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Hemodynamics, Shock, and Infection in Critical Care

May 14th, 2015 7:30 a.m. to 4:00 p.m.

Hennepin County Medical Center - Shapiro Building, Lower Level –

Room SL.180

Description/Purpose Statement 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 purpose of this class is to understand the principles behind hemodynamics and to look at the causes, symptoms, and types of shock. Assessment and management of patients with hemodynamic problems and shock will be addressed. Target Audience/Prerequisite This class was designed for the novice critical care or telemetry nurse who has already attended the Cardiovascular Critical Care and Neurological Critical Care classes.

Pre-requisite It is highly recommended that you attend the Cardiovascular Critical Care and Neurological Critical Care classes prior to attending this class.

Before You Come to Class You must complete the Understanding Adult Hemodynamics Primer and the Shock and Infection in Critical Care Primer. Please bring your primer post-tests to class with you for processing.

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 Trent Heather 12:15 – 1:00 p.m. Lunch 1:00 – 2:30 p.m. Infection in the ICU Environment and Sepsis and Septic Shock Trent Heather 2:30 - 2:45 p.m. Break 2:45 – 3:30 p.m. Neurogenic Shock Review and Anaphylactic Shock Trent Heather 3:30 - 4:00 p.m. Putting It All Together Trent Heather

For attending this class, you are eligible to receive:

8.4* or 7.00** contact hours (see below)

Criteria for successful completion: All participants must attend the program and complete verification and evaluation forms to receive contact hours. If you are an ANCC certified nurse, you must attend the ENTIRE activity to receive contact hours and complete the application process with TCHP. 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 primer for this class, you are eligible to receive an

additional:

2.0* or 1.66** contact hours (see below) per primer

Criteria for successful completion for all: You must read the primer, complete the post-test and evaluation, and submit it to TCHP for processing. If you are an ANCC certified nurse, you must complete the application process with TCHP.

*Denotes contact hours used for renewing licensure with the MN Board of Nursing or other Board that uses a 50 min/contact hour formula. These contact hours will be issued unless you request contact hours that comply with the ANCC formula. **Denotes contact hours used for renewing Nursing Certification with ANCC or other organization that uses the formula of 60 min/contact hour. You must request these contact hours if you need them.

Continued on next page

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://www.tchpeducation.com/coursebooks/coursebooks_main.htm

Please Read! • Check the attached map for directions to the class and assistance with parking. • Certificates of attendance will be distributed at the end of the day. • 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.

http://www.tchpeducation.com/

NOTE: the 5th Street

exit off 94 will be

permanently closed

March 30, 2015.

Follow revised “From the East” directions.

Finding the Shapiro (SL180) Conference Room at HCMC 701 South 8th Street, Minneapolis, MN 55401

Finding the classroom from Outside the Building:

Enter the main entrance of HCMC Blue building from South 8th Street (directly

across the street from the Parkside Professional Building). Once inside the door, take a right and head towards the information desk. Turn left and go past the gift shop and coffee stand to the open stairway on your right. Take the stairs to the lower level. Turn to your right at the bottom of the stairs. *Take a right at the first hallway, just past the vending area. The Shapiro (SL180) conference room will be on your right

Finding the classroom from the Hospital/Allied Ramp: Take the ramp elevators to the lower level. Follow the signs to the hospital. Follow the hallway past the stairway. Follow directions above from *.

Driving Directions to HCMC:

From the Northeast:

Take 35W south to Exit 17C (Washington Avenue). Turn right onto Washington. Follow

Washington Avenue to Chicago Avenue and turn left. Take a left onto 9th street. Turn left

again to enter the Allied Ramp. Take the ramp elevator to the lower level and follow the

instructions above.*

From the Northwest: Take I-94 east to exit 230 (4th Street). Follow 4th Street through

downtown to Chicago Avenue and turn right onto Chicago Avenue. Follow Chicago to 9th

Street and turn left. Turn left again to enter the Allied Ramp. Take the ramp elevators to

the lower level and follow the instructions above.*

From the East: Take I-94 W to the 11th Street (233A) exit. Take a right onto Grant Street.

