Jason Persoff, M.D., S.F.H.M. - CEConsultants,...

Jason Persoff, M.D., S.F.H.M.

•  None •  Mo'va'onal Disclosures

•  Controversies in current management o  Does the airway even matter? o  What drugs work (hint: none)? o  Monitoring for perfusion during

a code

•  Post-cardiac arrest treatment o  Therapeutic hypothermia o  Prognosis

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•  Events leading up to cardiac arrest o  Dispel myths about who

benefits and who doesn’t from CPR

o  Advanced directives o  Clues to imminent cardiac

arrest in hospitalized patients

•  Treatment during early cardiac arrest o  Pathophysiology o  Code leadership

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•  Identify knowledge gaps •  Improve delivery of emergency cardiac care •  Stir the pot of controversies in resuscitation •  Recommend further improvements in clinical

practice

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•  Knowledge Gaps o  Age and resuscitation outcome o  Cancer diagnosis and resuscitation outcome o  Overall prognosis in resuscitation

•  Controversies o  In whom is CPR/ACLS futile?

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•  Knowledge Gaps o  Vital signs most predictive of imminent cardiopulmonary arrest

•  Improving Care o  Rapid response teams and improvements in code status discussion o  Changing culture of vital sign derangements o  Predictive models for the Electronic Medical Record

•  Controversies o  Why don’t people call for help?

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•  How much 'me did that video take? o  Exactly 82 seconds

•  In the hospital, how long does it take to recognize cardiac arrest?

Herlitz et al. Resuscitation 2001. Herlitz et al. Resuscitation 2001.

•  Eberle confirmed our skills at pulse check •  Sensi'vity 90% •  Specificity 55% •  Accuracy 65%

o  Median 'me needed to iden'fy presence or absence of pulse: •  24 seconds overall, 32 seconds for pulse absent pa5ents

•  In 2009, Tibbells confirmed we’d only goMen a liMle beMer •  Sensi'vity 86% •  Specificity 64% •  Accuracy 78%

•  BoMom line: in controlled circumstances, we don’t know if a pa'ent has a pulse or not

Eberle et al. Resuscitation 1996 (33) Tibballs J and Russell Philip. Resuscitation

2009; 80: 61 Eberle et al. Resuscitation 1996 (33)

Tibballs J and Russell Philip. Resuscitation 2009; 80: 61

•  A code blue is called while you’re on the unmonitored unit of the hospital. As you enter the room, the nurses wheel in the code cart.

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Neurologically Intact Survival (CPC 0-1)

Survival to Hospital Discharge

Return of Spontaneous Circulation

Death

CPC Status

• 0 Normal • 1 Good • 2 Mod Disability • 3 Major Disability • 4 Persistent Vegetative State • Brain Death

88% of all In-Hospital Cardiac Arrests Occur on Patients with DNR Status

Hodgetts et al. Resuscitation 54: 2002




Death

CPC Status


54-76%

17-57%

58-75%

14-27% of Pediatric In-Hospital Arrests

24% of Adult In-Hospital Arrests Samson et al. NEJM 354: 2006

Nadkarni, et al. JAMA 295: 2006

Total Surviving Neurologically Intact ~12%




Death

CPC Status


53-52%

10-20%

61-62%

Usually preceded up to 8 hours prior to arrest by marked changes in SBP, HR, or oxygen saturation

Skrifvars et al. Resuscitation 70: 2006

Nadkarni, et al. JAMA 295: 2006

Total Surviving Neurologically Intact ~6.8%

Untreated V-Fib/VT

Electrical Phase

0-4 minutes

High Countershock Receptivity

Circulatory Phase

4-10 minutes

CPR Needed Before Shock

Metabolic Phase

10+ minutes

Comprehensive Multisystem Approach

After Mader T, Resuscitation 2007

Circulatory Collapse 0-3 Mins

• Pulse Check? • Call Code? • CPR?

Code Team Arrival

3-6 Mins

• How quickly does the team arrive and who leads?

CPR, Drugs, Intubation 6-10 Mins

• Arrhythmia Recognition?

• Airway, Breathing • Shocks • Drugs

Code Team Begins to Integrate 10+ Mins

• Kitchen Sink • Txfr or

Pronounced

Acute VF Arrest

Metabolic Phase

Electrical Phase

Circulatory Phase

Fibrillating myocardium deplete of ATP

Weisfeldt ML and Becher LB. JAMA 2002;

288: 3035.

