gained

popularity in health care. Checklists standardize the

tasks that must be completed and provide a transparent

framework to ensure protocol adherence, all while

establishing a process to share information and support

among caregivers.38

Checklist DevelopmentThe design of our checklist was motivated by our

desire to shorten the time required to reach the target

temperature and provide direction to managing the many

treatment interventions at each stage of the therapeutic

hypothermia protocol. Our existing guideline and order

template became the key interventions captured on the

checklist. Based on the American Heart Association’s

guidelines for postresuscitation care and our guidelines

of care for use of therapeutic hypothermia after cardiac

arrest, we divided interventions into the 4 stages of the

therapeutic hypothermia protocol. The first phase is the

“initiation of cooling” from 0 to 4 hours. The goal is that

the patient will reach the target temperature of 33°C

(91.4°F) within 4 hours of initiation of therapeutic

hypothermia. The next phase is “maintenance of cool-

ing” from 4 to 24 hours. Cooling is maintained for 24

hours from the initiation of therapeutic hypothermia.

Twenty-four hours after the initiation of therapeutic

hypothermia, the “rewarming” phase begins. Rewarming

is done very slowly at a rate of 0.25°C (0.5°F) per hour

and takes 12 to 16 hours. Once the patient reaches 37°C

(98.6°F), the last phase, “normothermia,” is maintained

for 48 hours. We were now able to identify all of the

interventions that needed to be completed to achieve

our first goal of target temperature within 4 hours.

The checklist is designed as 1 page to be kept at the

bedside. It is a quick, easy, just-in-time resource for

nurses, includes a box to be checked when each item is

completed, and is used during handoff communication.

The checklist was first pilot tested in the CCU and was

revised on the basis of staff feedback. We incorporated

the checklist into the hospital policy available online,

and we placed hard copies in a reference book on the unit

for nurses to integrate into patient care. This therapeutic

hypothermia checklist (Figure 2) for intensive care nurses

has been in use since September 2012.

Evaluation and AnalysisData are collected in real time by our research coor-

dinator. An initiation of therapeutic hypothermia report

is generated each time orders for therapeutic hypothermia

are implemented and is sent to all members of the thera-

peutic hypothermia committee for review. This report

includes patients’ demographics (eg, age), initial rhythm,

downtime, times from ROSC to arrival in the emergency

department, from emergency department to ICU admis-

sion, from ROSC to target temperature, from ICU

admission to target temperature, from ICU admission

to placement of Arctic Sun surface cooling device, and

from ICU admission to electroencephalography. The

reports allow us to accurately track the use of therapeu-

tic hypothermia throughout the hospital and to review

cases both as they occur and over time.

The development and implementation of the thera-

peutic hypothermia checklist have provided the nurs-

ing staff in all ICUs with an easy-to-follow reference to

facilitate compliance with the required interventions in

the therapeutic hypothermia protocol. Since 2009, we

have cared for 183 patients receiving therapeutic hypother-

mia at our institution. Despite the various systems in

place, the median time

to target temperature

from ROSC was 8 hours,

double our desired goal

of 4 hours. Since we

began using the checklist, we have reduced our time

from CCU admission to target temperature from a

median time of 5 hours 47 minutes (2009-2011) to 4

hours (2012-2013) in the CCU, where the checklist was

first pilot tested and used consistently. The time from

CCU admission to placement of the Arctic Sun cooling

device has decreased from 1 hour before use of the

checklist to 30 minutes since implementation of the

checklist (see Table).

Nurses report that the checklisthelps them prepare, prioritize,and organize their interventions.


Figure 2 Therapeutic hypothermia (TH) after cardiac arrest: ICU nursing checklist.

Abbreviations: ABG, arterial blood gas analysis; BBG, bedside blood glucose; BHIP, Brigham and Women’s Hospital intravenous insulin protocol; BICS OE, Brigham Inte-grated Computing System order entry; BIS, bispectral index monitoring; BSAS, Bedside Shivering Assessment Scale; Ca, calcium; CBC, complete blood cell count;CK, creatine kinase; CK-MB, creatine kinase–MB fraction; cTnt, cardiac troponin T; CVP, central venous pressure; D/C, discontinue; EEG, continuous electroen-cephalographic monitoring; Glu, glucose; ICU, intensive care unit; IVB, intravenous bolus; K, potassium; labs, samples for laboratory tests; MAP, mean arterial pres-sure; Mg, magnesium; NMBA, neuromuscular blocking agent; q, every; temp, temperature; TOF, train of four.

Courtesy Brigham and Women’s Hospital, Boston, Massachusetts.

This is intended to be a quick reference only—Refer to the ADM 1.4.18 and Nursing NCPM ICU-44 policies for detailson patient management of therapeutic hypothermia. This document is not part of the medical record.

Patient ID stamp Date/Time TH initiated:________

Initiation of cooling 0-4 hours(goal: target temp within 4 hours)

❒ BICS OE template completed by house staff♢ EEG ordered in Precipio

❒ Establish 2 sources of temperature Monitoring to Arctic Sun —preferred order is Foley, esophageal, rectal

❒ Place Arctic Sun pads onadmission to ICU

❒ Sedation infusion (propofol ormidazolam)

❒ Analgesia infusion (fentanyl or hydromorphone)

❒ BIS monitoring❒ Baseline TOF❒ Magnesium 4 g IVB over 4

hours❒ Cover head, hands, feet with

towels/blankets❒ BSAS every hour

♢ If BSAS ≥ 1, follow shiver-ing algorithm

❒ BBG q 1 hour♢ If Glu > 200, start modified

BHIP♢ Turn insulin OFF if

Glu < 200❒ Draw baseline admission labs:

Chem 20, CBC, CK, CK-MB, cTnt, lactic acid, ABG

____ ♢ 4 hours after initiation: serum GLU, K

❒ Target temp (91.4°F) achieved within 4 hours of initiating THIF NOT—refer to shivering algorithm and Arctic Sun troubleshooting chart/guidelines

❒ Document hourly: Patient temperature, Arctic Sun flow, water temperature

❒ Determine time to begin rewarming

Maintenance of cooling4-24 hours

❒ BIS monitoring❒ Continue sedation/analgesia

infusions❒ BSAS q 1 hour

♢ If BSAS ≥ 1, follow shivering algorithm

❒ BBG q 1 hour♢ If Glu > 200, start modified

BHIP♢ Turn insulin OFF if Glu < 200

❒ MAP goal > 75 mm Hg❒ CVP goal > 12 mm Hg❒ Document hourly: Patient temp,

Arctic Sun flow, water temp❒ EEG performed❒ Draw labs q 4 hours after TH

initiation at:____ ♢ 8 hours: Chem 7,

CBC, CK, CK-MB, cTnt, lactic acid, ABG

____ ♢ 12 hours: Glu, K, cultures: blood, sputum,urine

____ ♢ 16 hours: Chem 7, CBC, CK, CK-MB, cTnt, lactic acid, ABG

____ ♢ 20 hours: Glu, K____ ♢ 24 hours: Chem7,

CBC, CK, CK-MB, cTnt,lactic acid, ABG

❒ Hold K+ replacement 4 hours prior to rewarming (unless K < 3.5)

Normothermia x 48 hours AFTER target temp 98.6ºF

❒ Keep Arctic Sun pads on andtarget temp set at 98.6°F/37°C for 48 hours

❒ Wean/discontinue sedation/ analgesia infusions

❒ If NMBA infusion ♢ D/C NMBA infusion♢ Assess TOF every hour♢ When TOF 4/4, wean/

discontinue sedation/ analgesia

❒ Observe for temp spikes andrigors♢ Refer to normothermia

section of shivering algorithm

❒ Document hourly: patient temp, Arctic Sun flow, water temp

❒ Draw labs every 8 hours x 2:♢ Glu, K, Mg, Ca

_______ _______

Rewarming 24-38 hours Date/time:______

❒ Rewarming begins 24 hoursafter initiation of TH

❒ Set Arctic Sun to:♢ target temp of

98.6°F/37°C ♢ rewarm at rate of 0.5°F

(0.25°C) per hour (it will take 12-16 hours to rewarm)

♢ Refer to directions on Arctic Sun and in nursing policy

❒ Continue sedation/analgesia infusions

❒ Draw labs q 4 hours after TH initiation at:____ ♢ 28 hours: Glu, K____ ♢ 32 hours: Glu, K____ ♢ 36 hours: Glu, K❒ BIS monitoring❒ BSAS q 1 hour

♢ If BSAS ≥ 1, follow shivering algorithm during rewarming

❒ BBG q 1 hour♢ If insulin infusion, check

BBG every 30 minutes♢ Turn insulin OFF if

Glu < 200❒ Document hourly: Patient

temp, Arctic Sun flow, water temp

❒ Once target temp of 98.6°F/37°C achieved: Normothermia phase♢ Wean off of sedation


the management of shivering. The checklist has provided

an opportunity for case discussions with the clinical nurse

educator and has led to an increased understanding of

the rationale for the different therapeutic hypothermia

interventions, including the early use of electroencephalo-

graphic monitoring. We have noted a decrease in time

from CCU admission to initiation of continuous electroen-

cephalographic monitoring from 37.5 hours to 14.25

hours (see Table). The nurses have stated that the thera-

peutic hypothermia checklist aids in clinical decision

making by providing prompts to assist with maintaining

hemodynamic stability and preventing complications

from therapeutic hypothermia.

DiscussionThe use of the therapeutic hypothermia checklist helps

maintain consistent care of patients in the dynamic ICU

Observations of practice and feedback from the

nursing staff in all the ICUs all support the utility of the

therapeutic hypothermia checklist for intensive care

nurses. The checklist has been implemented in units

other than the CCU where therapeutic hypothermia is

used less often. Nurses have reported that using the

therapeutic hypothermia checklist helps them prepare,

prioritize, and organize their interventions when admit-

ting a critically ill patient. Nurses have reported that the

checklist guides nursing documentation and ensures

that future interventions remain on schedule, while also

supporting teamwork and communication. The check-

list helps the nurses to focus on the immediate tasks

and simultaneously view the entire process from begin-

ning to end so that they can anticipate changes as the

patient progresses. We have observed increased use of

the shivering algorithm and nursing documentation of

Mr C, a 55-year-old man, was out jogging one

evening when he experienced a witnessed ven-

tricular fibrillation cardiac arrest. Bystander

cardiopulmonary resuscitation was initiated, and EMS-

activated prompt defibrillation and ROSC were achieved

within 10 minutes. EMS initiated therapeutic hypothermia

with an infusion of iced normal saline (4°C) and ice packs

applied to the neck, axillae, and groin. Mr C arrived in the

emergency department at 9:05 PM with a body temperature

of 36.5°C (97.8°F). Despite Mr C’s history of hypertension

and coronary artery disease (drug-eluting stent to circumflex

artery 5 years earlier), the 12-lead electrocardiogram did

not show evidence of myocardial ischemia or infarction.

An assessment by the emergency department’s team and a

neurology consultant confirmed that Mr C met the criteria

for therapeutic hypothermia: he had experienced a ventric-

ular fibrillation cardiac arrest with ROSC after 10 minutes,

he was comatose (no meaningful response to verbal stimuli),

and there were no contraindications for therapeutic hypother-

mia. The emergency department continued cooling with

ice packs and initiated continuous infusions of propofol

and fentanyl.

Mr C was admitted to the CCU at 12:30 AM with a body

temperature of 35°C (95.2°F). The CCU nursing staff had

prepared for his arrival and anticipated Mr C’s care needs

by using the therapeutic hypothermia checklist. The physi-

cians had entered the therapeutic hypothermia order set and

the necessary equipment including the Arctic Sun surface

cooling device was ready for placement upon Mr C’s arrival

and was started at 12:40 AM. Interventions to prevent shiver-

ing and maintain comfort were initiated. Bispectral monitor-

ing was initiated, and a baseline train of 4 was obtained. Blood

samples for laboratory tests were collected per the therapeutic

hypothermia protocol. Mr C did experience some shivering

that was promptly treated by referring to the shivering algo-

rithm from the therapeutic hypothermia checklist and a target

temperature of 32.7°C (90.9°F) was achieved at 2 AM. Electroen-

cephalographic monitoring was initiated at 9 AM. Cooling

was maintained for 24 hours from the start of therapeutic

hypothermia. The nurse coming on for the next shift was

alerted that Mr C would be due to be rewarmed in 2 hours.

Using the checklist, the nurses reviewed the completed inter-

ventions during the maintenance phase. A potassium level of

3.2 mEq/L had been repleted per protocol 2 hours previously.

The glucose levels had remained less than 200 mg/dL, so

insulin had not been initiated during the cooling phase. Mr C

rewarmed at a rate of 0.25°C (0.5°F) per hour without signif-

icant hypotension, hypoglycemia, or hyperkalemia. Nor-

mothermia (37°C, 98.6°F) was achieved in 14 hours and

maintained per protocol for 48 hours. Mr C’s neurological

and cardiac status improved during his 5-day stay in the CCU,

and he was discharged home on day 10 after receiving an

implantable cardioverter defibrillator. He had good neurolog-

ical recovery as evidenced by a Cerebral Performance Category

score of 1. Mr C returned to work 2 weeks after discharge

from the hospital and resumed his exercise regimen.

CASE STUDY


environment, where many team members need to col-

laborate with one another. Further, it supports nursing

practice by decreasing the uncertainty for nurses less

familiar with implementing the protocol in this complex

time-pressured situation.

We have introduced a novel checklist for the imple-

mentation of therapeutic hypothermia and demonstrated

further support for the growing body of evidence indi-

cating that checklists and other types of cognitive aids

are effective in improving various complex processes.30

Using a checklist for therapeutic hypothermia has many

implications in addition to the potential to improve

patients’ outcomes. Given that checklists have been

documented as improving teamwork and communica-

tion, their use in therapeutic hypothermia could lead to

improved interdisciplinary collaboration. Further, this

type of support for nursing work increases nurses’

autonomy and allows them more time to focus on pro-

viding holistic care to patients and patients’ families.

LimitationsThis report of the implementation of an ICU nursing

checklist for therapeutic hypothermia to integrate the

evidence for therapeutic hypothermia into practice is

limited by the lack of control over possible confounding

variables that may have affected the time to achieve the

temperature target. Although our practice has improved,

we cannot conclude that this is solely a result of using

the checklist. Nonetheless, we easily integrated the

checklist into practice, and it can be adapted for use in

other institutions.

SummaryThus far, the therapeutic hypothermia checklist for

intensive care nurses has helped the CCU improve 2

metrics related to the implementation of evidence-based

practice of therapeutic hypothermia: the time from CCU

admission to achieving the target temperature and the

time from CCU admission to continuous electroen-

cephalographic monitoring.

Our next challenge will be to focus on the processes

within our system to continue the cooling initiated by

EMS and decrease the time from ROSC to ICU admis-

sion. Further evaluation of compliance with the thera-

peutic hypothermia checklist and the effects on

patients’ outcomes is needed for continuous quality

improvement. CCN

AcknowledgmentsThe authors thank Annmarie Chase, RN, MSN, CEN ED, clinical flow manager, Benjamin M. Scirica, MD, MPH (co-chair), and all members of the TherapeuticHypothermia Committee at Brigham and Women’s Hospital for their guidanceand support in the development of the therapeutic hypothermia checklist forintensive care nurses and the nursing staff of the CCU and medical ICU for theirfeedback on the implementation of the checklist.

Financial DisclosuresNone reported.

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CCN Fast Facts

Use of a Nursing Checklist to FacilitateImplementation of Therapeutic HypothermiaAfter Cardiac Arrest

CriticalCareNurseThe journal for high acuity, progressive, and critical care nursing

begins. Rewarming is done very slowly at a rate of

0.25°C (0.5°F) per hour and takes 12 to 16 hours.

• Once the patient reaches 37°C (98.6°F), the last

phase, “normothermia,” is maintained for 48 hours.

• The checklist is a quick, easy resource for nurses,

and is used during handoff communication. The

nursing checklist has provided all of the intensive

care nurses with an easy-to-follow reference to

facilitate compliance with the required steps in

the protocol for therapeutic hypothermia.

• Using a checklist for therapeutic hypothermia has

many implications in addition to the potential to

improve patients’ outcomes. Given that checklists

have been documented as improving teamwork

and communication, their use in therapeutic

hypothermia could lead to improved interdiscipli-

nary collaboration. Further, this type of support

for nursing work increases nurses’ autonomy and

allows them more time to focus on providing

holistic care to patients and patients’ families.

• Use of the checklist has helped reduce the time from

admission to the unit to reaching the target tem-

perature and the time from admission to continu-

ous electroencephalographic monitoring in the

cardiac intensive care unit. Evaluation of patients’

outcomes as related to compliance with the proto-

col interventions is ongoing. CCN

FactsTherapeutic hypothermia has become a widely

accepted intervention that is improving neurological

outcomes following return of spontaneous circulation

(ROSC) after cardiac arrest. This intervention is highly

complex but infrequently used, and prompt implemen-

tation of the many steps involved, especially achieving

the target body temperature, can be difficult.

• A checklist was introduced to guide nurses in

implementing the therapeutic hypothermia

protocol during the different phases of the inter-

vention (initiation, maintenance, rewarming,

and normothermia) in an intensive care unit.

• We divided interventions into the 4 stages of

the therapeutic hypothermia protocol so that we

were able to identify all of the interventions that

needed to be completed to achieve our first goal

of target temperature within 4 hours.

• The first phase is the “initiation of cooling” from

0 to 4 hours. The goal is that the patient will reach

the target temperature of 33°C (91.4°F) within 4

hours of initiation of therapeutic hypothermia.

• The next phase is “maintenance of cooling” from

4 to 24 hours. Cooling is maintained for 24 hours

from the initiation of therapeutic hypothermia.

• Twenty-four hours after the initiation of thera-

peutic hypothermia, the “rewarming” phase

Avery KR, O’Brien M, Pierce CD, Gazarian PK. Use of a Nursing Checklist to Facilitate Implementation of Therapeutic Hypothermia After Cardiac Arrest. Critical CareNurse. 2015;35(1):29-38.


Delirium has a substantial impact on health care. This complication is associated with a

15-day increase in hospital length of stay (LOS),1 a financial impact of $4 billion to $16 billion

annually,2 and a 19% increase in 6-month mortality.3 Delirium is common across all patient

settings; the prevalence, however, varies according to acuity of illness. Delirium develops in general

medicine patients at rates ranging from 11% to 42%.4 The highest prevalence of delirium, as high as 87%,

occurs in critically ill patients.5 Understanding the impact of delirium on hospitalized patients makes

prevention and optimal treatment of this complication a priority. Two approaches are used to manage

delirium: use of pharmacological agents and application of nonpharmacological therapies.

NonpharmacologicalInterventions to PreventDelirium: An Evidence-Based Systematic ReviewRYAN M. RIVOSECCHI, PharmD

PAMELA L. SMITHBURGER, PharmD, MS, BCPS

SUSAN SVEC, RN, BSN, CCRN

SHAUNA CAMPBELL, RN, BSN

SANDRA L. KANE-GILL, PharmD, MS


Feature

Development of delirium in critical care patients is associated with increased length of stay, hospital costs, and

mortality. Delirium occurs across all inpatient settings, although critically ill patients who require mechanical

ventilation are at the highest risk. Overall, evidence to support the use of antipsychotics to either prevent or

treat delirium is lacking, and these medications can have adverse effects. The pain, agitation, and delirium

guidelines of the American College of Critical Care Medicine provide the strongest level of recommendation

for the use of nonpharmacological approaches to prevent delirium, but questions remain about which non-

pharmacological interventions are beneficial. (Critical Care Nurse. 2015;35[1]:39-51)



1. Describe the nursing literature on nonpharmacological interventions to prevent delirium2. Discuss nonpharmacological interventions that have been shown to be effective in preventing delirium3. Explain the tools developed for the measurement of delirium in intensive care unit patients


The 2013 pain, agitation, and delirium guidelines6 of

the American College of Critical Care Medicine provide

recommendations for the use of pharmacological agents

in the prevention and treatment of delirium. Because of

a lack of compelling data, the guidelines do not provide

a recommendation for a pharmacological protocol or for

a combined nonpharmacological and pharmacological

protocol for prevention of delirium. Furthermore, the

guidelines give a -2C recommendation for pharmacologi-

cal prevention with either haloperidol or atypical

antipsychotics. The lack of evidence supporting the use

of pharmacological agents creates a void in the effective

management of delirium.

The guidelines6 give the highest grade within the

delirium section (1B) to a nonpharmacological preven-

tion strategy, meaning the recommendation is a strong

one backed by a moderate level of evidence. Unfortu-

nately, most of the literature is on nonpharmacological

interventions used in either general medicine, geriatric,

or perioperative patients.7-16 Although critically ill

patients certainly differ from most of the populations of

patients studied, one can reasonably assume that critically

ill patients, who are at the highest risk for delirium, would

also benefit from nonpharmacological interventions. Large

randomized controlled trials with a multi-interventional

approach that includes pharmacological and nonphar-

macological approaches to prevent delirium are needed.17

Any appropriate attempt at such a study requires a strong

understanding of nonpharmacological approaches. The

purpose of this systematic review is to summarize the

available literature on nonpharmacological management

of delirium among all populations of patients. The ulti-

mate goal is to identify which strategies are beneficial to

facilitate the development of a nonpharmacological pro-

tocol that could be implemented for critically ill patients.

MethodsA literature search was completed by using MEDLINE

and EMBASE. With PubMed, the following terms were

used to search MEDLINE for material from 1946 to

October 15, 2013: delirium AND (critically ill, intensive

care, ICU, intensive care unit, OR critical illness), AND

(treatment, prevention, prophylaxis, adjunctive therapy,

OR adjunct therapy). Additional searches in MEDLINE

were then performed with the terms (mobility, animation,

exercise, rehabilitation, physical therapy, OR bicycle),

(light, window, curtains, shades, OR blinds), (earplugs,

ear, noise, OR hearing aid), (sleep, sleep hygiene, OR

sleep deprivation), (eyeglasses, glasses, OR magnifying

lens), orientation, and hydration, each combined with

AND delirium, AND (critically ill, intensive care, ICU,

intensive care unit, OR critical illness). EMBASE was

searched by using the same strategy. The search was

restricted to studies conducted in humans and reported

in English. A second reviewer independently performed

the same search for validation. The titles of all citations

retrieved from the search were reviewed for relevance.

On the basis of the relevance of the title, articles were

selected to be reviewed at the abstract level. Abstracts were

considered for full-text review if delirium was measured

as an outcome (incidence or severity), and the screening

for delirium was completed by using a standardized screen-

ing tool. No further review of an abstract was done if the

study covered was not original research, addressed exclu-

sively pharmacological approaches, or used a combination

of pharmacological and nonpharmacological approaches.

If, after review, the abstract was still deemed applicable,

a full-text review was done in which the same inclusion


Ryan M. Rivosecchi is a second-year pharmacy resident in criticalcare at the University of Pittsburgh Medical Center, PresbyterianHospital, Pittsburgh, Pennsylvania.

Pamela L. Smithburger is an assistant professor of pharmacy andtherapeutics, University of Pittsburgh School of Pharmacy, Pittsburgh,Pennsylvania, and a clinical specialist in the medical intensive careunit at the University of Pittsburgh Medical Center, PresbyterianHospital.

Susan Svec is the clinical director of the medical intensive care unit,University of Pittsburgh Medical Center, Presbyterian Hospital. Sherecently graduated from the master’s of leadership and administrationprogram at California University of Pennsylvania, California,Pennsylvania.

Shauna Campbell is the nursing director of the medical intensive careunit at the University of Pittsburgh Medical Center, PresbyterianHospital.

