Download February 9, 2015 - Twin Cities Health Professionals Education

TCHP
Education
Consortium
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.
Cardiovascular Critical Care
February 9th, 2015
7:30 a.m. to 4:00 p.m.
Minneapolis VA Simulation Center
(Building in the parking lot North of the hospital)
Please read driving and parking directions carefully
Description/Purpose Statement
Cardiac and vascular diseases are becoming more and more common in American society. Critical care nurses routinely see patients with a wide
variety of cardiovascular problems. The purpose of this class is to learn how to assess and care for the patient experiencing problems such as angina,
myocardial infarction, peripheral vascular disease, hypertension, congestive heart failure, cardiomyopathy, and cardiogenic shock. Simulation will be
provided to reinforce course content.
Target Audience/Prerequisite
This class was designed for the novice critical care or telemetry nurse; however, other health care professionals are welcome to attend.
Before You Come to Class
You must complete the Cardiovascular Critical Care 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.
7:45 - 9:15 a.m.
9:15- 9:30 a.m
9:30 – 10:00 a.m.
10:00 a.m. -12:00 p.m.
12:00 - 12:45 p.m.
12:45 - 1:45 p.m.
1:45 - 2:00 p.m.
2:00 – 4:00 p.m.
Registration
Hypertensive Urgencies and Emergencies; Vascular Disease
Break
Congestive Heart Failure and Cardiomyopathies
Acute Coronary Syndrome (ACS)
Lunch
Cardiogenic Shock and SVO2
Break
Cardiac Simulations and Debriefing
Cleo Bonham
Cleo Bonham
Robin Rabey
Robin Rabey
Robin Rabey /Cleo Bonham
Continuing Education Credit
For attending
this class, you
are eligible to
receive:
8.4* or 7.00** contact hours (see below).
If you complete the primer
for this class, you are
eligible to receive an
additional:
2.0* or 1.66** contact hours per primer (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.
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.
Please Read!
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•
•
•
•
•
•
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.
Directions to the Minneapolis VA Simulation Center, Building 68,
Entry Door 68-2, Room 227, One Veterans Drive, Minneapolis, MN 55417
The VA Simulation Center is located on the second floor of Building 68 in Room 227
Please allow at least TEN minutes to get to the classroom from either the hospital or parking lots.
Driving Directions
th
Take Hwy. 55 to 54 Street and go
west. Go past the stop sign on
Minnehaha and turn left at the second
entrance into the VA parking lot.
Visitors should park in Lot 11 (overflow
lot) or in Lots 9 or 10.
Parking Directions
Head towards the building which is northwest of the hospital. Enter using the
southeast entrance that faces parking Lot 7. The door is to the right of the
smoking shelter (“68-2” sign located above the door). The northwest entrance
is for the daycare—do not go in this door. Entry to the second floor is only
available through the stairwell or elevator. Walk through the door directly
across from the elevator to the end of the hall to room 227.
There is a light rail station in front of the Minneapolis VA Health Care System. Check http://www.metrotransit.org/light-rail
for information on taking the light rail.
NOTE: There is not a cafeteria in this building. Please bring refreshments (snacks and drinks) for break time and consider
packing a lunch so that you don’t need to walk to and from the hospital. There is not a refrigerator available. Dress in
layers to accommodate fluctuations in temperature. Doors to the Simulation Center Room will not be open until
approximately 7:30 a.m. Doors to the building should be open by 7:00 a.m.
Map of surrounding roads to the Minneapolis VA Health Care System: Sim. Center
More detailed driving directions:
th
From the East (St. Paul): Take 35E south to West 7 /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
th
to the right and go to the next stoplight (54 ) and turn left.*
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
th
west. As you exit on 55 west, it will “Y” almost immediately. Stay to the right and go to the next stoplight (54 ) and
turn left.*
From the North: Take 35W south to 62 east. Get into the right lane on 62 and exit on 55 west. At the top of the exit
nd
th
ramp, turn left to continue on 55 west. Go to the 2 stoplight (54 ) and turn left.*
From the South: Take 35W north to 62 east. Get into the right lane on 62 and exit on 55 west. At the top of the exit
nd
th
ramp, turn left to continue on 55 west. Go to the 2 stoplight (54 ) and turn left.*
From the West: Take 494 east to 35W north. Take 62 east. Get into the right lane on 62 and exit on 55 west. At the
nd
th
top of the exit ramp, turn left to continue on 55 west. Go to the 2 stoplight (54 ) and turn left.*
*Go past the stop sign on Minnehaha and turn left at the second entrance into the VA parking lot. Visitors should park
in Lot 11 (overflow lot) or in Lots 9 or 10.
TCHP
Education
Consortium
This home study is pre-reading for a class.
Please complete this activity and bring your
post-test and evaluation to class with you.
Cardiovascular Critical Care Primer
© 2000 TCHP Education Consortium. Revised 2007, 2010, 2014
This educational activity expires March 27, 2015
All rights reserved. Copying, electronic transmission and sharing without permission is forbidden.
Introduction/Purpose Statement
Cardiac and vascular diseases are becoming more and
more common in American society. Critical care nurses
routinely see patients with a wide variety of
cardiovascular problems. The purpose of this home study
is to increase your understanding of the anatomy,
physiology, and pathophysiology of problems such as
angina, myocardial infarction, peripheral vascular disease,
congestive heart failure, and cardiomyopathy.
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.
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
March 27, 2015—your envelope must be
postmarked on or before that day.
Planning Committee/Editors*
*Linda Checky, BSN, RN, MBA, Program Manager for
TCHP Education Consortium.
Content Objectives
1.
2.
3.
4.
5.