Follow Grant Street; it will turn into East 14th Street. Turn left on Chicago Avenue. Follow

Downtown

East/Metrodome Light Rail Station

Hospital/ Allied Parking Ramp

B Building

Main Entrance

http://www.metrotransit.org/rail/stations/04_metrodome.asp



Chicago to 9th Street South and turn right. Turn left to enter the Allied Ramp (see map on

next page). Take the ramp elevators to the lower level and follow the instructions on the

previous page.*

From the South: Take 35W North to exit 16A (downtown exit). Take 5th Avenue exit;

follow 5th Avenue to 8th Street and turn right. Turn right on Chicago Avenue and in one

block, turn left on 9th Street. Take a left to enter the Allied Ramp. Take the ramp elevators

to the lower level and follow the instructions on the previous page.*

From the West: Take 394 east to exit 9B (6th Street). Follow 6th Street to Chicago

Avenue; turn right onto Chicago. Take Chicago Avenue to 9th Street and turn left. Turn left

again to enter the Allied Ramp. Take the ramp elevators to the lower level and follow the

directions on the previous page.*

Public transportation is another options for getting downtown. For bus schedules and

information, go to www.metrotransit.org. Light Rail Transit to HCMC: HCMC is located at

the corner of Park Ave. and 6th Street, conveniently located just 1-1/2 blocks south of the

Downtown East/Metrodome station of the Light Rail Transit line. Light Rail information is

available at www.metrotransit.org/rail/index.asp.

Parking:

There are various options for parking around HCMC, but we suggest you park in the

Hospital/Allied Ramp. Directions and maps guide you to and from this ramp. Meters are

available around the hospital and vary in price. Check www.mplsparking.com for rates. Parking rates are subject to change without notice, but the current cost of park in the Allied ramp is $11.00. (cash or credit using the payment kiosk as you exit). The program coordinator will have a limited number of discount coupons for the Hospital/Allied Ramp available for $6.00. You must pay with cash or check in the exact amount for the discount

coupon—change is not available.

-

Visit www.hcmc.org for

more maps and directions.

E = Hospital/

Allied Ramp

(*parking lot

entrance)

3 = HCMC, Blue

Building

E = Hospital/

Allied Ramp

(*parking lot

entrance)

3 = HCMC, Blue

Building

Visit www.hcmc.org for

more maps and directions.

http://www.metrotransit.org/

http://www.metrotransit.org/rail/index.asp

http://www.mplsparking.com/

http://www.hcmc.org/

http://www.hcmc.org/

From the East:

Take I-94 W to the 11th Street (233A) exit. Take a right onto Grant Street. Follow Grant

Street; it will turn into East 14th Street. Turn left on Chicago Avenue. Follow Chicago to 9th

Street South and turn right. Turn left to enter the Allied Ramp.

This home study is pre-reading for these TCHP classes:

• Cardiovascular Surgery Course • Hemodynamic Monitoring

Please complete this activity and bring your post-test and evaluation to class with you.

Understanding Adult Hemodynamics

A Primer for: Cardiovascular Surgery and

Hemodynamic Monitoring

© 11/2005 TCHP Education Consortium.

This educational activity expires March 27, 2015.

All rights reserved. Copying without permission is forbidden

TTCCHHPP Education Consortium


A Primer for: Cardiovascular Surgery and Hemodynamic Monitoring © TCHP Education Consortium October, 2005

Page 1

Understanding Adult Hemodynamics: A Primer for Cardiovascular Surgery and Hemodynamic Monitoring

Introduction/Purpose Statement

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 purpose of this home study program is to give a brief introduction to hemodynamic monitoring - how we do it, what the numbers mean, and how we can optimize the movement of blood in the body. You’ll also learn about a variety of pharmacologic strategies that are used to improve cardiac output.

• CV Surgery Class

All patients undergoing cardiovascular surgery will have some sort of hemodynamic monitoring. If you are unfamiliar with hemodynamic monitoring, you should read this primer to be able to understand content presented in the CV Surgery class.

• Hemodynamic Monitoring Class

This primer was developed to give you a starting point in learning how to manage patients with hemodynamic monitoring. This primer can be used as either a stand-alone educational activity or as an introduction to the "Hemodynamic Monitoring" class.

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, complete the post-test and evaluation, and submit them for processing.

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.

Relevant Financial Relationships and Resolution of Conflicts of Interest:



Page 2

If a conflict of interest or relevant financial relationship is found to exist, the following steps are taken to resolve the conflict:

1. Writers, content reviewers, editors and/or program planners will be instructed to carefully review the materials to eliminate any potential bias.

