TCHP Education Consortium · 2020. 1. 7. · Understanding Adult Hemodynamics ©TCHP Education...

Hemodynamics, Shock, and Infection in Critical Care

April 29th, 2020

7:30 a.m. to 4:00 p.m.

Minneapolis VA Health Care System,

Room 4U.106

(4th floor at the back of the Medical Library)

Description/Learning Outcomes

Health care professionals entering into critical care can be intimidated by the complexity of patients in the ICU. It is vital that the care giver understands

hemodynamics and how failure of the normal regulatory mechanisms in the body can lead to rapid and profound shock. The learning outcomes are for

the learner to have an improved ability to:

Link the principles behind hemodynamics to the selected treatment of hemodynamic problems

Assess and manage patients experiencing hemodynamic problems and shock

Identify the causes, symptoms, and types of shock

Target Audience

This class was designed for the novice critical care or telemetry nurse.

Before You Come to Class

It is highly recommended that you complete the Understanding Adult Hemodynamics and the Shock in Critical Care Primers prior to

attending. It will be assumed that you have this knowledge. You can find the primers on the TCHP website; it will be attached to your

pre-class materials: http://tchpeducation.com/coursebooks/preclass_docs.html. HCMC employees are encouraged to complete the

primer on the LMS.

Schedule

7:30 - 7:45 a.m. Registration

7:45 - 8:45 a.m. Introduction to Hemodynamic Monitoring Brett Fladager

8:45 - 9:00 a.m. Break

9:00 - 11:00 a.m. Pressure Monitoring (CVP), Arterial Line Monitoring, Minimally-Invasive

Pressure Monitoring (FloTrac)

Brett Fladager

11:00 a.m.– 12:15 p.m. Overview of Shock, Hypovolemic Shock and Cardiogenic shock review Lynelle Scullard

12:15 – 1:00 p.m. Lunch

1:00 – 2:30 p.m. Infection in the ICU Environment and Sepsis and Septic Shock Lynelle Scullard

2:30 - 2:45 p.m. Break

2:45 – 3:30 p.m. Neurogenic Shock Review and Anaphylactic Shock Lynelle Scullard

3:30 - 4:00 p.m. Putting It All Together Lynelle Scullard

For attending this

class, you are eligible to receive:

7.00 contact hours

Criteria for successful completion: All participants must attend the program and complete an online evaluation form to

receive contact hours. Note that you must attend the ENTIRE activity to receive contact hours.

The Twin Cities Health Professionals Education Consortium is an approved provider of continuing nursing education by the

Wisconsin Nurses Association, an accredited approver by the American Nurses Credentialing Center's Commission on

Accreditation.

If you complete the primers for this

class, you are eligible to receive additional contact hours.

Criteria for successful completion of primers: You must read the primer and complete the online post-test and evaluation.

Please Read!

Check the attached map for directions to the class and assistance with parking.

Certificates of attendance will be emailed to class participants once the online evaluation is completed.

You should dress in layers to accommodate fluctuations in room temperature.

Food, beverages, and parking costs are your responsibility.

If you are unable to attend after registering, please notify the Education Department at your hospital or TCHP at 612-873-2225.

In the case of bad weather, call the TCHP office at 612-873-2225 and check the answering message to see if a class has been cancelled. If a class has been cancelled, the message will be posted by 5:30 a.m. on the day of the program.

More complete class information is available on the TCHP website at www.tchpeducation.com.

You must print out your own course materials! None will be available at the class. Click on the link below to access:

www.tchpeducation.com/coursebooks/coursebooks_main.htm

If the link does not work, copy and paste the link (web page address)

into your internet browser. Available 1 week prior to class.

TCHP Education Consortium

http://tchpeducation.com/coursebooks/preclass_docs.htmlhttp://www.tchpeducation.com/http://www.tchpeducation.com/coursebooks/coursebooks_main.htm

Minneapolis VA Health Care System –4U-106 One Veterans Drive

Minneapolis, MN 55417

Directions to the MVAHCS

From the East (St. Paul): Take 35E south

to West 7th/Highway 5 exit. Turn right at the

top of the exit ramp. Continue on 5 to the

Fort Snelling exit and stay to the right as

you follow the exit around. You will “Y”

into traffic coming from the Mendota

bridge. Move to the right and exit on 55

west. As you exit on 55 west, it will “Y”

almost immediately. Stay to the left and go

straight through the stoplight. You will be

on Minnehaha. Follow Minnehaha to the

stoplight in front of the VA and turn left

into the parking lot. If you miss the “Y”

continue to the next stoplight (54th) and turn

left. Go to stop sign (Minnehaha) and turn

left again. Go to the stoplight in front of the

VA and turn right into the parking lot.

From the Southeast: Take 35E to 110

west. Take the 55 west/Fort Snelling exit.

Go to the far righthand lane as soon as you exit to continue on 55 west. Go over the Mendota Bridge, move to the

right lane and exit to follow 55 west. As you exit on 55 west, it will “Y” almost immediately. Stay to the left and go

straight through the stoplight. You will be on Minnehaha. Follow Minnehaha to the stoplight in front of the VA and

turn left into the parking lot. If you miss the “Y” continue to the next stoplight (54th) and turn left. Go to stop sign

(Minnehaha) and turn left again. Go to the stoplight in front of the VA and turn right into the parking lot.

From the North: Take 35W south to 62 east. *Follow directions below.

From the South: Take 35W north to 62 east. *Follow directions below.

From the West: Take 494 east to 35W north. Take 62 east. *Follow directions below.

*Directions, continued: Get into the right lane on 62 and exit on 55 west. At the top of the exit ramp, turn left to

continue on 55 west. Go to the stoplight (Minnehaha) and turn left. Follow Minnehaha to the stoplight in front of the

VA and turn left into the lot.

For All: Park in the Visitor’s Parking Lot to the left (parking is free). Enter through the outpatient entrance and take

the elevator to the 4th floor. Enter the Medical Library that is next to the bank of elevators. 4U-106 is located at the

back of the library.

Light Rail Transit: The LRT line stops right in front of the VA. Feel free to utilize the park and ride lots and take

the LRT to the VA. Go to the LRT website for information about where to park, fares, and how to ride:

http://www.metrocouncil.org/transit/rail/index.htm

https://www.google.com/maps/place/VA+Hospital/@44.8997554,-93.2144266,15z/data=!4m5!3m4!1s0x87f6296b50320a9f:0xd7cc25c43608f47!8m2!3d44.9015845!4d-93.2058821?hl=en

Understanding Adult Hemodynamics

© 11/2005 TCHP Education Consortium. Revised 2014; 10/2016; 1/2018

This educational activity expires January 31, 2021.

All rights reserved. Copying, electronically transmitting or sharing without permission is forbidden.


This home study is pre-reading for a class. Please complete before class time. If contact hours are desired, follow instructions at the end of the packet.


©TCHP Education Consortium, 10/2005; January 2018v.2 edition

Page 1

Understanding Adult

Hemodynamics

Introduction/Learning Outcomes

Aristotle started investigating it in the 4th century B.C.;

Galen in the 2nd century A.D. continued to investigate

it. The heart, blood vessels, and concepts of

hemodynamics were intriguing to Harvey, Malpighi

and van Leeuwenhoek in the 1600's. So what exactly

is hemodynamics? Heme means "blood", and

dynamus means "movement," so hemodynamic

means the movement of blood.

We care about the movement of blood, and monitor it,

because how the blood moves through the body will

determine how the tissues are replenished with oxygen

and nutrients and are able to excrete end-products of

metabolism.

The learning outcome of this home study program is

for the learner to self-report an improvement in their

knowledge base and critical thinking skills related to

hemodynamic monitoring - how we do it, what the

numbers mean, and how we can optimize the

movement of blood in the body through a variety of

pharmacologic strategies.

This home study is used as pre-reading for several

TCHP classes. You only need to complete it once if

taking multiple classes.

Target Audience

This home study was designed for the novice critical

care or telemetry nurse; however, other health care

professionals are invited to complete this packet.

Content Objectives

1. Identify non-invasive indicators of hemodynamic status.

2. List three indications for invasive hemodynamic monitoring.

3. Describe the relationships among preload, contractility, compliance, afterload, and cardiac

output.