6.
7.
*Lynn Duane, MSN, RN, Assistant Program Manager
for TCHP Education Consortium.
Identify the normal anatomy and physiology of the
cardiovascular system.
Describe the pathophysiology of an acute
myocardial infarction.
Describe the symptoms of heart failure.
Describe the pathophysiology of tamponade.
Identify the factors that favor the development of a
venous thrombosis.
Differentiate between dilated, hypertrophic, and
restrictive cardiomyopathy.
Differentiate between Buerger’s Disease and
Raynaud’s Syndrome.
Authors
Marie Langer, RN, MA, CCRN, Staff Nurse in the
CICU at Regions Hospital.
Karen Poor, MN, RN, Former Program Manager for the
TCHP Education Consortium.
Content Experts/Reviewers
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
Professionals Education Consortium to
balance, independence, and objectivity
educational activities sponsored by TCHP.
Robin Rabey, MSN, RN, Critical Care Educator at the
Minneapolis VA Health Care System.
Cleo Bonham, MSN, RN, Critical Care Educator at the
Minneapolis VA Health Care System.
Colleen Johannsen, RN, Staff Nurse in the Heart and
Vascular Care Unit at Regions Hospital.
Marie Langer, RN, MA, CCRN, Staff Nurse in the
CICU at Regions Hospital.
*Robin Rabey, MSN, RN, Critical Care Educator at the
Minneapolis VA Health Care System.
Sharon Stanke, MSN, RN, Critical Care Educator at the
Minneapolis VA Health Care System.
*Denotes reviewer of current edition
Health
provide
in all
Anyone
Cardiovascular Critical Care Primer
© 2000 TCHP Education Consortium; 2014 edition
Page 1
Contact Hour Information
For completing
this
Home
Study
and
evaluation,
you are eligible
to receive:
2.0* or 1.66** contact hours (see
below)
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.
*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 on the evaluation form if
you need them.
Please see the last page of the packet before the post-test
for information on submitting your post-test and
evaluation for contact hours.
Cardiovascular Critical Care Primer
© 2000 TCHP Education Consortium; 2014 edition
Page 2
Peripheral Vascular Disease
As opposed to cardiac or cerebrovascular disease,
peripheral vascular disease refers to problems within the
blood vessels in the extremities, thorax, and abdomen.
The majority of peripheral vascular disease problems are
caused by atherosclerosis, just like cardiac and cerebral
vascular disease.
Arterial Vascular Disease
There are three major problems that can arise in the
arterial vasculature: atherosclerotic occlusion, aneurysm,
and embolization.
femoral) are related to the lack of arterial flow. The distal
extremity becomes cool, pale or cyanotic, with poor or
absent pulses.
Pain often accompanies arterial
insufficiency because the distal tissues are starved for
oxygen. The symptoms of carotid arterial insufficiency
result from brain anoxia – ranging from transient ischemic
attacks to completed stroke.
Bruits are common in both ileofemoral and carotid artery
insufficiency. A bruit is the sound that is heard when the
pressure in the vessel prior to the lumen narrowing is
high, and the pressure after the narrowed area is low. The
resulting turbulent blood flow causes a low-pitched
“whooshing” sound.
Aneurysm
Atherosclerosis
Atherosclerosis – or arteriosclerosis in the artery – is the
primary cause of all vascular problems in the United
States. In this process, there is a gradual build up of
plaque on the intimal wall of the artery caused by
repeated injury, clotting, and scarring.
Problems in the arterial system arise when the amount of
plaque build up has grown to such as an extent that blood
is no longer able to pass easily through the narrowed
arterial diameter. This is called arterial insufficiency.
When blood cannot pass through at all, it is called arterial
occlusion.
Normal cross-section of an artery
Beginning of atheroma
Partial occlusion with clot formation
An aneurysm is a weak area in an arterial wall. This
weakening
can
be
caused
by
hypertension,
atherosclerosis, smoking, or may be congenital. There
are three layers of the artery: the intima, the media, and
the adventitia.
Intima
Adventitia
Media
While there is initially just a weakening in the media of
the arterial wall, eventually pressure will build up and
cause the weakened area of the artery to begin to balloon.
There are two main types of aneurysms: Saccular and
fusiform.
Fusiform aneurysms appear as a nearly symmetrical bulge
around the circumference of the weakened area of the
affected vessel. Saccular aneurysms appear as a blister on
one side of the vessel. They may be caused by trauma,
such as a motor vehicle crash.
Occluded vessel
Fusiform aneurysm
Although the most common sites of arterial insufficiency
and occlusion are the carotid, renal, popliteal, aortoiliac
and femoral arteries, any junction or branching area can
develop problems.
The symptoms of arterial insufficiency or occlusion in the
arteries that supply the legs (popliteal, aortoiliac, and
(side view of an artery)
There is a large dilation of the artery
closest to the heart with a gradual
narrowing.
Cardiovascular Critical Care Primer
© 2000 TCHP Education Consortium; 2014 edition
Page 3
Saccular aneurysm
reaches a branch through which it cannot travel.. At that
point, the embolus will block blood flow distal to the
occlusion.
(side view of an artery)
There is an outpouching on one
side of the artery
Venous Vascular Disease
The most common form of vascular disease related to the
venous system is the development of deep vein
thrombosis. Typically found in the lower extremities
(particularly the calves), a thrombus occludes venous
return to the heart. Pressure backs up from below the
thrombus, causing edema to form distal to the occlusion.
Many aneurysms lie dormant without symptoms for years.
Other aneurysms can continue to grow in size until their
mass causes symptoms or they rupture.
Although any artery can develop an aneurysm, the most
dangerous ones are in the aorta. The aorta is the major
artery in the body. It branches from the left ventricle and
traverses down through the thorax (thoracic aorta) and the
abdomen (abdominal aorta), giving off branches to supply