2. TCHP will review written materials to audit for potential bias.

3. Evaluations will be monitored for evidence of bias and steps 1 and 2 above will be taken if there is a perceived bias by the participants.

No relevant financial relationships have been disclosed to the TCHP Education Consortium.

Sponsorship or Commercial Support:

Learners will be informed of: • Any commercial support or

sponsorship received in support of the educational activity,

• Any relationships with commercial interests noted by members of the planning committee, writers, reviewers or editors will be disclosed prior to, or at the start of, the program materials.

This activity has received no commercial support outside of the TCHP consortium of hospitals other than tuition for the home study program by non-TCHP hospital participants.

If participants have specific questions regarding relationships with commercial interests reported by planners, writers, reviewers or editors, please contact the TCHP office.

Non-Endorsement of Products:

Any products that are pictured in enduring written materials are for educational purposes only. Endorsement by WNA-CEAP, ANCC, or TCHP of these products should not be implied or inferred.

Off-Label Use:

It is expected that writers and/or reviewers will disclose to TCHP when “off-label” uses of commercial products are discussed in enduring written materials. Off-label use of products is not covered in this program.

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 March 27, 2015—your envelope must be postmarked on or before that day.

Planning Committee/Editors Linda Checky, BSN, RN, MBA, Assistant Program Manager for TCHP Education Consortium.

Lynn Duane, MSN, RN, Program Manager for TCHP Education Consortium.

Authors

Karen Poor, MN, RN, Former Program Manager for the TCHP Education Consortium.

Sharon Stanke, MSN, RN, Nursing Instructor in Critical Care, Minneapolis VA Medical Center.

Content Experts

Denise Rogich, PharmD, Pharmacist at the Minneapolis VA Medical Center.

*Sharon Stanke, MSN, RN, Nursing Instructor in Critical Care, Minneapolis VA Medical Center.

Carrie Wenner, PharmD, Pharmacist at the Minneapolis VA Medical Center.

*Denotes reviewer of the current edition



Page 3

Contact Hour Information

For completing this Home Study and evaluation, you are eligible to receive:

2.0 MN Board of Nursing contact hours / 1.66 ANCC contact hours

Criteria for successful completion: You must read the home study packet, complete the post-test and evaluation, and submit them to TCHP for processing.

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 before the post-test for information on submitting your post-test and evaluation for contact hours.



Page 4

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.

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 = SV x HR 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. It 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



Page 5

• Vagal stimulation (bearing down)

• 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.

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."

Contractility increases (the heart squeezes harder) from:

• 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 6

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.

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

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



Page 7

• 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

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 system 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.

The Pulmonary Artery Catheter The pulmonary artery (PA) catheter is also known as the Swan Ganz catheter. It will measure three different pressures directly and is the method 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 placed 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 information about the left side 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:



Page 8

• 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. The normal value for RV pressure is 20-30 systolic/0-5 diastolic.

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/10-20 diastolic.

Increased pressures are found in:

• Atrial or septal defects

• Pulmonary hypertension

• LV failure

• Mitral stenosis

Pulmonary capillary wedge pressure

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 PCWP 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 PCWP is decreased with:

• Hypovolemia

• Vasodilation

The diastolic number of the PA pressure is often used instead of the PCWP, particularly in cardiac surgery patients. The PAD is always higher (by 1-4 mm Hg) than the PCWP, 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. 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

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

PCWP: 8-12 mm Hg Left heart preload



Page 9

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 - the heart rate, preload, contractility, and 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

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.

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 - acebutolol, atenolol, carteolol, labetalol, metoprolol, nadolol, oxprenolol, penbutolol, pindolol, propranolol, sotalol, timolol

• Calcium channel blockers - bepridil, diltiazem, felodipine, isradipine, nicardipine, nifedipine, verapamil

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. In special cases, dialysis may be indicated to remove excess fluid from the body.



Page 10

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 6-8 mm Hg and a PCWP of 12-14 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, isradipine, 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 to work much less hard to get the blood out.

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.



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Cardiac Output/Cardiac Index Decreased

Contractility (SV, RVSWI, LVSWI)

Preload (RAP, PCWP)

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



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Hemodynamic Pharmacology

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. 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.