4. Describe pharmacologic strategies that manipulate heart rate, preload, contractility, and

afterload to improve cardiac output.

Disclosures

In accordance with ANCC requirements governing

approved providers of education, the following

disclosures are being made to you prior to the

beginning of this educational activity:

Requirements for successful completion of this

educational activity:

In order to successfully complete this activity you

must read the home study and complete the online

post-test and evaluation.

Conflicts of Interest

It is the policy of the Twin Cities Health

Professionals Education Consortium to provide

balance, independence, and objectivity in all

educational activities sponsored by TCHP.

Anyone participating in the planning, writing,

reviewing, or editing of this program are expected

to disclose to TCHP any real or apparent

relationships of a personal, professional, or

financial nature. There are no conflicts of interest

that have been disclosed to the TCHP Education

Consortium.

Expiration Date for this Activity:

As required by ANCC, this continuing education

activity must carry an expiration date. The last day

that post tests will be accepted for this edition is

January 31, 2021—your post-test time stamp

must be on or before that day.

Planning Committee/Editors*

*Linda Checky, BSN, RN, MBA, Program Manager

for TCHP Education Consortium.

*Lynn Duane, MSN, RN, Assistant Program

Manager for TCHP Education Consortium.

Sharon Stanke, DNP, MSN, RN, Nursing Instructor

in Critical Care, Minneapolis VA Health Care System.



Page 2

Authors

Karen Poor, MN, RN, Former Program Manager for

the TCHP Education Consortium.

Sharon Stanke, DNP, MSN, RN, Nursing Instructor


Content Experts

Denise Rogich, PharmD, Pharmacist at the

Minneapolis VA Medical Center.

*Sharon Stanke, DNP, MSN, RN, Nursing Instructor


Carrie Wenner, PharmD, Pharmacist at the

Minneapolis VA Medical Center.

*Denotes the content expert for the current edition

Contact Hour Information

For completing

this Home Study and evaluation, you are eligible

to receive:

1.80 contact hours

Criteria for successful

completion: You must read the

home study packet and complete

the online post-test and

evaluation..

The Twin Cities Health Professionals

Education Consortium is an approved

provider of continuing nursing

education by the Wisconsin Nurses

Association, an accredited approver by

the American Nurses Credentialing

Center’s Commission on

Accreditation.

Please see the last page of the packet for information

on submitting your post-test and evaluation for contact

hours.



Page 3

The Concepts of Hemodynamics

The end-all and be-all of hemodynamic monitoring is

the cardiac output. The cardiac output (CO) is the

amount of blood ejected from the ventricle in one

minute. This amount of blood is adequate to supply

the body tissues with oxygenated blood. The purpose

of blood flow / CO is simply to deliver oxygen to all

cells in the body

Normally, the cardiac output is between

4-8 liters of blood every minute. Imagine

an organ the size of your fist pumping out

2-4 Coke bottles of blood every minute!

Two components multiply to make the cardiac output:

the heart rate and the stroke volume.

CO = HR x SV Of course, different sized folks need different amounts

of blood circulating. An 80-pound little old lady needs

less blood than a 350-pound linebacker, right? To

even things out a little bit, there is a calculation called

the "cardiac index."

The cardiac index (CI) is the cardiac output adjusted

for body surface area. CI should be between 2.5 - 4.2

liters of blood per minute per square meter of surface

area.

Heart rate The first component of the

cardiac output is the heart

rate. The heart rate and

stroke volume should work

like a teeter-totter. If one

goes up, the other should

go down, and vice versa.

This is the concept of the

compensatory heart rate.

The most common change in the heart rate to

compensate is for it to go faster (become tachycardic)

because of low stroke volume or increased tissue

oxygen needs.

Causes of compensatory tachycardia are:

Hypovolemia from dehydration, bleeding, loss of fluid

Low blood pressure

Anxiety, fear, pain, and anger cause the sympathetic nervous system to release

endogenous and exogenous catecholamines

Fever

Exercise

There are limitations to the compensation that

tachycardia can provide: heart rates above 180

beats/min in a normal heart, or above 120 in a diseased

heart, are too fast to compensate. If the stroke volume

continues to decline, the heart rate can only increase

so much to balance cardiac output.

On the other hand, the heart can go more slowly

(become bradycardic) to compensate for a high

cardiac output or high blood pressure. This can be

seen with seasoned athletes with "strong pumps," who

often have heart rates in the 40's-60's at rest.

Beyond the compensatory tachy- or brady-cardias,

there are those rhythms that hurt the hemodynamic

state of the patient.

Sinus tachycardias that are > 180 in the normal heart

or > 120 in the diseased heart are not compensatory

anymore because the heart can't fill adequately with

blood to pump out. Other dysrhythmias have the same

problem, but an additional one: they lose 20% of their

cardiac output because their atria are not contracting

in sync with the ventricles. These rhythms are:

Atrial tachycardia

Uncontrolled atrial flutter/atrial fibrillation

Junctional tachycardia

SVT

Ventricular tachycardia

Bradycardias that present problems to the

hemodynamic standing of the patient are:

Junctional rhythm

2nd degree AV block, type II

3rd degree AV block

Idioventricular rhythm

What can cause these kinds of bradycardias? The most

common causes are:

Myocardial infarction

Vagal stimulation (bearing down)



Page 4

Beta blocking and calcium channel blocking agents

Stroke volume The stroke volume is the amount of blood

ejected with each ventricular contraction.

Kinda makes sense, doesn't it? The

amount of blood per beat X the number of

beats in a minute is the amount of blood

that leaves the heart every minute (also

known as Cardiac Output or CO).

Three main factors determine stroke volume:

contractility, preload, and afterload.

Contractility Contractility is the force and velocity with

which ventricular ejection occurs,

independent of the effects of preload and

afterload. Huh? Think of contractility as the

"squeeze." Remember “squeeze” when we get

to pharmacology as it is synonymous with “intrope.”

Contractility increases (the heart squeezes harder)

from:

Sympathetic nervous system: The fight or flight response from fear, anxiety, stress,

pain, hypovolemia

Exercise

The bad thing about increased contractility is that

although it increases stroke volume, it will also

increase the demand of oxygen by the heart (MVO2).

This can be hazardous in someone with heart disease.

The prime example: the guy who has the heart attack

while shoveling snow -- all the exercise increased his

heart rate and his contractility and his heart couldn't

handle the extra work.

Decreased contractility decreases stroke volume and

MVO2. The causes might be:

hypoxia

hypercapnia

metabolic acidosis

hyperkalemia

hypocalcemia

myocardial infarction

cardiac surgery

Preload Preload is the amount of blood in

a ventricle before it contracts.

It's the "gas in the tank." Preload

is also known as "filling

pressures."

Preload is determined by:

1. The total circulating blood volume: how much blood is actually in the blood vessels?

2. The distribution of vascular volume: where is the blood and fluid? In the blood vessels, in the cells,

or in the "3rd space?"

3. Atrial systole: are the atria contracting in sync with the ventricles? If they are not, there is a

decrease in preload by 20%.

There is a theory that helps to explain how preload and

contractility are related: the Frank Starling Law. This

is what it says --

Imagine that you have a

rubber band in your hands

that you are stretching. If

you stretch out the rubber

band out about three inches, it will contract back pretty

well.

Now imagine that you stretch out

your rubber band just an inch or so.

What will happen now? It won't

contract back very fast or with very

much force. This is what happens when a person

becomes hypovolemic - they don't have a lot of stretch,

so they don't have a lot of squeeze.

Next, if you stretch out your rubber band six-eight

inches, it will contract back more strongly and faster.

This is the

principle

behind a

fluid challenge or fluid flush. If you give someone a

little fluid to stretch their heart, they should squeeze

back harder.



Page 5

The last idea in the Frank-Starling Law is that you can

overstretch the heart - by filling it so full of fluid that

the muscle fibers can't contract back well if at all. This

is what happens in congestive heart failure.

Preload is dependent on 2 factors

How full is the tank (ventricles)

AND

How much stretch to the ventricles

It is not an either /or -- it is both factors.

Compliance Compliance is part of the stroke

volume determination. It refers

to the distensibility of the

ventricular myocardium - or its

ability to stretch. People with

normal compliance have hearts

that are able to stretch with

volume loads - for example, you

would do fine if you chugged a 20 ounce glass of water

on a hot day - your heart would be able to

accommodate that change.