all of the body organs with blood.
Symptoms from an aortic aneurysm may include dyspnea,
stridor, hoarseness, hemoptysis, cough, or chest pain. All
of these symptoms are related to the mass of the aneurysm
impinging on other organs. Pain is the main symptom of
descending thoracic aortic aneurysm: pain in the shoulder,
lower back, abdomen, shoulders, arms, or neck. Finally,
abdominal aneurysms usually have no symptoms until
they leak or rupture.
Leaking or rupture of an aortic aneurysm is usually a lifethreatening emergency. If the wall is weakened enough,
the aneurysm will rupture, resulting in aortic blood being
pumped into either the chest or abdominal cavity. The
patient may bleed to death (exsanguinate) in a very short
time. More commonly, patients who complain of severe,
unrelenting pain, shortness of breath, faintness, etc., may
be experiencing the leaking of blood from the aneurysm.
Similar to aneurysms, an aortic dissection is more
common than an aortic aneurysm rupture. A dissection is
said to occur when there is a longitudinal split between
the intima and the media of the thoracic aorta. A
dissection may occur after trauma, or due to Marfan’s
syndrome,
increasing
age,
hypertension,
or
atherosclerosis.
Embolization
The third cause of peripheral vascular insufficiency is
embolism. An embolus can begin as either a clot formed
in the heart or as a piece of dislodged plaque. An
embolus will travel through the arterial system until it
Cardiovascular Critical Care Primer
© 2000 TCHP Education Consortium; 2014 edition
Page 4
The first stage of deep vein thrombosis (DVT) formation
is injury.
The second stage is intravascular clot
formation. If that clot (thrombus) does not become
detached and form an embolus, it will adhere to the vein
wall within 24-48 hours and eventually be lysed.
The three components needed to cause a DVT are defined
in Virchow’s triad:
1. Hypercoagulability of the blood: blood dyscrasias,
trauma, cancer, estrogen therapy, systemic infection,
smoking
2. Venous stasis: heart disease (CHF), dehydration,
immobility, incompetent leg vein valves
3. Intimal damage: trauma, infection, venipuncture, IV
infusion of irritant solutions.
Buerger’s Disease and Raynaud’s
Syndrome
Buerger’s Disease, or Thromboangiitis Obliterans, (TOA)
is a rare condition that presents as an inflammation and
eventual blockage of the small vessels of the extremities.
In rare cases, internal organs are affected. Unlike other
vascular diseases, it is neither an embolic nor an
atherosclerotic disease. The classic patient is a 20-40 year
old smoker, usually male. Non-smoking tobacco users are
at risk as well. There is likely a genetic component to it,
as it is far more prevalent in certain ethnic groups.
TOA is characterized by reduced blood flow to the
extremities, with collateral circulation developing in an
ineffective corkscrew pattern (visible on angiogram).
Symptoms are related to lack of blood flow: coldness of
the extremity, intermittent claudication (pain or cramping
that occurs in the legs when walking), and numbness,
tingling, and burning sensations. Symptoms start at the
tips of the fingers and toes and progress upward. As the
disease progresses, there is ulceration of the tips of the
digits, and eventually gangrene. Amputation of the digits
can only be avoided by abstaining from all forms of
tobacco.
Exposure to cold worsens the symptoms. The extremity is
sensitive to loss of blood flow caused by elevation above
the level of the heart. Care to avoid cold and constricting
medications is important. Treatments such as
sympathectomies, (a surgical procedure that destroys
nerves in the sympathetic nervous system provide only
temporary relief, as do vasodilating drugs).
The cause is unknown, but tobacco is thought to be a
trigger for an autoimmune or inflammatory process. TOA
is often accompanied by Raynaud’s Syndrome.
Treatment is generally aimed at control of symptoms.
This involves avoiding offending drugs, including
caffeine and tobacco. Protection of the extremities by
keeping warm in cold weather and when handling cold
and frozen objects can prevent attacks. Patients also need
to be aware that significant cooling after exercise can
trigger an attack, making it important to cool down
slowly.
Some drugs, such as topical nitroglycerin, Viagra, ace
inhibitors, and calcium channel blockers may relieve
symptoms. Open wounds, blackening of the skin, breaks
in the skin, and joint soreness surrounding the affected
areas need to be evaluated and treated.
Figure 2 Raynaud's Syndrome (eMedicine.com)
Figure 1: Buerger’s Disease with thrombophlebitis of the
great toe. (emedicine.medscape.com)
In Raynaud’s Syndrome, the arterioles of the extremities
constrict in response to exposure to cold or stress. There
is a cyclical response, with the fingers, toes, and the tips
of the nose and ears turning pale due to lack of blood
flow. As oxygen is consumed, the color turns to bluish.
Then, as the arterioles relax and blood refills, the
extremity becomes flushed, and then returns to normal
color. Attacks may last minutes or hours.
Primary Raynaud’s occurs with no associated cause, and
is generally a milder form, with little pain. Secondary
Raynaud’s may be associated with vasoconstricting drugs,
frostbite, repetitive motion or vibration injury, smoking,
or thoracic outlet syndrome. Secondary Raynaud’s is
more painful and may also be associated with Buerger’s
disease.
Hypertension & Hypertensive Crisis
Mr. Jerome Atwater enters the Emergency Department
with complaints of headache, dizziness, and chest pain.
He has a 30 year history of hypertension. His initial vital
signs are: HR of 145, sinus tachycardia; BP of 210/138
mm Hg; RR of 24/minute. The initial diagnosis is
hypertensive crisis.
What is blood pressure?
The arterial blood pressure is the pressure within the
arteries that drives blood into the circulation. The blood
pressure is determined by the cardiac output multiplied by
the systemic resistance. There are three main elements to
blood pressure:
Cardiovascular Critical Care Primer
© 2000 TCHP Education Consortium; 2014 edition
Page 5