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.

Diuretics: Decreasing Preload

According to the algorithm on page 8, preload is one of the three factors affecting cardiac output. When preload is too high (i.e., high RAP and PCWP), 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.



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Expected Hemodynamic Outcome for Lasix® and Bumex®

Heart rate

Preload (RA,PAW, PAD)

Contrac-tility

Afterload

(SVR)

Blood pressure

Dopamine: Renal-Dose and Low-Dose 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 causes an increase in urine output and results in a decreased preload. This is referred to as “renal-dose dopamine.” Although renal-dose and low-dose dopamine increases urine output it does not prevent renal dysfunction or death.

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,PAW, PAD)

Contractility Afterload

(SVR)

Blood pressure

Vasodilators: Decreasing Afterload and Preload

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



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discarded after 12 hours. An arterial line is beneficial for continuously monitoring the blood pressure.

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, PAW,

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, PAW,

PAD)


(SVR)

Blood pressure

Positive Inotropes: Improving Contractility

Contractility or “squeeze” is the third component that affects cardiac output. Drugs that have beta 1 effects increase the contractility o 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.

Dobutamine also has beta 2 effects which cause vasodilation, resulting in a decrease in afterload / systemic vascular resistance. Dobutamine may also decrease PAW or preload to the L side of the heart.



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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 every 5- 10 minutes to obtain the desired B/P.

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, PAW,

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


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.

Because milrinone does not cause vasoconstriction, it may be infused peripherally.

Expected hemodynamic outcome for milrinone

Heart rate

Preload

(RA, PAW,

PAD)


(SVR)

Blood pressure

Dopamine: Medium-Dose Remember “renal-dose” dopamine? 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.

Receptors stimulated by medium-dose dopamine

Alpha

(Vaso-constriction)

Beta 1


Beta 2

(Vaso-dilatation)

Dopaminergic

(Renal dilation )

The medium-dose range is about 5-10 mcg/kg/min.

Expected hemodynamic outcome for medium-dose dopamine

Heart rate

Preload

(RA, PAW,

PAD)


(SVR)

Blood pressure

Inotropes/ Vasopressors: Increasing Afterload

Many times critically ill patients have problems with low blood pressure. To ensure that all the body’s



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organs are being perfused properly, it is necessary to keep the blood pressure in an acceptable range.

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 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


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.

Expected hemodynamic outcome for high-dose dopamine

Heart rate

Preload

(RA, PAW,

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.

Receptors stimulated by Levophed®

Alpha

(Vaso-constriction)

Beta 1


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



Page 17

not increase blood pressure. Levophed is an especially good medication for septic shock.

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, PAW,

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


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®. phenylephrine 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

(RA, PAW,

PAD)


(SVR)

Blood pressure

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


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, PAW,

PAD)


(SVR)

Blood pressure



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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


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 V1 vascular smooth muscles receptors causing constriction. 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. If blood pressure management is indicated, it is best to use other medications.

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, PAW,

PAD)


(SVR)

Blood pressure

Applying Concepts to Case Examples

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 (PAW: 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 19

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.

Directions for Submitting Your Post Test for Contact Hours

You have received this packet as pre-reading to prepare you for attending a TCHP class. If you have paid to attend the class, the cost of this home study is covered by your course tuition. Please fill out the attached post-test and evaluation and bring them with you to class. The program coordinator will process your post-test for contact hours and return it to you with a certificate of completion.

HCMC employees only: it is preferred that you complete this home study on the HCMC intranet if it is available. TCHP home studies can be accessed under My Learning Center.

If you are unable to complete the post-test and evaluation prior to class, you can mail it in later to TCHP:

HCMC – TCHP Office

701 Park Avenue – Mail Code SL Minneapolis, MN 55415*

Please make a copy of your post-test prior to mailing as it will not be returned to you. Paid participants may request contact hours for this home study without a processing charge up to 3 months after you have taken the class.

*Please check the TCHP website for updates to our address: www.tchpeducation.com



Page 20

Post- Test: Understanding Adult Hemodynamics Please print all information clearly and sign the verification statement:

Name

(please print legal name above)

Birth date (required)

Format: 01/03/1999 M M D D Y Y Y Y

Email:________________________________________________

For TCHP Consortium Hospital employees only:

Hospital Unit

Personal verification of successful completion of this educational activity (required):

I verify that I have read this home study and have completed the post-test and evaluation.