CPR Initiated >1-2 Minutes

After Collapse

Survival ↓ 34% to 14%

Herlitz et al. Resuscitation

49: 2001

Cooper et al. Resuscitation

68: 2006

Code Team Arrival > 3

Minutes After Collapse

Survival ↓ Starts

@ 2Mins Survival 0%

@ 6 Mins

Skrifvars et al. Resuscitation

70: 2006

ACLS Training Status of Nurses

SHD 31% vs. 20%

30 day 26% vs. 5.9%

1 year 21% vs. 0%

Moretti et al. Resuscitation

72: 2007

Quality of CPR Lots o’ Stuff

Chest Compressions

Start Now

Good Recoil

Push Hard

Pump Fast

CPR when done perfectly provides only… – 1/3 normal cardiac output – 10-15% normal cerebral blood flow – 1-5% normal cardiac blood flow

Sanders et al. Resuscitation 1985.

•  Compressions too shallow 62.6% of the 'me

•  Compressions too slow 71.9% of the 'me

* p < 0 .0083

* 75% 25%

ROSC No ROSC Quartile 1

95.5 - 138.7 cpm

* 24% 76% Quartile 2

87.1 – 94.8 cpm

58% 42% Quartile 3

72.4 – 87.1 cpm

* 42% 58% Quartile 4

40.3 – 72.0 cpm

Abella. Circulation 2005; 111:428-34

*

62%

0%

42%

0% 20% 40% 60% 80%

% Too Shallow

% Too Deep

% Incomplete

Release

Wik et al. JAMA 2005: 293:299-304

Yu et al. Circulation 2002; 106:368-72

•  Compression depth inversely correlates with likelihood of successful defibrilla'on

•  Mechanisms of why this may happen o  Rapid drops in aor'c diastolic pressure

o  Expansion of the right heart (compromising leW ventricular size and flow)

•  Delays in resuming chest compressions following defibrilla'on decrease ROSC and neurological intact survival

Edelson DP, et al. Resuscitation 2006; 71: 137. Yu et al. Circulation 2002; 106: 368. Chamberlain D, et al. Resuscitation 2008; 77: 10. Berg RA, et al. Resuscitation 2008; 78: 71.

•  AEDs o  Widely available but with long hands-‐off 'mes

•  Shock ‘Em NOW!

Chan PS, et al. NEJM 2008; 358: 9. Lloyd MS, et al. Circulation 2008; 117: 2510. Op Ed: Perkins GD. Resuscitation 2008; 79: 1.

•  Risk of shock: negligible o  Brave volunteers didn’t die

o  Few case reports

Op Ed: Perkins GD. Resuscitation 2008; 79: 1.

•  Wrong…Zoll (among other manufacturers have accelerometer pads that “zero out” compressions

•  Delayed defibrilla'on o  Black race associated with delays in defibrilla'on (p<0.001)

o  Small hospital size (<250 beds)

o  “AWer hours” (nights/weekends)

o  Non-‐monitored bed

Chan PS, et al. NEJM 2008; 358: 9. Herlitz et al. Resuscitation 2001.

•  Con'nuous capnography o  Increasingly appears to be predic've of excellent perfusion

o  Markers of perfusion include a sudden increase in PCO2

o  Ven'la'ons can be 'trated to accommodate for EtCO2 of 35-‐40mmHg

Oxygen is Rapidly

Consumed

• 2-4 Minutes • Asymmetric distribution

Switch to Anaerobic Metabolism

• Hepatic perfusion necessary to clear • pKa, pH and other

changes change medication effects

CO2 Rapidly Rises

• Adds to acid burden • Needs lung perfusion

and ventilation to clear

Low Flow

• Functional reductions in compression-

assisted forward flow • Arteriole failure with

low effective blood volumes

Hypoxia

Circulatory Collapse

Lactic Acidosis

Hypercarbia

“The Drain”

•  “Iatrogenic hypotension” –  Over-zealous BVM use due to

•  Desire to correct hypoxia •  Belief that hyperventilation will correct acid-base derangements

•  What is the appropriate tidal volume for a patient in cardiopulmonary arrest?

•  Roughly 750cc

•  What is the volume of an adult bag-valve-mask?

•  1.5 liters •  Designed for 1-handed operation

New Paradigm: CCR

Michard F. Anesthesiology 2005

•  Phenomenon of auto-‐PEEP usually referred to pa'ents on a ven'lator

•  Rate exceeded at least 60.9% of the 'me in humans

•  In swine models, hyperven'la'on results in… •  …increased intrathoracic pressure •  …decreased coronary perfusion pressures •  …lower survival

• Abella. Circulation 2005; 111:428-34.

•  Aufderheide, et al. Resuscitation 2004.

•  Contraindicated in conscious pa'ents o  Can premote retching and laryngospasm

o  Trauma

•  Pa'ents gasp during cardiac arrest •  Gasping…

o  …is a forceful agonal respira'on

o  …is a marker of improved prognosis

o  …increases cerebral blood flow

o  …decreases intracranial pressure

o  …improves upper airway patency

o  …generates cardiac output

• Yang, et al. Crit Care Med 1994; 22: 879.

