tchp education consortium · 2020. 1. 7. · understanding adult hemodynamics ©tchp education...
TRANSCRIPT
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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
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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
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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.
TCHP Education Consortium
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.
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Understanding Adult Hemodynamics
©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.
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Understanding Adult Hemodynamics
©TCHP Education Consortium, 10/2005; January 2018v.2 edition
Page 2
Authors
Karen Poor, MN, RN, Former Program Manager for
the TCHP Education Consortium.
Sharon Stanke, DNP, MSN, RN, Nursing Instructor
in Critical Care, Minneapolis VA Health Care System.
Content Experts
Denise Rogich, PharmD, Pharmacist at the
Minneapolis VA Medical Center.
*Sharon Stanke, DNP, MSN, RN, Nursing Instructor
in Critical Care, Minneapolis VA Health Care System.
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.
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Understanding Adult Hemodynamics
©TCHP Education Consortium, 10/2005; January 2018v.2 edition
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)
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Understanding Adult Hemodynamics
©TCHP Education Consortium, 10/2005; January 2018v.2 edition
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.
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Understanding Adult Hemodynamics
©TCHP Education Consortium, 10/2005; January 2018v.2 edition
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
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Understanding Adult Hemodynamics
©TCHP Education Consortium, 10/2005; January 2018v.2 edition
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
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Understanding Adult Hemodynamics
©TCHP Education Consortium, 10/2005; January 2018v.2 edition
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
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Understanding Adult Hemodynamics
©TCHP Education Consortium, 10/2005; January 2018v.2 edition
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
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Understanding Adult Hemodynamics
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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.
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Understanding Adult Hemodynamics
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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
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Understanding Adult Hemodynamics
© 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.
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Understanding Adult Hemodynamics
© TCHP Education Consortium 10/ 2005; January 2018 edition
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.
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Understanding Adult Hemodynamics
© TCHP Education Consortium 10/ 2005; January 2018 edition
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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)
Contractility Afterload
(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)
Contractility Afterload
(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
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Understanding Adult Hemodynamics
© TCHP Education Consortium 10/ 2005; January 2018 edition
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)
Contractility Afterload
(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)
Contractility Afterload
(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)
Contractility Afterload
(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.
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Understanding Adult Hemodynamics
© TCHP Education Consortium 10/ 2005; January 2018 edition
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)
Contractility Afterload
(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®.
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Understanding Adult Hemodynamics
© TCHP Education Consortium 10/ 2005; January 2018 edition
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)
Contractility Afterload
(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)
Contractility Afterload
(SVR)
Blood
pressure
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Understanding Adult Hemodynamics
© TCHP Education Consortium 10/ 2005; January 2018 edition
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)
Contractility Afterload
(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
-
Understanding Adult Hemodynamics
© TCHP Education Consortium 10/ 2005; January 2018 edition
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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you are paying for. You can also pay online
http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=23269127http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=23269127http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3724452/http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3724452/
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Understanding Adult Hemodynamics
© TCHP Education Consortium 10/ 2005; January 2018 edition
Page 19
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Shock in Critical Care Primer
© 2000 TCHP Education Consortium. Revised 2007, 2015, 12/2017
This educational activity expires December 31, 2020. All rights reserved. Copying, electronic transmission and sharing without permission is forbidden.
TCHP Education Consortium
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.
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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,
TCHP Education Consortium
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.
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Shock in Critical Care Primer
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
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Shock in Critical Care Primer
2000 TCHP Education Consortium; 2017 edition Page 3
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
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Shock in Critical Care Primer
2000 TCHP Education Consortium; 2017 edition Page 4
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.
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Shock in Critical Care Primer
2000 TCHP Education Consortium; 2017 edition Page 5
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