People who have increased compliance, though, run

the risk of overstretching and not being able to contract

back well. Conditions that have increased compliance

are:

Congestive heart failure

Dilated cardiomyopathy

On the flip side, people with decreased myocardial

compliance don't stretch well to accommodate

changes in load. People who have:

a myocardial infarction,

a stunned myocardium from surgery or trauma, or

restrictive cardiomyopathy

may all have difficulty handling increased loads of

fluid.

Afterload

The last concept is afterload. Afterload is how

hard the heart (either the right or the left side) has

to push to get the blood out. Afterload is also

thought of as the resistance to flow or how

clamped the blood vessels are.

Afterload is determined by:

The compliance of the aorta

Mass/viscosity of blood: how thick or thin it is

Vascular resistance: whether the blood vessels are constricted or dilated

Oxygen level: hypoxemia will cause vasoconstriction

Monitoring hemodynamics the old fashioned way

Long before there were monitors, cables, and lines,

health care providers had to look, listen, and feel the

patient to determine their hemodynamic status.

Because all tissues are dependent on oxygenated

blood, a deficiency in delivery will affect each organ

system.

The "first things to go" when the blood circulation is

not what it should be are the skin and the gut.

Indicators of diminished blood supply to these organs

are:

Cool, clammy skin

Pale, ashen, or cyanotic skin color

Diminished bowel sounds

Diarrhea or constipation

Increased NG tube drainage

The "second things to go" are the kidneys and lungs.

Failure to get blood to these organs has much more

serious consequences:

Increased respiratory rate and effort

Shortness of breath

Decreased PaO2 on ABG or decreased SaO2

Crackles in the lungs from heart failure

Decreased urine output

Increased urine concentration

Elevated BUN/creatinine/potassium



Page 6

Finally, the brain and the heart are very greedy for

oxygenated blood. They are the first and last organs

to be perfused. When they fail, indicators may be:

Decreased or altered level of consciousness

Disorientation

Slowly reacting pupils

Chest pain/pressure

Tachy or brady-dysrhythmias, ectopy

ST segment elevation

Monitoring Using Tools

Why do we sometimes choose to use invasive lines

instead of monitoring the patient in non-invasive

ways?

Well, our patients are not always straight-forward,

textbook cases. They are complicated and complex

and can be difficult to diagnose. Secondly, invasive

monitoring can help determine what kinds of treatment

should be started, as well as evaluating how well the

treatment is working. And last, treatment for another

problem may affect how the blood circulates; invasive

line monitoring can also measure those effects.

There are four types of invasive lines:

1. Arterial line

2. CVP

3. Pulmonary artery catheter

4. Left atrial line (rarely used)

Of course, not everyone who is admitted to an ICU

needs to have invasive arterial lines. Virtually all post-

open heart surgery patients, however, will have at least

an arterial line, if not a PA or CVP line in too. There

are certain conditions where invasive monitoring is

quite helpful:

Complicated MI

Unstable MI with drug titration

CHF/pulmonary edema

Multisystem failure/ shock

High risk cardiac patient for surgery or procedure

High risk OB

Respiratory failure

The Arterial Line The arterial line transmits a systolic and diastolic

pressure through a transducer that turns the pressure

into an electrical waveform and a number. In short,

the arterial line gives us a blood pressure. In cardiac

surgery patients, the mean arterial pressure is

followed, with a desired MAP between 60-80 mmHg.

However, the arterial line blood pressure is not the

same as a cuff pressure. There appears to be

differences between direct (arterial) and indirect non-

invasive (cuff) readings measuring systolic blood

pressure during hypotension. The differences between

these 2 measures (direct/internal versus

indirect/external) is similar to the differences observed

between an axillary temperature and a rectal

temperature. The mean blood pressure from both

techniques is considered a more reliable means of

assessing prognosis and is the preferred metric to use

for diagnosis and treatment decisions in the ICU.1

Note that an arm cuff pressure is more likely to under-

estimate MAP/blood pressure than to over-estimate it.2

The Pulmonary Artery Catheter The pulmonary artery (PA) catheter is also known as

the Swan Ganz catheter. It will directly measure three

different pressures and is used to obtain the cardiac

output, contractility, and afterload information.

The PA catheter is floated through a major vein into

the superior or inferior vena cava. From there, it is

floated through the heart and into the pulmonary

artery. It has a pressure sensor in the right atrium and

another one in at the distal end of the catheter to

measure the pulmonary artery pressure. When the

balloon at the end of the catheter is inflated, pulmonary

capillary wedge pressure is obtained to give



Page 7

information about the left side of the heart. With the

catheter in correct position we can monitor pressure on

both sides of the heart. The left side and the right side.

We can gain very useful clinical information when we

assess both sides of the heart.

Right atrial pressure

The right atrial pressure (RAP) measures the venous

return to the right heart. It is a right heart preload

measurement.

The RAP is essentially the same pressure that is

obtained with a CVP on a triple lumen catheter.

Normally, the RAP will be between 2 and 6 mm Hg.

It can be increased in:

Fluid overload

Cardiac tamponade

Right heart dysfunction

Pulmonary problems

The RAP is decreased with:

Dehydration/volume loss

Venodilation

Right ventricular pressure This pressure is not documented routinely, as it should

only be seen during the passage of the catheter on

insertion and removal. The normal value for RV

pressure is 20-30 systolic/0-5 diastolic. RV pressures

should only be seen on insertion or removal of the

catheter. Seeing RV pressure waveforms during

monitoring or regular patient care would be a

complication. This could happen when your patient is

moved or repositioned; the catheter could have

accidently been tugged a bit to cause the catheter to

dislodge slightly. You will need to notify a physician

of this complication.

Pulmonary artery pressure The pulmonary artery pressure (PAP) is measured at

the distal end of the catheter. The normal values for

PAP are 20-30 systolic (PAS)/10-20 diastolic (PAD).

Increased pressures are found in:

Atrial or septal defects

Pulmonary hypertension

LV failure

Mitral stenosis

Pulmonary capillary obstructive pressure (PAOP)

Often called the "wedge," this pressure is obtained

when the balloon on the end of the PA catheter is

inflated. This blocks off all pressures from the right

side of the heart, allowing the pressure sensor at the tip

of the catheter to see, indirectly, the pressures on the

left side of the heart. It is a left heart preload

measurement.

Normally, the PAOP is between 8 and 12 mm Hg. It

is increased in:

Fluid overload

Mitral valve stenosis

Aortic stenosis or regurgitation

LV failure

Constrictive pericarditis or tamponade

The PAOP is decreased with:

Hypovolemia

Vasodilation

The diastolic number of the PA pressure is often used

instead of the PAOP, particularly in cardiac surgery

patients. The PAD is always higher (by 1-4 mm Hg)

than the PAOP, but is a close approximation.

Cardiac Output

The cardiac output can be measured by using the PA

catheter. When the procedure has been finished, the

computer will generate a bunch of numbers. You will

first gather your direct readings of PAP, RA, and

PAOP, and measure the CO. You can then obtain the

rest of the hemodynamic picture using computer

generated values based on mathematical formulas.

Here are the numbers with the normal values and what

they measure:

Cardiac output: 4-8 L/min

Cardiac index: 2.5 - 4.0 L/min/m2 (keep > 2.1)

Stroke volume: 60-100 ml/beat Contractility

Systemic vascular resistance (SVR): 800-1200

dynes/s/cm-5 Left heart afterload



Page 8

Pulmonary vascular resistance (PVR): 50-150

dynes/s/cm-5 Right heart afterload

The direct measurements from the PA catheter give

information on the preload status of the heart.

RAP: 2-6 Hg Right heart preload

PAOP: 8-12 mm Hg Left heart preload

Manipulation of Cardiac Output

Well, okay, now we've got all of these numbers - what

do we do with them? Here's the overall idea:

We want to get blood to the tissues without

beating the heart to death.

To optimize cardiac output, we need to optimize each

of the components of cardiac output. There are four

components:

1. heart rate, 2. preload, 3. contractility, and 4. afterload.

Here are the strategies for the different components.