Sandra L. Kane-Gill is an associate professor of pharmacy andtherapeutics at the University of Pittsburgh School of Pharmacy.She has secondary appointments in the School of Medicine in theClinical Translational Science Institute, Department of CriticalCare Medicine, and the Department of Biomedical Informatics.She is also the critical care medication safety pharmacist at the Uni-versity of Pittsburgh Medical Center in the Department of Pharmacy.

Corresponding author: Sandra Kane-Gill, 918 Salk Hall, 3501 Terrace St, Pittsburgh,PA 15261 (e-mail: [email protected]).

To purchase electronic or print reprints, contact the American Association of Critical-Care Nurses, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or (949)362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].

Authors

and exclusion criteria were applied

to the text of the article. No inclusion

restrictions were placed on the study

setting or population of patients

(critically ill or not critically ill).

Studies with mixed nonpharmaco-

logical interventions, including non-

pharmacological protocols with

many interventions, were included.

The exclusion of any involvement of

pharmaceuticals was necessary to

evaluate the true benefit of a non-

pharmacological protocol and mini-

mize confounding variables. The

references of the included articles

were reviewed to ensure a compre-

hensive assessment.

ResultsAll Studies

A total of 17 articles7-24 met the

inclusion criteria and were selected

for review (see Figure and Tables 1

and 2). Seven studies18-24 were done

in critically ill patients, 5 in geriatric

general medicine patients,9-13 3 in postoperative patients,14-16

and 2 in patients who had a hip fracture.7,8 A total of 13

of the studies were prospective investigations,7-11,13,15,16,18,21-24

and 4 were randomized control trials.14-16,24 The Confusion

Assessment Method or the Confusion Assessment Method

for the Intensive Care Unit (CAM-ICU) was the most fre-

quently used tool and was used in 10 studies.7-10,13,19-23 The

Neelon and Champagne Confusion Scale was used in 4

evaluations,14-16,24 and the Intensive Care Delirium Screen-

ing Checklist,18 the Diagnostic and Statistical Manual of

Mental Disorders (Fourth Edition; DSM-IV),12 and the

Delirium Screening Scale12 were each used once. The

frequency of delirium screening ranged from less than

daily to 3 times per day.

The incidence of delirium was determined in 12

studies.7-15,18-21 Among these, 9 revealed a benefit of the

nonpharmacological intervention.8-10,12-15,20,21 Table 3 gives

the interventions used in the individual studies. Among

the interventions that were beneficial, the mean reduc-

tion in the incidence of delirium was 24.7%, with a

range of 9.7% to 31.8%. In 6 studies,7,8,10,11,22,23 the dura-

tion of delirium decreased after the addition of the

nonpharmacological intervention. Additionally, among

the 6 evaluations7-10,13,18 of the severity of delirium, all but

1 study9 indicated a reduction in severity. Patients’ LOS

was examined in 6 studies.7,8,11,18-20 Of the 6 studies, the

results of 2 revealed a decrease in LOS.11,19 Among the 3

studies18-20

done in the

ICU, only 1

indicated a

reduction in

LOS.19 When

any outcome related to delirium (incidence, duration,

severity) was examined, only 2 studies11,19 did not show

any benefit from the addition of a nonpharmacological

intervention.

A total of 28 unique nonpharmacological interven-

tions were used in the clinical studies. The most com-

mon interventions associated with any clinical benefit

were mobilization,8,10,20-23 reorientation,9,10,13,18,21 education

of nurses,7,10,12,18,23 and music therapy.9,16,18,20,21 A single

nonpharmacological intervention was examined in 5

studies,12,14-16,24 and multiple nonpharmacological inter-

ventions were examined in 12 investigations.7-10,11,13,18-23

Delirium is associated with multiple negativeconsequences, including increased lengthof stay, higher health care costs, and evenincreased mortality.


Figure Breakdown of articles selected in literature search.

44 Excluded▪ 24 were not original research▪ 6 did not measure delirium or did not

use standard delirium measurement▪ 5 contained pharmacological intervention▪ 5 were not full-text articles▪ 4 did not involve an intervention

Abstracts screened outcomes, delirium screening, and pharmacologicalinterventions

Limit to English and humans 821

54 Selected for full-textreview

17 Included in review

10 Included

References reviewed for inclusion

7 Included

89 Selected for further review of abstract

EMBASE1540 citations

MEDLINE1104 citations

Titles screened for relevance


Reference,year

Milisen et al,7

2001

Marcantonio et al,8 2001

Inouye et al,9

1999

Vidán et al,10

2009

Lundström et al,11 2005

Tabet et al,12

2005

Caplan andHarper,13 2007

Ono et al,14

2011

Taguchi et al,15

2007

McCaffrey,16

2009

Design

Prospective

Prospective,randomized,double-blind

Prospective,individualmatching

Prospective,controlled

Prospective

Case-control,single-blind

Prospective

Randomized,randomizedcontrolled trial

Prospective,randomizedcontrolled trial


Screening tool used (frequency)

CAM, modified CAM

CAM (daily)

CAM (daily)

CAM (daily)

DSM-IV criteria(days 1, 3, and 7)

Delirium Rating Scale

CAM (every other day)

MDAS for severity ifCAM positive

NEECHAM (no com-ment on how often)

NEECHAM (twice a day)

NEECHAM (daily for 3 days)

Population (N)

Hip fracture, emergencydepartment/trauma, (26)

Hip fracture, ≥ 65 years old(126)

General medicine,> 70 years old(852)

Geriatric unit, age> 70 years (542)

Age > 70 years,geriatric unit (400)



Esophagectomy(22)

Esophagectomy(11)

Hip or knee surgery, > 75years old (22)

Notable exclusions

Metastatic cancer,life expectancy < 6 months

Inability to completeinterview, low riskfor delirium

Expected hospitalstay <48 hours

None

Patient not presenton unit duringassessment

Severe dementiaDischarged within 48

hours

Nonpharmacological interventions

Nursing educationPoster in units

Module: dehydration, dentures, nutrition supplements, mobilization (physical/occu-pational therapy), glasses, hearing aids,clock, calendar, family presence

Protocol: orientation with care-team namesand day’s schedule, cognitive stimulationactivities, sleep protocol (warm drink,relaxing music, back massage, noise reduction, medication reschedule), mobilization, visual aids, adaptive equipment,hearing aids, hydration

Staff educationPoster in unitsOrientation: clock, calendar, reason for

admission, date, place, family letterGlasses, hearing aidsSleep: warm drink, reschedule medications

and proceduresMobilization: out of bed, catheter removal,

change positions, avoid restraintsHydration: schedule water if ratio of blood urea

nitrogen to serum level of creatinine > 40Nutrition

Medical team educationReorganization of nursing staff

Medical team education

ReorientationCognitive stimulation activitiesFeeding assistanceHydrationVision protocolHearing protocol

Bright light therapy

Bright light therapy

Music therapy

Table 1 Studies included that involved patients who were not critically ill

Abbreviations: CAM, Confusion Assessment Method; DSM-IV, Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition); LOS, length of stay;MDAS, Memorial Delirium Assessment Scale; NEECHAM, Neelon and Champagne Confusion Scale.


Outcomes

No difference in incidence3-day reduction in duration Reduction in the severity (2.94 points)No difference in LOS

18% reduction in incidence17% reduction in severity1.2-day reduction in durationNo difference in LOS

5.1% reduction in incidence56 fewer days delirious28 fewer episodes No difference in severity No difference in recurrence

6.8% reduction in incidence0.4 decrease in severity2.5-hour reduction in durationNo difference in recurrenceNo difference in functional declineNo difference in death

No difference in prevalence at 24 and 72 hours4-day reduction in LOS

9.7% reduction in point prevalence of delirium

31.8% reduction in incidence3.9-point reduction in MDAS score

31.7% reduction in prevalence

34% reduction in incidence at day 3

Decrease in delirium each of the 3 days

Comments

Used resource study nursesScreened only patients with CAM if NEECHAM identified them as

high riskScreened only on days 1, 3, 5, and 8

Recommendations by geriatric consultant based on moduleRecommendations not made if team was already doing them

Less than 50% screened met inclusion criteriaUsed research nursesGeared intervention against risk factorsSame medical team provided care to both groups

Must have risk factor for inclusion Disposition to either geriatric or general medicine decided by

emergency department physicianBaseline characteristics not very similarNote intervention more helpful in intermediate risk

Extensive nursing training for the intervention

Investigators had no role in day-to-day managementUse of daytime assessment and point prevalence could be

underestimated

Patient must have 1 risk factor for enrollmentMean intervention time 14-19 h/wkVery small sample sizeCost analysis

Mean LOS 24.8 daysTwo dropped out because light was too brightAll male populationScreening stopped on postoperative day 5

All male population

All patients received standard pain, mobilization protocolMusic set to play 4 times a day for 1 hour; patients could do

more if they wished to

Antipsychotic use

Not reported

Yes

Not reported

Not reported

Not reported

Not reported

Not reported

Not reported

Not reported

Not reported

In 6 of those studies,8-10,13,20,21 the interventions were

incorporated into a protocol. The mean number of

interventions used per study was 4.1.

ICU StudiesOf the 7 studies18-24 (Table 2) conducted in ICU patients,

6 investigations18,20-24 indicated a benefit in at least 1

delirium-related outcome, including incidence, duration,

or severity. In the remaining study,19 a 0.6-day reduction

in ICU LOS occurred. Only 1 study18 indicated a reduction

in subsyndromal delirium. In all but 1 study,24 more than

1 nonpharmacological intervention was used; mobiliza-

tion, a noise-reduction protocol, and a sleep protocol

were used most often. All studies20-24 that included either

mobilization or noise-reduction or sleep protocols indi-

cated a statistically significant benefit in at least 1 delirium-

related outcome.

DiscussionICU delirium is associated with numerous adverse

consequences, ranging from increased cost to mortality.3,5

As in a multitude of other ailments, prevention is the opti-

mal strategy, especially when effective treatment options

are unavailable. Haloperidol has been studied for preven-

tion and treatment of ICU delirium, but the results have

been inconclusive.25,26 Because of the unconvincing evidence


Reference,year

Skrobik et al,18

2010

Arenson et al,19

2013

Kamdar et al,20

2013

Colombo et al,21 2012

Schweickert et al,22 2009

Needham et al,23 2010

Van Rompaeyet al,24 2012

Design

Prospective

Randomized,cohort

Observational,pre-postdesign

Prospective,observational,2 stage

Prospective,randomized

Prospective


Screening tool used (frequency)

ICDSC (3 times a day)

CAM, CAM-ICU (3 times a day)

CAM-ICU (2 times a day)

CAM-ICU (2 times a day)

CAM-ICU (daily)

CAM-ICU (daily)

NEECHAM (daily)

Population (N)

Medical-surgicalICU (1133)

Cardiac surgery(ICU/medicine)(1010)

Medical ICU (300)

Medical-surgicalICU (314)

Medical ICU (104)

Medical ICU (57)

ICU (136)

Notable exclusions

Inpatient death, preexisting structuralbrain disease

Visual or hearingimpairment

Absent limbs, 6-month mortality<50%, cardiac arrest

No exclusions

Minimum score of 10 on GlasgowComa Scale

Hearing impairmentSedation

Nonpharmacological interventions

Nursing educationRadio or compact disc player, reorientation

Private room, no barriersWindows

Sleep: minimize overhead page, turn off television, dim hallway, group care activities

Open blindsPrevent nappingMobilizationMinimize caffeine before bed Sleep: earplugs, eye mask, music

Reorientation: follow mnemonic—use firstname, give information about location, LOS,and illness

ClockRead paper or book, music, radioReduction of night noise

Mobilization, physical/occupational therapyPassive range-of-motion exercises

Mobilization, physical/occupational therapyNursing education

Ear plugs

Table 2 Studies included that involved patients who were critically ill

Abbreviations: CABG, coronary artery bypass graft; CAM, Confusion Assessment Method; ICDSC, Intensive Care Delirium Screening Checklist; ICU, intensive care unit;LOS, length of stay; NEECHAM, Neelon and Champagne Confusion Scale; RASS, Richmond Agitation-Sedation Scale.

for pharmacological management of delirium, nonphar-

macological strategies need to be further evaluated.

The nonpharmacological intervention specifically

discussed in the pain, agitation, and delirium guidelines6

of the American College of Critical Care Medicine is

early mobilization. Our review fully supports this recom-

mendation, and we think early mobilization should be

included, when feasible, in any nonpharmacological

prevention protocols implemented across all practice

settings. Some type of mobilization was used in 6 stud-

ies,8,10,20-23 and 4 of the types8,10,20,21 were included in proto-

cols with many interventions. The 2 studies22,23 in which

mobilization was not part of a protocol were conducted

in medical ICU patients receiving mechanical ventilation,

and the results showed benefits for all outcomes evaluated.

The onus then switches to the development of a

nonpharmacological protocol to prevent delirium, but

the ideal protocol has not yet been developed. One start-

ing point would be to use the known risk factors for

delirium and target interventions to patients who have

these risk factors. This strategy was used by Inouye et al,9

who created a standardized protocol to combat 6 risk

factors: cognitive impairment, sleep deprivation, immo-

bility, visual impairment, auditory impairment, and

dehydration. The observational PRE-DELIRIC (PREdic-

tion of DELIRium in ICu patients) study27 was done in


Outcomes

No difference in rate of delirium8.7% reduction in ICDSC score = 08.4% reduction in subsyndromal deliriumNo difference in LOS (patients with delirium)

No difference between environmentsDay 3 median day of onset0.6-day reduction in ICU LOS

5% increase in delirium-free or coma-free days20% reduction in incidence of delirium or comaNo difference in ICU mortalityNo difference in ICU LOS

13.5% reduction in incidenceMean onset on day 2Delirium increased ICU LOS by 2 days

2-day reduction in ICU delirium days24% decrease in ICU time with delirium13% decrease in hospital days with delirium

8% reduction in days delirious32% increase in days not delirious24% decrease in days unable to assess

2-point reduction on NEECHAM score25% reduction when delirium and mild confusion

grouped together

Comments

Hospital does not provide cardiac surgery or trauma careNurses could give haldoperidol if ICDSC score > 3No difference in antipsychotic administered

Same anesthetic used63.9% underwent CABG, 71.7% men6.2% delirium in < 65-year-olds vs 21.4% in > 65-year-oldsBaseline characteristics very different

Primary outcome delirium-coma combination according toCAM/RASS

Delirium secondary outcomeCompared ICU with post-ICUPrimarily respiratory failure patientsPrimary outcome of sleep quality: no difference

Used research nursesStandardized sedation protocolAll treatment haloperidol or olanzapineMedical ICU significantly higher rates of deliriumMidazolam use hazard ratio of 2.145

All patients received mechanical ventilationLess than 10% of patients in medical ICU includedDelirium a secondary outcome

Inclusion was mechanical ventilation ≥ 4 daysRoutine delirium screening not part of standard care before

project startedNo delirium assessments on 15 (pre) and 28 (post) patient days

NEECHAM scorer blinded to use of ear plugsLowest NEECHAM score used for calculation of incidence

Antipsychotic use

Yes

Not reported

Yes

Yes

Yes

Not reported

Not reported

an ICU, and multivariate logistic regression analysis

indicated that 10 of the 25 risk factors evaluated were

predictive of delirium. Unfortunately, the majority of

the predictors, such as age and scores on the Acute

Physiology and Chronic Health Evaluation II, were

characteristics

that could not

be altered by

use of a

nonpharmaco-

logical inter-

vention. Although creation of a protocol based on risk

factors is an excellent starting point, efforts must be

directed toward modifiable health care–associated

exposures and not nonmodifiable susceptibilities.

Protocols with many interventions would be needed

in order to include the many risk factors for delirium

identified through the literature and to combat each fac-

tor appropriately. Marcantonio et al8 attempted to devise

such a protocol. They developed a geriatric consultation

that encompassed 10 modules with at least 2 recommen-

dations to be made for each module. Collectively, 31

recommendations potentially could have been used.

Implementation of the appropriate recommendations

for each patient resulted in one of the largest reductions

in both incidence and severity of delirium. Vidán et al10

also used a multicomponent intervention and had results

similar to those of Marcantonio et al.8 The inevitable

follow-up question becomes, Is a certain aspect of these

multicomponent interventions leading to the positive

results, and, if so, what aspect?

The importance of a protocol that includes multiple

interventions is evident when the outcomes of studies with

2 or fewer interventions7,11,12,14-16,18,19,22-24 are compared with

the outcomes of studies with many interventions.8-10,13,20,21

For incidence of delirium, the multi-interventional pro-

tocols resulted in a 15.9% mean reduction, whereas those

with 2 or fewer interventions showed an 11% reduction.

The 11% reduction is slightly misleading because 4 of the

11 studies7,11,18,19 with 2 or fewer interventions did not


Implementation of the appropriate recommendations for each patientresulted in one of the largest reductionsin both incidence and severity of delirium.

Table 3 Interventions showing benefita

a Key: X, trial in patients who were not critically ill; #, trial in critically ill patients.

Refe

renc

e

Nurs

ing

educ

atio

n

Visu

al d

ispl

ays

Hydr

atio

n

Dent

ures

Nutri

tion

Mob

ility

Eye

prot

ocol

Hear

ing

prot

ocol

Cloc

k

Cale

ndar

Fam

ily

Reor

ient

atio

n

Mus

ic

Daily

sch

edul

e

Cogn

itive

stim

ulat

ion

War

m d

rink

Back

mas

sage

Ligh

t the

rapy

Nois

e re

duct

ion

Med

icat

ion/

proc

edur

e re

sche

dule

Adap

tive

equi

pmen

t

Cath

eter

rem

oval

Avoi

danc

e of

rest

rain

ts

Open

blin

ds

Min

imiza

tion

of c

affe

ine

befo

re b

ed

Eye

mas

k

Dim

hal

lway

s at

nig

ht

7 X X8 X X X X X X X X X18 # # #9 X X X X X X X X X X X X X10 X X X X X X X X X X X X X20 # # # # # # #21 # # # # # #22 #23 # #12 X13 X X X X X X14 X15 X24 #16 X

indicate any difference in the incidence of delirium,

whereas all 6 of the multi-interventional studies8-10,13,20,21

indicated a reduction in incidence of at least 5.1%.

Another strategy, included in 6 studies,7,10-12,18,23 was

extensive education of nurses. The specifics of the educa-

tion were typically not reported, but the material tended

to focus on the effects of delirium, screening for delirium,

and, at times, implementation of the investigators’ pro-

tocol. This strategy was used as the sole intervention in

2 studies.11,12 Milisen et al7 used education of nurses and

prominent display of educational material, both of which

resulted in no difference in the incidence of delirium or

the LOS, but a positive reduction in both the duration

and the severity of delirium. Tabet et al12 concentrated

on an education-only strategy for both nurses and

physicians and reported a 9.7% reduction in the point-

prevalence of delirium. However, the investigators used

the Delirium Rating Scale, a screening tool that is not

recommended in the guidelines6 of the American College

of Critical Care Medicine. Whether or not the results

would be the same if either the Intensive Care Delirium

Screening Checklist or the CAM-ICU were used is not

clear. Last, Lundström et al11 used a similar strategy but

also included a reorganization of the nursing staff. These

investigators noted no difference in the prevalence of

delirium at 24 or 72 hours. Patients in the study were

tested for delirium by using the DSM-IV on hospital days

1, 3, and 7. Because the DSM-IV is a set of diagnostic

criteria and not a delirium screening tool, whether or

not these results can reliably be compared with the

results of other studies in which screening for delirium

was used is unclear.12

We would be remiss if we did not address the notion

that perhaps the best protocol simply involves high-level

nursing care. Most of the unique interventions used in

the studies reviewed could be easily incorporated into

everyday nursing for every patient regardless of the

patient’s risk factors for delirium. Notable exceptions

would be early mobility, nutrition, and catheter removal.

An inability to determine if certain aspects of a newly

implemented protocol were already routine nursing

practice before the protocols were implemented is a lim-

itation of most published studies of nonpharmacological

interventions. Unfortunately, a study that could indicate

a true level of the benefit of each intervention would not

be feasible, because such a study would require nurses

to stop providing standard care. Additionally, any future

studies must include use of a standardized screening

tool, preferably either the CAM-ICU or the Intensive

Care Delirium Screening Checklist, to allow accurate

interpretation of the impact of any future interventions

or protocol.

Implications for Critical Care NursesAlthough we reviewed of studies of both critically ill

and non–critically ill patients, we think that a variety of

interventions that benefit patients who are not critically

ill would still be useful in an ICU. The evidence shows

that targeting interventions to prevent or treat known

risk factors for delirium have the greatest benefit (eg,

cognitive stimulation, reorientation), and a great deal

of overlap exists between risk factors for both critically

and non–critically ill patients. A wide variety of patients

are treated in ICUs, and the variety of specialized ICUs

can be as unique as the patients treated within the units.

For these reasons, strong consideration should be given

to having ICUs implement nonpharmacological inter-

ventions that have been beneficial for patients who were

not critically ill.

Multicomponent intervention protocols to combat

delirium have proved beneficial. On the basis of guideline

recommendations and the strength of literature, these

protocols should include early mobilization, education

of nurses, and cognitive stimulation with reorientation.

Depending on the severity of a patient’s illness, a variety

of ways can

be used to

accomplish

early mobi-

lization.

Mobilization can be as complete as full physical or occu-

pational therapy treatments or merely passive range-of-

motion exercises. Bedside nurses and other members of

the medical team work together to decide the level of

mobilization a patient can complete. Additionally, nurses

can advocate for removal of tubes, catheters, or restraints

that may prevent early mobilization.

Second, education of nurses is an essential component

of the success of any new intervention or initiative. The

literature describes a variety of strategies for educating

nurses, including didactic lectures, visual displays, and

one-on-one sessions. In order to include the potentially

large number of nurses who need to be educated, educa-

tion should be directed at all types of learners.28,29 Last,


All studies that included mobilization, noise-reduction, or sleep protocols displayeda benefit in the reduction of delirium.

cognitive stimulation and reorientation is a rather broad

term that allows each nurse to develop a strategy that

works for him or her. Still, each nurse’s intervention

should incorporate a few key components, such as

determining how the patient would like to be addressed,

frequent reorientation to date and time, providing updates

on the patient’s schedule and clinical status, and convers-

ing with the patient in a manner that requires memory

recall by the patient.

The implementation of a new intervention or initiative

is often met with resistance to change. In order to mini-

mize this resistance, obtaining nurses’ acceptance of and

willingness to support the change becomes imperative.

One strategy to eliminate high levels of resistance is to

educate nurses about the dangers and implications of

the development of delirium while stressing that patients

become increasingly difficult to care for once delirium

occurs. Another frequent reason for resistance is an

overall lack

of time during

the nursing

shift to add

additional

tasks to be completed; however, most interventions we

have mentioned in this review could be worked into a

nurse-implemented protocol that would require no more

than 5 to 10 minutes per nursing shift to accomplish.

Assembling a multidisciplinary team (physician, nurse,

pharmacist, and respiratory therapist) to determine

which nonpharmacological interventions are feasible

within each specific unit is important. Ultimately the

success of a nonpharmacological protocol to prevent

delirium lies with the bedside nurses, who have the

most frequent contact with patients.

ConclusionUse of nonpharmacological interventions is essential

for the prevention of delirium. These interventions can

be a low-risk, low-cost strategy that has shown a benefit

in most studies. Nonpharmacological therapy also has

the potential to decrease the off-label use of antipsychotics

for the treatment of delirium. The largest challenge in

developing a nonpharmacological protocol is determin-

ing what interventions to include. Although a “one-size-

fits-all” protocol may not be available, a strong body of

evidence supports the inclusion of education of the med-

ical team, reorientation with cognitive stimulation, and

early mobility in any protocol created. ICU staff should

assemble a multidisciplinary team to review interven-

tions of known benefit to determine which ones can be

implemented within the staff ’s specific unit. CCN


References1. Salluh JI, Soares M, Teles JM, et al; Delirium Epidemiology in Critical

Care Study Group. Delirium epidemiology in critical care (DECCA): an international study. Crit Care. 2010;14(6):R210. doi:10.1186/cc9333.