The systolic blood pressure (SBP) is the pressure
in the arteries that occurs with ejection from the
left ventricle.

The diastolic blood pressure (DBP) is the
pressure that has been “stored up” in the arteries
during the relaxation of the heart.
The
sympathetic nervous system (SNS) maintains the
muscle tone in the arteries.

The mean arterial pressure (MAP) is the average
blood pressure in the systemic circulation.
vasoconstricts the blood vessels and stimulates the
kidneys to reabsorb water.
Hypertension is defined as...
Although definitions may vary, the American Heart
Association defines hypertension as a consistently
elevated blood pressure of > 140 mm Hg systolic and/or >
90 mm Hg diastolic.
What causes hypertension?
How is blood pressure controlled?
There are many mechanisms that work to control the
blood pressure.
Baroreceptors: receptors in the aortic arch and carotid
artery bodies that are sensitive to pressure. Stimulation of
these receptors occurs with either a low or high BP.
Information sent to the medulla results in a change in the
heart rate and vascular tone of the arteries.
Chemoreceptors:
situated near the baroreceptors,
chemoreceptors are sensitive to changes in the pH, PaO 2,
and PaCO2. The chemoreceptors are stimulated when the
PaCO2 rises and when the pH and PaO2 falls with
hypotension. Information is sent to the medulla.
Autonomic nervous system:

The parasympathetic nervous system decreases
cardiac output (CO) and BP by decreasing the heart
rate.

The sympathetic nervous system increases the CO by
increasing the heart rate and cardiac contractility, and
by vasoconstricting the blood vessels, thus increasing
BP.
Renin-Angiotensin-Aldosterone system:
Renin is
released by the kidneys in response to a decrease in blood
pressure. Renin combines with angiotensinogen to form
angiotensin I, which is then converted to angiotensin II.
Angiotensin II causes massive vasoconstriction and
stimulates aldosterone. Aldosterone causes the kidney
tubules to reabsorb water and sodium.
Renal prostaglandins: These hormones weaken the
action of the renin-angiotensin-aldosterone system.
Vasopressin: Also known as antidiuretic hormone
(ADH), vasopressin is released with a decrease in blood
volume or an increase in serum osmolality.
It
Cardiovascular Critical Care Primer
© 2000 TCHP Education Consortium; 2014 edition
Page 6
Ninety to ninety-five percent of hypertension is called
“primary” or “essential” hypertension. There is no known
cause for primary hypertension. Risk factors that are
suspected in the development of primary hypertension
are:









Family history
Advancing age
Race
High sodium intake
Obesity
Excess alcohol consumption
Low intake of potassium, calcium, magnesium
Stress
Use of oral contraceptive drugs
The remaining cases of hypertension are lumped into the
category of “secondary hypertension.” Causes for this
type
of
hypertension
include
renal
disease,
arteriosclerosis,
coarctation
of
the
aorta,
pheochromocytoma, elevated levels of adrenocortical
hormones, and brain lesions.
Why is hypertension harmful?
The main problem with hypertension is that it places a
larger burden on the heart and blood vessels than they are
built for. The workload of the heart increases because it
has to pump harder against resistance to push blood out.
This leads to ventricular muscle hypertrophy, which
increases myocardial oxygen demand. Eventually the
oxygen demand outstrips the supply, leading to angina,
myocardial infarction, and congestive heart failure.
The arteries throughout the body are also affected by
hypertension.
Hypertension appears to speed the
development of atherosclerosis, affecting the coronary
arteries and renal vasculature. An elevated blood pressure
can also cause an outpouching in a weak part of an
arterial wall. This outpouching is called an aneurysm.
Aneurysms can occur in any blood vessel in the body;
especially the aorta, the retina, and the brain.
What is occurring with Mr. Atwater?
Mr. Atwater is experiencing a hypertensive crisis.
Hypertension is a “crisis” when the diastolic BP increases
above 120 mmHg, and when there is organ damage. It is
generally accompanied by renal disorders, vascular
changes and retinopathy. The extremely high pressure
causes an intense reflex vasoconstriction in the brain, in
the brain’s attempt to preserve itself. This measure is
often not successful, and cerebral edema develops,
causing papilledema (swelling of the optic nerve at the
point of its entrance into the eye), headache, restlessness,
confusion, stupor, motor and sensory deficits, and visual
disturbances. The continued high BP injures the walls of
the arterioles, especially in the kidney and retina. Retinal
hemorrhage and kidney failure occur as a result.
Cardiomyopathy
What is cardiomyopathy?
Cardiomyopathy is a term that is used to describe a
problem with the functioning of the heart muscle. There
are three forms:
1. Dilated (congestive)
2. Hypertrophic
3. Restrictive
to dilated cardiomyopathy, sometimes called alcoholic
cardiomyopathy. Other potential causes: pregnancy,
viral infections, certain chemotherapy drugs, and a
hereditary disposition.
What causes the signs and symptoms of dilated
cardiomyopathy?
Some people with dilated cardiomyopathy can live for a
long time without symptoms. When symptoms do begin,
however, they resemble those of congestive heart failure.
As the left heart fails, the left ventricle is not able to pump
out the blood that is filling it. The pressure in the left
ventricle rises, eventually causing fluid to back up into the
pulmonary system. As the pressure in the pulmonary
system rises, fluid is forced out of the capillary bed into
the alveoli. Pulmonary edema ensues, with shortness of
breath, cough with frothy or blood tinged sputum, and
crackles bilaterally.
As the right heart fails, the right ventricle cannot pump
out its share of blood, leading to increased pressure in the
venous system. Fluid is forced out of the venous system
into the peripheral circulation, causing edema of the
extremities.
People with dilated cardiomyopathy can also develop
cardiac dysrhythmias, particularly atrial fibrillation and
ventricular dysrhythmias.
Dilated Cardiomyopathy
Hypertrophic Cardiomyopathy
Dilated cardiomyopathy is the most common form of
cardiomyopathy. In this form, the heart muscle fibers are
stretched beyond their normal size.
This stretching
causes the heart chambers to become dilated and the walls
of the heart to become thinner. The stretched muscle
fibers are not able to contract well, resulting in poor
cardiac contractility and inadequate ejection of blood.
This eventually leads to increased dilation, and
eventually, to congestive heart failure.
Hypertrophic cardiomyopathy is the second most
common form of cardiomyopathy. In this type of
cardiomyopathy, there is an abnormal overgrowth of
muscle fibers, leading to decreased ventricular chamber
size and increased ventricular wall size.
As the
cardiomyopathy progresses, there is little room for blood
in the ventricles, and limited relaxation of the ventricles
during diastole, causing a decreased amount of blood to
be pumped into the circulation with each beat.
See how the ventricles are
enlarged and the walls surrounding
them are thin?
Note how the ventricle
chamber size is about the
same
as
the
atrial
chamber size (much too
small) and the walls of the
ventricle are very thick.
What are the causes of dilated cardiomyopathy?
The majority of cases of dilated cardiomyopathy are
idiopathic – that is, no one knows why they have
developed this condition. Alcohol abuse has been linked
Another name for hypertrophic cardiomyopathy is
hypertrophic obstructive cardiomyopathy (HOCM).
Cardiovascular Critical Care Primer
© 2000 TCHP Education Consortium; 2014 edition
Page 7
What are the causes of hypertrophic cardiomyopathy?
About 50% of all cases seem to be related to a genetic
abnormality transmitted by one or both parents. The other
cases do not have an identifiable cause. Hypertrophic
cardiomyopathy is not caused by exercise; the
conditioned heart has more muscle mass, but the
ventricular chamber size remains adequate, as does the
ability to contract and relax.
What are the signs and symptoms caused by?
The cause of the symptomology of hypertrophic
cardiomyopathy is related to inadequate stroke volume
(the amount of blood pumped out of the left ventricle with
each contraction). The patient’s heart rate may be normal
or even fast, but the patient cannot get enough blood to
the vital organs. Symptoms arising from inadequate
blood supply are: shortness of breath, fainting during
activity, palpitations, chest pain, or fatigue. Ventricular
fibrillation can be the first indicator of a problem, and
may lead to sudden death.
Congestive Heart Failure
Mr. Wood enters the hospital after a three-day history of
chest pain. The EKG indicates that Mr. Wood has had an
anterior wall MI. The day after admission, Mr. Wood
begins to show the signs and symptoms of heart failure.
He is hypotensive and tachycardic, with a respiratory rate
of 26. His respirations are labored; rales are auscultated
in the middle and lower lobes of his lungs. He is anxious.
What is heart failure?
The term “heart failure” indicates that the heart has been
damaged so that it does not pump blood adequately,
causing decreased tissue perfusion and back up into the
peripheral circulation. Although heart failure can be
classified as left or right in etiology, the failure of one
side of the heart usually leads to failure on the opposite
side. The pathophysiology for both left and right heart
failure is the same, as shown below:
As the condition progresses to the severe stage,
congestive heart failure results as the pressure in the heart
rises to such an extent that blood “backs up” into the
lungs and periphery.
Heart pumps
ineffectively
Blood backs up
into the venous system
There is insufficient
blood going to the tissues
Venous pressure
increases
Kidneys retain
sodium and water
Capillary pressure
Blood volume
Restrictive Cardiomyopathy
Restrictive cardiomyopathy is rare in the United States.
In this case, there is no chamber size or ventricle wall size
change; rather, the walls of the ventricle become stiff and
noncompliant. Abnormal tissue, caused by amyloidosis,
hemochromatosis, or sarcoidosis, invades the walls of the
ventricle, causing the contractility to be compromised.
The chamber and
wall
sizes
are
normal;
however,
the wall itself is rigid
and noncompliant.
Fluid leaks from the
capillaries into the
tissues
Edema develops
The signs and symptoms of restrictive cardiomyopathy
are essentially the same as dilated cardiomyopathy:
weakness, fatigue, shortness of breath, edema, nausea and
bloating.
Tissues become hypoxic
What is the route of blood through the
heart?
The right side of the heart is a low pressure, high capacity
venous system. Blood enters the right atrium from the
superior and inferior vena cava. Passive filling and
active contraction of the atria pushes the blood through
Cardiovascular Critical Care Primer
© 2000 TCHP Education Consortium; 2014 edition
Page 8
the tricuspid valve into the right ventricle. As the right
ventricle fills, it actively expels the blood through the
pulmonic valve into the pulmonary artery and into the
lungs for re-oxygenation.
The renin-angiotensin-aldosterone system is also
stimulated, causing further vasoconstriction and the
retention of water and sodium.
Rales and Respiratory Rate
The left side of the heart is a high pressure arterial system
whose size is regulated by different muscle walls.
Arteries have the ability to dilate and constrict as
stimulated by the sympathetic nervous system in a
response to baroreceptor reflexes, oxygenation status,
presence of hypercarbia, and CNS stimulation.
When the blood exits the pulmonary circulation through
the pulmonary vein, it enters the left atrium. From the
left atrium, the blood is expelled through the mitral valve
into the left ventricle, and is then ejected through the
aortic valve. The aorta is the gateway into the systemic
circulation from the aorta’s origin on the left ventricle.
Aorta
Superior vena
cava
Pulmonary
artery
Left atrium
Right atrium
Left ventricle
Inferior
vena cava
Right ventricle
What are the pathophysiologic
mechanisms for Mr. Wood’s symptoms?
Hypotension and Tachycardia
As Mr. Wood’s heart fails to pump adequately, the
baroreceptors located in the aortic arch and carotid bodies
sense a decreased blood pressure. This will stimulate the
Sympathetic Nervous System (SNS) to release the
catecholamines (epinephrine and norepinephrine), which
increases the heart rate and the pumping action
(contractility) of the heart, and constricts the peripheral
blood vessels to attempt to get more blood into the central
system.
The inadequate pumping of Mr. Woods’ heart causes a
backup into the lungs from the left side of the heart. The
pressure inside the pulmonary blood vessels increases to
such a point that fluid (plasma) escapes into an area of
less pressure - the alveoli and smaller airways. This is
known as cardiogenic pulmonary edema. Fluid in the
airways will “bubble” with respiration, causing the
crackling sound of rales. This fluid also impairs gas
exchange, which triggers the medulla to increase
respiratory rate and effort.
Anxiety
The decrease in oxygenation from pulmonary edema and
the actions of the catecholamines combine to cause
anxiety in the heart failure patient. In severe cases, these
physiologic mechanisms can cause a feeling of
“impending doom.”
What signs and symptoms indicate left
sided heart failure?
All patients with heart failure will exhibit fatigue and
weakness, and an S3 and S4 may be auscultated. The
patient with left-sided heart failure will exhibit signs that
relate to the arterial flow of blood.
Symptoms of Left-Sided Heart Failure