Heart rate If the patient is in a non-compensatory

tachycardia, such as atrial fibrillation,

atrial flutter, supraventricular

tachycardia (SVT), or paroxysmal

atrial tachycardia (PAT), the first interventions are

usually pharmacological:

Beta blocking agents: such as atenolol, metoprolol, propranolol, sotalol, or esmolol

Calcium channel blockers, such as diltiazem and verapamil

Adenosine

Amiodarone

If drugs don't work, or the patient is unstable,

synchronized cardioversion is the treatment of choice.

Ventricular tachycardia is another non-compensatory

tachycardia that should be treated immediately. If the

patient is stable, lidocaine or amiodarone are the drugs

of choice. A second line drug is procainamide. If

drugs don't convert the v-tach, or if the patient is

unstable, he/she is cardioverted.

Bradycardia is a bit more straight forward. If the heart

rate is too slow to support the cardiac output, it needs

to speed up. The drug of choice is atropine.

Epinephrine and dopamine may also be tried. Usually,

though, if atropine doesn't work, the patient is either

put on a transcutaneous pacemaker or has a

transvenous pacemaker placed.

Contractility If low contractility is the problem, the interventions

take two paths: either to increase the stretch or to

increase the strength.

Increasing the stretch goes right back to the Frank

Starling Law - if you stretch further, you should

contract back better. Crystalloids, such as normal

saline, lactated Ringers, or D5NS, will stay in the

vascular space and will stretch the myocardium.

Colloids, such as albumin, Dextran, Hespan, fresh

frozen plasma, or packed RBC's, are also used.

Colloids are preferable in situations where there is

edema, as they will act to pull fluid out of the "3rd

space" and put it back into the vasculature.

Increasing the strength should start with fixing what's

causing the decreased squeeze, such as

correcting hypoxia, hypercapnia, and

electrolyte imbalances. The squeeze can

also be increased by giving positive

inotropic drugs, like moderate dose

dopamine, dobutamine, epinephrine, or milrinone

(see page 4 to review squeeze/contractility/inotrope).

Sometimes the problem is that the contractility is too

high - the heart is squeezing harder than it has to.

Because increased contractility increases the

myocardial oxygen consumption, angina or MI may

result. Drugs are used to decrease contractility:

Beta blockers - atenolol, labetalol, metoprolol, propranolol, sotalol, timolol

Calcium channel blockers - diltiazem, felodipine, nicardipine, nifedipine, verapamil



Page 9

Preload Problems with preload fall

into two categories: there's

too much or there's too

little. If there is too much

preload, furosemide or

other diuretics are the first

choice to "unload" the heart. Renal dose dopamine

(2-5 mcg/kg/min) may be given (you may see this

given in practice, however, this practice is not

evidence-based). In special cases, dialysis may be

indicated to remove excess fluid from the body.

If there is not enough preload, it's simple - give some!

The rule of thumb is to replace like-for-like. If they

lost blood, give them PRBC's. If they've had diarrhea

and vomiting for a week, give them crystalloids.

Most cardiac surgery patients are kept on the high end

of preload with a RAP of 10 mm Hg and a PAOP of

15 mm Hg.

Afterload Just like preload, afterload can either be too high

or too low. If the afterload is too high - an SVR

> 1200, the heart is working really hard to pump

out its blood. Drugs are the first choice to

decrease a high SVR:

Nitroglycerin IV

Nitroprusside IV

If the patient is more stable, calcium channel blockers: diltiazem, felodipine, nicardipine,

nifedipine, verapamil

If pharmacologic management isn't doing the trick, an

intra-aortic balloon may be inserted. The IABP helps

to decrease SVR by deflating the balloon just before

ventricular contraction, creating almost a "vacutainer"

effect that allows the heart move blood through the

system with much less effort.

On the flip side, the SVR can be too low. A really low

SVR indicates venous pooling, in which case, the

preload drops. Vasoconstricting drugs can do the trick

to increase SVR:

Norepinephrine (Levophed®)

Phenylephrine (Neosynephrine®)

Algorithm of Treatment

Please see the algorithm on the next page for

recommended treatments to optimize cardiac output.



Page 10

Cardiac Output/Cardiac Index

Decreased

Contractility (SV, RVSWI, LVSWI)

Preload (RAP, PAOP)

Afterload (SVR, PVR)

High Low High Low High Low

Beta Blockade

Calcium

channel

blockade

Positive Inotropes:

•dobutamine

•dopamine

•milrinone

•digoxin

Dilators:

•nitroglycerin

•nitroprusside

•milrinone

•alpha and

calcium

channel

blockers

Diuretics:

•furosemide

•bumetanide

•ethacrynic acid

•mannitol

Volume:

•colloids

•crystalloids

•blood

•hetastarch

Dysrhythmia

control:

•drugs

•pacemaker

•AICD

Dilators:

•nitroglycerin

•nitroprusside

•milrinone

•alpha and

calcium

channel

blockers

IABP

increase

augmentation

Pressors:

•epinephrine

•norepinephrine

•dopamine

•neosynephrine

IABP

decrease

augmentation


© TCHP Education Consortium 10/ 2005; January 2018 edition

Page 11

Introduction Now let’s take a look at the medications that are used

to manipulate cardiac output. First data is gathered to

determine what aspects of the cardiac output need

adjustment. Patient history, physical assessment, vital

signs, and key hemodynamic parameters from the PA

catheter all contribute to the assessment data. Once

we’ve determined what the problems are, we are ready

to determine which vasoactive drugs will benefit our

patient. Remember, the primary goal is to optimize

cardiac output/index. To do that, we need to optimize

each of the components of cardiac output - the heart

rate, preload, contractility, and afterload. In order to

choose the appropriate medication, we need to keep in

mind the physiological response that these

medications produce and to titrate those effects using

the MAP and SV.

Let’s review a few relevant terms before we continue

to discuss individual medications.

Inotropic: affects contractility

A positive effect increases contractility

A negative effect decreases contractility

Chronotropic: affects the heart rate

A positive effect increases the heart rate

A negative effect decreases heart rate

Dromotropic: affects conductivity

The hemodynamic effects of vasoactive drugs occur as

a result of their interactions with receptors in the heart

and vascular system. These receptors are:

Alpha-receptors:

Are located in the blood vessels and cause vasoconstriction in most vessels, especially

the arterioles.

Increase afterload by causing peripheral vasoconstriction and increasing blood

pressure.

Beta 1 receptors:

Are located in the heart.

Have inotropic, chronotropic, and dromotropic effects.

Because of their inotropic, chronotropic, and

dromotropic effects, stimulation of the Beta 1

receptors increases contractility and heart rate,

thus increasing cardiac output.

Beta 2 receptors:

Are located in the bronchial and vascular smooth muscles.

Cause bronchodilation, and vasodilatation.

Reduce afterload.

Dopaminergic receptors:

Are located in the renal and mesenteric artery bed.

Dilate renal and mesenteric arteries.

Reduce preload by inducing diuresis /natriuresis.

According to the algorithm on page 10, preload is one

of the three factors affecting cardiac output. When

preload is too high (i.e., high RAP and PAOP),

medications are used to reduce the preload.

Medications that are used to reduce preload are

diuretics and vasodilators.

Furosemide (Lasix®) and Bumetanide (Bumex®)

Lasix®

and Bumex®

are diuretics that act on the loop

of Henle in the kidney. These medications decrease

the preload by increasing urine output, thus reducing

the work of the heart. They are used for acute

pulmonary edema, CHF, peripheral edema, and HTN.

Monitor serum electrolytes such as potassium closely

because potassium is depleted as the patient diureses.



Page 12

Expected Hemodynamic Outcome

for Lasix®

and Bumex®

Heart

rate

Preload

(RA,PAOP, PAD)

Contrac-

tility

Afterload

(SVR)

Blood

pressure

Dopamine: Renal-Dose and Low-Dose Renal-dose dopamine is used in clinical practice from

time to time. Current evidence does not support renal

dose dopamine as effective. However, the practice

persists due to the following beliefs:

Dopamine will cause different vasoactive effects depending on the dose infused. At low

doses, dopamine stimulates the dopaminergic

receptors in the arteries located in the

kidneys, abdomen, heart and brain.

The vasodilatation of renal and mesenteric arteries will cause an increase in urine output

and results in a decreased preload.

Renal-dose and low-dose dopamine are rarely used,

but the effects are listed below.