2. Pun BT, Ely EW. The importance of diagnosing and managing ICUdelirium. Chest. 2007;132(2):624-636.

3. Ely EW, Shintani A, Truman B, et al. Delirium as a predictor of mortal-ity in mechanically ventilated patients in the intensive care unit. JAMA.2004;291(14):1753-1762.

4. Siddiqi N, House AO, Holmes JD. Occurrence and outcome of deliriumin medical in-patients: a systematic literature review. Age Ageing. 2006;35(4):350-364.

5. Balas MC, Rice M, Chaperon C, Smith H, Disbot M, Fuchs B. Managementof delirium in critically ill older adults. Crit Care Nurse. 2012;32(4):15-26.

6. Barr J, Fraser GL, Puntillo K, et al; American College of Critical Care Med-icine. Clinical practice guidelines for the management of pain, agitation,and delirium in adult patients in the intensive care unit. Crit Care Med.2013;41(1):263-306.

7. Milisen K, Foreman MD, Abraham IL, et al. A nurse-led interdisciplinaryintervention program for delirium in elderly hip-fracture patients. J AmGeriatr Soc. 2001;49(5):523-532.

8. Marcantonio ER, Flacker JM, Wright RJ, Resnick NM. Reducing deliriumafter hip fracture: a randomized trial. J Am Geriatr Soc. 2001;49(5):516-522.

9. Inouye SK, Bogardus ST Jr, Charpentier PA, et al. A multicomponentintervention to prevent delirium in hospitalized older adults. N Engl JMed. 1999;340(9):669-676.

10. Vidán MT, Sánchez E, Alonso M, Montero B, Ortiz J, Serra JA. An inter-vention integrated into daily clinical practice reduces the incidence ofdelirium during hospitalization in elderly patients. J Am Geriatr Soc.2009;57(11):2029-2036.

11. Lundström M, Edlund A, Karlsson S, Brännström B, Bucht G,Gustafson Y. A multifactorial intervention program reduces the dura-tion of delirium, length of hospitalization, and mortality in deliriouspatients. J Am Geriatr Soc. 2005;53(4):622-628.

12. Tabet N, Hudson S, Sweeney V, et al. An educational intervention canprevent delirium on acute medical wards. Age Ageing. 2005;34(2):152-156.

13. Caplan GA, Harper EL. Recruitment of volunteers to improve vitality inthe elderly: the REVIVE study. Intern Med J. 2007;37(2):95-100.

14. Ono H, Taguchi T, Kido Y, Fujino Y, Doki Y. The usefulness of brightlight therapy for patients after oesophagectomy. Intensive Crit Care Nurs.2011;27(3):158-166.

15. Taguchi T, Yano M, Kido Y. Influence of bright light therapy on postop-erative patients: a pilot study. Intensive Crit Care Nurs. 2007;23(5):289-297.

16. McCaffrey R. The effect of music on acute confusion in older adultsafter hip or knee surgery. Appl Nurs Res. 2009;22:107-112.

17. Khan BA, Zawahiri M, Campbell NL, et al. Delirium in hospitalizedpatients: implications of current evidence on clinical practice and futureavenues for research—a systematic evidence review. J Hosp Med. 2012;7(7):580-589.


Multicomponent protocols targetingknown risk factors for delirium appear tohave benefits over single interventions.


To learn more about caring for patients with delirium, read“Impact of a Delirium Screening Tool and Multifaceted Educationon Nurses’ Knowledge of Delirium and Ability to Evaluate It Correctly” by Gesin et al in the American Journal of Critical Care,January 2012;21:e1-e11. Available at www.ajcconline.org.

18. Skrobik Y, Ahern S, Leblanc M, Marquis F, Awissi DK, Kavanagh BP.Protocolized intensive care unit management of analgesia, sedation,and delirium improves analgesia and subsyndromal delirium rates[published correction appears in Anesth Analg. 2012;115(1):169]. AnesthAnalg. 2010;111(2):451-463.

19. Arenson BG, MacDonald LA, Grocott HP, Heibert BM, Arora RC. Effectof intensive care unit environment on in-hospital delirium after cardiacsurgery. J Thorac Cardiovasc Surg. 2013;146(1):172-178.

20. Kamdar BB, Yang J, King LM, et al. Developing, implementing, andevaluating a multifaceted quality improvement intervention to promotesleep in an ICU. Am J Med Qual. 2014;29(6):546-554.

21. Colombo R, Corona A, Praga F, et al. A reorientation strategy for reducingdelirium in the critically ill: results of an interventional study. MinervaAnestesiol. 2012;78(9):1026-1033.

22. Schweickert WD, Pohlman MC, Pohlman AS, et al. Early physical andoccupational therapy in mechanically ventilated, critically ill patients: arandomised controlled trial. Lancet. 2009;373(9678):1874-1882.

23. Needham DM, Korupolu R, Zanni JM, et al. Early physical medicineand rehabilitation for patients with acute respiratory failure: a qualityimprovement project. Arch Phys Med Rehabil. 2010;91(4):536-542.

24. Van Rompaey B, Elseviers MM, Van Drom W, Fromont V, Jorens PG.

The effect of earplugs during the night on the onset of delirium andsleep perception: a randomized controlled trial in intensive care patients.Crit Care. 2012;16(3):R73.

25. Wang W, Li HL, Wang DX, et al. Haloperidol prophylaxis decreasesdelirium incidence in elderly patients after noncardiac surgery: a ran-domized controlled trial. Crit Care Med. 2012;40(3):731-739.

26. Page VJ, Ely EW, Gates S, et al. Effect of intravenous haloperidol on theduration of delirium and coma in critically ill patients (Hope-ICU): arandomised, double-blind, placebo-controlled trial. Lancet Respir Med.2013;1(7):515-523.

27. van den Boogaard M, Pickkers P, Slooter AJ, et al. Development and val-idation of PRE-DELIRIC (PREdiction of DELIRium in ICu patients)delirium prediction model for intensive care patients: observationalmulticentre study. BMJ. 2012;344:e420.

28. Devlin JW, Marquis F, Riker RR, et al. Combined didactic and scenario-based education improves the ability of intensive care unit staff to recog-nize delirium at the bedside. Crit Care. 2008;12(1):R19.

29. Gesin G, Russell BB, Lin AP, Norton HJ, Evans SL, Devlin JW. Impact ofa delirium screening tool and multifaceted education on nurses’ knowl-edge of delirium and ability to evaluate it correctly. Am J Crit Care. 2012;21(1):e1-e11.


CCN Fast Facts

Nonpharmacological Interventions to Prevent Delirium: An Evidence-Based Systematic Review

CriticalCareNurseThe journal for high acuity, progressive, and critical care nursing

patient can complete. Additionally, nurses can advo-

cate for removal of tubes, catheters, or restraints that

may prevent early mobilization.

• Education of nurses is an essential component of the

success of any new intervention. In order to include

the potentially large number of nurses who need to

be educated, education should be directed at all

types of learners.

• Cognitive stimulation and reorientation is a broad

term that allows each nurse to develop an individual

strategy. Still, each nurse’s intervention should

incorporate a few key components, such as deter-

mining how the patient would like to be addressed,

frequent reorientation to date and time, providing

updates on the patient’s schedule and clinical status,

and conversing with the patient in a manner that

requires memory recall by the patient.

• Obtaining nurses’ acceptance of and willingness to

support the new intervention is imperative.

• One reason for resistance is a lack of time during the

nursing shift to add additional tasks. Assembling a

multidisciplinary team (physician, nurse, pharma-

cist, respiratory therapist) to determine which non-

pharmacological interventions are feasible within

each specific unit is important.

• Ultimately the success of a nonpharmacological protocol

to prevent delirium lies with the bedside nurses, who

have the most frequent contact with patients. CCN

FactsDevelopment of delirium in critical care patients is

associated with increased length of stay, hospital costs,

and mortality. The pain, agitation, and delirium guide-

lines of the American College of Critical Care Medicine

provide the strongest level of recommendation for the

use of nonpharmacological approaches to prevent

delirium, but questions remain about which nonphar-

macological interventions are beneficial.

• Prevention is the optimal strategy, especially

when effective treatment options are unavailable.

Haloperidol has been studied for prevention and

treatment of intensive care unit (ICU) delirium,

but the results have been inconclusive.

• A variety of interventions that benefit patients

who are not critically ill would still be useful in

an ICU. The evidence shows that targeting inter-

ventions to prevent or treat known risk factors

for delirium have the greatest benefit (eg, cogni-

tive stimulation, reorientation), and a great deal

of overlap exists between risk factors for both

critically and non–critically ill patients.

• Multicomponent intervention protocols to

combat delirium have proved beneficial. These

protocols should include early mobilization,

education of nurses, and cognitive stimulation

with reorientation.

• Mobilization can be as complete as full physical

or occupational therapy treatments or merely

passive range-of-motion exercises. Bedside nurses

and other members of the medical team work

together to decide the level of mobilization a

Rivosecchi RM, Smithburger PL, Svec S, Campbell S, Kane-Gill SL. Nonpharmacological Interventions to Prevent Delirium: An Evidence-Based Systematic Review.Critical Care Nurse. 2015;35(1):39-51.


CNE Test Test ID C1512: Nonpharmacological Interventions to Prevent Delirium: An Evidence-Based Systematic ReviewLearning objectives: 1. Describe the nursing literature on nonpharmacological interventions to prevent delirium 2. Discuss nonpharmacological interven-tions that have been shown to be effective in preventing delirium 3. Explain the tools developed for the measurement of delirium in intensive care unit patients







7. Which of the following is the nonpharmacological intervention specificallydiscussed in the pain, agitation, and delirium guidelines of the AmericanCollege of Critical Care Medicine?a. Music therapyb. Reorientationc. Nursing educationd. Early mobilization

8. Which of the following is used to allow accurate interpretation of theimpact of future interventions to reduce delirium?a. Biostatisticsb. Multiple regression analysisc. Bonferroni multiple comparison testd. Standardized screening tool

9. The evidence-based literature supports which of the following nonphar-macological interventions to combat delirium?a. Nursing education, mobility, and cognitive stimulation with reorientationb. Nursing education, mobility, and art therapyc. Mobility, cognitive stimulation with reorientation, and art therapyd. Mobility, exercise therapy, and cognitive stimulation with reorientation

10. Which of the following nonpharmacological interventions allows eachnurse to develop a strategy that works for him or her?a. Mobilizationb. Nursing educationc. Cognitive stimulation and reorientationd. Music therapy

11. Which of the following is a strategy for educating nurses about non-pharmacological interventions that help reduce delirium?a. Visual displaysb. Case study analysisc. Excel spread sheetd. PowerPoint self-learning modules

12. Which of the following is essential for the prevention of delirium?a. Pharmacological therapyb. Nonpharmacological interventionsc. Occupational therapyd. Speech therapy




Test ID: C1512 Form expires: February 1, 2018 Contact hours: 1.0 Pharma hours: 0.0 Fee: AACN members, $0; nonmembers, $10 Passing score: 9 correct (75%) Synergy CERP Category A Test writer: Lynn C. Simko, PhD, RN, CCRN

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Signature




1. �a �b �c �d

12. �a �b �c �d

11. �a �b �c �d

10. �a �b �c �d

9. �a �b �c �d

8. �a �b �c �d

7. �a �b �c �d

6. �a �b �c �d

5. �a �b �c �d

4. �a �b �c �d

3. �a �b �c �d

2. �a �b �c �d

1. The highest prevalence of delirium occurs in which of the followingpatient populations?a. Nursing home patientsb. Critically ill patientsc. General medicine patientsd. Perioperative patients

2. Exclusion criteria of the research described in this manuscript includewhich of the following?a. Not original researchb. Delirium measured as an outcomec. Screening for delirium using a standardized screening toold. Incidence or severity of delirium was an outcome measure

3. Excluding any manuscripts involved with pharmaceuticals was necessaryto evaluate the true benefit of a nonpharmacological protocol and to minimizewhich of the following?a. Validity and reliability issuesb. Hierarchies of evidencec. Confounding variablesd. Cleaning and coding data

4. Which of the following tools was used most frequently in the deliriumresearch?a. Delirium Screening Scaleb. Neelon and Champagne Confusion Scalec. Intensive Care Delirium Screening Checklistd. Confusion Assessment Method for the Intensive Care Unit

5. In several studies, the duration of delirium decreased after the additionof which of the following?a. Nonpharmacological interventionsb. Pharamacological interventionsc. Haloperidold. Lorazepam

6. Which of the following factors were examined in outcomes related todelirium?a. Incidence, duration, and severityb. Decreasing length of stayc. Mobilityd. Reorientation

Heat stroke is a persistent problem among firefighters,1 athletes,2 and militarypersonnel,3 all of whom have occupations that require physical exertion inhumid or hot environments. Military occupations in particular involve physically

demanding tasks, such as carrying heavy loads for extended periods, often with

unpredictable rest periods.4 When protective equipment such as body armor is

worn, heat dissipation is further blocked.5 These extreme conditions place US military personnel

and the military nurses who care for them at risk for heat injuries.6

Heat stress is determined by environmental (ie, radiant and ambient temperature, air movement,

and humidity) and behavioral (eg, ergogenic agents, work intensity, and protective clothing) factors.7,8

Just a few of these risk factors combined can quickly lead to an exertional heat injury. The less severe

conditions can be treated on site with the person resuming normal activities the same day. Conversely,

exertional heat stroke (EHS) is a life-threatening emergency, and rapid cooling must be administered

immediately to ensure survival.9 The high incidence of heat illnesses3 in the US military might indicate

that rapid recognition of heat injury and use of sound clinical nursing practices are not being applied

consistently from ship to ship or unit to unit. Because EHS morbidity and mortality are preventable,

it is important that critical care nurses in the Navy and other branches of the military rapidly recognize

Exertional Heat Stroke inNavy and Marine Personnel:A Hot TopicCARL W. GOFORTH, RN, PhD, CCRN

JOSH B. KAZMAN, MS


Military Critical Care Nursing: Navy

Although exertional heat stroke is considered a preventable condition, this life-threatening emergency affects

hundreds of military personnel annually. Because heat stroke is preventable, it is important that Navy critical

care nurses rapidly recognize and treat heat stroke casualties. Combined intrinsic and extrinsic risk factors

can quickly lead to heat stroke if not recognized by deployed critical care nurses and other first responders.

In addition to initial critical care nursing interventions, such as establishing intravenous access, determining

body core temperature, and assessing hemodynamic status, aggressive cooling measures should be initiated

immediately. The most important determinant in heat stroke outcome is the amount of time that patients

sustain hyperthermia. Heat stroke survival approaches 100% when evidence-based cooling guidelines are fol-

lowed, but mortality from heat stroke is a significant risk when care is delayed. Navy critical care and other

military nurses should be aware of targeted assessments and cooling interventions when heat stroke is sus-

pected during military operations. (Critical Care Nurse. 2015;35[1]:52-59)


and treat patients with potential EHS during military

operations. Previous military reviews have focused on

organizational practices and the onus of responsibility

for EHS up the chain of command.10 For critical care mil-

itary nurses, however, it is crucial to rapidly recognize

and treat heat stroke in the field. Therefore, the aim of

this column is to discuss the definition, risk factors,

treatment, and nursing implications of EHS.

Definition of Heat StrokeHeat stroke is a life-threatening emergency charac-

terized by a rapid increase in the body’s core temperature

(Tcore) to greater than 40°C (104°F), multiple organ dys-

function,9 and central nervous system abnormalities (eg,

delirium, confusion, agitation),11 with a mortality rate as

high as 18% in military populations.12 Exertional heat

stroke, especially when combined with strenuous activity,

can occur during exposure to hot or mild climates. Con-

versely, classic heat stroke occurs only in hot climates.

The heat injury spectrum is listed in Table 1.

Incidence of Exertional Heat StrokeEHS mortality is significant in athletes and certain

occupations, such as agricultural workers.14 Among

athletes, EHS is the third leading cause of mortality.15

Moreover, among athletes and military personnel, the

frequency of EHS continues to increase despite safety

measures.12,15-18 Despite knowledge of EHS risk factors,

the incidence of heat stroke or heat exhaustion in the

US military has not decreased in the past 5 years, esti-

mated in 2013 at 0.25 and 1.57 per 1000 person years,

respectively.3 Highly motivated individuals might be

tempted to ignore heat safety rules, especially during

Authors

Carl Goforth is the clinical subject matter expert for the Marine CorpsCombat Development Command located in Quantico, Virginia.He has more than 20 years of combined Navy and Marine serviceand has deployed as a critical care and flight nurse attached to USMarine units overseas.

Josh Kazman is a research associate with the Consortium for Healthand Military Performance at Uniformed Services University of theHealth Sciences. He has worked on a variety of projects and publi-cations related to health disparities, heat tolerance, cardiovasculardisease, and injury prevention.

Corresponding author: CDR Carl Goforth, Combat Development & Integration,HQMC, 3300 Russell Road, Quantico, VA 22134-5001 (e-mail: [email protected]).

To purchase electronic or print reprints, contact the American Association of Critical-Care Nurses, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or(949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].

Clinical condition

Heat syncope

Heat cramps

Heat exhaustion

Classic heat stroke

Exertional heat stroke

Core temperature

Normal

Normal or elevatedbut < 40°C (104°F)

37°C-40°C (98.6°F-104°F)

> 40°C (104°F)

> 40°C (104°F)

Related symptoms

Generalized weakness,syncope

Painful muscle contrac-tions (commonly in calf,quadriceps, or abdominalmuscles)

Fatigue, nausea, vomiting,headache

Heat exhaustion symptomspresent before mentalstatus changes

Heat exhaustion symptomspresent before mentalstatus changes

Related signs

Postural syncope with rapidrecovery once supine

Affected muscles are stiffand tender to palpation

Flushed, profuse sweatingwith or without clammyskin, normal mental status

Hot skin with or withoutsweating, mental statuschanges (disorientation,ataxia, loss of conscious-ness); can develop slowlyover several days

Hot skin with or withoutsweating, mental statuschanges (disorientation,ataxia, loss of conscious-ness); rapid onset

Definitiona

Dizziness or fainting in a hotenvironment due to pos-tural blood pooling in lowerextremities

Painful muscle spasms during exercise in the heat

Diminished physical activityin the heat due to cardio-vascular compromise

Severe hyperthermia primarilydue to heat exposure

Severe hyperthermia primarilydue to strenuous exercise

Table 1 Heat-related illness criteria

a Definitions from Pryor et al9 and Epstein and Roberts.13


dangerous operations, placing them at even greater risk

of EHS.10 Military units’ awareness of heat injury is also

important. One military unit or ship might place greater

emphasis on work/rest cycles, environmental monitor-

ing, and so on than another unit.

Risk FactorsRecognizing inherent risk factors can help Navy criti-

cal care nurses make informed clinical decisions during

training and deployments. Additionally, US Navy medical

missions, such as

disaster response,

usually include the

care of diverse, vul-

nerable popula-

tions, such as the young and the elderly.19 EHS risk factors

(Table 2) are commonly classified into 1 of 2 areas:

intrinsic (related to the individual) and extrinsic (envi-

ronmental, task-related, or contextual).

Intrinsic Risk FactorsIn addition to a history of heat illness, intrinsic risk

factors can range from sickle cell trait to high motiva-

tion.6,16,22,23 Military training includes the indoctrination

of military culture, such as “mission first,” which can

lead motivated persons to ignore important physiologi-

cal warning signs. Other data from the US military show

that overweight military personnel have a higher risk

for sustaining heat injuries.22 Low aerobic fitness has

been cited as a predisposing factor for EHS.24 Poorly

conditioned athletes must work harder to keep up with

fit teammates and thus may ignore warning signs such

as dehydration, tachycardia, or sweating cessation.

Numerous classes of medications have also been impli-

cated in heat stroke (Table 3).

The mechanism by which common medications

contribute to heat stroke depends on the class of drug.

Anticholinergics (antihistamines, antidepressants, or

antipsychotics) decrease production of sweat.11 Cardio-

vascular agents, such as antihypertensives or diuretics,

decrease the natural physiological responses to dehy-

dration and hyperthermia.25 Of special concern to

young, healthy populations is the recent increase in

use of dietary supplements.

Recent publications indicate that US Marines are

among the highest military users of dietary supplements.26

Ergogenic stimulants, such as amphetamines or ephedra,

increase heat production. Ephedra, from the Chinese plant

ma-huang,27 along with 1,3-dimethylamyamine (DMAA),

is associated with serious heat injury in athletes28,29 and

with EHS30 and death31 in the military. Although the exact

mechanism underlying heat injury in many ergogenic

aids is not fully characterized, published reports clearly

Table 2 Risk factors for heat illnessa

Intrinsic (internal) factors

History of heat-related event

Age (< 15 or > 65 years)

Alcohol consumption

Existing medical conditions (ie, respiratory, hematologic,or cardiovascular)

Dehydration

Sleep deprivation

Medications or supplements

Obesity

Overmotivation

Inadequate acclimatization, pooraerobic conditioning, or both

Recent illness

Sickle cell trait

Extrinsic (environmental) factors

Level of exertion

Excess clothing or protectiveequipment

Lack of water

Temperature (ambient)

Humidity

Wet bulb globe temperature

a Based on information from Armstrong et al,2 Epstein et al,10 Casa et al,17

Glahn et al,20 and Wallace et al.21

Table 3 Medications implicated in exertional heat illnessa

Effect

Reduces rate of sweating

Alters skin blood flow

Lowers cardiac contractility

Increases heat production(ergogenic), hypothalamic setpoint, or both

Type of medication

AntihistaminesAnticholinergics

Calcium channel blockersFemale reproductive hormonesCapsaicin

β-Blocking medicationsCalcium channel blockers

SympathomimeticsAmphetaminesEphedra1,3-dimethylamyamine(sympathomimetic properties)

Salicylates (supratherapeuticdoses)

a Based on information from Howe and Boden,11 Seto et al,25 Kao et al,26 Lee,27

Lopez and Casa,28 Fink et al,29 Oh et al,30 and Eliason et al.31


Exertional heat stroke develops as aresult of many complex factors andcan vary from person to person.

indicate that US Navy and other critical care nurses should

screen EHS patients for recently used medications or

ingestion of dietary supplement.

Extrinsic Risk FactorsProfessions in the US Armed Forces are particularly

hazardous, with constant exposure to strenuous physical

exertion and climate extremes. For instance, summer

temperatures in Afghanistan routinely reach 51°C (124°F).32

During military operations, personnel perform tasks while

wearing body armor, which weighs a mean of 12.3 kg

(27 lbs),33 often without sufficient rest. Because of the

nature of military operations, these factors are difficult to

modify and might place military personnel in scenarios

that exceed their physical capacity. Therefore, these indi-

viduals are at increased risk when subjected to individual

and environmental factors that predispose them to EHS.

It is clear from the evidence that EHS develops as a

result of many complex factors and can vary from per-

son to person. However, hyperthermia is always the

common denominator underlying any risk factor.6

HyperthermiaHyperthermia is an increase in Tcore above the body’s

natural set point.6 Human homeostasis requires a narrow

operating temperature around 37°C.34 To accomplish this,

a thermoregulatory system composed of compensatory

and noncompensatory systems communicate together for

thermoregulation when Tcore fluctuates.35 During strenu-

ous physical activity, body temperature increases in

healthy persons, but as metabolic processes and/or envi-

ronmental conditions exceed cardiovascular and central

nervous system compensation, hyperthermia (Tcore >

40°C) ensues13 and the risk of EHS increases.10

Temperatures as high as 46.5°C (116°F) have been

reported in patients who have recovered from heat stroke,36

but survival at such an extreme Tcore is rare. The severity

of tissue injury due to hyperthermia depends on the crit-

ical thermal maximum,37 defined as the maximum inten-

sity and duration of tissue heating before cellular death

occurs.38 At extreme core temperatures, thermoregulatory

mechanisms are overwhelmed, cellular proteins begin

denaturing, and apoptosis (programmed cellular death)

can occur within 5 minutes.39,40 Failure to promptly rec-

ognize and treat hyperthermia can lead to EHS within

minutes, a life-threatening medical emergency. The inte-

grated effects of hyperthermia leading to derangement

of the central nervous system and multiorgan dysfunc-

tion are typical of EHS (Figure 1). More extensive reviews

are available.13

Clinical ManagementThe extent and severity of EHS might not be read-

ily apparent in the chaos of military operations.