Anxiety
Orthopnea, dyspnea, tachypnea
Cough with frothy sputum
Diaphoresis
Basilar rales, rhonchi
Cyanosis, hypoxia, respiratory acidosis
Elevated Pulmonary Artery Diastolic Pressure (PA
diastolic), Pulmonary Capillary Wedge Pressure (PCWP)
Nocturia
Mental confusion
Pulsus alternans (arterial pulse waveform that has
alternating strong and weak beats, and almost always
indicates left ventricular systolic impairment)
Cardiovascular Critical Care Primer
© 2000 TCHP Education Consortium; 2014 edition
Page 9
What signs and symptoms indicate right
sided heart failure?
Right-sided heart failure manifests in the venous side of
blood flow.
Symptoms of Right-Sided Heart Failure









Hepatomegaly / splenomegaly
Dependent pitting edema
Venous distention, hepatojugular reflux (an alternative
method to measure venous pressure through distension of
the internal jugular vein)
Bounding pulses
Oliguria
Dysrhythmias
Elevated Central Venous Pressure (CVP), Right Atrial
(RA), and Right Ventricle (RV) pressures
Kussmaul’s sign (A rise in jugular venous pressure on
inspiration)
Abdominal pain, anorexia, weight gain
From the Core Curriculum for Critical Care Nurses, J. Alspach
(ed.).
Angina and Myocardial Infarction
Mr. Caleb Ash presents to his family physician with the
complaint of chest pain that “comes and goes.” His
physician suspects that Mr. Ash may have angina. He
orders a stress test and echocardiogram.
What is angina?
Angina is a "warning sign" of myocardial damage.
Because the heart has no direct pain receptors or
messengers, the pain of myocardial ischemia is through
nerves sent back to the spinal cord. The spinal cord sends
out the urgent pain messages through other spinal nerves,
which may manifest as chest pressure; tightness; arm,
back or jaw pain; or GI distress may be the patients'
symptoms. Whatever manifestation the warning takes,
the symptoms are known as "angina."
1.
2.
3.
4.
5.
Age: Males > 45 years; Females > 55 years or
premature menopause without estrogen therapy
History of premature coronary artery disease (CAD)
in a first degree relative (parent, sibling)
Current cigarette smoking
Hypertension > 140/90 or on medication
High density lipid (HDL) count < 35
The factor that is “negative” or is likely to subtract
another risk factor is:
1. High density lipid (HDL) count > 60
How is angina diagnosed?
Mr. Ash’s physician has ordered two of the most common
tests for diagnosis of angina.
The stress
electrocardiogram is a test which combines electrical
rhythm monitoring with exertion. The patient is placed
on a treadmill or other exercise machine and exercises
until either angina is experienced or there are EKG - ST
depression/ T wave inversion changes.
An echocardiogram is a noninvasive diagnostic test that
bounces sound waves from the probe off of the structures
below it, i.e., the heart. A visual picture forms on the
echocardiogram screen. Cardiac wall movement
abnormalities, chamber size, valve function, and blood
flow can be assessed using this test.
Although the resting echocardiogram was normal, Mr.
Ash’s stress test was abnormal. His physician ordered a
coronary angiogram for the next week.
The most common angiographic procedure done is the
coronary angiogram. The term "coronary angiogram" is
commonly used to describe a number of diagnostic tests
that can be performed in the cardiac catheterization lab.
Included in these diagnostic tests are:
What causes angina?
Left main c. a.
Circumflex c.a.
Angina is caused by myocardial ischemia. Causes of
myocardial
ischemia
include
atherosclerosis,
hypertension, anemia, dysrhythmias, shock, congestive
heart failure, and coronary artery spasm. Atherosclerosis
is the most common cause of myocardial ischemia.
Right
c.a.
Left anterior
descending c.a.
What are the risk factors for Atherosclerosis?
The risk factors that are “positive” or are likely to cause
atherosclerosis include:
Cardiovascular Critical Care Primer
© 2000 TCHP Education Consortium; 2014 edition
Page 10