• Ristagno G, et al. Resuscitation 2007; 75: 366.

• Xie J, et al. Crit Care Med 2004; 32:238.

• Srinivasan V, et al. Resuscitation 2006; 69: 329.

• Ewy GA and Kern KB. J Am Coll of Cardiol 2009; 53:147.

Rats! A hemorrhagic

model of PEA in rats

Suzuki M, et al. Resuscitation 2009; 80:109.

•  Why hypothermia? o  Superoxide genera'on post-‐resuscita'on o  Calcium influx into cells o  Decreased available glucose o  Increased oxida've phosphoryla'on o  Cooling preserves mitochondria

o  The only “brain preserving” therapy post-‐arrest •  Hazards

o  Coagulopathy o  Impaired WBC func'on o  Decrease in cardiac index o  Hyperglycemia (Real)

•  Requires o  Con'nuous bladder or central monitoring of temperature o  Target 32-‐34°C

A. Aguila et al. / Resuscitation 81 (2010) 1621–1626

After data from SA Bernard, et al. NEJM 2002; 346: 557-63.

After data from THACASG. NEJM 2002; 346: 549-56.

After THACASG. NEJM 2002; 346: 549-56.

•  Therapeu'c Hypothermia o  Depression in cardiac index from TH means pressors are indicated

•  Maintenance of MAP 90-‐100mmHg

•  Oddo M, et al. Crit Care Med 2006 o  Paralysis is recommended but must be combined with seda'on

•  Paralysis is stopped once core temp is >35°C

o  TH causes selec've increases in CK-‐MB

•  Standard resuscita'on peak ~100 at 6 hrs •  TH resuscita'on peak ~300 at 12 hrs •  Nevertheless, STEMI or suspicion of MI should NOT preclude PCI

•  Therapeu'c Hypothermia o  Goal: RAPID decrease in core temp to 32-‐34 Deg C

o  Average 6 hours to achieve targets •  Oddo M, et al. Crit Care Med 2006

o  Cold LR 30mL/kg bolus plus external cooling in comatose pa'ents post-‐resuscita'on

o  BoMom Line: HIGHER CPC SCORES, SIMILAR SURVIVAL

•  CPC 0-‐1 seen in 54% of those treated vs. 30% of controls •  Review: Bro-‐Jeppensen J, et al. Resuscita*on 2009; 80: 171.

o  Theore'cal decrease in diminishment of ECG VF to asystole

o  Cooling DURING arrest seems to improve ROSC, but not survival •  Pre-‐Arrest and Intra-‐Arrest Hypothermia and VF. Menegazzi JJ, et al.

Resuscita*on 2009; 80: 126.

Shockable Rhythm? Yep

V-Fib

Pulseless VT

Have no idea

Nope

PEA

Asystole

360J Mono

150J Biphasic

150J Biphasic

or

5 Cycles

(150 Compressions)

Pressor (Epi vs. Vaso)

Shock

Drug

Shock

Antiarrhythmic (Amiodarone)

•  You come across an unconscious pa'ent who appears unarousable and not par'cularly lively. As a group, determine: o  Who will lead the code

o  Determine interven'ons prior to defibrillator arrival

o  When the defibrillator arrives, how would you set it up?

•  Group leader, discuss what chaos ensued •  How did you figure out to use the defibrillator? •  How did you decide on a collec've course of ac'on? •  What areas of uncertainty existed? •  Take 2: new group leader, same exercise

•  Peripheral vs. Central Lines •  Precordial Thumps •  Cough CPR •  Pulse Checks

Shockable Rhythm? Yep

V-Fib

Pulseless VT

Have no idea

Nope

PEA

Asystole

360J Mono

150J Biphasic

150J Biphasic

or

5 Cycles

(150 Compressions)

Pressor (Epi vs. Vaso)

Shock

Drug

Shock

Antiarrhythmic (Amiodarone)

Desbiens NA, Crit Care Med 2008; 36:391.

•  All pa'ents in PEA should receive: o  IVF wide open to “fill the tank”

•  Pa'ents will go into vascular collapse commonly as shock ensues increasing the rela've vascular volume by many liters

o  Oxygen •  Systemic hypoxia causes vasoconstric'on of the pulmonary arteries leading to RV dysfunc'on and thus decreases in LV preload

o  Epinephrine •  Peripheral alpha-‐agonist can clamp down the vessels effec'vely but will also increase myocardial workload via beta-‐agonist effects. This is a short-‐term fix

o  Chest Compressions •  Already discussed

•  Your team arrives on a pa'ent who is agonally breathing but appears to have a very faint, rapid pulse. o  At what point would you ins'tute chest compressions?

o  What interven'ons should you ini'ate immediately and why?

o  Name some immediate causes that could have led to this collapse

•  What were the difficul'es this go around in deciding course of ac'on?