Because mild forms of heat illness, if not recognized,

might rapidly progress to EHS, immediate evaluation

is necessary to assess the severity of symptoms and, if

needed, to initiate cooling rapidly. When cooling is

provided immediately, survival is near 100%.18 Reduc-

ing Tcore to less than 40.5°C in less than 30 minutes is

the current recommendation.9

Supportive InterventionsThe initial priorities most relevant to EHS are

hemodynamic status, Tcore, and mental status. Upon

presentation of EHS, critical care nursing staff must

assess and stabilize vital signs, correctly recognize

signs and symptoms of EHS, and begin cooling. The

hallmark of EHS is altered function of the central

nervous system, such as confusion and combativeness.

Nursing management for EHS starts with assessing air-

way, breathing,

and circulation

(ABCs). Baseline

consciousness

should also be

immediately established, along with an initial score on

the Glasgow Coma Scale. Additional assessments

include, when possible, medical history, medications,

and/or dietary supplements used, body temperature at

admission and maximum known temperature, clinical

features apparent at admission, and vital signs. Critical

care nursing interventions also include advanced

hemodynamic monitoring and initiating fluid resuscita-

tion with crystalloid intravenous solutions per the insti-

tution’s protocol, preferably chilled (4°C) 0.9% sodium

chloride solution.41 Lactated Ringer solution is not

used, because liver function can be suppressed by over-

heated tissues, leading to unmetabolized lactate and

worsening lactic acidosis.20 Numerous studies42-44 have

demonstrated that axillary, aural (tympanic), oral, and

skin temperatures often indicate a falsely low Tcore,

especially after intense exercise in the heat. Rectal tem-

perature remains the reference standard for assessment

Central nervous system abnormalitiessuch as confusion and agitation oftenare the first signs of heat stroke.


of Tcore in a potential EHS patient and the end point is

a Tcore less than 39°C (102°F).

CoolingOnce hyperthermia is confirmed by rectal temperature,

or if a high suspicion of hyperthermia exists while one is

waiting for positive confirmation, cooling measures should

begin without delay. Effective heat dissipation relies on

the rapid transfer of heat from the body’s core to the skin

and from the skin to the environment.9

The most important determinant in an EHS out-

come is the amount of time that patients’ core body

temperature is above the threshold (38.6°C) for cellular

damage.45 Reducing the Tcore to less than 40°C within

30 minutes or less is critical.6 When in doubt, the maxim

“cool first, transport second” should be employed to ensure

rapid treatment.

The fastest way to decrease Tcore is to remove restrictive

clothing and equipment and immerse the body (trunk

and extremities) in a pool or tub of cold water (approxi-

mately 1°C-14°C, or 35°F-57.2°F).46 Once the patient is

immersed in cold water, aggressive stirring or continu-

ous water motion will replace warmed water at the skin

with cold water. Additionally, wrapping a cold, wet towel

Figure 1 The event sequence leading to heat stroke and death from the compensatory to the uncompensable phase. Physicalactivity, especially during hot conditions, initiates a “compensable” thermoregulatory response (above the dashed horizontal line).When individual ability to compensate is surpassed, central venous pressure decreases, core temperature increases leading tothermoregulatory failure if prompt treatment is not initiated. This thermoregulatory failure triggers cellular death, intracellularimbalance (energy depletion), and circulatory failure. The multiple body system failures, if not immediately treated, lead to death.

Abbreviations: ATP, adenosine triphosphate; CNS, central nervous system; DIC, dissemiated intravascular coagulation.

Adapted with permission from Epstein and Roberts,13 ©2011, John Wiley and Sons A/S.

Com

pens

ator

yNo

ncom

pens

ator

yIntrinsic factors

Sweat

Hypovolemia Central venous pressure decreases

Core temperature increase

Systemic inflammation

Blood brain barrier breakdown

CNS derangement

ATP depletion

Cellular anoxia

*Liver dysfunction*Renal failure*Coagulopathy (DIC)*Cardiac dysrythmia*Myoglobin release*Intestinal permeability

Circulatory collapse

Increased metabolic rate


Cardiac output increase

Extrinsic factors

Heat stroke

Death

Heat stress



around the top of the head will enhance rapid cooling

further.45 It is recognized that cold water is not always

available in remote areas. One alternative, when resources

are limited, is to douse the victim with immediately

available water. This method can reach a cooling rate of

0.1°C to 0.2°C per minute.47 Cooling rates for the most

common cooling methods are presented in Figure 2.9

Civilian Nursing ImplicationsHeat exposure is one of the most deadly natural

hazards in the United States. The Centers for Disease

Control and Prevention48 estimates that between 1992

and 2006, heat stroke claimed the lives of 423 Americans,

more than hurricanes, lightning, floods, tornados, and

earthquakes combined. These injuries require aggressive

clinical treatments consisting of rapid cooling and sup-

portive nursing care, such as fluid resuscitation to preserve

organ function. Therefore, although this article is focused

on Navy critical care nursing, the concepts of rapid recog-

nition and cooling are universal and apply to any critical

care nurse caring for a heat stroke victim.

ConclusionEHS requiring critical care nursing intervention rep-

resents a substantial risk of morbidity and mortality to

Navy and Marine Corps personnel. With military EHS

rates at high levels despite scientific advances, never

before has it been so clinically important to recognize

and rapidly treat potential EHS casualties. EHS rates in

the Marine Corps, for instance, were more than 5 times

higher than the rates in other military branches in

2011.49 Data also suggest that military heat stroke sur-

vivors have twice the mortality risk from cardiovascular,

kidney, and liver failure within 30 years of initial hospi-

talization compared with military survivors of nonheat

injuries.21 According to the best evidence available, ice-

water or cold-water immersion is the most effective cool-

ing treatment and is recommended as the definitive

treatment.46 If this method is unavailable, case reports

demonstrate that continual water dousing combined

with fanning is a practical alternative until advanced treat-

ment is available. Practical resources for the implemen-

tation of EHS prevention and emergency procedures can

Figure 2 Relative cooling rates by heat stroke nursing intervention. Optimal cooling rates (> 0.155°C/min), acceptable coolingrate (> 0.079°C/min and < 0.154°C/min), or unacceptable cooling rates (< 0.078°C/min).

Abbreviation: IVF, intravenous fluids.Adapted with permission from Pryor et al,9 ©2013 with permission from Elsevier.

Mea

n co

olin

g ra

te, º

C/m

in

2ºC cold-water immersion

0.00

0.05

0.10

0.15

0.20

0.25

Unac

cept

able

Acce

ptab

leOp

timal

0.30

0.35

0.40

4ºC cooling blanket



Chilled IVF and water-room temperature immersion

Ice packs at major arteries

Gastric lavage

Ice-water immersion

IVF-room temperature, ice packs at major arteries

IVF-room temperature only


be found in multiple locations (Table 4). The evidence

underscores the need for prompt identification of poten-

tial EHS victims and aggressive cooling measures in the

field as key critical care nursing actions. CCN

AcknowledgmentsThe views expressed are those of the authors and do not reflect the officialpolicy or position of the US Marine Corps, the Uniformed Services Universityof the Health Sciences, the Department of Defense, or the US government.

Financial DisclosuresWork on this manuscript was funded by the Office of Naval Research, grantno. N0001411MP20023.

References1. Murakoshi M, Sekine M. Measures by local government—actions to

take in dealing with heat stroke for firefighters. Nihon Rinsho. 2012;70(6):1052-1056.

2. Armstrong LE, Johnson EC, Casa DJ, et al. The American football uniform:uncompensable heat stress and hyperthermic exhaustion. J Athl Train.2010;45(2):117-127.

3. Update: Heat Injuries, Active Component, US Armed Forces, 2012. MSMR.2013;20(3):17-20.

4. Simpson R, Gray S, Florida-James G. Physiological variables and perform-ance markers of serving soldiers from two “elite” units of the BritishArmy. J Sports Sci. 2006;24(6):597-604.

5. Chinevere T, Cadarette B, Goodman D, Ely B, Cheuvront S, Sawka M.Efficacy of body ventilation system for reducing strain in warm and hotclimates. Eur J Appl Physiol. 2008;103(3):307-314.

6. Casa D, Armstrong L, Kenny G, O’Connor F, Huggins R. exertional heatstroke: new concepts regarding cause and care. Curr Sports Med Rep.2012;11(3):115-123.

7. Epstein Y, Moran D. Thermal comfort and the heat stress indices. IndHealth. 2006;44(3):388-398.

8. Haller C, Benowitz N. Adverse cardiovascular and central nervous systemevents associated with dietary supplements containing ephedra alkaloids.N Engl J Med. 2000;343(25):1833-1838.

9. Pryor RR, Casa DJ, Holschen JC, O’Connor FG, Vandermark LW. Exertionalheat stroke: strategies for prevention and treatment from the sports fieldto the emergency department. Clin Pediatr Emerg Med. 2013;14(4):267-278.

10. Epstein Y, Druyan A, Heled Y. Heat injury prevention—a military per-spective. J Strength Cond Res. 2012;26:S82-S86.

11. Howe AS, Boden BP. Heat-related illness in athletes. Am J Sports Med.2007;35(8):1384-1395.

12. Carter R III, Cheuvront S, Williams J, et al. Epidemiology of hospitaliza-tions and deaths from heat illness in soldiers. Med Sci Sports Exerc. 2005;37(8):1338-1344.

13. Epstein Y, Roberts W. The pathopysiology of heat stroke: an integrative viewof the final common pathway. Scand J Med Sci Sports. 2011;21(6):742-748.

14. Centers for Disease Control. Heat-related deaths among crop workers—United States, 1992-2006. MMWR. 2008;57:649-653.

15. Stearns R, O’Connor F, Casa D, Kenny G. Exertional Heat Stroke. Sudbury,MA: Jones and Bartlett Learning, LLC; 2011.

16. Armstrong L, Casa D, Millard-Stafford M, Moran D, Pyne S, RobertsWO. American College of Sports Medicine position stand: exertionalheat illness during training and competition. Med Sci Sports Exerc. 2007;39(3):556-572.

17. Casa D, Almquist J, Anderson S. Inter-association task force on exertionalheat illnesses consensus statement. NATA News. 2003;6:24-29.

18. Casa D, Guskiewicz K, Anderson S, et al. National Athletic Trainers’Association position statement: preventing sudden death in sports. J Athl Train. 2012;47(1):96-118.

19. Faulk J, Hanly M. Tales From the Sea: Critical Care Nurses Serving Aboardthe USNS Comfort and USNS Mercy. Crit Care Nurse. 2013;33(4):61-67.

20. Glahn K, Ellis F, Halsall P, et al. Recognizing and managing a malignanthyperthermia crisis: guidelines from the European Malignant Hyperther-mia Group. Br J Anaesth. 2010;105(4):417-420.

21. Wallace RF, Kriebel D, Punnett L, Wegman DH, Amoroso PJ. Prior heatillness hospitalization and risk of early death. Environ Res. 2007;104(2):290-295.

22. Bedno S, Li Y, Han W, et al. Exertional heat illness among overweightUS Army recruits in basic training. Aviat Space Environ Med. 2010;81(2):107-111.

23. Carter R, Cheuvront S, Sawka M. Heat related illnesses. Sports Sci Exchange.2006;19(3):1-6.

24. Gardner JW, Kark JA, Karnei K, et al. Risk factors predicting exertionalheat illness in male Marine Corps recruits. Med Sci Sports Exerc. 1996;28(8):939-944.

Now that you’ve read the article, create or contribute to an online discussion aboutthis topic using eLetters. Just visit www.ccnonline.org and select the article youwant to comment on. In the full-text or PDF view of the article, click “Responses”in the middle column and then “Submit a response.”

To learn more about military critical care nursing, read “Tales Fromthe Sea: Critical Care Nurses Serving Aboard the USNS Comfortand USNS Mercy” by Faulk and Hanly in Critical Care Nurse,August 2013;33:61-67. Available at www.ccnonline.org.

Resource

Uniformed Services University, Consortiumfor Health and Military Performance

US Army Research Institute of Environmental Medicine

US Army Medical Department

American College of Sports Medicine

US Marine Corps Heat Injury PreventionProgram

Description

Clinical consultation for exertional heat illnessand related conditions such as exertional rhabdomyolysis

Army clinical and educational resources regardingheat physiology, acclimation, and related operational issues

Provides a link to Medical Aspects of Harsh Environments, Volume 1

Civilian guidelines and consensus regarding exertional heat illness

Marine Corps resource for the prevention of heatinjury guidance per MCO 6200.1E, includingacclimatization and work-rest cycles

Website

http://champ.usuhs.mil

http://www.usariem.army.mil

http://www.cs.amedd.army.mil

www.acsm.org

http://www.imef.marines.mil/portals/68/Docs/IMEF/Surgeon/MCO_6200.1E_W_CH_1_Heat_Injury_Prevention.pdf

Table 4 Military and civilian resources for exertional heat illness guidelines


25. Seto C, Way D, O’Connor N. Environmental illness in athletes. Clin SportsMed. 2005;24(3):695-718.

26. Kao T-C, Deuster PA, Burnett D, Stephens M. Health behaviors associatedwith use of body building, weight loss, and performance enhancingsupplements. Ann Epidemiol. 2012;22(5):331-339.

27. Lee M. The history of Ephedra (ma-huang). J R Coll Physicians Edinb.2011;41(1):78-84.

28. Lopez R, Casa D. The influence of nutritional ergogenic aids on exercise heattolerance and hydration status. Curr Sports Med Rep. 2009;8(4):192-199.

29. Fink E, Brandom BW, Torp KD. Heatstroke in the super-sized athlete.Pediatr Emerg Care. 2006;22(7):510-513.

30. Oh R, Henning J. Exertional heatstroke in an infantry soldier takingephedra-containing dietary supplements. Mil Med. 2003;168(6):429-430.

31. Eliason M, Eichner A, Cancio A, Bestervelt L, Adams B, Deuster P. Casereports: death of active duty soldiers following ingestion of dietary sup-plements containing 1, 3-dimethylamylamine (DMAA). Mil Med. 2012;177(12):1455-1459.

32. NOAA. Climate of Afghanistan. http://www.ncdc.noaa.gov/oa/climate/afghan/afghan-narrative.html. Accessed November 11, 2014.

33. Konitzer L, Fargo M, Brininger T, Lim Reed M. Association betweenback, neck, and upper extremity musculoskeletal pain and the individualbody armor. J Hand Ther. 2008;21(2):143-148.

34. Hall J. Guyton and Hall Textbook of Medical Physiology. 12th ed. Philadelphia,PA: Saunders: Elsevier; 2011.

35. Ha S, Talbott E, Kan H, Prins CA, Xu X. The effects of heat stress and itseffect modifiers on stroke hospitalizations in Allegheny County, Pennsyl-vania. Int Arch Occup Environ Health. 2014;87(5):557-565.

36. Ghaznawi H, Ibrahim M. Heat stroke and heat exhaustion in pilgrimsperforming the Haj (annual pilgrimage) in Saudi Arabia. Ann Saudi Med.1987;7(3):323-326.

37. Sherwood SC, Huber M. An adaptability limit to climate change due to

heat stress. Proc Natl Acad Sci U S A. 2010;107(21):9552-9555.38. Lutterschmidt WI, Hutchison VH. The critical thermal maximum: history

and critique. Can J Zool. 1997;75(10):1561-1574.39. Bouchama A, Knochel J. Heat stroke. N Engl J Med. 2002;346(25):1978-1988.40. Leon L, Helwig B. Heat stroke: role of the systemic inflammatory response.

J Appl Physiol. 2010;109(6):1980-1988.41. Badjatia N. Hyperthermia and fever control in brain injury. Crit Care Med.

2009;37(7):S250-S257.42. Casa DJ, Becker SM, Ganio MS, et al. Validity of devices that assess body

temperature during outdoor exercise in the heat. J Athl Train. 2007;42(3):333-342.

43. Ganio MS, Brown CM, Casa DJ, et al. Validity and reliability of devicesthat assess body temperature during indoor exercise in the heat. J AthlTrain. 2009;44(2):124-135.

44. Ronneberg K, Roberts W, McBean A, Center B. Temporal artery temper-ature measurements do not detect hyperthermic marathon runners.Med Sci Sports Exerc. 2008;40(8):1373-1375.

45. Gagnon D, Lemire BB, Casa DJ, Kenny GP. Cold-water immersion andthe treatment of hyperthermia: using 38.6ºC as a safe rectal temperaturecooling limit. J Athl Train. 2010;45(5):439-444.

46. McDermott BP, Casa DJ, Ganio MS, et al. Acute whole-body cooling forexercise-induced hyperthermia: a systematic review. J Athl Train. 2009;44(1):84-93.

47. Rav-Acha M, Hadad E, Epstein Y, Heled Y, Moran D. Fatal exertionalheat stroke: a case series. Am J Med Sci. 2004;328(2):84-87.

48. Centers for Disease Control and Prevention. Preventing heat-relatedillness or death of outdoor workers. Workplace Solutions. 2013. http://www.cdc.gov/niosh/docs/wp-solutions/2013-143/. Accessed November11, 2014.

49. Update: Heat injuries, active component, U.S. Armed Forces, 2011.MSMR. 2012;19(3):14-16.


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It is only fitting that the first neonate to be supported by extracorporeal membraneoxygenation (ECMO) was named Esperanza, which when translated from Spanishmeans hope.1 Indeed, to the more than 50 000 patients who have survived because of ECMO,

this revolutionary treatment has provided hope where there was none before.2 In the past 5

decades, the use of artificial oxygenation and perfusion has revolutionized the care of critically

ill patients, both in the operating room and in the intensive care unit. Use of artificial oxygenation and

perfusion has evolved from bypass during cardiac surgery to advanced life support, to complex extracorpo-

real cardiopulmonary resuscitation (ECPR). Within the past 20 years, ECPR has been initiated when

traditional resuscitation methods have failed and has proven its effectiveness with a survival to discharge

rate of approximately 40%.3-13 However, the appropriate use of this therapy and delineated criteria for

initiating and withdrawing this therapy have yet to be defined. Furthermore, implementation of this

Extracorporeal Membrane Oxygenationfor Pediatric Cardiac ArrestJENNIE RYAN, MS, CPNP-AC


Pediatric Care

Extracorporeal cardiopulmonary resuscitation (ECPR) remains a promising treatment for pediatric patients

in cardiac arrest unresponsive to traditional cardiopulmonary resuscitation. With veno-arterial extracorporeal

support, blood is drained from the right atrium, oxygenated through the extracorporeal circuit, and transfused

back to the body, bypassing the heart and lungs. The use of artificial oxygenation and perfusion thus provides

the body a period of hemodynamic stability, while allowing resolution of underlying disease processes. Survival

rates for ECPR patients are higher than those for traditional cardiopulmonary resuscitation (CPR), although

neurological outcomes require further investigation. The impact of duration of CPR and length of treatment

with extracorporeal membrane oxygenation vary in published reports. Furthermore, current guidelines for

the initiation and use of ECPR are limited and may lead to confusion about appropriate use of this support.

Many ethical concerns arise with this advanced form of life support. More often than not, the dilemma is not

whether to withhold ECPR, but rather when to withdraw it. Although clinicians must decide if ECPR is

appropriate and when further intervention is futile, the ultimate burden of choice is left to the patient’s care-

givers. Offering support and guidance to the patient’s family as well as the patient is essential. (Critical Care

Nurse. 2015;35[1]:60-70)


1. Determine the difference between venovenous and venoarterial extracorporeal membrane oxygenation (ECMO)2. Describe the benefits of extracorporeal cardiopulmonary resuscitation3. Discuss the ethical considerations related to management of patients undergoing ECMO



extraordinary therapy introduces

many ethical dilemmas concerning

advanced life support. This article

addresses the use of ECMO during

CPR, as well as the ethical problems

we face with the continued advance-

ment of end-of-life care.

Extracorporeal Cardiopulmonary Resuscitation

ECPR is considered the initiation

of ECMO, following refractory cardiac

arrest unresponsive to conventional

cardiopulmonary resuscitation (CPR).

During the initiation of ECPR, tradi-

tional resuscitation measures are con-

tinued, including chest compressions

and emergency administration of

medication. Practitioners initiating

this treatment should aim to maxi-

mize cardiac output and flow to opti-

mize outcomes. While traditional

resuscitation continues, surgeons place the ECMO cannu-

las in large arterial and venous vessels. Location of can-

nula placement is based on the type of ECMO that the

patient will receive. There are 2 forms of ECMO, venove-

nous and venoarterial. During venovenous ECMO, blood

is drained from the right atrium, oxygenated through the

circuit, then perfused back into the right atrium where the

heart pumps it to the rest of the body, bypassing only the

lungs. However, this form of ECMO requires adequate

cardiac function, which is always severely impaired or

absent in ECPR patients.14 Therefore, venoarterial extra-

corporeal support is initiated for ECPR patients. In this

technique, 1 cannula is placed for venous drainage,

similar to venovenous ECMO, but the oxygenated blood

is returned to the aorta, bypassing both the lungs and

heart (see Figure). Placement of the cannulas is depend-

ent on the ease of access and the size of the patient.14 If

access to intracardiac placement is available, such as

with postoperative cardiac patients, this method is usu-

ally preferable, with direct cannulation of the right atrium

and aorta. Other methods include the cannulation of the

femoral artery and vein. However, this use is restricted

to adolescents and adults because the size of their vessels

is large enough to support adequate drainage and reinfu-

sion.14 Still, the most common method of cannulation is

venous access through the internal jugular vein directly

into the right atrium and arterial access through the

right carotid artery into the aorta.3

Once a patient is successfully cannulated, the patient

is immediately connected to the ECMO circuit. For this

reason, most centers have developed a “rapid deployment

system,” in which a circuit is preprimed with a crystalloid

solution or is able to be primed with blood products within

a very short period, usually 10 to 20 minutes.15 Although

a large immediate infusion of crystalloid solution can be

tolerated by older children and adolescents, some centers

are reluctant to administer such an infusion to a neonate

because of the significant hemodilution.15 However, the

Author

Jennie Ryan in a nurse practitioner in the intensive care unit atNemours Cardiac Center. She is also a per diem faculty member inthe Helene Fuld Pavillion Simulation Lab at the University ofPennsylvania, School of Nursing, in Philadelphia.

Corresponding author: Jennie Ryan, MS, CPNP-AC, Nemours Cardiac Center, A. I. duPont Hospital for Children, 1600 Rockland Road, Wilmington, DE 19803 (e-mail: [email protected]).

To purchase electronic or print reprints, contact the American Association of Criti-cal-Care Nurses, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or(949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].

Figure Venoarterial extracorporeal support for extracorporeal cardiopulmonaryresuscitation.

Venous cannula

Rightatrium

Leftatrium

Rightventricle

Leftventricle

Aortic cannula

Aorta

Superior venacava


benefits of immediate end-organ perfusion often outweigh

the risks of low hematocrit, which can be resolved with

blood transfusions once the circuit has been established.15

The Benefits of ECPRThe postresuscitation phase in pediatric patients

remains a high-risk period, complicated by significant

myocardial dysfunction, hyperthermia, hyperglycemia,

impaired autoregulation of blood pressure, and ischemia/

reperfusion response.14-16 Upon return of spontaneous

circulation and reperfusion, a decrease in contractility

of the heart, known as myocardial stunning, often occurs.