Coronary arteriogram:
viewing the coronary
arteries through the use of dye

Right heart cath: obtaining volumes and pressures
in the right heart

Left heart cath: obtaining volumes and pressures in
the left heart

Aortogram: obtaining information about the size,
function, and pressure of the aorta

Ventriculogram: through the use of dye, obtaining
the ejection capability of the heart
During the weekend, Mr. Ash had several episodes of
angina. On Sunday evening, the angina was not relieved
with three nitroglycerin tablets. As instructed by his
physician, his wife called 911. Mr. Ash was brought into
the Emergency Room, where he was evaluated for an
acute myocardial infarction (AMI).
What is a myocardial infarction?
A myocardial infarction, or MI, is the end result of tissue
ischemia. An MI indicates that cells in the myocardium
have been anoxic and have died. There are three phases
in the evolution of an MI: ischemia, injury, and
infarction.
In ischemia, the myocardium is deprived of oxygen
and/or blood. At this point, if the blood supply or oxygen
is returned, the myocardium will return to normal. Injury
is the next phase of an MI, where the cells have become
damaged from the lack of oxygen. If interventions are
started in time, the myocardium will return to normal.
Infarction occurs when the cells are deprived of oxygen
long enough to die. Infarction is irreparable.
Immediately to 7 days after an MI, the infarcted area is
"mushy" and friable. The cells are dead, and no longer
contract or move. After about seven days, collagen scar
tissue forms over the area, making the infarcted region
more stable. Stretching of the dead tissue before seven
days can lead to either a ventricular aneurysm and rupture
or to remodeling (thickening of the muscle) of the
expanded area, which will lead to congestive heart failure.
What arteries supply the heart?
The heart needs oxygenated blood like any other tissue in
the body. All of the coronary arterial blood supply arises
from two "holes" in the root of the aorta, called coronary
ostia. During contraction of the ventricles, the coronary
ostia are compressed. Coronary arteries are supplied with
blood only during diastole.
The right coronary artery arises from the right ostia and is
located between the right atrium and right ventricle. The
right coronary artery is also known as the RCA.
The RCA artery supplies:

the sinoatrial node (SA) node in 55% of hearts

the atrioventricular node (AV) node in 90% of
hearts

the RA and RV heart muscle

the inferior-posterior wall of the LV
For most people, the RCA divides into two branches: the
posterior descending artery, which supplies the RV and
inferior wall of the LV; and the marginal acute branch,
which supplies the inferior surface of the RV.
The left coronary artery comes off of the left coronary
ostia as the left main coronary artery (LMCA). It quickly
branches into the left anterior descending artery (LAD)
and the circumflex artery. The LAD supplies the:

anterior part of the interventricular septum

the anterior wall of the LV

the right bundle branch of the conduction system

part of the left bundle branch.
The circumflex artery, and its major branch, the obtuse
marginal, supplies:

the AV node in 10% of all hearts

the SA node in 45% of all hearts

the lateral posterior surface of the left ventricle.
The coronary arteries supply all of the layers of the heart,
which means that they do not lay just on the outside
surface of the heart. The large part of the artery lies on
the surface of the heart, with smaller branches entering
into the myocardial and subendocardial tissue layers to
supply all parts of the heart.
Mr. Ash complains of severe painful pressure in the
center of his chest and radiating down his left arm and up
his jaw. He is diaphoretic and pale. He complains of
some nausea. He is given morphine and started on a
nitroglycerin drip, but does not have significant pain
relief.
Cardiovascular Critical Care Primer
© 2000 TCHP Education Consortium; 2014 edition
Page 11
What is causing Mr. Ash’s symptoms?
Chest Pressure and Radiation
Because the heart has no direct pain receptors or
messengers, the pain of myocardial ischemia is shunted
through the spinal nerves of its dermatome. The warning
sent by the heart may manifest in many different ways,
according to which spinal nerves were stimulated. Chest
pressure, tightness; arm, back, or jaw pain; or GI distress
may result.
Diaphoresis and Pallor
As the injury has occurred to his heart, Mr. Ash’s
sympathetic nervous system has kicked into high gear.
The catecholamines (epinephrine and norepinephrine) that
were released in response to SNS stimulation cause
peripheral vasoconstriction and sweating, resulting in
cool, clammy, and pale skin.
divided into the fibrous and serous pericardium. The
epicardium is a component of the serous pericardium and
covers the heart and great vessels. The myocardium is
the muscular portion of the heart which contains
conduction fibers, atrial muscle fibers, and ventricular
muscle fibers. The endocardium is the innermost surface
of the heart that covers the chambers of the heart.
What are the possible mechanisms of
tamponade in Ms. Comparo’s case?
Pericarditis is an inflammation of the pericardial sac,
usually as a result of a more generalized disease process,
such as an MI or leukemia. Pericarditis will not cause the
heart to pump less effectively; however, the complications
of pericarditis will cause pericardial effusions and fibrin
deposits.