Renal-dose dopamine is used for patients who have a

high preload or low urine output. This often occurs in

patients with CHF.

Receptors stimulated by

renal and low-dose dopamine

Alpha

(Vaso-constriction)

Beta 1

(Heart rate and

contractility)

Beta 2

(Vaso-

dilatation)

Dopaminergic

(Renal dilation )

Renal-dose dopamine is generally considered to be in

the range of approximately 0.5-2mcg/kg/min.

When further reduction in preload is needed,

dopamine may be titrated up into the “low dose” range.

Low dose dopamine is approximately 2-5mcg/kg/min.

and is titrated by 1-2 mcg/kg/min every 5-10 min.

Low dose dopamine will have little to no effect on the

heart rate or blood pressure.

Expected hemodynamic outcome

for renal and low dose dopamine

Heart

rate

Preload

(RA,PAOP,

PAD)

Contractility Afterload

(SVR)

Blood

pressure

Vasodilators are used to reduce afterload and, to a

somewhat lesser extent, reduces preload. Reducing

afterload decreases the amount of squeeze needed to

circulate blood, conserving myocardial O2

consumption. Reducing preload involves getting rid

of excess fluid in the system. This decreases the

amount of blood in the right atrium prior to contraction

of the atria during the cardiac cycle. The two

medications discussed here are nitroprusside and

nitroglycerine.

Nitroprusside or Nipride Nipride is used for hypertensive emergencies to reduce

blood pressure.

Nipride relaxes the arterial and venous smooth

muscles causing vasodilatation thus decreasing

afterload. The primary effect is arterial vasodilatation.

This is a very potent medication and can quickly drop

the BP and the SVR (afterload). Monitor closely when

making any dose changes.

This medication works very quickly, which means

when you start the medication there are immediate

effects. The half-life is so short that when you stop the

medication its effects are gone.

The dosage range is 0.5 to 5 mcg/kg/min. and the

average dose is 2 mcg/kg/min. Start nipride at 0.5mcg

/kg/min and titrate by 0.25-0.5 mcg/kg/min every 2

min to achieve the desired parameters determined by

the physician. Nipride may be titrated to B/P or SVR.

Use a volumetric infusion pump to administer this

medication. Nipride may be infused in a peripheral IV.

As a vasodilator, nipride will not cause tissue damage

upon infiltration as can occur with vasopressors such

as dopamine.

Do not flush or bolus in the IV site of nipride because

the blood pressure will drop immediately. Nipride

tends to deteriorate in the presence of light. To protect

nipride from light, the container should be covered

with foil, or another opaque material and discarded

after 12 hours. An arterial line is beneficial for

continuously monitoring the blood pressure.



Page 13

At high doses or with long term therapy (>72 hours),

nipride converts to thiocyanate and may result in

cyanide toxicity. Do not exceed 10mcg/kg/min. for

longer than 10 minutes or it will increase the risk for

cyanide toxicity. If infused at this high of a rate it must

be turned off because of the potential for cyanide

toxicity.

One of the risks associated with nipride administration

is a precipitous drop in blood pressure. Sometimes

dopamine is needed to keep the blood pressure in a

therapeutic range, while providing afterload reduction.

Expected hemodynamic outcome for nipride

Heart

rate

Preload

(RA,

PAOP,

PAD)


(SVR)

Blood

pressure

Nitroglycerin Nitroglycerin is used for patients with angina and

hypertension.

This medication is a venodilator; dilating the venous

system. When the veins are dilated blood moves more

easily through the system, reducing the pressure

needed to circulate the blood around. Coronary

perfusion will increase, and both preload and afterload

will decrease.

Nitroglycerin may be infused in a peripheral IV. Use a

volumetric infusion pump. The usual dosage starts at

5-10 mcg/min. The range is 10-200 mcg /min. Titrate

nitroglycerine by 10 mcg every 5 minutes to achieve

the goal blood pressure or relief of chest pain.

The dosage of nitroglycerin may also be based on the

patient’s weight. The normal range is 0.5 –1.5 mcg

/kg/min. Titrate by 0.1 –0.2 mcg /kg every 5 minutes.

It is common to have complaints of a headache

because of the dilation happening in the cerebral

vasculature. Acetaminophen is usually effective for

headaches caused by nitroglycerine.

Expected hemodynamic outcome for Nitroglycerin

Heart

rate

Preload

(RA,

PAOP,

PAD)


(SVR)

Blood

pressure

Contractility or “squeeze” is the third component that

affects cardiac output. Drugs that have beta 1 effects

increase the contractility of the heart.

Dobutamine

Dobutamine is used for patients experiencing heart

failure, cardiogenic shock, and sometimes following

cardiac surgery for patients requiring intravenous

inotropic support.

Receptors stimulated by dobutamine

Alpha

(Vaso-

constriction)

Beta 1

(Heart rate

and

contractility)

Beta 2

(Vaso-

dilatation)

Dopaminergic

(Renal

dilation)

Minimal

Dobutamine increases cardiac contractility (a positive

inotropic effect) because of the beta 1 effect of the

medication. By increasing the squeeze of the heart or

contractility, it will help to increase the blood pressure

and cardiac output.

These same beta 1 effects also increase heart rate and

may lead to an increased myocardial oxygen demand

due to tachycardia. However, keep in mind that

dobutamine may have a lesser effect on tachycardia

than dopamine. So, if the patient is already

tachycardic, dobutamine would be your first choice

over dopamine.

Dobutamine also has beta 2 effects which cause

vasodilation, resulting in a decrease in afterload /

systemic vascular resistance. Dobutamine may also

decrease PAOP or preload to the L side of the heart.

The usual dosage is 2.5 to 20 mcg/kg/min. Start at 2

mcg/kg/min. Titrate dobutamine by 1-2 mcg/kg/min



Page 14

every 5- 10 minutes to obtain the desired MAP and

SV.

Dobutamine should be infused in a central line

because it does have some alpha (vasoconstrictive)

effects. There may be tissue necrosis if infiltration

occurs. Use a volumetric infusion pump. An arterial

line is beneficial for continuously monitoring the

blood pressure.

Expected hemodynamic outcome for dobutamine

Heart

rate

Preload

(RA,

PAOP,

PAD)


(SVR)

Blood

pressure

Milrinone (Primacor®) Milrinone is used for low cardiac output due to poor

contractility. This is commonly seen in patients with

acute, decompensated right heart failure. Milrinone is

a good medication for CHF as a short-term therapy.

Receptors stimulated by milrinone

Alpha

(Vaso-

constriction)

Beta 1

(Heart rate

and

contractility)

Beta 2

(Vaso-

dilatation)

Dopaminergic

(Renal

dilation )

none none none none

Milrinone is a good medication for improving

contractility but the mechanism of action is different

than the medications we have already discussed. It

does not stimulate the alpha or beta cells. Milrinone

increases the cyclic-AMP concentrations in the cell

which improves contractility and vasodilatation

(afterload reduction).

While milrinone increases contractility and decreases

afterload, it has minimal effect on the heart rate. This

means that it increases cardiac output without an

increase in heart rate or oxygen consumption.

Recommended dosage is a 50 mcg/kg load over 10

minutes, followed by a maintenance dose of 0.375 to

0.75 mcg/kg/min. The dose will vary depending on

renal function. Use a volumetric infusion pump and

monitor MAP and SV. Because milrinone does not

cause vasoconstriction, it may be infused peripherally.

Expected hemodynamic outcome for milrinone

Heart

rate

Preload

(RA,

PAOP,

PAD)


(SVR)

Blood

pressure

Dopamine: Medium-Dose The medium-dose range is about 5-10 mcg/kg/min.

Titrate dopamine by 1-2 mcg/kg at a time. When the

dose of dopamine is increased the beta 1 and 2

receptors are stimulated causing an increase in heart

rate, contractility and, to a lesser extent,

vasodilatation.

A medium dose of dopamine is used to achieve a

positive inotropic effect in patients with heart failure.

Heart rate also increases. When used in this fashion,

the effects are similar to dobutamine. Monitor MAP

and SV.