Signature

1) Components that make up cardiac output are:

a) Heart rate x preload b) Stroke volume x afterload c) Stroke volume x heart rate d) Heart rate x contractility

2) Cardiac index refers to:

a) Cardiac output adjusted for body surface area

b) Classification of system for MIs c) Cardiac vessel disease d) Both B & C

3) All of the following are main factors for stroke

volume except:

a) Contractility b) Heart rate c) Afterload d) Preload

4) Afterload is determined by

a) Compliance of the aorta b) How thick or thin the blood is c) SVR d) Both A & B e) All of the above

5) The RAP is:

a) Decreased with volume loss b) Preload to the heart c) Normally between 2-6 mm Hg d) All of the above

6) Which of the following is used to increase

preload?

a) Giving volume b) Using vasodilators c) Using vasopressors

Match the medication to the action below:

7. ____ Low dose dopamine

8. ____ Epinephrine

9. ____ Medium-dose dopamine

10. ____ Nitroprusside

11. ____ Nitroglycerin

12. ____ Levophed®

a) Reduces BP

b) Increases urine output but does not prevent renal dysfunction or death.

c) Venodilator

d) Increases “squeeze”

e) Vasoconstrictor

f) Alpha, beta 1 & 2 stimulant

Expiration date: The last day that post tests will be accepted for this edition is March 27, 2015—your envelope must be postmarked on or before that day.

Primer completed with Class



Page 21



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Evaluation: Understanding Adult Hemodynamics Please complete the evaluation form below by placing an “X” in the box that best fits your evaluation of this educational activity. Completion of this form is required to successfully complete the activity and be awarded contact hours.

At the end of this home study program, I am able to: Strongly Agree

Agree Neutral Disagree Strongly Disagree

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.

5. The teaching / learning resources were effective. If not, please comment:

The following were disclosed in writing prior to, or at the start of, this educational activity (please refer to the first 2 pages of the booklet). Yes No

6. Notice of requirements for successful completion, including purpose and objectives

7. Conflict of interest

8. Disclosure of relevant financial relationships and mechanism to identify and resolve conflicts of interest

9. Sponsorship or commercial support

10. Non-endorsement of products

11. Off-label use

12. Expiration Date for Awarding Contact Hours

13. Did you, as a participant, notice any bias in this educational activity that was not previously disclosed? If yes, please describe the nature of the bias:

14. How long did it take you to read this home study and complete the post test and evaluation:

______hours and ______minutes.

15. Did you feel that the number of contact hours offered for this educational activity was appropriate for the amount of time you spent on it?

____Yes

____No, more contact hours should have been offered

____No, fewer contact hours should have been offered.

Expiration date: March 27, 2015

This home study is pre-reading for this TCHP class:

• Shock and Infection in Critical Care Please complete this activity and bring your post-test and evaluation to class with you.

Shock and Infection in Critical Care Primer © 2000, 2007 TCHP Education Consortium. This educational activity expires March 27, 2015. All rights reserved. Copying without permission is forbidden.

TTCCHHPP Education Consortium

Shock and Infection in Critical Care Primer

© 2007 TCHP Education Consortium Page 1

Introduction Introduction/Purpose Statement Failure of the normal regulatory mechanisms in the body can lead to rapid and profound shock. The purpose of this home study is to review the pathophysiology of cardiogenic, hypovolemic, anaphylactic, and neurogenic shock. A brief review of sepsis and septic shock is also covered. 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 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, complete the post-test and evaluation, and submit them for processing. 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. Relevant Financial Relationships and Resolution of Conflicts of Interest:

If a conflict of interest or relevant financial relationship is found to exist, the following steps are taken to resolve the conflict:

1. Writers, content reviewers, editors and/or program planners will be instructed to carefully review the materials to eliminate any potential bias.

2. TCHP will review written materials to audit for potential bias.

3. Evaluations will be monitored for evidence of bias and steps 1 and 2 above will be taken if there is a perceived bias by the participants.

No relevant financial relationships have been disclosed to the TCHP Education Consortium. Sponsorship or Commercial Support: Learners will be informed of:

• Any commercial support or sponsorship received in support of the educational activity,

• Any relationships with commercial interests noted by members of the planning committee, writers, reviewers or editors will be disclosed prior to, or at the start of, the program materials.