Decreased function of the heart can lead to hypotensive

shock, with further damage arising from increased pro-

duction of inflammatory mediators and nitric oxide.16

Treatment of hypotension and myocardial dysfunction

often requires aggressive hemodynamic support with

fluid resuscitation and vasoactive agents including epi-

nephrine, dobutamine, and dopamine.16

In contrast, mechanical circulation via ECMO

allows the body a period of hemodynamic stability

and the possibility of resolution of underlying disease

processes.15,16

Perfusion of

organs with

fully oxygenated

blood via the

ECMO circuit

allows decreased myocardial oxygen demand, gener-

ally without the use of high-dose vasoconstrictors and

inotropic agents.15 This stability in the postresuscita-

tion period may further improve survival rates.17

Large, multi-institutional studies16-18 show that overall

survival to discharge rates in pediatric patients resusci-

tated with conventional CPR remains at approximately

25% to 27%. However, survival statistics for ECPR are

more encouraging, with a general rate of success of near

40% to 60%.2-5,7-13,19-26 Multi-institutional data obtained in

2012 from the Extracorporeal Life Support Organization

(ELSO), an international registry and database of ECMO

treatment, demonstrated that ECPR was successful for

934 out of 2236 neonatal and pediatric patients, with

survival to discharge of 39% for neonates and 40% for

children. Other retrospective, single-institution studies

have shown survival rates as high as 72% to 80%.25,27-29

The Table provides more detailed information from the

current studies of ECPR in pediatric patients. Critical

analysis of this information is imperative when deter-

mining the utility of ECPR.

Most studies rate ECPR’s success solely on survival to

discharge statistics; only a few studies address neurologi-

cal outcome. A void remains in the literature as far as

addressing quality of life after ECPR. Furthermore, “good

neurological outcome” is often a subjective measure,

with terminology varying among researchers. Some

studies have shown that ECPR patients have an increased

likelihood of central nervous system complications

developing compared with patients treated with ECMO

without CPR.4 Other studies examining ECPR patients

have shown favorable neurological outcomes, as meas-

ured by the Pediatric Cerebral Performance Category

Scale, with a score of 2 or less in most patients.8,9,19,20,32

Further investigation into long-term neurological seque-

lae is needed and should be included in future studies.

When to Initiate Therapy?In 2005, the American Heart Association recom-

mended the use of ECPR for in-hospital patients in car-

diac arrest when the duration of no-flow arrest is brief

and the condition leading to the cardiac arrest is

reversible.35 This broad recommendation does not offer a

definition of “brief,” nor does it differentiate between

time of no-flow arrest and duration of traditional CPR.

More recent recommendations from the 2010 Interna-

tional Consensus on Cardiopulmonary Resuscitation36

specifies that ECPR is appropriate for patients with heart

disease that is “amenable to treatment or heart trans-

plantation,” where the cardiac arrest occurs in the inten-

sive care unit in a facility with the personnel, equipment,

and training to provide ECPR. Use of ECPR is indicated

in only 1 situation after out-of-hospital cardiac arrest,

which is in cases of environmentally induced severe

hypothermia (< 30°C), again, only if the appropriate

equipment and expertise are available.36 Medical institu-

tions providing ECPR should have established protocols

for its implementation and use. Often centers lacking

these resources are unable to offer ECPR at all.

The advantages of ECPR after prolonged conven-

tional resuscitation remain a source of controversy.

Despite the large number of studies performed regarding

ECPR use, no criteria or guidelines for timing of initia-

tion of this therapy have been clearly established. The

International Consensus on Cardiopulmonary Resuscita-

tion recognizes that evidence is insufficient for establishing


Mechanical circulation via extracorporealmembrane oxygenation allows the bodya period of hemodynamic stability andthe possibility of resolution of underlyingdisease processes.

Reference

Aharon et al28

Alsoufi et al21

Alsoufi et al30

Cengiz et al4

Chan et al5

Chrysostomous et al29

Conrad et al3

de Mos et al10

Del Nido23

Delmo Walter et al11

Duncan et al22

Huang et al13

Huang et al9

Joffe et al19

Kane et al20

Kelly and Harrison31

Kumar et al12

Population ofpatients

Postoperative, cardiac


ICU and cardiac

ELSO registry

ELSO registry ofcardiac patients

Cardiac

ELSO registry

ICU

Cardiac

ICU

Cardiac

Pediatric

Pediatric

Meta-analysis

Cardiac

Pediatric and cardiac


No. ofpatients

10

48

80

161

492

40

151 Neonatal

282 Pediatric

5

11

42

11

54

27

762

172

31

29

No. (%) ofsurvivors todischarge

8 (80)

23 (46)

27 (34)

64 (40)

208 (42)

30 (75)

Neonatal: 65 (43)

Pediatric: 111 (39)

2 (40)

6 (55)

17 (40.4)

6 (55)

25 (46)

11 (41)

361 (49)

88 (51)

7 (23)

12 (41)

Duration of cardiopulmonaryresuscitation, min

Mean (range), 42 (5-110)

> 30 min associated with poor survival

Not reported

Median (range)Survivors: 46 (14-95) Nonsurvivors: 41 (19-110)

Not reported

Not reported

Median (IQR)Survivors: 40 (25-50)Nonsurvivors: 37 (35-50)

Not reported

RangeAll: 31-77Survivors: 35-48

Mean (SD): 65 (9)

Mean (SD)Survivors: 35 (1.3)Nonsurvivors: 46 (4.2)

Median (range)55 (20-103)

Mean (SD)Survivors: 39 (17)Nonsurvivors: 52 (45)

Median (IQR)Survivors: 45 (25-50)Nonsurvivors: 60 (37-81)

Not reported

Median (interquartile range)Survivors: 32 (25-41)Nonsurvivors: 36 (21-45)

MedianSurvivors: 40Nonsurvivors: 47

Mean (SD)Survivors: 42 (8)Nonsurvivors: 51 (10)

Duration of ECMO therapy

Not reported

Not reported

4 days for both survivors andnonsurvivors

Mean (SD)Survivors: 4.7 (3.5) daysNonsurvivors: 4.4 (6.4) days

Median (IQR) Survivors: 87 (51-137) hours Nonsurvivors: 87 (37-171) hours

Median (IQR)Survivors: 53 (29-98) hoursNonsurvivors: 48 (28-102) hours

Not reported

Not reported

Mean (SD): 112 (18) hours

Mean (SD)Survivors: 4.0 (2.2) days Nonsurvivors: 6.0 (0.9) days

Not reported

Not reported

Median (IQR), rangeSurvivors: 102 (68-135), 43-

419 hoursNonsurvivors: 89.2 (26.9-221),

6-637 hours

Not reported

Median (interquartile range)Survivors: 84 (52-118) hoursNonsurvivors: 119 (57-183)

hours

MeanSurvivors: 4 daysNonsurvivors: 6 days

Not reported

Continued

Table Retrospective pediatric studies of extracorporeal membrane oxygenation (ECMO) in cardiopulmonary resuscitation


any specific threshold for CPR duration beyond which

survival is unlikely.36

A substantial amount of debate can be found in pub-

lished reports about when ECPR should be initiated and

when further intervention would be futile. Several pedi-

atric studies have shown increased mortality rates for

patients cannulated after 30 minutes of conventional

CPR.7,11,28,34 However, other retrospective studies8-10,12,20,26,27,29,31,32

of pediatric patients have shown positive outcomes with

median CPR duration of 30 to 50 minutes. Even more

interesting are the multiple case reports24,27,30,32,37 of suc-

cessful cannulation and survival to discharge in patients

receiving CPR of up to 90 to 220 minutes.

Other research has focused on parameters that may

act as predictors for positive outcome. ECPR patients

with a preexisting diagnosis of cardiac illness have

shown improved survival outcomes, when compared

with patients with noncardiac illnesses.5,6,8,30,32 Perhaps

patients with cardiac illness have less multiorgan dysfunc-

tion before cardiac arrest and therefore are more likely to

Reference

Morris et al32

Paden et al2

Polimenakos et al26

Prodhan et al27

Raymond et al8

Shah et al33

Sivarajan et al34

Thiagarajan et al6

Tajik and Cardarelli7

Wolf et al24

Thourani et al25

Population ofpatients

ICU

ELSO registry

Cardiac single ventricle,neonates

ICU, cardiac

AHA/NRCPR

Cardiac

Cardiac

ELSO registry

Meta-analysis

Cardiac

Cardiac

No. ofpatients

64

Neonatal: 784

Pediatric: 1562

14

32

199

27

37

682

288

90

15

No. (%) ofsurvivors todischarge

21 (33)

Neonatal: 304 (39)

Pediatric: 630 (40)

8 (57)

24 (72)

87 (44)

9 (33)

14 (38)

261 (38)

114 (39.6)

50 (55.5)

11 (73.3)

Duration of cardiopulmonaryresuscitation, min

Median (range)Survivors: 50 (5-105)Nonsurvivors: 46 (15-90)

Not reported

Mean (SD)Survivors: 38.6 (6.3)Nonsurvivors: 42.1 (7.7)



Not reported

MedianSurvivors: 15 Nonsurvivors: 40

Not reported

Not reported

Survivors: 42 (16-98)Nonsurvivors: 43 (20-75)

Not reported

Duration of ECMO therapy

Median (range)Survivors: 55 (2-359) hoursNonsurvivors: 64 (1-506) hours

Not reported in ECPR group

Median (IQR)Survivors: 4 (3-6.5) daysNonsurvivors: 8 (5-11.5) days

Median (range)Survivors: 122 (41-816) hoursNonsurvivors: 59 (7-905)

hours

Not reported

Mean (SD)Survivors: 79.3 (40.7) hoursNonsurvivors: 128.6 (193.3)

hours

Not reported

Median (interquartile range)Survivors: 88 (51-140) hoursNonsurvivors: 66 (26-157)

hours

Median (range)4.3 (0.03-90) days

Median (range)Survivors: 3 (1-20) daysNonsurvivors: 5 (1-21) days

Median (range)66 (18-179)

Table Continued

Abbreviations: AHA/NRCPR, American Heart Association/National Registry of Cardiopulmonary Resuscitation; ELSO, Extracorporeal Life Support Organization; ICU,intensive care unit; IQR, interquartile range.


survive after treatment with ECPR.8 Few published data

support preexisting measurements as indicators for sur-

vival. Arterial blood gas values have been postulated to

be predictive variables in several studies, with pH less

than 7.2 associated with higher mortality.4,19,20,34 However,

Thiagarajan et al6 noted that although pre-ECMO arterial

pH less than 6.9 was strongly associated with negative

outcome, 12% of children who survived after ECPR use

had a pre-ECMO pH less than 6.9.6 Multiple studies5,6,8,9,19,20

have shown that preexisting renal insufficiency and

metabolic electrolyte abnormalities are associated with

worse survival to discharge.

This discordance in published results is of extreme

importance to practitioners initiating ECPR in pediatric

patients. The absence of clearly defined parameters and

inconsistencies in published reports may lead some cli-

nicians to initiate ECPR when attempts may be futile,

but also may inhibit its use when there is the possibility

of success.

When to Withdraw ECMO?Transition from ECPR to standard ECMO care occurs

once the child is cannulated and placed on the ECMO

circuit. Further management of the patient focuses on

treatment of underlying disease processes. The use of

artificial oxygenation and perfusion in this time allows

the child a period of hemodynamic stability and decreased

myocardial oxygen demand, during which vital organ

function may return. However, the precise amount of

time it takes the organs to regain adequate function to

support the body remains unknown. Several studies4,5,30

of duration of ECMO after CPR show similar amounts of

time on the circuit for both survivors and nonsurvivors.

Historically, data in pediatric patients indicate that

ECMO for cardiac failure after cardiothoracic surgery

continued beyond 3 to 6 days results in poor outcomes,

and ECMO beyond 2 weeks may not improve respiratory

failure.33 However, a recent review38 of ELSO data in car-

diac ECMO patients shows no significant difference in

survival to discharge between patients who receive

ECMO for 14 to 20.9 days (25% survival) and patients

who received ECMO for 21 to 27.9 days (23% survival);

but, survival decreased significantly after 28 days to

13%.38 In pediatric patients receiving ECMO for acute

respiratory failure, review of ELSO data showed survival

rates were inversely related to duration of ECMO.

Patients receiving ECMO support for 3 weeks or longer

had a survival to discharge rate of 38%, significantly

decreased from the rate of survival of patients who

received ECMO support for 2 weeks or less (61%).39

If separation from the ECMO circuit is not possible

because of ongoing cardiac or pulmonary failure, then

transition to other modes of mechanical support may be

an option. Patients with prolonged pulmonary failure

but recovery of cardiac function may be transitioned to

venovenous extracorporeal support, potentially decreas-

ing the risk of oxygenator-associated thrombi. Patients

with continued cardiac dysfunction may be converted to

a ventricular assist device to act as a bridge for transplant.

To date, only 2 ventricular assist devices are approved

for pediatric use, the Berlin Heart and HeartWare. How-

ever, no current research supports the use of a ventricu-

lar assist device in children after cardiac arrest.

The only clear indicator for withdrawal of ECMO

support is neurological devastation evidenced by brain

death, in which termination of all life support is war-

ranted. Other clear criteria for withdraw of ECMO

include hemorrhagic stroke or intraventricular hemor-

rhage in which anticoagulation must be discontinued to

prevent wors-

ening intracra-

nial bleeding.

Other indica-

tors for termi-

nation of

ECMO

include wors-

ening end-organ dysfunction. Renal insufficiency follow-

ing ECPR is a poor prognostic factor.5,6,8,9,19 Acute renal

injury can occur during cardiac arrest and resuscitation

as a result of hypoperfusion of the kidneys. Again, the

question of how long it will take for these organs to recover,

or if recovery is possible at all, has yet to be answered.

Ethical ConsiderationsThe judicious use of ECPR in pediatric critical care is

complicated by a vast number of factors, including the

high cost of care, questionable effectiveness, and intensi-

fied emotions of families and providers caring for a criti-

cally ill child. ECPR is an advanced form of life support,

so its use in patient care must be in accordance with the

principles of medical ethics. The first principle is benefi-

cence, which requires that practitioners offer care that

is beneficial to their patients.40 Unnecessary surgical

The use of artificial oxygenation and perfusion allows a period of hemodynamicstability, during which vital organ functionmay return. However, the amount of timeit takes the organs to regain adequatefunction remains unknown.


procedures and unauthorized research are common

problems that arise when addressing beneficence.41 The

second principle is nonmaleficence, meaning do no

harm. This principle requires that the benefits of a treat-

ment must outweigh the potential negative aspects such

as overburdensome pain and unavoidable suffering.40

When discussing the continued use of ECMO, practi-

tioners must decide if prolonged therapy to enhance the

possibility of survival prevails over the risk of unneces-

sary discomfort and extended suffering of the child. The

third ethical principle is autonomy, which refers to the

patient’s right to decide what is appropriate in their

care. In critically ill pediatric patients, a dependent

child’s autonomy is delegated to the surrogate decision

maker, most often the parents.40 Their values and judg-

ments must be respected by practitioners and incorpo-

rated into decision making at every level.

The fourth principle is justice, which is often a source

of controversy in modern medicine.40 This principle

demands that therapies be provided equally to all

patients despite differences in socioeconomic status,

race, gender, and

so on. However,

medical resources

are not limitless,

and societies must

strive to ensure appropriate distribution of health care.40

Median hospital charges of ECPR patients has been

quoted at $310824, which is significantly greater than

charges for propensity-matched conventional CPR

patients, which are $147817.42 Financial burdens of

ECMO support may far exceed reimbursement from

insurance companies and may place the hospital at

financial risk.40,43 Offering excess treatment in one

patient may conceivably lead to a decrease in resources

for another patient.43

Taking into account the ethical principles of medicine,

practitioners in the intensive care unit must be acutely

aware of the potential for benefit and the medically

futility of the therapies they provide. Most often, such

awareness means that advanced life support is initiated

and removed appropriately depending on the patient’s

chance of survival and the desires of the patient’s family.

These concepts are more commonly known as initiating,

withholding, and withdrawing treatment.

Ethical guidelines have determined that, withholding

and withdrawing life support are no different.44,45 However,

many professionals recognize that a psychological differ-

ence clearly exists.44 Based on this assumption, the Presi-

dent’s Commission on Ethical Problems in Medicine

concluded that, contrary to widespread feelings on the

matter, withdrawing treatment was preferable to with-

holding treatment for 2 reasons.45,46 Primarily, withdraw-

ing allows a time-limited trial of therapy in which the

patient’s status can be reassessed and prognosis deter-

mined.45,46 Second, a traditional reluctance to withdraw

treatment had led many practitioners to forgo lifesaving

therapies altogether for fear of eventual “failure.”44 For

this reason, most intensivists now offer advanced life

support to their patients with the hope that therapies

will be successful, or at the very least “buy some time.”44

Withholding ECPR is often a debate between physi-

cians involved in the patient’s care. Most families are not

aware of ECPR and would not know to request that their

child be treated with ECPR. Often ECPR is recommended

by a physician, and therefore withholding ECPR may

come to mean simply not offering it. Withholding ECPR

often becomes an intraprofessional dilemma, where the

effectiveness of treatment is controversial. As discussed

previously, the lack of parameters to guide physicians is

detrimental to evidence-based practice, and decisions in

this scenario are often based on personal reasoning,

experience, and values. In these difficult situations, prac-

titioners most often decide to treat, possibly against their

better judgment.44 Solomon et al44 examined perceptions

of physicians and nurses caring for critically ill children

and reported that 80% of critical care attending physicians

agreed that “sometimes I feel we are saving children who

should not be saved,” whereas only 8% agreed that

“sometimes I feel we give up on children too soon.”

The ethical dilemma of ECPR is therefore most often

not whether to withhold it, but when to withdraw it.

Again, the literature does not support a definitive

timetable for withdrawal of ECMO. Obviously, neurolog-

ical devastation as evidenced by brain death is a defini-

tive indicator for withdrawal of treatment. But no other

parameters exist, and the decision to withdraw is often

at the recommendation of the provider.40,47 Maintaining

ethical principles at this time is essential for practitioners

as they address the medical futility of further treatment.40

There must be a level of assurance that prolonged time

on ECMO will enhance patients’ outcomes and that this

possibility outweighs the risks of further suffering and

discomfort for the child.47


The ethical dilemma of ECPR is mostoften not whether to withhold support,but when to withdraw it.

The Final DecisionAlthough clinicians must decide if ECMO is appro-

priate and when further intervention is futile, the ultimate

burden of choice is left to the patient’s parents. As prac-

titioners, we must be aware of, and respect, the tremendous

responsibility of this decision. ECPR is initiated as the

most advanced form of life support available to patients,

when death without ECMO is most certainly imminent.

Furthermore, many patients remain alive purely through

the use of ECMO and cannot be supported with traditional

medicine. Removal of the pump often equates to death.

In 2003, Curley and Meyer48 examined parental

experiences with ECMO and reported that 61% of par-

ents felt that they had no other choice but to consent to

treatment, since death was the only other option. In the

study, most parents understood that ECMO was an

extraordinary intervention, even in the technologically

dominant intensive care unit environment.

As practitioners, we must be aware of our communi-

cation with parents in this very difficult and anxious time.

Honesty concerning the many complications and uncer-

tainties of ECMO is paramount to effective discussions.48

Furthermore, when a decision is made to treat a child

with ECMO, parents must be cautioned that its use

involves a time-limited trial.48 Reasonable expectations of

length of duration and outcome must be clear to par-

ents.47 Finally, all members of the team must be prepared

to answer questions and provide support throughout the

use of ECMO.47 The importance of offering support and

guidance can never be underestimated in this setting,

where parents are very aware that every moment with

their child may be their last.

Nursing ImplicationsThe use of ECMO during CPR is a technologically

advanced and complex treatment that requires extensive

knowledge from every member of the health care team.

Bedside nurses should be well educated on the physiol-

ogy of the patient, as well as the mechanical aspects of

the ECMO pump. Centers providing this treatment must

offer educational programs to train nurses in rapid

deployment of the ECMO circuit. Familiarity with the

circuit and experience with the cannulation procedure

will ensure a smooth transition from cardiopulmonary

resuscitation to artificial circulation.

Once the patient is cannulated, highly skilled nurses

are needed to manage daily treatment. Nursing care of

ECMO patients is both physically and mentally demand-

ing. These patients require frequent laboratory and

physical assessments, as well as frequent neurological

checks. Neurological injury is common in ECMO patients

owing to the acuity of their illness and the risk of cerebral

vascular injury from stroke or hemorrhage. Daily ultra-

sound imaging of the head are routine in most centers,

and continuous electroencephalographic monitoring is

also implemented with concerns for subclinical seizure

activity. Because

of the immense

workload associ-

ated with ECMO

patients, 2

nurses are gener-

ally needed to

care for these acutely ill children. One nurse is tasked

with the care of the patient, while the other nurse tends

to the needs of the ECMO pump. Most centers have

implemented the use of perfusionists and specially

trained respiratory therapists to manage the ECMO cir-

cuit in an effort to reduce the strain on nursing staffing.

Furthermore, the bedside nurse is often depended on

to provide support to patients’ families. This responsibil-

ity is difficult and challenging, and it requires a large

amount of dedication. Most intensive care nurses are well

versed in end-of-life care and must continue to use this

skill during ECMO trials. Although the physical care of

these patients can be burdensome, bedside nurses must

strive to ensure that time is allocated for family support.

When needed, nurses should be aware of the resources

available for patients’ families, including palliative care

teams, social workers, and chaplain services. These serv-

ices can help by offering assistance to family members

during periods of critical illness and end of life.

The Future of ECPRUse of ECMO as a final therapy during CPR in the

care of critically ill patients remains promising. As

providers continue to broaden the boundaries of use of

ECMO, it is imperative that judicious decision making

be maintained in the clinical setting. Further data and

research are needed to create guidelines and parameters

for withholding and withdrawing ECMO. It is essential

that clinicians providing this treatment be thoroughly

educated and knowledgeable about the literature, so that

decisions are based on evidence.

The importance of offering support andguidance can never be underestimatedin this setting, where parents are veryaware that every moment with theirchild may be their last.


Finally, as with all end-of-life care, it is essential that

all members of the health care team be aware of parental

presence and concern. Support must be provided to

patients’ families on a constant basis to ensure that their

needs are met. It is very easy for physicians and nurses

to become overwhelmed by the technical aspects of

caring for these critically ill patients and focus solely on

maintaining life. However, a holistic approach to care

should remain a focus, with appropriate support of the

patient as well as the patient’s family. CCN


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extracorporeal membrane oxygenation for children with respiratoryfailure. Pediatr Crit Care Med. 2012;13(4):e294-e254.

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CNE Test Test ID C151: Extracorporeal Membrane Oxygenation for Pediatric Cardiac ArrestLearning objectives: 1. Determine the difference between venovenous and venoarterial extracorporeal membrane oxygenation (ECMO) 2. Describe thebenefits of extracorporeal cardiopulmonary resuscitation 3. Discuss the ethical considerations related to management of patients undergoing ECMO







7. The use of ECPR in pediatric critical care is complicated by all except which of

the following?

a. High cost of care

b. Questionable effectiveness

c. Intensified emotions of families and providers

d. Absence of standardized clinical guidelines for withdrawal

8. Which of the following is the term for the concept of initiating and removing

advanced life support?

a. Initiating

b. Withholding

c. Withdrawing

d. All of the above

9. Nursing care of patients receiving ECMO include which of the following?

a. Neurologic assessment

b. Highly skilled nursing care

c. Early mobility

d. A and B

10. Which of the following can help nurses assist families with emotional

support during hospitalization?

a. Child life specialists

b. Palliative care, social workers, and chaplain services

c. Physician support

d. Leadership support

11. Studies examining parents’ experiences with ECMO report which of the

following?

a. Parents felt they had no other choice as death was the only other option.

b. ECMO is one of several treatments available to improve their child’s condition.

c. Parents preferred optimistic reports on their child’s condition over reasonable prognosis.

d. Parents relied heavily on the physicians to guide them through the daily stressors

of having a child undergoing supportive measures.