Receptors stimulated by medium-dose dopamine

Alpha

(Vaso-

constriction)

Beta 1

(Heart rate

and

contractility)

Beta 2

(Vaso-

dilatation)

Dopaminergic

(Renal

dilation )

Expected hemodynamic outcome for

medium-dose dopamine

Heart

rate

Preload

(RA,

PAOP,

PAD)


(SVR)

Blood

pressure

Many times critically ill patients have problems with

low blood pressure. To ensure that all the body’s

organs are being perfused properly, it is necessary to

keep the blood pressure in an acceptable range.



Page 15

Vasopressors are used to increase the blood pressure

by constricting the arterial blood vessels. Constricting

the vascular system also increases the afterload and

cardiac output. Vasopressors are used to manage such

situations as severe hypotension and cardiac arrest.

In general, all vasoactive medications should be given

in a central IV port. If a vasoconstrictor infiltrates,

tissue necrosis may occur. If this happens, notify the

physician immediately. The recommended treatment

is Phentolamine, infiltrated subcutaneously at the

extravasation site.

Vasoconstrictors clamp down or shunt blood away

from the periphery in order to give blood to the more

important organs and systems. Monitor the circulation

to the extremities as part of your routine assessments.

Dusky and/or mottled extremities that are cool or cold

to the touch can occur with peripheral

vasoconstriction. There may be a loss of the pulse

oximeter signal if blood vessels in the fingers, toes,

and ears are clamped down. There are times when the

need to maintain BP outweighs the need to maintain

good circulation to the extremities. The physician will

try to balance these needs as much as possible.

Use a volumetric infusion pump. An arterial line is

beneficial for continuously monitoring the blood

pressure.

Dopamine: High-dose (10-20 mcg/kg/min) High-dose dopamine is reserved for the treatment of

severe hypotension that is not related to hypovolemia.

Receptors stimulated by high-dose dopamine

Alpha

(Vaso-

constriction)

Beta 1

(Heart rate

and

contractility)

Beta 2

(Vaso-

dilatation)

Dopaminergic

(Renal

dilation )

In high doses, dopamine stimulates the alpha-receptors

causing vasoconstriction. This effect tends to override

the other effects that occur at lower doses (including

the vasodilator effect).

When high-dose dopamine clamps down on the blood

vessels, internal organs are not perfused as well and

the “renal effect” is lost; urine output may decrease.

Systemic vascular resistance increases and the amount

of squeeze needed to circulate the blood also increases.

Couple that with an increase in heart rate and it is easy

to see why there is also an increase of myocardial

oxygen demand.

A dopamine infusion is usually started at 5

mcg/kg/min and is titrated at 1-2 mcg/kg/min. every 5-

15 minutes until adequate results are achieved.

When you are administering high doses of dopamine,

you may want to consider using norepinephrine

(Levophed®

) in addition to dopamine, or as an

alternative. Use caution with high dose dopamine

when dealing with tachycardia.

Expected hemodynamic outcome for

high-dose dopamine

Heart

rate

Preload

(RA,

PAOP,

PAD)


(SVR)

Blood

pressure

Norepinephrine (Levophed®)

Levophed®

is used for profound hypotension caused

by such conditions as myocardial infarction,

septicemia, transfusion reactions and drug reactions. It

is the drug of choice for septic shock.

Receptors stimulated by Levophed®

Alpha

(Vaso-

constriction)

Beta 1

(Heart rate

and

contractility)

Beta 2

(Vaso-

dilatation)

Dopaminergic

(Renal

dilation )

Minimal

Levophed®

is a potent vasoconstrictor used to increase

blood pressure. The primary effects are alpha-

adrenergic effects, resulting in vasoconstriction. Used

mainly for pressor effects indicated in severe

hypotension secondary to low peripheral resistance.

When using Levophed®

, always correct hypovolemia

first. Vasoconstriction when the “tank” is dry will not

increase blood pressure. It is important to have an

adequate preload prior to the initiation of Levophed®.



Page 16

The loading dose for Levophed®

is 8-12 mcg/min.,

followed by a maintenance dose of 2-4 mcg/min. The

therapeutic dosage range is 2-12 mcg/min. Titrate by

1-2 mcg every 5-10 minutes to achieve the desired

effect.

Levophed®

has the potential to cause end-organ renal

damage with prolonged use due to vasoconstriction.

Because of the possibility of causing extreme

hypertension, monitor vital signs closely.

Expected hemodynamic outcome for Levophed®

Heart

rate

Preload

(RA,

PAOP,

PAD)


(SVR)

Blood

pressure

Phenylephrine (Neosynephrine®) Phenylephrine is used in the management of

hypotension caused by shock, anesthesia or

hypersensitivity reactions to drugs.

Receptors stimulated by phenylephrine

Alpha

(Vaso-

constriction)

Beta 1

(Heart rate

and

contractility)

Beta 2

(Vaso-

dilatation)

Dopaminergic

(Renal

dilation )

Phenylephrine has a powerful effect on the alpha-

receptors causing potent vasoconstriction, although it

is not as potent as Levophed®

. Pphenylephrine

completely lacks the chronotropic and inotropic

effects on the heart.

The usual dose of phenylephrine starts at 100-180

mcg/min then decreases to 40-60 mcg/min once

stabilized. The usual dose range is 20-200 mcg/min.

Like Levophed®

, phenylephrine also has the

possibility of causing end organ damage with

prolonged use due to vasoconstriction.

Expected hemodynamic outcome for phenylephrine

Heart

rate

Preload Contractility Afterload

(SVR)

Blood

pressure

(RA,

PAOP,

PAD)

Epinephrine (Adrenaline)

Epinephrine is naturally occurring hormone secreted

by the adrenal glands. A sympathomimetic, it imitates

almost all the actions of the sympathetic nervous

system (the “fight or flight” response). This

medication is commonly used intravenously during

cardiac arrest, and as an infusion for severe

hypotension.

Receptors stimulated by epinephrine

Alpha

(Vaso-

constriction)

Beta 1

(Heart rate

and

contractility)

Beta 2

(Vaso-

dilatation)

Dopaminergic

(Renal

dilation )

Epinephrine has mixed effects on the receptors of the

sympathetic nervous system. It stimulates alpha, beta

1 and beta 2 receptors.

The results of alpha stimulation are vasoconstriction

and an increase in blood pressure. An increase in

contractility and heart rate occur as a consequence of

beta 1 stimulation. Myocardial oxygen demand is

increased as a result.

The usual dose is 1-8 mcg/min. or 0.01-0.05

ug/kg/min. Titrate epinephrine by 1mcg/min or 0.01

mcg/kg every 5 minutes. Monitor blood pressure

every 5 minutes.

Expected hemodynamic outcome for epinephrine

Heart

rate

Preload

(RA,

PAOP,

PAD)


(SVR)

Blood

pressure



Page 17

Vasopressin (Pitressin®) Vasopressin is most commonly used for vasodilator

shock, GI bleeding, and organ donor management.

Receptors stimulated by vasopressin

Alpha

(Vaso-

constriction)

Beta 1

(Heart rate

and

contractility)

Beta 2

(Vaso-

dilatation)

Dopaminergic

(Renal

dilation )

Other

none none none none

Vasopressin is a naturally occurring anti-diuretic

hormone most commonly used in the treatment of

diabetes insipidus. The hormone is released in the

presence of a low blood volume and has direct effect

on Vasopressin 1 vascular smooth muscles receptors

causing constriction and keeps the fluid in the vascular

system (hence, anti-diuretic hormone). When

vasopressin is administered at higher doses,

vasoconstrictive effects occur due to vasopressin’s

action on vasopressin receptors.

The usual dosage is quite low, at about 0.04 units /min.

with the usual dosage range of 0.01-0.1 units/min.

Vasopressin is not usually titrated; rather it is left at a

set dose. This is very important- Vasopressin at a set

dose allows for active titration and weaning of

catecholamine drips using MAP as a guide.

Higher doses have been used with GI Bleeding,

although there is some evidence that the higher dose

may increase mortality.

Be careful in the transcription and administration of

this medication. Because of the small dosages, decimal

point errors are common when orders are written and

transcribed. A single decimal point mistake results in

a dose that is TEN TIMES what was intended.

Expected hemodynamic outcome for vasopressin

Heart

rate

Preload

(RA,

PAOP,

PAD)


(SVR)

Blood

pressure

slightly

Now let’s take a look at the different medications you

will use to manage your patient’s hemodynamic status.