•  Ul'mately, what did your group decide was the e'ology for the collapse and how did you approach it?

•  What algorithms do you think may have helped you perform beMer?

•  Effect of CCR on Alveolar Collapse and Recruitment o  More Atelectasis

o  More Hypoxemia

o  Worse Hemodynamics

o  Effects Persist Even AWer Resump'on of IPPV

o  But…the pigs used were anesthe*zed

•  Markstaller K, et al. Resuscita*on 2008; 79: 125.

Methyl-Prednisolone 40mg

IV after Epinephrine

Hydrocortisone 300mg qd x 7 days

Mentzelopoulos SD, et al. Arch Int Med

2009; 169: 15.

Steroids

Low Relative Cortisol Levels

Sillberg VAH, et al. Resuscitation 2008; 79: 380.

Wyer, et al. Ann Emergency Med

2006; 48: 86.

Koshman, et al. Ann of

Pharmacology 2005; 39: 1687.

Vasopressin

Non-Adrenergic Vasoconstrictor


Yup in animals, not so in humans largely due to study design

heterogeneity.

Epinephrine plus

Vasopressin

Smoke if You Got ‘Em


Epinephrine

α/β Agonist

•  Why hypothermia? o  Superoxide genera'on post-‐resuscita'on o  Calcium influx into cells o  Decreased available glucose o  Increased oxida've phosphoryla'on o  Cooling preserves mitochondria o  The only “brain preserving” therapy post-‐arrest

•  Hazards o  Coagulopathy o  Impaired WBC func'on o  Decrease in cardiac index o  Hyperglycemia (Real)

•  Requires o  Con'nuous bladder or central monitoring of temperature o  Target 32-‐34°C

After data from SA Bernard, et al. NEJM 2002; 346: 557-63.

After data from THACASG. NEJM 2002; 346: 549-56.

After THACASG. NEJM 2002; 346: 549-56.

•  Therapeu'c Hypothermia o  Depression in cardiac index from TH means pressors are indicated

•  Maintenance of MAP 90-‐100mmHg

•  Oddo M, et al. Crit Care Med 2006 o  Paralysis is recommended but must be combined with seda'on

•  Paralysis is stopped once core temp is >35°C

o  TH causes selec've increases in CK-‐MB

•  Standard resuscita'on peak ~100 at 6 hrs •  TH resuscita'on peak ~300 at 12 hrs •  Nevertheless, STEMI or suspicion of MI should NOT preclude PCI

•  Therapeu'c Hypothermia o  Goal: RAPID decrease in core temp to 32-‐34 Deg C

o  Average 6 hours to achieve targets •  Oddo M, et al. Crit Care Med 2006

o  Cold LR 30mL/kg bolus plus external cooling in comatose pa'ents post-‐resuscita'on

o  BoMom Line: HIGHER CPC SCORES, SIMILAR SURVIVAL

•  CPC 0-‐1 seen in 54% of those treated vs. 30% of controls •  Review: Bro-‐Jeppensen J, et al. Resuscita*on 2009; 80: 171.

o  Theore'cal decrease in diminishment of ECG VF to asystole

o  Cooling DURING arrest seems to improve ROSC, but not survival •  Pre-‐Arrest and Intra-‐Arrest Hypothermia and VF. Menegazzi JJ, et al.

Resuscita*on 2009; 80: 126.

•  Post-CA Brain Injury •  Post-CA Myocardial Dysfunction •  Systemic Reperfusion Response •  Precipitating Causes

»  Review: Nolan JP, et al. Resuscitation 2008; 79: 350.

•  Does an RRT decrease mortality and frequency of codes: Maybe

•  Yes: Downey AW, et al. Crit Care Med 2008; 36: 477. o  Measured altera'on in mental status

o  Delay in MET call resulted in death (37% vs. 22%)

•  Yes: Dacey MJ, et al. Crit Care Med 2007; 35: 2076.

•  Yes: Sebat F, et al. Crit Care Med 2007; 35: 2568.

•  Yes: Sharek PJ, et al. JAMA 2007; 298: 2267.

•  No: Chan PS, et al. JAMA 2008; 300: 2506. o  Single hospital before and aWer interven'on, no differences in mortality, but decrease in ICU admission rate

•  No: MERIT Study. Crit Care Resusc 2007; 9: 206. o  MET not called for >15 mins prior to CA

•  “Why doesn’t anyone call for help?” •  Buist M. Crit Care Med 2008; 36: 634.

•  Implementa'on of an RRT improves vital sign recording •  Chen J, et al. Resuscita*on 2009; 80: 35.

Isn’t Orientation over yet????

Jason Persoff, M.D., S.F.H.M. - CEConsultants,...

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