12. Which of the following statements is true regarding treatment of neonates

with ECMO?

a. Large immediate infusion of crystalloids is a standard of care for neonates.

b. Immediate infusion with crystalloids is well tolerated by neonates.

c. Benefits of immediate end-organ perfusion often outweigh the risks of low hematocrit.

d. Hemodilution is not a significant risk with neonates.




Test ID: C151 Form expires: February 1, 2018 Contact hours: 1.0 Pharma hours: 0.0 Fee: AACN members, $0; nonmembers, $10 Passing score: 9 correct (75%) Synergy CERP Category A Test writer: Tina Cronin

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1. �a �b �c �d

12. �a �b �c �d

11. �a �b �c �d

10. �a �b �c �d

9. �a �b �c �d

8. �a �b �c �d

7. �a �b �c �d

6. �a �b �c �d

5. �a �b �c �d

4. �a �b �c �d

3. �a �b �c �d

2. �a �b �c �d

1. Venoarterial extracorporeal membrane oxygenation (ECMO) is the preferred

extracorporeal support for extracorporeal cardiopulmonary resuscitation

(ECPR) patients over venovenous ECMO because of which of the following?

a. Risk of hemodilution in neonates

b. Absence of adequate cardiac function

c. Impaired renal function

d. None of the above

2. Complications in the postresuscitation phase in pediatric patients include all

except which of the following?

a. Impaired autoregulation of blood pressure

b. Myocardial dysfunction

c. Increased contractility of the heart

d. Hyperglycemia

3. Benefits of mechanical circulation via ECMO include which of the following?

a. Decreased risk of hypotensive shock

b. Decreased risk of aggressive vasoactive resuscitation

c. Promotion of autoregulation of blood pressure in the initial resuscitation period

d. Promotion of hemodynamic stability

4. ECPR is recommended for use in which of the following types of patient settings?

a. Heart transplant surgery

b. Brief no-flow cardiac arrest in the hospital setting

c. Severe hyperthermia

d. Prolonged cardiopulmonary resuscitation with spontaneous return of circulation

5. Which of the following preexisting measurements can help determine survival

potential?

a. Preexisting diagnosis of cardiac illness has shown to improve survival outcomes

b. A pre-ECMO pH of less than 7.2 is associated with higher mortality

c. A pre-ECMO pH of less than 6.9% is associated with negative outcomes

d. All of the above

6. Which of the following is the only clear indicator for withdrawal of ECMO

support?

a. Neurological deterioration

b. Ongoing cardiac dysfunction

c. Ongoing pulmonary failure

d. Oxygenator-associated thrombi

Carol Rauen, RN, MS, CCNS, CCRN, PCCN, CEN, RN-BC, the department editor,

is an independent clinical nurse specialist in The Outer Banks of North Carolina.

Carol welcomes feedback from readers and practice questions from potential

contributors at [email protected].

Kirtley Ceballos, MSN, RNC-NIC, PCNS-BC, clinical nurse specialist in the

neonatal intensive care unit at University of Colorado Hospital, University of

Colorado Health, Colorado Institute for Maternal Fetal Health, Aurora, Colorado,

contributed the pediatric CCRN questions.

Steve Risch, RN, MSN, CCRN, CCNS, a critical care clinical nurse specialist at

Holy Cross Hospital, Silver Spring, Maryland, contributed the adult CCRN

questions.

Adult CCRN Practice Questions1. Following a craniotomy, a

patient has a decreased serum

sodium level. Which other labo-

ratory findings would lead the

nurse to suspect syndrome of

inappropriate antidiuretic hor-

mone (SIADH)?

A. High serum osmolality and low

urine sodium

B. Low serum osmolality and high

urine sodium

C. High urine specific gravity and

high urinary output

D. Low urine specific gravity and

low urinary output

Test plan topic: Endocrine, 6% of the

CCRN questions

2. A multiple trauma patient has

received 4 L of normal saline and

2 units of packed red blood cells

but continues to be hypotensive.

Which recent assessment finding

of this patient would best reflect

improving tissue perfusion?

A. Increasing creatinine level

B. Increasing hematocrit

C. Decreasing heart rate

D. Decreasing lactic acid levels

Test plan topic: Multisystem, 8% of

the CCRN questions

3. A patient who continues to

experience full-body tonic-clonic

Contributors

Celebrate and Be Proud!


Certification Test Prep

RAUEN

Thirty years ago this month (February 1985) I took the CCRN

exam. Achieving and maintaining my critical care certification

is one of the accomplishments, in my 34 years as a critical care

nurse, of which I am most proud. Many of the nurses who are read-

ing this column were not yet born when I became certified. My

efforts to help others prepare for and achieve this coveted certifica-

tion is exciting and humbling. The recent changes that have

occurred in the eligibility criteria have allowed more nurses to

obtain and maintain their CCRN certification. Now all nurses who

affect the care of critically ill patients and their families, whether

electronically (CCRN-e), in the classroom, at the bedside, or from an

administrative office (CCRN-K), can proudly wear the CCRN creden-

tial. I feel honored to be a member of this group. Please join me in

celebrating my anniversary and remember to celebrate your own!


CEBALLOS RISCH

Test plan topic: Cardiovascular, 20% of the CCRN questions

Correct Answers and Rationales for Adult CCRN Practice Questions1. Correct Answer: B

RationaleSIADH or diabetes insipidus (DI) can develop after

craniotomy. The posterior lobe of the pituitary gland,

which is regulated by the hypothalamus, releases antidi-

uretic hormone (ADH). In SIADH, increased release of

ADH causes fluid retention. The fluid retention causes

the patient to have a low urinary output, low serum

osmolality, low serum level of sodium, high specific

gravity of urine, and high sodium level in the urine.

SourceMorton P, Fontaine D. Critical Care Nursing: A Holistic Approach. 10th ed.

Philadelphia, PA: Lippincott, Williams & Wilkins; 2013:391.

2. Correct Answer: D

RationaleThe best indicator of improved oxygen delivery to

the cells during resuscitation is a decreasing level of lactic

acid, which is a byproduct of anaerobic metabolism.

Creatinine and hematocrit are not good indicators of oxy-

genation at the cellular level, and a decrease in heart rate

can reflect adequate resuscitation, but is not as specific

an indicator of tissue perfusion as are lactic acid levels.


Philadelphia, PA: Lippincott, Williams & Wilkins; 2013:1408-1418.

3. Correct Answer: C

RationaleStatus epilepticus is a seizure that is continuous for a

prolonged period of time and typically does not respond

to single/initial administration of antiepileptic medica-

tion and benzodiazepine. Simple and partial complex

seizures last only 5 to 7 minutes. Myoclonic seizures are

associated with hypoxic brain injury and have a single

jerklike presentation, not full-body involvement.

SourcesBardwaj A, Mireski M. Handbook of Neurocritical Care. 2nd ed. New York, NY:

Springer; 2012:499.Morton P, Fontaine D. Critical Care Nursing: A Holistic Approach. 10th ed.

Philadelphia PA: Lippincott, Williams & Wilkins; 2013:902.

movements with no apparent response despite

administration of lorazepam (Ativan) and pheny-

toin (Dilantin) is most likely experiencing which

type of seizure?

A. Partial complex

B. Simple complex

C. Status epilepticus

D. Myoclonic seizure

Test plan topic: Neurological, 12% of the CCRN questions.

4. A patient who sustained a cervical (C5) spinal

cord injury 8 weeks ago and is quadriplegic has

sudden development of hypertension, blurred

vision, flushing, and diaphoresis of the face and

neck. The nurse should immediately:

A. Lower the head of the bed to flat position

B. Coach the patient to breathe deeply and cough

effectively

C. Check the patient’s temperature and administer an

antipyretic as needed

D. Irrigate the patient’s urinary catheter

Test plan topic: Neurological, 12% of the CCRN questions.

5. A patient has these hemodynamic findings after

mitral valve replacement:

Heart rate (HR), 65/min

Systolic blood pressure (SBP), 70 mm Hg

Mean arterial pressure (MAP), 55 mm Hg

Cardiac output (CO), 3.8 L/min

Cardiac index (CI, calculated as CO in liters per

minute divided by body surface area in square

meters), 1.8

Central venous pressure (CVP), 12 mm Hg

Pulmonary artery occlusion pressure (PAOP),

15 mm Hg

Which of the following interventions should the

nurse perform?

A. Increase epinephrine infusion from 4 μg/min to

6 μg/min.

B. Decrease the norepinephrine infusion from 8 μg/min

to 4 μg/min

C. Prepare to administer a 1-L bolus of normal saline

D. Attach the epicardial pacing wires to a pacemaker

and begin ventricular (VVI) pacing



RationaleThe most common cause of autonomic dysreflexia is

obstruction of the urinary catheter, so irrigation might

correct the problem. The head of the bed (A) should be

elevated, not lowered. Although C5-level quadriplegics

must be monitored carefully for airway and pulmonary

issues, assisting the patient with effectively coughing (B)

will not help to treat the current problem. Fever (C) is

not a symptom of autonomic dysreflexia.

SourcesBardwaj A, Mireski M. Handbook of Neurocritical Care. 2nd ed. New York, NY:

Springer; 2012:499. Morton P, Fontaine D. Critical Care Nursing: A Holistic Approach. 10th ed.


5. Correct Answer: A

RationaleIncreasing the epinephrine infusion would further

increase - and -receptor stimulation to increase heart

rate, contractility, and blood pressure. Decreasing the

norepinephrine (B) could further decrease the blood

pressure. The CVP and the PAOP are both high, indicat-

ing that more volume (C) is not needed at this time. No

need to pace for a heart rate of 65/min.



Pediatric CCRN Practice Questions1. A 13-year-old is now permanently disabled after a

motor vehicle collision (MVC) in which the

mother was driving. What is an effective way for

the nurse to promote coping for this patient and

family?

A. Instruct the parents to recognize how different the

child will be from their peers.

B. Discourage expression of feelings of anger by the

patient toward the mother.

C. Provide information about other children in similar

situations who are doing well.

D. Do not include the child in discussions or decisions

about care.

Test plan topic: Professional Caring and Ethical Practices,

20% of the pediatric CCRN questions

2. A 3-week-old infant is newly admitted to the

pediatric intensive care unit (PICU) with a heart

rate of 246/min. The parents report the baby has

refused feeding for 8 hours and is difficult to

console. The infant is pale and sweating. What

intervention will be tried first?A. Digoxin

B. Applying ice to the face

C. Synchronized cardioversion

D. Intravenous (IV) adenosine

Test plan topic: Cardiac, 14% of the pediatric CCRN

questions

3. An 11-year-old admitted for bacterial meningitis

has complained of headache and abdominal pain

for the past 4 hours and is now febrile, tachy-

cardic, and vomiting. The nurse contacts the

physician immediately because the nurse suspects:

A. Acute adrenocortical insufficiency

B. Appendicitis

C. Hyponatremia

D. Cushing syndrome

Test plan topic: Neurological, 14% of the pediatric CCRN

questions

4. A 6-kg infant is in the PICU after 6 days of having

bloody diarrhea, vomiting, and fever at home.

Urine output in the past 12 hours is 10 mL and is

amber in color. Blood pressure is 110/85 mm Hg.

What diagnostic test do you expect to evaluate

these new symptoms?

A. Liver function tests

B. Magnetic resonance imaging

C. Renal scan

D. Echocardiogram

Test plan topic: Renal, 6% of the pediatric CCRN questions

5. An 8-year-old recovering from an open femoral

fracture is moved from the medical-surgical unit

to the PICU because of signs of infection. What

symptom of osteomyelitis may be masked by

treatment of the primary injury?


A. Local signs infection

B. Fever

C. Dehydration

D. Pain

Test plan topic: Multisystem, 11% of the pediatric CCRN

questions

Correct Answers and Rationales for Pediatric CCRN Practice Questions1. Correct Answer: C

RationaleFostering hopefulness (C) may help improve the

patient’s sense of well-being. It is important to promote

normalization by emphasizing abilities, rather than

focusing on differences (A). If the child is not allowed to

express anger (B), this family will not be able to develop

a nurturing environment. Allowing the patient to partic-

ipate in decisions (D) will encourage a positive self-image.

SourceHockenberry MJ, Wilson D. Wong's Nursing Care of Infants and Children. St

Louis, MO: Elsevier Health Sciences; 2013:857-858.

2. Correct Answer: B

RationaleThis patient has clinical signs of supraventricular

tachycardia (SVT). A vagal maneuver, like applying ice

to the face, can immediately reverse SVT. IV adenosine

(D) may be used in the emergency setting when vagal

maneuvers fail. Digoxin (A) is first-line medical man-

agement for chronic SVT. Synchronized cardioversion

(C) can be used to treat SVT in the ICU setting if cardiac

output is compromised.

SourceHockenberry MJ, Wilson D. Wong's Nursing Care of Infants and Children. St Louis,

MO: Elsevier Health Sciences; 2013:1400.

3. Correct Answer: A

RationaleAlthough rare, acute adrenocortical insufficiency

can be caused by damage of the adrenal gland from

meningococcemia. Early symptoms include headache,

diffuse abdominal pain, nausea, and vomiting. Although

abdominal pain and vomiting can be symptoms of

appendicitis (B), classic signs include anorexia and peri-

umbilical pain followed by nausea and pain in the right

lower quadrant. Hyponatremia (C) should always be con-

sidered in patients with central nervous system infection

and can be a result of adrenal insufficiency. Cushing syn-

drome (D) is rare in children and most often caused by

steroid therapy.

SourceHockenberry MJ, Wilson D. Wong's Nursing Care of Infants and Children. St

Louis, MO: Elsevier Health Sciences; 2013:1586.

4. Correct Answer: C

RationaleOliguria, amber urine, and hypertension are clinical

manifestations of hemolytic-uremic syndrome (HUS),

the leading cause of acute renal failure in infants and young

children. HUS generally follows an episode of gastroenteritis.

A renal scan to assess renal perfusion is an expected diag-

nostic procedure.

SourcePotts NL, Mandleco BL. Pediatric Nursing: Caring for Children and Their Families.

Independence, KY: Cengage Learning; 2011:723.


RationaleBecause the patient is most likely receiving pain med-

ication for the fracture, increased pain and tenderness may

not be perceived. The nurse should monitor for signs of

acute infection and alterations in thermoregulation while

continuing to provide pain-relief measures.

SourcePotts NL, Mandleco BL. Pediatric Nursing: Caring for Children and Their Families.

Independence, KY: Cengage Learning; 2011:1312.

AACN Certcorp publishes a study bibliography that

identifies the sources from which items are validated. The

document may be found in the AACN Certification exam

handbook. The contributor of each question written for

this column has listed the source used in developing each

item. CCN


Barbara McLean is a critical care clinicalnurse specialist at Grady Health Systemsin Atlanta, Georgia.

complexity of variables requires a

physiological appreciation of a

constellation of signs and symp-

toms, not just the blood pressures

or the mean pressure.1

In 1896, the mercury sphyg-

momanometer was designed and

then adopted and disseminated in

part by Harvey Cushing. In 1905,

Korotkoff developed methods for

auscultating Korotkoff sounds,

which were related primarily to

diastolic pressures. The clinical

techniques of direct measurement

of blood pressure by intra-arterial

cannula were initially developed

in the 1930s but were not used

effectively until the 1950s. These

measurements were soon accepted

as representing true systolic and

diastolic pressures.2 Since that time,

a significant amount of research

and engineering has produced a

variety of invasive and alternative

indirect methods of measuring

blood pressure. Following a brief

summary of the current methods

of evaluating blood pressure, a

simple overview of validation of

invasive arterial blood pressure

will simplify the comparisons.

Providers can indirectly moni-

tor blood pressure by using a num-

ber of techniques, most of which

describe the external pressure

of correlating with the NIBPvalues so often, it makes mewonder if I have misunder-stood my previous trainingon arterial catheters.

A Barbara McLean, RN, MN,

CCNS-BC, NP-BC, CCRN,

replies:

Many critically ill patients are

monitored with continuous blood

pressure measurements, which

provide clinicians with the impor-

tant measures of systolic blood

pressure (reflecting the change of

pressure in the artery related to

ventricular stroke volume) and

diastolic blood pressure (related

to vascular tone), as well as the

calculated mean arterial pressure

and pulse pressure. The physiology

of blood pressure monitoring is

quite complex, and the meanings

of the different values are often

misunderstood. Although most

providers use target end points for

pressure monitoring and interven-

tion, little evidence supports the

use of a single blood pressure tar-

get. When measuring noninvasively,

the points of measure are static,

versus the invasive measures, which

are dynamic (beat to beat). The

Author

Corresponding author: Barbara McLean, RN, MN,

CCNS-BC, NP-BC, CCRN, Grady Health Systems, 80 JesseHill Jr. Drive SE, Atlanta, GA 30303 (e-mail:[email protected]).

To purchase electronic and print reprints, contact theAmerican Association of Critical-Care Nurses, 101Columbia, Aliso Viejo, CA 92656. Phone, (800) 809-2273 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].

Comparing Blood Pressure Measures: Does One Measurement Equal Another?

Is it prudent to corre-late noninvasive bloodpressure (NIBP) meas-urements with arterialblood pressure meas-urements? My under-standing is that theaccuracy of arterialblood pressure meas-urements is assessedby doing the square-wave test and level-ing, not by correlatingthe arterial measure-ments with the NIBPvalues. However, Iobserve the practice

©2015 American Association of Critical-Care Nursesdoi: http://dx.doi.org/10.4037/ccn2015557

Ask the Experts

Q


applied to block flow to an artery

distal to the occlusion. These

methods actually detect the effects

of blood flow, not intra-arterial

pressure. These differences in what

is actually measured are the major

points of discrepancy between

direct and indirect measurements.

Five methods are currently used

for noninvasive monitoring of blood

pressure: Doppler flow, infrasound,

oscillometry, the volume clamp

technique, and arterial tonometry.

Doppler FlowSystems that operate on the

Doppler principle take advantage

of the change in frequency of an

echo signal when there is move-

ment between 2 objects. Doppler

devices emit brief pulses of sound

at a high frequency that are reflected

back to the transducer. In an uncom-

pressed artery, the small amount

of motion of the artery wall does

not cause a change in frequency of

the reflected signal. The compressed

artery exhibits a large amount of

wall motion when flow first appears

in the vessel distal to the inflated

cuff, which changes the frequency

of the signal, causing what is known

as a Doppler shift. The first appear-

ance of flow in the distal part of the

artery represents systolic pressure.

When the Doppler shift in the echo

signal disappears, that represents

diastolic pressure.

InfrasoundInfrasound devices use a

microphone to detect low-frequency

(20-30 Hz) sound waves associated

with the oscillation of the arterial

wall. These sounds are processed by

a minicomputer, and the processed

signals are usually displayed in

digital form.

OscillometryMost automated NIBP devices

are based on oscillometry. Oscillo-

metric devices operate on the same

principle as manual oscillometric

measurements. The cuff senses

pressure fluctuations caused by

vessel wall oscillations in the pres-

ence of pulsatile blood flow. Maxi-

mum oscillation is seen at mean

pressure, whereas wall movement

greatly decreases below diastolic

pressure. As with the other auto-

mated methods described, the

signals produced by the system

are processed electronically and

displayed in numeric form.3 In

oscillometry, variations in cuff

pressure resulting from arterial

pulsations during cuff deflation

are sensed by the monitor and

used to determine arterial blood

pressure values. The pressure at

which the peak amplitude of arte-

rial pulsations occurs corresponds

closely to directly measured mean

arterial pressure, and values of

systolic and diastolic pressure are

derived from proprietary formulas

that examine the rate of change of

the pressure pulsations. Conse-

quently, systolic and diastolic val-

ues obtained with this technique

are less reliable than mean arterial

pressure values.

Indirectly measured pressures

vary depending on the size of the

cuff used. Cuffs of inadequate width

and length can provide falsely ele-

vated measurements. Bladder width

should equal 40% and bladder

length at least 60% of the circum-

ference of the extremity measured.

When a cuff is slowly deflated and

blood first begins to flow through

the occluded artery, the artery’s

walls begin to vibrate. This vibra-

tion can be detected as an oscilla-

tion in pressure and has served as

the basis for the development of

several automated devices for mon-

itoring blood pressure. The disad-

vantages include the inability to

measure diastolic pressure, poor

correlation with directly measured

pressures, and lack of utility in

situations in which Riva-Rocci

(auscultation) measurements are

also unobtainable.4

Volume Clamp TechniqueThe volume clamp method

avoids the use of an arm cuff. A

finger cuff is applied to the proxi-

mal or middle phalanx to keep

the artery at a constant size. The

pressure in the cuff is changed as

necessary by a servocontrol unit

strapped to the wrist. The feed-

back in this system is provided by

a photoplethysmograph that esti-

mates arterial size. The pressure

needed to keep the artery at its

unloaded volume can be used to

estimate the intra-arterial pressure.5

Arterial TonometryArterial tonometry provides

continuous noninvasive measure-

ment of arterial pressure, includ-

ing pressure waveforms. It slightly

compresses the superficial wall of

an artery (usually the radial artery).

Pressure tracings obtained in this

manner are similar to intra-arterial

tracings. A generalized transfer


function can convert these tracings

to an estimate of aortic pressure.

This method has not yet achieved

widespread clinical use.

In summary, automated non-

invasive measurement of blood

pressure is a major component of

modern critical care monitoring.

Oscillometric and Doppler-based

devices are adequate for frequent

blood pressure checks in patients

without hemodynamic instability,

in patient transport situations

where arterial catheters cannot be

easily used, and in patients with

severe burns, in whom direct arte-

rial pressure measurement would

be associated with an unacceptably

high risk of infection. Automated

NIBP monitors have a role in fol-

lowing trends of pressure change;

however, the averaging over time is

the value-laden data, not the single

measure, or its comparison to

invasive arterial pressure. In gen-

eral, such automated devices have

significant limitations in patients

with rapidly fluctuating blood

pressures, and blood pressure val-

ues obtained with such devices

may differ substantially from

directly measured intra-arterial

pressures.

Given these limitations, critical

care practitioners should be wary

of relying solely on NIBP measure-

ments in patients with rapidly

changing hemodynamics or in

whom very exact measurements

of blood pressure are important.6

It is vital to remember that regard-

less of the method by which blood

pressure is measured, it is a poor

surrogate for the true value of con-

cern, that is, the stroke volume

that forces itself (via cardiac ejec-

tion) into the resistant arteries. For

most trials conducted in humans

or animals, blood pressure meas-

ures obtained by using a wide vari-

ety of methods correlate poorly with

invasive arterial pressure measure-

ments, particularly in patients

with edema, who are receiving

vasoactive medications, or who

have significant hypoperfusion.7-9

In the clinical environment,

monitoring of direct arterial

pressure uses an underdamped

catheter-transducer system. The

arterial response to ventricular

ejection is a frequency response,

that is, the stroke volume bolus of

blood goes into the artery, gener-

ating a vibration column that emits

many responses (arterial wall

oscillations) that are averaged into

the systolic pressure. These frequen-

cies transmit into the system,

which transmits the frequencies

through the fluid-filled tubing and

transducer.10 Nowadays, monitors

offer internal calibration, filtering

of artifacts, and printouts of the

display. The digital display shows

an average of values over time and

thus does not show beat-to-beat

variability accurately. Beat-to-beat

differences in amplitude can be

measured precisely by freezing the

monitor display with on-screen

calibration, allowing assessment

of the effect of ectopic beats on

blood pressure, variations in pulse

pressure or systolic pressure, and

the severity of pulsus paradoxus.