Please fill in your answers in the spaces provided.

Compare your answers to those at the end of the case

studies.

Case 1:

Bob has an Anterior Wall Myocardial Infarction (AWMI) with sustained hypotension SBP < 85 and a low cardiac output due to poor contractility. There is an elevated preload to the left side of the heart (PAOP: pulmonary artery wedge), and an elevated afterload (SVR: systemic vascular resistance).

In order to manage Bob’s hemodynamics each component should be addressed.

Bob’s preload is elevated In order to optimize Bob’s preload you may want to use a.________.

Bob also has an elevated afterload (SVR).

In order to reduce the resistance the heart has to work against, afterload reducers or ________are a good choice.

In order to help Bob with the low contractility, a _______ _______medication would be beneficial.

Case 2 Your next patient, Joe, is admitted with a necrotic bowel. He has a fever of 39.8º C and a WBC of 26,000. His cardiac output is very high (9.6 L /min) and his B/P is very low: 68/ 40. His afterload or SVR is low: 480.

In order to maintain adequate arterial pressure and organ perfusion ____________are needed.

Answers: (Case 1) diuretic, vasodilators, positive inotropic. (Case 2) vasoconstrictors or pressors



Page 18

Summary

Understanding the concepts behind hemodynamics

can help you plan, implement, and evaluate your

interventions when working with patients who have

disturbances in their hemodynamic status. Every set

of numbers needs to be compared to your physical

examination of the patient and interventions are

planned accordingly. It takes continued monitoring

and intervention adjustment to maintain an optimal

outcome for the patient. We hope that this program

gave you some knowledge about hemodynamics: Why

and how we do hemodynamic monitoring, and

common vasoactive medications used in critically ill

patients.

References

1. Lehman, L., et.al., (July 2013). Methods of Blood

Pressure Measurement in the ICU, Crit Care Med. Jan

2013; 41(1): 34–40. Manuscript available online:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3724

452/

2. Lakhal, K, et.al. (2012). Noninvasive monitoring of

blood pressure in the critically ill: Reliability

according to the cuff site (arm, thigh, or ankle). Crit

Care Med, 40: 1207-1213.

Bibliography

Gahart, B. and Nazareno, A. (2017). 2017 Intravenous

Medication, 33rd ed. Elsevier, Inc., St. Louis, MO.

ISBN: 9780323297394.

Hitner, H. and Nagle, B. (2012). Pharmacology, 5th ed.

McGrawHill Publishing, Inc., NY. ISBN: 978-0-07-

352086-5.

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Shock and Infection in Critical Care Primer

© 2000 TCHP Education Consortium; 2017 edition

Page 1

Introduction

Introduction/Learning Outcomes Failure of the normal regulatory mechanisms in the

body can lead to rapid and profound shock. The

learning outcome of this home study is for learners to

self-report an improvement in their knowledge base

related to the pathophysiology of cardiogenic,

hypovolemic, anaphylactic, neurogenic, and septic

shock.

Target Audience This home study was designed for the novice critical

care or telemetry nurse; however, other health care

professionals are invited to complete this packet.

Content Objectives 1. List the classifications of shock. 2. List the functions of the cell and the

microcirculation.

3. Describe the stages of shock. 4. Describe three major mechanisms put into action

to compensate for shock.

5. Define terms related to shock.

Disclosures

Requirements for successful completion of this

educational activity: In order to successfully complete this activity you

must read the home study and complete the online

post-test and evaluation.

Conflicts of Interest It is the policy of the Twin Cities Health Professionals

Education Consortium to provide balance,

independence, and objectivity in all educational

activities sponsored by TCHP. Anyone participating in

the planning, writing, reviewing, or editing of this

program are expected to disclose to TCHP any real or

apparent relationships of a personal, professional, or

financial nature. There are no conflicts of interest that

have been disclosed to the TCHP Education

Consortium.

Expiration Date for this Activity:

As required by ANCC, this continuing education

activity must carry an expiration date. The last day that

post tests will be accepted for this edition is December

31, 2020—your envelope must be postmarked on or

before that day.

Planning Committee/Editors*

*Linda Checky, BSN, RN, MBA, Program Manager

for TCHP Education Consortium.

*Lynn Duane, MSN, RN, Assistant Program

Manager for TCHP Education Consortium.

Trent Heather, BSN, BA, Clinical Care Supervisor, SICU, Hennepin County Medical Center.

Author Karen Poor, MN, RN, Former Program Manager,


Content Experts Trent Heather, BSN, BA, Clinical Care Supervisor, SICU, Hennepin County Medical Center.

*Kelly Kreimer, MSN, RN, ICU Educator,

Minneapolis VA Health Care System.

Lynelle Scullard, BSN, RN, CCRN, Nurse Manager,

SICU, Hennepin County Medical Center.

*Denotes expert for current edition

Contact Hour Information

For completing

this Home Study and evaluation, you are eligible

to receive:

1.50 contact hours (see

information that follows)

Criteria for successful

completion: You must read the

home study and complete the

online post-test and evaluation.

The Twin Cities Health Professionals

Education Consortium is an approved

provider of continuing nursing

education by the Wisconsin Nurses

Association, an accredited approver by

the American Nurses Credentialing

Center’s Commission on

Accreditation.

Please see the last page of the packet for information

on submitting your post-test and evaluation for contact

hours.


2000 TCHP Education Consortium; 2017 edition Page 2

An Overview of Shock

Definition

Shock is a state of inadequate perfusion relative to

tissue demands.

Classification

The integrity of the circulatory system is dependent

on: (1) an efficient cardiac pump to circulate blood (2)

an adequate blood volume, and (3) a healthy vascular

bed where gas, nutrients and waste are exchanged.

The loss of any one of these three essential

components leads to one of the three major classes of

shock:

Cardiogenic: loss of an efficient cardiac pump

Hypovolemic: inadequate circulating blood volume

Distributive (neurogenic, anaphylactic, and septic): a dysfunctional vascular bed

The cascading events of shock begin with an insult,

leading to inadequate oxygen transport and cellular

dysfunction, proceeding to tissue and vascular

disturbances, and ending with organ dysfunction or

failure.

Oxygen Transport

Oxygen transport has two components: oxygen

delivery (DO2) and oxygen utilization /consumption

(VO2). Oxygen delivery (DO2) is the product of

cardiac output and arterial oxygen content.

Calculation of the arterial oxygen content depends on

(1) the hemoglobin content of blood, (2) the oxygen

saturation of hemoglobin, and (3) the amount of

oxygen bound to hemoglobin. Changes in any of these

three factors and/or changes in cardiac output alters

oxygen delivery to tissues.

Normally, systemic oxygen delivery is five times

greater than oxygen consumption. In other words, 20

percent of DO2 is absorbed (VO2), while 80 percent of

DO2 remains in returning venous blood. The body

adjusts to maintain this ratio; usually by increasing or

decreasing cardiac output.

Tissue oxygen utilization cannot be directly measured;

however, the calculation of VO2 (which can also be

obtained as the SVO2 reading from a Swan-Ganz

catheter) helps infer the amount of oxygen being used

at the cellular level and serves as a guide to the

adequacy of tissue perfusion and cellular metabolism.

Factors that determine VO2 are: (1) DO2, (2) state of

microcirculation, and (3) cellular milieu.

Other components that affect carried and released

oxygen are pH, temperature and CO2. This

relationship can be mapped with the oxyhemoglobin

dissociation curve.

Life at the Cellular Level

The cell is the unit, or building block, of all living

things. The cell has several structures that are vital for

functioning:

1. Cell membrane: a barrier with selective permeability between plasma and interstitial

fluid that allows interchanges to occur between

the cell and its environment. When damaged, it

becomes permeable to almost anything.

2. Nucleus: controls the biochemical reactions; site of cellular reproduction.

3. Cytoplasm: the protoplasm within the cell but outside of the nucleus that surrounds the

organelles; site of most cellular activity.

4. Organelles: “small cellular organs” or specialized metabolic machinery of the cell that

produce and store protein, detoxify contents, aid

in phagocytosis, and provide cellular energy.