This activity has received no commercial support outside of the TCHP consortium of hospitals other than tuition for the home study program by non-TCHP hospital participants. If participants have specific questions regarding relationships with commercial interests reported by planners, writers, reviewers or editors, please contact the TCHP office. Non-Endorsement of Products: Any products that are pictured in enduring written materials are for educational purposes only. Endorsement by WNA-CEAP, ANCC, or TCHP of these products should not be implied or inferred. Off-Label Use: It is expected that writers and/or reviewers will disclose to TCHP when “off-label” uses of commercial products are discussed in enduring written materials. Off-label use of products is not covered in this program.



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 March 27, 2015—your envelope must be postmarked on or before that day.

Planning Committee/Editors

Linda Checky, BSN, RN, MBA, Assistant Program Manager for TCHP Education Consortium.

Lynn Duane, MSN, RN, Program Manager for TCHP Education Consortium.

Author Karen Poor, MN, RN, Former Program Manager, TCHP Education Consortium Content Expert Lynelle Scullard, BSN, RN, CCRN, Clinical Care Supervisor, SICU, Hennepin County Medical Center.

Contact Hour Information

For completing this Home Study and evaluation, you are eligible to receive:

2.0 MN Board of Nursing contact hours / 1.66 ANCC contact hours Criteria for successful completion: You must read the home study packet, complete the post-test and evaluation and submit them to TCHP for processing. 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 before the post-test for information on submitting your post-test and evaluation for contact hours.



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: (a) efficient cardiac pump, (b) an adequate blood volume, and (c) a healthy vascular bed. 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 blood volume • Distributive (neurogenic, anaphylactic, and

septic): an unhealthy vascular bed The cascading events of shock begin with inadequate oxygen transport and cellular dysfunction, which proceed to tissue and vascular disturbances, and end 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 infers utilization 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.

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; site of most cellular activity.

4. Organelles: 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) 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. The artery has a strong, smooth muscle wall, and directs blood to capillary beds and controls 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, is made by the sympathetic innervation and vasomotor influences. 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. 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), (2) humoral, (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+ ion, 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 also no clinical signs or symptoms except elevated lactate levels. In the initial stage of shock, the cell switches from aerobic metabolism to anaerobic metabolism, which causes decreased energy production and increased lactic acid levels. Diminished blood flow to the microcirculation reduces oxygen delivery and sequesters metabolic by-products, thereby reducing 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 stimulates the sympathetic nervous system. 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 contractility 5. Increase the rate and depth of breathing 6. Dilate the pupils

Hormonal Compensation Mediated through the sympathetic nervous system, humoral 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 arteriole to the effects of catecholamines. The posterior pituitary releases 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 “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, 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 scant amounts of blood. 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 causes 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 makes 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 ashen to cyanotic. The potential for skin breakdown is enormous.

Kidneys The low blood pressure is seen as a decreased glomerular filtration rate (GFR) by the kidney. 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 Hyperpnea occurs 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. Resultant decreased ventilation and impeded gas exchange 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 its metabolic and detoxification functions. Loss of clotting factors induce coagulopathies such as DIC.

Pancreas Shock induces the release of amylase and lipase into the circulation. A chemical called myocardial depressant factor (MDF), released from the pancreas, decreases myocardial contractility.

Cardiogenic Shock Cardiogenic shock is caused by inadequate myocardial contractility from acute myocardial infarction, coronary artery disease, or mechanical factors (valvular regurgitation, low output syndrome, arrhythmias).

Pathophysiology of Cardiogenic Shock In cardiogenic shock, the left ventricle has been injured in some way, leading to impaired pumping.

Decreased tissue perfusion

Decreased BP

Decreased C.O

Decreased S.V.

Pulmonary interstitial edemaIntra-alveolar edema

Increased pulmonarycapillary pressure

Increased pulmonaryvenous pressure

IncreasedLAP

Elevated left ventricularfilling pressure

Inadequate systolic emptying

Impaired pumping abilityof the left ventricle

Because the pumping is ineffective, less blood is pushed out with each heartbeat, leading to a decreased stroke volume*. The heart rate increases to compensate for a low cardiac output and blood pressure, but will eventually be insufficient to compensate for the decreased stroke volume. The tissues begin to be inadequately perfused. The impaired pumping also leads to less blood being pushed from the ventricle during systole. The left ventricle gradually fills with more and more blood, causing an elevated pressure within the LV and left atrium. This pressure “backs up” into the pulmonary vasculature, causing an increased pulmonary capillary pressure. * Stroke volume = the amount of blood pumped out of the left ventricle with each contraction.