Direct measurement of arterial

blood pressure requires that the

pressure waveform from the can-

nulated artery be reproduced

accurately on the bedside monitor.

The displayed pressure signal is

markedly influenced by the meas-

uring system, including the arterial

catheter, extension tubing, stop-

cocks, flush devices, transducer,

amplifier, and recorder.

Zeroing and leveling are com-

mon procedures for most providers,

but the importance of the dynamic

response to fluid flush is not gen-

erally well understood or used to

test the accuracy of the system.

The length, width, and compliance

of the tubing all affect the system’s

response to change. Small-bore

catheters are preferable because

they minimize the mass of fluid

that can oscillate and amplify the

pressure. The compliance of the

system (the change in volume of

the tubing and the transducer for

a given change in pressure) should

be low. In addition, bubbles in the

tubing can affect measurements

in 2 ways. Large amounts of air in

the measurement system damp

the system response and cause

the system to underestimate the

pressure. Large amounts of air

are usually easily detectable.

Small air bubbles cause an increase

in the compliance of the system

and can markedly amplify the

reported pressure.

Testing the Accuracy ofthe Monitoring SystemZero Reference

When pressure measurements

seem inaccurate or differ markedly

from indirect measurements, the

system’s accuracy can be checked

quickly. The most likely source of

error is improper zeroing of the


system, which can be caused either

by a change in the patient’s position

or by zero drift. Opening the trans-

ducer stopcock to air and aligning

the transducer with the midaxillary

line should confirm that the moni-

tor displays zero (a transducer that

is below the zero reference line will

result in falsely high measurements

and vice versa). The monitor should

be zeroed whenever the patient’s

position changes, when blood pres-

sure changes significantly, and rou-

tinely every 6 to 8 hours because

of zero drift. Disposable pressure

transducers are standardized and

do not require calibration. If zero

referencing is correct, a fast-flush

test can be done to assess the sys-

tem’s dynamic response.10,11

Square-Wave TestTwo major factors affect the

validity of pressures measured:

resonant frequency response, the

vibration of the fluid column in

response to a change in the system

(eg, flush), and the damping coef-

ficient, evaluating the end of the

vibrations.

Overdamped tracings are usu-

ally caused by problems that are

correctable, such as air bubbles,

kinks in tubing, clots, overly

compliant tubing, loose connec-

tions, a deflated pressure bag, or

anatomical factors that affect the

catheter. An underdamped trac-

ing results in systolic overshoot

and can be due to excessive tub-

ing length or patient-related fac-

tors such as increased inotropic

or chronotropic state, as the vessel

wall is more rigid and oscillates

at a higher level. Many monitors

can be adjusted to filter out fre-

quencies above a certain limit,

which can eliminate frequencies

in the input signal that are caus-

ing ringing, although elimination

of important frequencies will result

in inaccurate measurements.10

Although other techniques can

be used, the easiest way to test the

damping coefficient and resonant

frequency of a monitoring system

is by doing a fast-flush test (also

known as a square-wave test). This

test is performed at the bedside

by briefly opening and closing the

continuous flush device, producing

a square-wave displacement on

the monitor followed by a return

to baseline, usually after a few

smaller oscillations. Visual inspec-

tion is usually sufficient to ensure

a proper frequency response. An

optimal fast-flush test causes an

undershoot followed by a small

overshoot, then settles back into

the patient’s waveform (Figure 1).

When air is present in the tubing,

a clot is on the tip of the catheter,

or the catheter is not properly

positioned, the waveform will

Figure 1 Crisp systole, dicrotic notch, and diastole. When flush test is applied, 2 oscillations follow before return to baseline.

300 mm Hg

DicroticnotchSystole

Diastole

Systolic

MeanDiastolic

Time →

Pres

sure→

“Square wave” or flush test,natural resolution to normal oscillation,only 2 oscillations before return to baseline


appear more rounded and less

defined. When the square-wave

flush is applied, no resonance is

seen (Figure 2). Finally, when the

system is underdamped, the tub-

ing is too long, or the catheter is

the wrong size, multiple oscilla-

tions are apparent after the square-

wave test is applied (Figure 3).

Dynamic response validation by

fast-flush test should be performed

frequently: at least every 8 hours,

with every significant change in

the patient’s hemodynamic status,

after each opening of the system

(zeroing, blood sampling, tubing

change), and whenever the wave-

form appears damped.

Components of the monitoring

system are designed to optimize

the frequency response of the entire

system. The 18- and 20-gauge

catheters used to gain vascular

access are not a major source of

distortion but can become kinked

or occluded by thrombus, resulting

in overdamping of the system.

Standard, noncompliant tubing

is provided with most disposable

transducer kits and should be as

short as possible to minimize sig-

nal amplification (overdamping).

Air bubbles in the tubing and con-

necting stopcocks are a notorious

source of overdamping of the trac-

ing and can be cleared by flushing

through a stopcock.

Despite technical problems,

direct arterial pressure measure-

ment offers several advantages.

Arterial catheters actually measure

the end-on pressure propagated by

the arterial pulse. In contrast, indi-

rect methods report the external

pressure necessary either to obstruct

flow or to maintain a constant

transmural vessel pressure. Arterial

catheters can also detect pressures

at which Korotkoff sounds are

either absent or inaccurate. Arte-

rial catheters provide a continuous

measurement, with heartbeat-to-

heartbeat blood pressures.

Problems With ComparingNoninvasive and InvasivePressure Monitoring

Indirect methods of measur-

ing blood pressure estimate the

arterial pressure by reporting

the external pressure necessary to

either obstruct flow or maintain a

constant transmural vessel size. A

recently published meta-analysis12

of 28 studies involving 919

patients concluded that

inaccuracy and imprecision

of continuous noninvasive

arterial pressure monitoring

devices are larger than what

was defined as acceptable.

This may have implications

Figure 2 When the arterial pressure loses its sharp visualization or the digital measure is lower than oscillated or anticipated,check the patient first. Then check all connections on the monitoring system, starting at the patient all the way to the transducerand then the pressure bag. An overdamped picture can occur when connections are loose, the pressure bag is inflated at lessthan 300 mm Hg, there is air in the tubing, or a clot forms on the tip. Validate the mean pressure of both the arterial catheterand the oscillated pressure.

300 mm Hg

Normalsystole

Normal diastole

Constantmean

Underestimatedsystole

Overestimateddiastole

Comparing normalwith overdamped

Systolic

Oscillations absent,indicates overdamping

Mean

Diastolic

Time →

Pres

sure→

“Square wave” or flush test


for clinical situations where

continuous noninvasive arte-

rial pressure is being used for

patient care decisions.

Direct arterial catheters measure

the end-on pressure propagated by

the arterial pulse with every beat.

They are not measuring the same

end points as indirect methods

measure. Rigorous validation of

the accuracy of the monitoring

system can be done with the square-

wave flush test, but that does not

ensure the value of the blood

pressure measurements, just the

accuracy of the system.11

Direct arterial pressure meas-

urement offers several advan-

tages in many but not all patients.

Although an invasive catheter is

required, the reported risk of com-

plications is low. Arterial catheters

provide a heartbeat-to-heartbeat

measurement, can detect pressures

at which Korotkoff sounds are

either absent or inaccurate, and

do not require repeated inflation

and deflation of a cuff. Regardless

of the method used, the mean

arterial pressure should generally

be the value used for decision

making in most critically ill

patients, because it is the most sta-

ble (least affected) measurement

(calculation) across all methods of

blood pressure monitoring.

So to answer the first question,

“Is it prudent to correlate NIBP

measurements with arterial blood

pressure measurements?” No.

Most noninvasive methods provide

an average calculation for systolic

and diastolic blood pressures,

based on a measured mean pres-

sure. Compare the mean pressures

and consider the tested and zeroed

invasive arterial pressure to be the

true measure whether you like the

numbers or not. These 2 types of

measurements evaluate something

quite different: direct pressure

monitors beat-to-beat pressure

pulse, whereas the commonly used

noninvasive methods measure

peak oscillations related to blood

flow. Especially in patients treated

with vasopressors, inotropic agents,

and vasodilators, these measure-

ments may differ significantly.

The second question was, “My

understanding is that the accuracy

of arterial blood pressure meas-

urements is assessed by doing the

square-wave test and leveling, not

by correlating the arterial meas-

urements with the NIBP values.

However, I observe the practice of

correlating with the NIBP values

so often, it makes me wonder if I

have misunderstood my previous

training on arterial catheters.”

Leveling and square-wave test-

ing provide an evaluation of the

system and validation of system

acceptability. Neither test validates

the patient’s arterial pressure, but

the tests validate the integrity of

Figure 3 Spiked systole with a lower diastole should alert the provider to a possible underdamping issue. Underdamping usuallyoccurs when the tubing is too long or the catheter is the wrong size. The problem is usually not physiologic. Reduce the tubinglength and stabilize or replace the catheter. Observe that the mean pressure remains constant between oscillated and invasive.

300 mm Hg

Normalsystole

Normaldiastole

Constantmean

Overestimatedsystole

UnderestimateddiastoleComparing normal

with underdamped

Systolic

“Ringing oscillations”indicate underdamping

Mean

Diastolic

Time →

Pres

sure→

“Square wave” or flush test


the monitoring system that meas-

ures the pressure. If zeroing is

performed and the square-wave

test is passed, you can rest assured

that the direct pressure is being

monitored correctly. When inva-

sive arterial pressure monitor is

zero referenced, leveled, and passes

the frequency response test, then

the invasive pressure is what should

be monitored. At the very best,

correlation can be made between

noninvasive and invasive meas-

urements at the mean pressure

measure only.

Remember that the primary

role of the circulation is to provide

tissues with dissolved and bound

oxygen as well as other energy

substrates, so it is always best to

correlate pressure readings with

indicators of tissue perfusion, no

matter what method(s) you choose

for monitoring. Recommendations

for pressure targets must take into

consideration the site and method

of measurement as well as the true

value of blood pressure versus

oxygen adequacy. Trends in blood

pressure and the relationship to

metabolic measures are the most

important measures in today’s

critical care environment. CCN


References1. Magder SA. The highs and lows of blood

pressure: toward meaningful clinical targetsin patients with shock. Crit Care Med. 2014;42(5):1241-1251.

2. Pierce EC. Percutaneous arterial catheteriza-tion in man with special reference to aortog-raphy. Surg Gynecol Obstet. 1951;93:56.

3. Borow KM, Newberger JW. Non-invasiveestimation of central aortic pressure usingthe oscillometric method for analyzingsystemic artery pulsatile blood flow: com-parative study of indirect systolic, dias-tolic, and mean brachial artery pressurewith simultaneous direct ascending aorticpressure measurements. Am Heart J.1982;103:879.

4. Bruner JM, Krenis LJ, Kunsman JM, Sher-man AP. Comparison of direct and indirectmethods of measuring arterial blood pres-sure: Pt III. Med Instrum. 1981;15(3):182-188.

5. Bogert LW, van Lieshout JJ. Non-invasivepulsatile arterial pressure and stroke volumechanges from the human finger. Exp Physiol.2005;90:437-446.

6. Van Egmond J, Hasenbros M, Crul JF. Inva-sive v. non-invasive measurement of arterialpressure. Br J Anaesth. 1985;57(4):434-444.

7. Aarnes TK, Hubbell JAE, Lerche P, Bed-narski RM. Comparison of invasive andoscillometric blood pressure measurementtechniques in anesthetized sheep, goats, andcattle. Vet Anaesth Analg. 2014;41:174-185.

8. Hohn A, Defosse JM, Becker S, et al. Non-invasive continuous arterial pressure moni-toring with Nexfin does not sufficientlyreplace invasive measurements in criticallyill patients. Br J Anaesth. 2013;111(2):178-184.

9. Stover JF, Stocker R, Lenherr R, et al. Non-invasive cardiac output and blood pressuremonitoring cannot replace an invasivemonitoring system in critically ill patients.BMC Anesthesiol. 2009;9:6.

10. Troy P, Smyrnios NA, Howell MD. Routinemonitoring of critically ill patients. In:Irwin RS, Rippe JM, eds. Irwin and Rippe’sIntensive Care Medicine. Philadelphia, PA:Lippincott Williams & Wilkins; 2011:258-276.

11. McGhee BH, Bridges EJ. Monitoring arte-rial blood pressure: what you may notknow. Crit Care Nurse. 2002;22(2):60-79.

12. Kim SH, Lilot M, Sidhu KS, Rinehart J, YuZ, Canales C, Cannesson M. Accuracy andprecision of continuous noninvasive arterialpressure monitoring compared with invasivearterial pressure: a systematic review andmeta-analysis. Anesthesiology. 2014;120(5):1080-1097.

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Ask the ExpertsDo you have a clinical, practical,or legal question you’d like to haveanswered? Send it to us and we’llpass it on to our Ask the Expertspanel. Questions may be mailed toAsk the Experts, Critical Care Nurse,101 Columbia, Aliso Viejo, CA 92656;or sent by e-mail to [email protected] of the greatest generalinterest will be answered in thisdepartment each and every issue.

www.ccnonline.org

Melody R. Campbell is a critical care clinical nurse specialist and trauma programmanager at Kettering Medical Center, Kettering, Ohio.

Julie Fisher is a physical therapist and the lead therapist in the physical medicineand rehabilitation department at Good Samaritan Hospital, Dayton, Ohio.

Lyndsey Anderson is an occupational therapist in the physical medicine and rehabilitation department at Good Samaritan Hospital, Dayton, Ohio.

Erin Kreppel is a physical therapist in the physical medicine and rehabilitationdepartment at Little Company of Mary Hospital, Evergreen Park, Illinois.

Corresponding author: Melody R. Campbell, RN, DNP, CEN, CCRN, CCNS, Trauma Program, Kettering MedicalCenter, 3535 Southern Blvd, Kettering, Ohio 45429 (e-mail: [email protected]).

To purchase electronic or print reprints, contact the American Association of Critical-Care Nurses, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].

Literature Review,Appraisal, and Synthesis

Electronic databases searched for

evidence included Cochrane, PubMed,

and CINAHL. Key words included

mechanical ventilation, critically ill,

critical illness, early mobilization proto-

col, delirium, intensive care unit, early

mobility, sedation, physical rehabilita-

tion, and physical therapy. In CINAHL,

limits included research, English,

human, and all adults. Related cita-

tions were reviewed in PubMed with

limitations of clinical trials, human,

English, and publication between 2007

and 2012. References from key articles

were reviewed to search for additional

evidence. Articles were included in

the appraisal if content focused on

early mobility in critically ill patients

receiving mechanical ventilation.

Articles were rated by strength of

evidence.4 Level 1 evidence, that estab-

lished by meta-analysis or systemic

review (and also the highest level of

evidence) was not found. No Cochrane

reviews or national practice guidelines

that were related to the subject had

been published between 2007 and

2012. Since that time, a clinical practice

guideline2 related to pain, agitation,

and delirium in the critically ill has

Anew bundle of interventions to improve the care of critically ill

patients receiving mechanical ventilation has been identified.1,2

This bundle incorporates performance and coordination of

spontaneous awakening trials and spontaneous breathing trials; careful

selection of sedatives; assessment, prevention, and management of delir-

ium; and early exercise with progressive mobility.1,2 In collaboration with

the Institute for Healthcare Improvement, and as a part of a critical care

collaborative, our hospital had implemented many parts of the bundle,

but early exercise and progressive mobility had not yet been incorpo-

rated into care. In this article, we share our process for literature review,

appraisal, and synthesis along with protocol development. An evidence-

based performance improvement (EBPI) model was used to plan, imple-

ment, and disseminate the change.3 High-fidelity human simulation

boosted confidence and teamwork and also underscored important

safety aspects before implementation. Unit champions and daily multi-

disciplinary rounding assisted with culture change.

Authors

Implementation of Early Exercise and Progressive Mobility: Steps to Success


In Our Unit

Melody R. Campbell, RN, DNP, CEN, CCRN, CCNSJulie Fisher, PT, MPTLyndsey Anderson, MOT, OTR/LErin Kreppel, PT, MPT


been published. Seven keeper articles

were identified.5-11

The articles were shared and

discussed with our multidiscipli-

nary team. From these articles, the

team determined that early activity

had been demonstrated to be safe

and feasible7,8 and that early mobil-

ity was associated with an increase

in both delirium-free days and

ventilator-free days.5,6,10 Some stud-

ies noted that the implementation

of early mobility contributed to

decreases in length of stay in both

intensive care units (ICUs) and

hospitals.9,10 An additional article11

discussed barriers and facilitators

to implementation of early mobility.

Barriers included sedation, decreased

level of consciousness, and agitation.

Factors that facilitated change were

the presence of a protocol and the

presence of unit champions.11 The

multidisciplinary team decided that

the evidence was sufficient for us to

implement the practice of early

mobility for our patients.

Planning for ChangeWhile our team was planning

implementation of early mobility,

we elected to be a part of an expedi-

tion on early mobility sponsored by

the Institute for Healthcare Improve-

ment. The expedition was a series of

webinars that included presenta-

tions of the science surrounding early

mobility and assisted with protocol

development and implementation

planning. We invited various depart-

ments (respiratory therapy, physical

and occupational therapy, pharmacy)

and our medical director to attend

the webinars. We ensured that ICU

nursing staff, who would act as unit

champions, could attend. The webi-

nar communicated the importance

of early mobility and the evidence

supporting the change.

Our early mobility protocol

(Figure 1) was developed after careful

reading of 2 key articles: a random-

ized controlled trial and a descriptive

study that detailed the intervention

arm of that same trial.5,6 The protocol

was reviewed by the multidisciplinary

team and by several critical care

intensivists. The protocol included

contraindications to initiating early

mobility designated by a yellow text

box indicating caution. Once the

patient had no contraindications,

preparation of early mobility would

begin, designated by a green text box

indicating that the patient was ready

to go. Preparing for early mobility

would include assessing and securing

all devices, stopping tube feeding, and

moving all catheters, intravenous

pumps, and the urinary catheter

drainage bag to the side of the bed

with the ventilator. Activity would

progress from active range-of-motion

exercises to bed mobility exercises

(lateral rolling, move from semire-

cumbent to upright), sitting on the

edge of the bed, sitting to/from stand-

ing and bed to/from chair transfers,

and finally ambulation. An addi-

tional red box was included in the

protocol that delineated contraindi-

cations to continuing early mobility.

If the patient experienced physiolog-

ical changes such as hemodynamic

instability, or oxygen desaturation,

activity would be stopped.

An additional flowchart (Figure

2) was created to visualize and teach

others how early mobility would fit

into our process of coordination of

spontaneous awakening trials and

spontaneous breathing trials.

Our plan for implementation was

written and reviewed by our hospital’s

Human Institutional Review Com-

mittee and the university’s institu-

tional review board. We wanted to

collect patient data during the imple-

mentation of our project to monitor

process and outcomes and wanted

to ensure the safety of that data col-

lection and dissemination of results.

The final aspects of planning for

practice change included creating

an aim statement. Using our EBPI

model, an aim statement would

help us to know whether we had

reached a short-term goal in our

implementation. Working with our

medical director, we determined

that our aim statement would be:

By month 3 of the project, early

mobility would be incorporated

into the care of 25% of patients

receiving mechanical ventilation

(as appropriate). The implementa-

tion steps in accordance with our

EBPI model are listed in Table 1.

Practicing With High-Fidelity Human Simulation

One of our physical therapists

had read an article about the use of

high-fidelity human simulation to

teach physical therapy students.

Training with simulation helped

improve the students’ confidence

before they started getting clinical

experience in an actual ICU.13 The

physical therapist expressed a

desire to try our protocol by using

simulation first so that the team

could practice together to ensure

that the protocol was easy to under-

stand and that safety concerns were

addressed. Her main concern was

related to accidental extubation of

a patient, and she wanted us to plan

the steps of how we would care for

a patient who experienced that seri-

ous adverse event. We developed 3


simulation scenarios (see Table 2 for

examples):

• Assessment of the patient to

determine whether any contraindi-

cations for beginning early mobility

were present.

• Preparation of the patient and

beginning activity with recognition

of changes in condition that would

require stopping activity.

• Inadvertent extubation during

activity.

The project leader/clinical nurse

specialist worked with the personnel

in the simulation laboratory to pre-

pare for practice. Intravenous pumps,

a tube feeding pump, a sequential

compression device, a ventilator, a

manual resuscitation bag, a cardiac

monitor, a walker, and a transport

ventilator were transported to the

laboratory. The simulation labora-

tory was set up with the appropriate

equipment to look like one of our

ICU rooms. Nursing unit champions,

physical therapists, occupational

therapists, and respiratory thera-

pists participated. The clinical

nurse specialist reviewed the draft

protocol, including the sections on

contraindications for early mobil-

ity, preparation of the patient,

progression of activity, and when

to stop activity if the patient’s

condition changed. Additionally,

the flowchart of how early mobility

Figure 1 Early mobility protocol.

Contraindications to initiating early mobility5,6

1. Mean arterial pressure, < 65 mm Hg2. Heart rate, < 60/min or > 120/min3. Respiratory rate, < 10/min or > 32/min4. Oxygen saturation (pulse oximetry), < 90%5. Actively undergoing a procedure6. Patient’s agitation requiring increased sedation in past 30 minutes7. Insecure airway device or difficult airway

Contraindications to continuing earlymobility5,6

1. Mean arterial pressure, < 65 mm Hg2. Heart rate, < 60/min or > 120/min3. Respiratory rate, < 10/min or > 32/min4. Oxygen saturation (pulse oximetry),

< 90%5. Marked patient-ventilator dyssynchrony6. Patient distress

a. Evidenced by nonverbal cues and gestures

b. Physically combative7. New arrhythmia8. Concern for myocardial ischemia9. Concern for airway integrity

10. Fall to knees11. Inadvertent removal of endotracheal

tube12. Judgment of nurse, physical thera-

pist, or occupational therapist

Prepare for early mobility5,6

1. Assess all devices before beginning2. Secure all devices3. Stop tube feeding4. Remove or detach unnecessary

devices (eg, sequential compres-sion systems)

5. Move urinary catheter drainagebag, intravenous poles, and fecal collection bag to side of bed next toventilator

6. Always mobilize to side of bed nextto ventilator

7. For ambulation, use transport venti-lator. Always have wheelchairbehind patient to use in event ofweakness, intolerance of activity.

Prepare for early mobility

Active or active assisted range-of-motion exercises

Bed mobility exercises: lateral rolling, move semirecumbent to upright

Sitting balance activities, apply gaitbelt, assist to sit at side of bed,

incorporate activities of daily living

Improve standing balance and tolerance: reach, march in place, weight shift

Ambulation with assistance

Work on transfers: sit to stand, bed to chair, bed to commode, repetition


would be incorporated into our

current process was reviewed and

discussed.

The simulation began and the

group focused on how to begin to

move the patient. Discussion was

intense, with brainstorming about

the roles and responsibilities of

each of the team members. When

the patient needed to move from

sitting at the edge of the bed to

standing or transfering to a chair, a

team member was substituted for

the patient simulator so that the

team could practice standing the

patient at the bedside and ambula-

tion in the hallway. Proper body

mechanics and safe handling of

patient were emphasized. The group

thoroughly enjoyed the simulation

and found that the “hands-on”

approach boosted confidence. Four

priorities were identified for imple-

mentation of the protocol with a

“real” patient:

• The nurse caring for the patient

could begin to prepare all tubes

and catheters anticipating the

other team members’ arrival.

Doing so decreased the prepa-

ration time for the other disci-

plines, thereby increasing the

number of other patients that

they were able to see in their

work day.

• One person should be desig-

nated to communicate with

the patient and provide direc-

tion to the team during early

mobility. The physical thera-

pist or occupational therapist

was positioned immediately


Figure 2 Incorporation of early mobility into our current process.