Cellular metabolism refers to all chemical and energy

transformations that occur in the body, including

anabolic and catabolic reactions. Carbohydrates,

proteins, and fats are oxidized, producing CO2, H2O,

heat, and chemical energy. This oxidation

(catabolism) is a complex, slow process which

liberates energy (ATP) which is then utilized by the

cells in small, usable amounts.

The Microcirculation

The term microcirculation is used to describe a group

of blood vessels within the tissues that acts as an

independent organ unit in regulating blood supply to

the tissues. The functions of the microcirculation are

to:

Deliver nutrients to, and remove wastes from, cells

Adjust blood flow in response to tissue metabolic needs



Maintain intravascular/interstitial osmotic equilibrium

The portion of the vascular bed lying between the

arterioles and the venules is considered the

microcirculation. There are no distinct boundaries

between the divisions, and the arrangement and

distribution differ from tissue to tissue depending on

architecture and function.

Arteries have strong, smooth muscle walls that direct

blood to capillary beds and control the pressure of the

blood delivered to those beds. Arterioles are referred

to as “resistance vessels.” Adjustments to the blood

flow, and therefore, tissue perfusion pressure, are

made by the sympathetic innervation of these vessels.

The arteries branch into the metarterioles, and from

there into the pre-capillary sphincters. The capillaries

at the end of the arterial system form a junction with

the venous system.

It is in the capillary system that nutrients, oxygen and

waste products are exchanged from the arterial side to

the venous side. Once that process is complete, the

blood exists into the venules and finally the veins for

return to the heart and lungs.

The microcirculation is controlled by the metabolites

from surrounding tissues. These metabolites have an

intrinsic capacity to regulate blood flow to compensate

for changes in the perfusion pressure and metabolic

needs. There is a delicate balance between blood flow

and tissue demand that is maintained by the (1)

autonomic nervous system (modulates vascular tone)

and (2) hormonal, (3) chemical, and (4) metabolic

influences.

Moment to moment redistribution of blood flow

through the microcirculation is known as

autoregulation. Actively metabolizing cells release

local mediators such as K+, H+ ions, CO2, and lactic

acid, causing local vasodilatation in order to deliver

greater blood flow to vascular beds with higher

metabolic activity.

Pathophysiology of Shock: Initial Stage

This is the stage in which there are (theoretically)

cellular changes in response to shock. There are no

clinical signs or symptoms except elevated lactate

levels.

In the initial stage of shock, the cell switches from

aerobic metabolism to anaerobic metabolisn, which

causes decreased energy production and increased

lactic acid levels. Diminished blood flow to the

microcirculation and sequestration of metabolic by-

products reduces oxygen delivery and utilization. The

cell metabolism suffers, and the cell begins to

deteriorate.

Compensatory Stage of Shock

The homeostatic compensatory mechanisms of the

body are activated by decreased cardiac output.

Compensation is mediated through neural, hormonal,

and chemical changes.

Neural Compensation

Baroceptors located in the aorta and carotid bodies

sense a decrease in the blood pressure. Messages are

sent to the medullary vasomotor center that stimulate

the sympathetic nervous system (SNS). The SNS uses

the endogenous catecholamines (epinephrine and

norepinephrine), which are released from the adrenal

medulla, to:

1. Constrict the blood vessels in the skin, GI tract and kidneys

2. Dilate the blood vessels in the skeletal muscles and coronary arteries

3. Sweat 4. Increase the heart rate and cardiac contractility 5. Increase the rate and depth of breathing 6. Dilate the pupils

Hormonal Compensation

Mediated through the sympathetic nervous system,

hormonal compensation begins. The anterior

pituitary releases ACTH, which causes a release of

mineralocortocoids and glucocorticoids. The

mineralocorticoids balance the sodium and water

levels. The glucocorticoids regulate the metabolic

function of the body through the stress response.

Cortisol sensitizes the muscle of the arterioles to the

effects of catecholamines.

The posterior pituitary releases anti-diuretic

hormone (ADH), causing vasoconstriction and renal

retention of water.

The kidneys, which are flow dependent, also sense the

decreased blood pressure. The kidneys release renin



in response, which then stimulates the angiotensin and

aldosterone systems. These hormones cause:

Retention of sodium and water

Increased blood volume in the major blood vessels because of water retention and

vasoconstriction of the smaller blood vessels

Decreased urine volume and sodium excretion

Increased potassium excretion and increased urine osmolarity

Chemical Compensation

Hypoxemia and cellular hypoxia cause an increase in

respiratory depth and rate. The acid-base balance is

disturbed with the excessive “blowing off” of CO2,

which leads to respiratory alkalosis. The combination

of hypoxemia and alkalosis adversely affects the level

of consciousness.

Progressive Stage of Shock

In this stage of shock, previously helpful

compensatory responses are no longer effective.

Severe hypoperfusion to all organ systems causes

multi-organ dysfunction syndrome (multi-system

organ failure). The microcirculation loses the ability

to autoregulate blood flow, causing pooling in the

periphery and leading to decreased blood volume

returning to the central blood vessels. This causes

further organ hypoperfusion.

Refractory Stage of Shock

This final and irreversible stage reflects the very last

part of a patient’s life. The cellular and organ

destruction has been so severe that death is inevitable.

Essential versus Non-essential Organs

The body long ago developed a priority list for which

organs are perfused first when blood volume or

transport is insufficient. On the top of the list:

Brain Heart Lungs

These organs will receive the most blood possible

during shock through stimulation of the beta receptors,

which cause vasodilation.

The other organs of the body, such as the skin and gut,

have primarily alpha-receptors, which when

stimulated cause vasoconstriction. They are

considered to be “non-essential organs.”

Organ-Specific Effects of Shock

Brain - Essential Organ

Beta adrenergic stimulation dilates cerebral vessels to

attempt to maintain enough flow for a MAP of 50.

Late in shock, the vasomotor center fails to recognize

and respond to sympathetic stimulation. Early

symptoms of hypoperfusion are irritability and

agitation, replaced by unresponsiveness in late stages.

Heart - Essential Organ

In all forms of shock except cardiogenic shock, the

myocardium experiences a protective flow.

Autoregulation maintains coronary flow as long as

arterial pressure does not fall below 70 mm/Hg. The

deterioration of heart function may eventually make

shock irreversible.

All other organs are considered

biologically expendable.

Skeletal Muscle, Fat, Skin

Vasoconstriction from alpha receptor stimulation

results in muscle weakness, cramping, and fatigue.

The skin becomes cool; its color becomes ashen, then

cyanotic. The potential for skin breakdown is

enormous.

Kidneys

The kidneys view a low blood pressure as a decreased

glomerular filtration rate (GFR). In order to increase

flow, the kidneys activate the renin-angiotensin-

aldosterone compensatory mechanism. Metabolic

acidosis created by cellular increases of lactic acid is

perpetuated by the kidneys’ inability to break down

and excrete lactic acid.

Lungs

Respiratory rate increases occur as a compensatory

response to sympathetic stimulation, hypoxia, and

metabolic acidosis. The increased respiratory rate

increases pulmonary muscle oxygen consumption.



Coupled with primary damage from centrally

mediated chemicals to pulmonary capillary

endothelial cells, increased capillary permeability

results in interstitial and intra-alveolar edema and

decreased pulmonary compliance. The decreased

ventilation and impeded gas exchange that result

further decrease oxygen delivery to cells.

Mesentery

In early stages of shock, there is a marked decrease in

blood flow to the gut manifested by nausea, vomiting,

and hypoactive bowel sounds. Later, intestinal

damage and necrosis by digestive enzymes cause

damage to the protective mucosal barrier. Bacteria

and toxins are released into the bloodstream.

Hypoperfusion to the intestines also enhances the

formation and absorption of endotoxins released from

native gram negative bacteria. When released, these

endotoxins cause extensive vascular dilatation, greatly

increasing cellular metabolism despite inadequate

oxygen and nutrients to cells.

Liver

The liver filters and detoxifies drugs, metabolites, and

coagulation products. The liver also stores glucose as

glycogen. The metabolic rate of the liver is very high

with consumption of large quantities of oxygen and

nutrients. In shock, the catecholamines stimulate liver

activity. Glucose is made available to the cells, which

are unable to use it, resulting in hyperglycemia.

Hepatic ischemia results in a decrease in the liver’s

metabolic and detoxification functions. Loss of

clotting factors induce coagulopathies such as DIC.

Pancreas

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