Hypovolemic Shock In hypovolemic shock, there is a critical depletion of intravascular volume from hemorrhage (most common), plasma loss due to burns, dehydration, traumatic shock due to blood loss and major tissue damage.



Pathophysiology of Hypovolemic Shock The pathophysiologic process of hypovolemic shock is straight-forward. Blood and/or fluids have left the body, causing a decreased amount of volume in the blood vessels.

Inadequate tissue perfusion

Decreased cardiac output

Decreased stroke volume

Decreased ventricular filling

Decreased venous return

Decreased intravascular volume

Venous return is decreased because of the lack of fluid in the vascular space, causing decreased ventricular filling. The ventricles do not have as much blood as normal to pump out, so the stroke volume is decreased. The heart rate will increase to compensate for the diminished stroke volume and resulting poor cardiac output and blood pressure. Eventually, if the fluid or blood loss continues, the heart rate will not be able to compensate for the decreased stroke volume. The end result of hypovolemic shock is inadequate tissue perfusion.

Neurogenic Shock Neurogenic shock is caused by the loss of sympathetic control (tone) of resistance vessels, resulting in the massive dilatation of arterioles and venules. Neurogenic shock can be caused by general or spinal anesthesia, spinal cord injury, pain, and anxiety.

Pathophysiology of Neurogenic Shock

Tissue perfusion

Cardiac output

Stroke volume

Venous return

Venous dilation

Peripheral vascularresistance

Arteriolar dilation

Massive vasodilation

Loss of sympathetic tone

In neurogenic shock, there has been an insult to the nervous system so that impulses from the sympathetic nervous system (the fight or flight response) cannot maintain normal vascular tone or stimulate vasoconstriction. The lack of SNS stimulation causes a massive venous and arterial vasodilation. On the venous side, blood pools in the distensible veins and does not return to the larger veins. Because of this pooling, there is a diminished amount of blood that returns to the heart. Stroke volume, cardiac output, and blood pressure all fall. On the arterial side, there is decreased peripheral vascular resistance, which actually helps the heart to pump with less energy. The drawback is that with decreased peripheral pressure, there is not the driving force to get blood, oxygen, and nutrients to the cells. This also causes a small degree of arterial blood pooling, which decreases the amount of blood returning to the heart.



Anaphylactic Shock Shock due to the severe allergic antigen-antibody reaction to substances such as drugs, contrast media, blood products, or insect or animal venom is called anaphylactic shock. Food products such as seafood, nuts, peanuts, peanut butter, and MSG can also cause anaphylactic shock.

Pathophysiology of Anaphylactic Shock

Venous & arterial dilation

Massivevasodilation

Interstitial edemaRelative hypovolemia

Capillarypermeability

Release of vaso-active mediators

Antigen-antibody reaction

Activation ofsensitized antibodies

Exposure to antigen

The immune system goes “haywire” in anaphylactic shock in an extreme allergic reaction. At some point, the individual is exposed to the substance and develops antibodies against it. On subsequent exposure to the substance (the antigen), these antibodies will aggressively bind to the antigen, forming an antigen-antibody complex. This complex causes the release of chemicals that cause vasodilation (in particular, histamine). Both veins and arteries vasodilate, leading to decreased blood returning to the heart. The capillaries become permeable to nearly everything, allowing fluids, proteins, and sometimes blood to pass through into the interstitial space. This causes massive interstitial edema. The vasodilation and fluid sequestration in the interstitium causes a relative hypovolemia.

Septic Shock Sepsis is a condition that occurs in many critically ill patients. Sepsis is the systemic response to infection. Many types of organisms can cause sepsis, including gram-negative bacteria, gram-positive bacteria, and fungi. The infections can occur anywhere in the body; urinary tract infections are probably the most common cause of sepsis. Septic shock is said to occur when the sepsis has progressed to the point where it is affecting many organ systems.