Considerations for spontaneous breathing trial6,12:

(1) spontaneous breathing trial should be done daily when indicated, (2) coordinate tim-ing of early mobility with spontaneous breathing trial: (a) perform spontaneous breath-ing trial earlier in day, (b) perform early mobility session later in day after spontaneousbreathing trial if trial is unsuccessful, (c) patient to be extubated? Extubate, and dophysical/occupational therapy later in day

Proceed with early mobility withphysical/occupational therapist6

Patient meets criteria for spontaneous awakening trial12

Assess wakefulness

Patient is awake and calm: (1) opens eyes to voice,

(2) squeezes hand of nurse, (3) sticks out tongue6

Patient with decreased responsiveness5:(1) perform passive range-of-motionexercises, (2) continue sedation vaca-tion, (3) continue to monitor and assess

Agitation: restart sedation at half dose6,12

Perform spontaneous awakening trial

in front of the patient while

the patient was moving and

the group determined that

this team member would

direct the patient and lead

communications for the team.

The goal was to help the

patient understand what to

do next and to decrease con-

fusion for team members.

• Additional roles were delineated.

The respiratory therapist would

be responsible at all times for

monitoring endotracheal tube

security and oxygenation status.

The nurse would monitor other

tubes and catheters as well as

vital signs. The physical and

occupational therapists would

assess and monitor motor

strength, balance, and toler-

ance of activity. The decision

to stop the intervention and

return the patient to a supine

position would be a team

decision led by the nurse. The

patient also could stop the

activity.

• Specific equipment would

be helpful for mobilization.

A reclining-back manual

wheelchair would be posi-

tioned behind the patient

when walking in the hall in the

event of change of condition.

This specific type of wheel-

chair would allow supine posi-

tioning for ease in transferring

the patient back into the bed.

The transport ventilator would

be used when the patient was

ambulating in the hall.

ImplementationSmall tests of change were used

to begin the implementation. After

each test, the multidisciplinary

team reviewed how things went.

The protocol flowed well and was

easily understood. The team, having

gained confidence through the use

of simulation, worked well together

and the patients were safe. Next steps

involved teaching others about early

mobility and disseminating the

practice. The physical medicine and

rehabilitation department conducted

several in-service training sessions

with their staff and added written

and oral competencies to ensure staff

knowledge and patient safety. Nurses

and respiratory therapists conducted

training during staff meetings as

well as special educational confer-

ences focused on the bundle. We

used a slogan of “Mobility Is Medi-

cine” and provided slogan buttons

to those staff members who had

cared for a patient during early

mobility. We also purchased cook-

ies shaped like feet and emphasized

“Feet to the Floor.” This added fun

and helped create some excitement

regarding the change. Daily multi-

disciplinary rounding helped to

determine which patients were ready

for early mobility and supported

staff during implementation. The

team met every 2 weeks in conjunc-

tion with the medical director. Prob-

lems encountered with the practice

change were discussed and methods

to improve implementation were

developed. Constant communica-

tion with all the specialties involved

was done through staff meetings,

electronic mail, bulletin boards,

and departmental publications.

The patient’s experience was

also explored. One patient whom

we interviewed after he had been

extubated indicated that he enjoyed

being up while connected to the

ventilator. He had severe chronic

obstructive disease and had received

mechanical ventilation before. He

felt that he was ready to move

before the team was ready, and

when he began to ambulate out of

his room, he felt that he could

have walked much further but the

team was “nervous.” He walked

the next day around the whole

perimeter of the ICU. He stated

that “it felt good to get out and walk

because there is nothing else to do

in the ICU” and “it made it more

interesting.” The exercise made

him feel like he was improving.

Table 1 Plan for implementing the evidence-based performance improvement modela

1. Describe the problem: Need for implementation of early mobility into practice.

2. Formulate focused clinical question: What is the effect of an early mobility protocolon delirium and length of stay in the intensive care unit over the course of 3 months?

3. Search for evidence.

4. Appraise and synthesize evidence.

5. Develop aim statement: By month 3 of project, early mobility will be incorporatedinto care of 25% of patients receiving mechanical ventilation (as appropriate).

6. Engage in small tests of change.• Ensure safety: high-fidelity human simulation• Ensure safety and reproducibility: protocol refinement

7. Disseminate practice to all staff and patients.

8. Utilize plan-do-study-act process to monitor/evaluate implementation of new practice.a Based on information from Levin et al.3


Sustaining PracticeCreating organizational memory

and knowledge reservoirs were

important mechanisms in our

hospital to help with sustaining

practice.14 In our electronic medical

record, we were able to create files

to hold resource documents. Our

early mobility protocol was placed

Cardiac monitor

Normal sinusrhythm

Heart rate = 80/minNoninvasive blood

pressure = 130/80mm Hg

Oxygen saturation(pulse oximetry) =98%

Respiratory rate =16/min

Change in conditionSinus tachycardiaHeart rate=116/minNoninvasive blood

pressure =150/84 mm Hg

Oxygen saturation(pulse oximetry) =90%

Respiratory rate =30/min

Instructor content

Patient is improv-ing. Yesterdaypatient was ableto sit and danglelegs at bedside,sit to stand with2-person assist.Gait was steady.Plan for today isto march in place,weight shift, and determine if patient canambulate in room.

Patient’s conditionhas changed.Please work as a team to remedythe situation.

Expectations of student group

Verbalize the contraindi-cations to initiating early mobility. Examinepatient and infusions.Review ventilator settingsand vital signs.

Verbalize preparing patientfor early mobility.

Prepare patient for sit tostand, march in place,weight shift, possibleambulation in room.Verbalize:• Secure all devices• Turn off tube feeding• Move urinary catheter,

and intravenous poles to side of bed next to ventilator.

• Remove unnecessary devices (eg, sequentialcompression system)

• Obtain portable ventilator• Walker with support

for portable cardiac monitor

• Recumbent wheelchair

Nurse: talks to patient andassures them of theirsafety, tells them whatwill happen.

Team assists patient backto bed.

Respiratory therapistapplies face mask 100%oxygen. Team assessespatient’s tolerance ofextubation. Nurse notifiesphysician/provider ofextubation.

Important learning considerations

Have chart of contraindica-tions for early mobilityavailable for team toreview.

Note that patient has nocontraindications.

Have chart of items forconsideration for plan-ning for early mobility.

Discuss roles and responsibilities of different personnel.

Respiratory therapist:responsible for endotra-cheal tube and tubing toventilator. Setup ofportable ventilator.

Nurse: responsible forintravenous poles andintravenous catheters.Cardiac monitor ontowalker.

Patient care technician:remove sequential com-pression device, andmove urinary drainagebag to side of bed byventilator. Attach towalker. Emphasize main-taining drainage bagbelow level of bladder.

Physical/occupationaltherapist: apply gait belt,instruct patient. Assesstrunk stability, balance.Assist to sit at side ofbed. Determine whethermay sit to stand, marchin place, begin ambula-tion in room.

Calm approach to patientvery important.

Indications that patientmay need reintubation:

Tachypnea, decreasedoxygen saturation, circumoral cyanosis,tachycardia, hypotension.

Resources for reintubation:nurse practitioner, physi-cian, or anesthesiologist.

Ventilator

Assist controlFraction of

inspired oxygen=40%

Positive end-expiratorypressure =5 cm H2O

Low pressurealarm fromventilator

Simulation

Oral endotrachealtube to subglotticsuction

Sequential com-pression device(both legs)

Nasogastric tube–tube feeding/pump

Urinary catheter

Peripherallyinserted centralcatheter

Infusions:Dexmedetomidine

(Precedex)0.7 μg/kg per hour

Inadvertent endotrachealtube removal,patient is anxious, tachypneic.

Table 2 Simulation scenario 3 for early mobility: inadvertent removal of endotracheal tube


in these files for ease of reference at

each computer terminal. We revised

our mechanical ventilator order set

(computer physician order entry) to

include prechecked orders for early

mobility as well as consultation with

physical and/or occupational thera-

pists for evaluation and treatment.

Then when the patient met criteria

for initiation of early mobility, the

appropriate orders were there. We

also used documents called standards

of nursing practice. These docu-

ments were a blend of nursing art

and science that helped to delineate

the important aspects of nursing

care for a specific type of patient.

They were used to help with orien-

tation of new staff. Our standard of

nursing practice for patients receiv-

ing mechanical ventilation was

updated to include concepts related

to early mobility. Lectures for criti-

cal care class also were updated to

include early mobility.

Lessons LearnedAfter 3 months, we were excited

that we had met our aim. More

than 25% of critically ill patients

receiving mechanical ventilation in

that third month had received early

mobility. No serious adverse events

had occurred. Staff were not only

readily identifying patients who were

appropriate for early mobility but

also were obtaining orders for

physical and occupational therapy

for patients who were not receiving

mechanical ventilation. A physical

therapist and an occupational ther-

apist were assigned to the ICU daily.

We had collected data related to

incidence and duration of delirium

and found a problem with the flow-

sheet design in our electronic medical

record. Additional changes were

the intensive care unit. Crit Care Med. 2013;32(4):15-26.

3. Levin RF, Keefer JM, Marren J, et al. Evidence-based practice improvement: merging 2paradigms. J Nurs Qual. 2010;25(2):117-126.

4. Melynk BM, Fineout-Overholt E. Evidence-BasedPractice in Nursing and Healthcare: A Guide toBest Practice. 2nd ed. Philadelphia, PA: Wolters/Kluwer/Lippincott Williams & Wilkins.

5. Schweikert WD, Pohlman MC, Pohlman AS,et al. Early physical and occupational therapyin mechanically ventilated, critically ill patients:a randomized controlled trial. Lancet. 2009;373(9678):1874-1882.

6. Pohlman MC, Schweickert WD, PohlmanAS, et al. Feasibility of physical and occupa-tional therapy beginning from initiation ofmechanical ventilation. Crit Care Med. 2010;38(11):2089-2094.

7. Bailey P, Thomsen GE, Spuhler V, et al. Earlyactivity is feasible and safe in respiratorytherapy. Crit Care Med. 2007;35(1):139-145.

8. Thomsen GE, Snow GL, Rodriguez L, et al.Patients with respiratory failure increase ambu-lation after transfer to an intensive care unitwhere early activity is a priority. Crit Care Med.2008;138(5):1224-1233.

9. Morris PE, Goad A, Thompson C, et al. Earlyintensive care unit mobility therapy in thetreatment of acute respiratory failure. CritCare Med. 2008;36(8):2238-2243.

10. Needham DM, Korupolu R, Zanni JM, et al.Early physical medicine and rehabilitationfor patients with acute respiratory failure: aquality improvement project. Arch Phys MedRehabil. 2010;91(4):536-542.

11. Winkelman C, Peereboom K. Staff-perceivedbarriers and facilitators. Crit Care Nurse. 2010;30(2):S13-S16.

12. Girard TD, Kress JP, Fuchs BD, et al. Efficacyand safety of a paired sedation and ventilatorweaning protocol for mechanically ventilatedpatients in intensive care units (awakeningand breathing trial): a randomized controlledtrial. Lancet. 2008;371(9607):126-134.

13. Shoemaker MJ, Riermersma L, Perkins R.Use of high fidelity simulation to teach physi-cal therapist decision-making skills for theintensive care setting. Cardiopulm Phys Ther J.2009;20(1):13-18.

14. Virani T, Lemieux-Charles L, Davis DA, et al.Sustaining change: once evidence-based prac-tices are transferred, what then? Healthcare Q.2009;12(1):89-96.

made to add detail to the 4 features of

the Confusion Assessment Method-

ICU (CAM-ICU) to support critical

thinking and accuracy of documen-

tation. We also noted problems with

sedation and analgesia practices and

are in the process of implementing a

nonverbal pain assessment tool and

an analgesia-first approach. As always,

change continues.

SummaryOur purposeful approach to the

implementation of early mobility by

using an EBPI model resulted in sus-

tainment of the practice a year later.

Critical appraisal and synthesis of

the literature resulted in a good pro-

tocol for early mobility. High-fidelity

human simulation built confidence

with working together, and this

translated to experiences with early

mobility in actual patients. Lessons

learned from others related to the

use of unit champions and multidis-

ciplinary rounding to help support

the practice change. We continue to

find opportunities to improve our

practice related to the care of patients

receiving mechanical ventilation. CCN

AcknowledgmentsThe authors acknowledge the leadership and sup-port of Mary Jo Trout, PharmD, RPh, BCPS, Robyn R.Razor, RN, MSN, and Thomas M. Yunger, Jr, MD,

FCCP, DABSM.


References1. Vasilevskis EE, Ely EW, Speroff T, et al.

Reducing iatrogenic risks: ICU-acquireddelirium and weakness—crossing the qual-ity chasm. Chest. 2012;138(5):1224-1233.

2. Barr J, Fraser GL, Puntillo K, et al. Clinicalpractice guidelines for management of pain,agitation and delirium in adult patients in

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In Our UnitIn Our Unit highlights uniquepractices, innovations, research, orresourceful solutions to commonlyencountered problems in criticalcare areas and settings where criti-cally ill patients are cared for. Ifyou have an idea for an In OurUnit article, send it to Critical CareNurse, 101 Columbia, Aliso Viejo,CA 92656; e-mail, [email protected].



Book Reviews

I had this book all those years agowhen I was becoming nursey so Iwould not have been so surprised byhow different working as a nurse,responsible and accountable for thecare of really sick patients, was fromwhat I learned in school. Second, Ihave had some great preceptorsthrough the years and I wish Kati Kleber had been one of them. Third, Iwish this book was available to give toall new nurses who crossed my path.It will make them feel as though theyare not alone, prepare them for whatis to come, and allow them to makeinformed choices as they move fromschool to becoming nursey.

Mary Pat Aust is a clinical practicespecialist at the American Associationof Critical-Care Nurses in Aliso Viejo,California.

©2015 American Association of Critical-CareNurses doi: http://dx.doi.org/10.4037/ccn2015997

Anatomy ofResearch forNursesHedges C, Williams B.

Indianapolis, IN: Sigma

Theta Tau International;

2014. Paperback; 352

pages. ISBN-13: 978-1938835117

This book is part of the Anatomyseries, published by Sigma Theta TauInternational, that uses the concept ofanatomical structure and function todevelop the content. The foundationof the book rests on distinguishingresearch from quality improvement andevidence-based practice, with additionaldiscussion about where these 3 com-ponents intersect.

through school, transi-tioning to working as anurse in a hospital,and transitioning fromthe acute care medical-surgical unit to aneuro/trauma intensivecare unit.

Kleber’s confident,compassionate, andwitty demeanor isevident throughoutthe book, as she dis-cusses combining thetechnical and emo-tional work of nursingand how to find yourplace along the con-tinuum. She offers tipsfor conquering study-ing for the NCLEXexam and strategiesfor landing a job. She

calls out some of the most fright-ening things about being a newnurse (eg, calling physicians,rounding with physicians, givingand receiving report from col-leagues, and assessing patients)and provides very practical, action-able tips.

Kleber offers advice on somecommon areas where new nursesstumble, such as time management,shift work, and, the ultimate in stress,the code blue. With wit and wisdom,she shares stories from her ownexperiences. She also shares herperspective on the work-life bal-ance, which is essential to becom-ing a resilient nurse.

As a nurse with more than 30years of experience, I had 3 wishesafter reading this book. First, I wish

Becoming NurseyKleber K. Portland, OR: Book Baby

Publishing; 2014. Paperback; 186 pages;

$12.99 (print), $7.99 (eBook). ISBN-13:

978-1483542460

Reviewed by Mary Pat Aust, RN, MS

The decision to become a nurseis a long-term commitmentthat sends nursing students on

a potentially confusing and frighten-ing journey. The transition betweenthe safety and structure of nursingschool and becoming a licensedhealth care provider in a hospitalnever seems long or structuredenough to avoid the inevitable fearand anxiety associated with it. Inher book, Becoming Nursey, Klebercovers topics such as getting

Many well-known names in theworld of nursing research haveauthored chapters in this book.Their contributions are significantlysupported by the inclusion of amedical librarian who coauthoredthe chapter on conducting the litera-ture search and review. In addition tothe process of conducting research,the book includes legal and ethicalaspects, research involving specialand vulnerable populations, where tofind funding, and the impact of theInternet and social media on theconduct of research.

Foundations ofClinical NurseSpecialist Practice2nd editionFulton JS, Lyon BL,

Goudreau KA, eds.

New York, NY: Springer Publishing; 2014.

Paperback; 512 pages. ISBN-13: 978-

0826129666

This book is both a text for edu-cating new clinical nurse specialists(CNSs) and for the benefit of CNSsin practice to continue their profes-sional development journey. Whilegiving the history and context of therole, this edition reaches into thepresent and future opportunitieswithin the health care system for theunique contributions of the CNS. Ashealth care continues to change, sodo the ways in which a CNS affectspatients and families, nurses, andsystems in the 3 spheres of influence.

The authors also discuss entre-preneurship, billing and reimburse-ment, and regulation of practice.Finally, short exemplar chaptersdemonstrate how the CNS role canbe implemented to achieve positiveoutcomes in multiple settings.

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Palliative CareNursing: QualityCare to the End of Life4th editionMatzo M, Sherman DW,

eds. New York, NY:

Springer Publishing; 2015. Hardcover;

704 pages. ISBN-13: 978-9826196354

This statement in the preface ofthe 4th edition truly describes therole and function of palliative care:

Unlike hospice care, pallia-tive care is not dependenton prognosis and can beprovided in the context ofcurative treatments, curingwhat can be cured, but withthe concurrent attempt ofalleviating symptomscaused by disease or itstreatment.

Palliative Care Nursingdescribes the ethical and legalaspects of palliative and end-of-lifecare, and presents the process ofproviding that care within the frame-work of the whole person (includingfamily and caregivers). Provision ofnursing care is divided into 2 sec-tions: (1) addressing the physicalaspects of dying for particular diag-noses and (2) addressing symptommanagement for all patients. Pallia-tive care nursing is a crucial aspectof providing care across patients’life span, whether faced with con-genital issues, chronic disease, oraging. CCN

www.ccnonline.org

Education Directory

FLORIDAMiamiCCRN/PCCN Review CourseDate: February 20-21, 2015. Place: Nova Southeastern University.Address: 8585 SW 124th Ave, FL 33183. Keynote Speaker: Mary Ann“Cammy” Fancher. Sponsor: Greater Miami Area Chapter of AACN.Contact: Joe Falise. Phone: (954) 594-1427. E-mail: [email protected]. Fee: Members, $140; nonmembers, $170; groups of 3 or more,$130/person; 1-day course (all attendees), $100. Credits: 14 CEUs

MiamiSCRN (Stroke Certified Registered Nurse) Review CourseDate: February 20-21, 2015. Place: Nova Southeastern University.Address: 8585 SW 124th Ave, FL 33183. Keynote Speaker: KendraKent. Sponsor: Greater Miami Area Chapter of AACN. Contact:Ruth Salathe. Phone: (305) 586-4203. E-mail: [email protected]: Members, $150; nonmembers, $175; groups of 3 or more,$140/person (applies only if registration received together); 1-daycourse (all attendees), $100. Credits: 14 CEUs

OrlandoCertification in Legal Nurse Consulting (5-day Seminar and Online)Date: April 13-17, 2015. Place: Marriott Orlando Airport. Address:7499 Augusta National Dr, Orlando, FL 32822. Keynote Speaker:Vickie L. Milazzo. Sponsor: Vickie Milazzo Institute. Phone: (800)880-0944. Fax: (713) 942-8075. E-mail: [email protected]: www.LegalNurse.com. Fee: Varies. Credits: 25.3 CEUs(5-day seminar); 40 CEUs (online)

Plantation40th Annual Spring SeminarDate: April 18, 2015. Place: Renaissance Hotel. Address: 1230 SouthPine Island, Plantation, FL 33324. Keynote Speakers: Teri Lynn Kiss,Kendra Menzies-Kent, Douglas Houghton, Mary Ann “Cammy”Fancher. Sponsor: Broward County Chapter of AACN. Contact:Patty Kelly. Phone: (954) 722-8020. E-mail: pattykelly7 @att.net.Fee: Members, $75; nonmembers, $100 before April 1, 2015. Credits: 6.5 CEUs

ILLINOISItascaMidwest ConferenceDate: March 23-24, 2015. Place: Eaglewood Resort and SPA.Address: 1401 Nordic Rd, Itasca, IL 60143. Keynote Speakers: TBA.Sponsor: Midwest Chicago Area Chapter of AACN. Contact: JennyA. Zaker. Phone: (847) 309-0662. E-mail: [email protected]: TBA. Credits: TBD


OREGONEugenePCCN/CCRN ReviewDate: February 11-12, 2015. Place: Valley River Inn. Address:1000 Valley River Way, Eugene, OR 97401. Keynote Speaker:Nicole Kupchik. Sponsor: Willamette Valley Chapter of AACN.Contact: Denise Hendrickson. Phone: (541) 868-6620. E-mail:[email protected]. Credits: Applied

TEXASTylerCCRN/PCCN ReviewDate: February 26-27, 2015. Place: Wisenbaker ConferenceCenter, Trinity Mother Frances Hospital, Tyler, TX. KeynoteSpeaker: Julie Miller. Sponsor: Greater East Texas Chapter ofAACN. Contact: Kim Thompson. E-mail: [email protected].

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make a positive difference in the life of someone who issuffering is truly a blessing.

What are the challenges you encounter andhow do you overcome them?

Fear of failing to do my very best as a nurse is thegreatest challenge I face every day. I turn to God forstrength and I pray diligently that He continues to useme to help improve patients’ lives.

What has your journey as a nurse been like?My journey as a nurse has been a beautiful educa-

tional experience and a true blessing. There have been(and will continue to be) challenging days when I havedone all I can do and nothing helps, but knowing I didmy best gives me some satisfaction.

At the end of a busy day, how do you find balance in your life?

I find balance in my faith and belief in God. I tryto live my life and treat others as I want to be treated.

What would we be surprised to know about you?

I am a vegetarian!

How has AACN played a role in your career?AACN has played a major role in my career. I look to

AACN for standards and resources, and I use the con-tinuing nursing education to evolve and learn as a nurse.AACN mandates excellence and I accept the challengeto uphold, meet, and exceed this mandate. CCN

I Am a Critical Care Nurse

Why did you become a nurse?I was made to be a nurse. It is in my nature to

care for, assess, troubleshoot, reassure, and encour-age patients. Being a nurse is all I have ever wantedto do.

What about your job as a nurse makes you happy?

Seeing my patients make progress and recovermakes me happy. The patients I care for are burnvictims and they are very close to death. When thesepatients take a turn for the better by just openingtheir eyes for the first time in the unit, it is nothingshort of a miracle. As a nurse, I can be a changeagent and I can bring hope to the hopeless, deliverhealing to the resistant, encourage and teach thenoncompliant, and see miracles happen at the bed-side. This is why I am so excited about my job.

Tell us about an extraordinary experienceyou’ve had as a critical care nurse.

I cared for a very ill, severely burned, and heav-ily sedated patient for months. While caring for her,I used to get close to her ear and whisper, “You cando it. I’m here for you. I’m praying for you.” Sheslowly improved and one day, when she was able tosit up in bed, she said, “Thank you for encouragingme. I heard everything you said.” It felt incredibleto find out that she heard me all those times when Iwhispered reassuring words to her. To be able to

Jacqueline Kramer, RN, isa staff nurse in the ICU/Burn Unitat Detroit Receiving Hospital inDetroit, Michigan.

©2015 American Association of Critical-Care Nurses doi:http://dx.doi.org/10.4037/ccn2015150


I Am a Critical Care Nurse features the extraordinaryin a critical care nurse’s ordinary experiences. To befeatured in this department, contact Critical Care Nursevia e-mail at [email protected].

Complete Issue Critical Nursing

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