Pathophysiology of Septic Shock The immune and inflammatory response begins to try to combat the organism that is causing an infection. The body releases multiple chemicals into the blood stream, including cytokines, vasodilators, complement factors, and free radicals. In septic shock, this response is not adequate to eliminate the infection and actually causes increased damage. The organism itself also releases substances called endotoxins or exotoxins, which further harm the organs and tissues. The combination of these chemicals and toxins cause: (1) peripheral vasodilation – interstitial edema and decreased blood return to the heart, and (2) decreased ability of the cells and tissues to take up oxygen and nutrients. The heart tries harder and harder to get oxygen and nutrients to the cells by increasing the heart rate and contractility initially, sometimes driving the cardiac output twice to three times its normal amount. Eventually, however, the immune response and compensatory mechanisms may not enough to combat the infection and resulting cellular destruction. The patient may develop multi-organ dysfunction syndrome (MODS); AKA multi-system organ failure (MSOF).

Conclusion Patients with a wide variety of problems can develop shock. Knowing the underlying pathophysiology may help guide you in assessing and managing the care of the patient with cardiogenic, hypovolemia, and distributive types of shock.



Resources 1. Barone, J., and Snyder, A. (1991). Treatment

strategies in shock: Use of oxygen transport measurements. Heart and Lung, 20(1), 81-86.

2. Rice, V. (1992). Shock, a clinical syndrome: An update. Part 1: An overview of shock. Critical Care Nurse, 11(4), 20-27.

3. Rice, V. (1992). Shock, a clinical syndrome: An update. Part 2: The stages of shock. Critical Care Nurse, 11(5), 74-82.

4. Rice, V. (1992). Shock, a clinical syndrome: An update. Part 3: Therapeutic Management. Critical Care Nurse, 11(6), 34-39.

5. Rice, V. (1992). Shock, a clinical syndrome: An update. Part 4: Nursing care of the shock patient. Critical Care Nurse, 11(7), 28-38.

Recommended Reading 1. Brozenee S, Russell SS. (1999). Core

Curriculum for Medical-Surgical Nursing, 2nd ed. Academy of Medical-Surgical Nurses, Janetti NJ.

2. Phipps WJ, Sands JK, Marek JF, eds. (1999)..Medical-Surgical Nursing: Concepts & Clinical Practice, 6th ed. St. Louis: Mosby, Inc.

3. Seidel HM, Ball JW, Dains JE et al, eds.(2002) Mosby's Guide to Physical Examination, 5th ed. St. Louis: Mosby, Inc.

4. Stillwell, S. (2002). Mosby’s Critical Care Nursing Reference. 3rd ed. St. Louis, Mo: Mosby/Elsevier.

5. Smeltzer SC, Bare BG, eds. (2002) Brunner & Suddarth's Textbook of Medical-Surgical Nursing, 10th ed. Philadelphia: Lippincott William and Wilkins.

6. Wiegand, D.J.L. & Carlson, K.K. (eds.) (2005). AACN Procedure Manual fro Critical Care. 5th ed. Philadelphia: Elsevier.

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1) The sympathetic nervous system will do all of

the following actions in response to a low cardiac output except: a) increase cardiac rate and contractility b) constrict the pupils c) dilate blood vessels in the skeletal muscles

and coronary arteries d) sweat

2) Which organ is considered essential in relation to

blood supply in the shock states? a) gastrointestinal tract b) kidneys c) heart d) lungs

3) The two pathophysiologic processes that occur in cardiogenic shock are: a) anoxia and decreased tissue perfusion b) decreased stroke volume and inadequate

systolic emptying c) low cardiac output and high urine output d) pulmonary edema and decreased stroke

volume 4) What is the most common cause of hypovolemic

shock? a) dehydration b) burns c) hemorrhage d) vomiting

5) The massive vasodilation that occurs in

neurogenic shock results in: a) venous dilation b) arteriolar dilation c) decreased cardiac output d) all of the above

6) What of the following will NOT cause

anaphylactic shock? a) a first bee sting b) blood products c) peanut butter d) contrast media

7) The most common cause agent of septic shock

is: a) upper respiratory infection b) urinary tract infection c) central line infection d) none of the above

Expiration date: The last day that post tests will be accepted for this edition is March 27, 2015—your envelope must be postmarked on or before that day.

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Expiration date: March 27, 2015

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