In a pericardial effusion, fluid leaks from the blood
vessels supplying the pericardial sac into the space
between the fibrous and serous layers. As the
effusion grows, the sac becomes "full". When there
is no further room for expansion to the outside of the
heart, the effusion will either stop, or will continue to
grow, causing a decreased pulse pressure and
tamponade.

Fibrin deposition on the serous pericardium from
pericarditis causes constrictive pericarditis. The
constriction does not allow expansion or effective
contraction of the heart, rendering it unable to adjust
to minute to minute changes in volume and pressure.
Nausea
Gastrointestinal distress and heartburn are two of the
many symptoms of an MI. Nausea and vomiting,
however, are commonly seen with an RCA occlusion.
The RCA supplies the AV node, which is also stimulated
by the vagus nerve. Irritation of the vagus nerve occurs
when the AV node is deprived of oxygen, resulting in
nausea. An inferior MI can be the direct result of an RCA
occlusion and will often coincide with symptoms of GI
upset.
Mr. Ash is transferred to the CCU after a bolus of a
thrombolytic agent is given.
Pericarditis/Pericardial
Tamponade
Ms. Louise Comparo is a 36 year old woman who has
been undergoing radiation therapy for breast cancer. She
enters the ER at approximately 2:30 a.m. complaining of
chest pressure, dizziness, and shortness of breath. The
assessment shows: distended neck veins, normal breath
sounds, distant heart sounds, BP 86/62 mm Hg, HR 156,
RR 32. The preliminary diagnosis is cardiac tamponade.
What structures are involved with
pericarditis and cardiac tamponade?
There are four layers of the heart: the pericardium,
epicardium, myocardium, and endocardium.
The
pericardium is the outermost layer of the heart and
makes up a sac that surrounds the heart. This sac is
Cardiovascular Critical Care Primer
© 2000 TCHP Education Consortium; 2014 edition
Page 12
Pericardial tamponade is the end result of either
pericardial effusion, constrictive pericarditis or pericardial
hemorrhage. Cardiac tamponade occurs when the heart is
unable to fill or pump adequately, leading to:
Decreased filling and contractility of the heart

Decreased cardiac output and BP

Compensatory mechanisms for low BP results in:
Vasoconstriction & Tachycardia

Increased workload for the heart

Decreased perfusion of the tissues as blood is shunted
away from the periphery and towards central organs

Tissues lack oxygen to produce ATP, forcing a change
from aerobic to anaerobic cellular metabolism in an
attempt to produce energy and preserve life

Lactic acidosis develops from anaerobic metabolism

Cardiac failure and shock results if the oxygen
deprivation is not fixed
What caused Ms. Comparo’s symptoms?
Because the heart was being compressed by the fluid in
the pericardium, it was not able to pump effectively,
causing less and less blood to enter into the system. The
net result: hypotension. The response of the SNS causes
tachypnea, and tachycardia. Fluid in the pericardium
will uniformly compress the heart, not just one side. This
causes an equalization in pressures between the right side
and the left side of the heart. This equalization translates
into a narrow pulse pressure, or a diastolic pressure that
is very close to the systolic pressure.
was given to form a foundation of knowledge to apply to
clinical practice.
Recommended Reading and
References
1.
Brozenee S, Russell SS. (2004). Core Curriculum for
Medical-Surgical Nursing, 3rd 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. (2011).
Mosby's Guide to Physical Examination, 5th ed. St.
Louis: Mosby, Inc.
4. Stillwell, S. (2006). Mosby’s Critical Care Nursing
Reference. 3rd ed. St. Louis, Mo: Mosby/Elsevier.
5. Smeltzer SC, Bare BG, eds. (2012). Brunner &
Suddarth's Textbook of Medical-Surgical Nursing,
10th ed. Philadelphia: Lippincott William and
Wilkins.
6. Wiegand, D.J.L. (ed). (2011). AACN Procedure
Manual for Critical Care.
7. Functional peripheral arterial disease: Raynaud’s
Syndrome. (2008). Retrieved March 13, 2010, from
http://www.merck.com/mmhe/sec03/ch034/ch034c.ht
ml#sec03-ch034-ch034c-1045
8. Hanly, E. J. (2009, May 1). Buerger Disease
(Thromboangiitis Obliterans) Retrieved March 13,
2010, from,
http://emedicine.medscape.com/article/460027overview
9. Occlusive peripheral arterial disease:
Thromboangiitis Obliterans. (2008). Retrieved March
13, 2010 from,
http://www.merck.com/mmhe/sec03/ch034/ch034b.ht
ml#sec03-ch034-ch034b-1029
10. American Association of Critical Care Nurses (2005).
The Cardiovascular System. J. Alspach. Core
curriculum for critical care nursing (6th edition).
Philadelphia: Saunders.
Summary
This program presented information regarding the normal
anatomy and physiology of the heart and blood vessels
and compared the normal state of affairs to pathological
states. Information on angina, myocardial infarction,
congestive heart failure, pericarditis, and cardiomyopathy
Cardiovascular Critical Care Primer
© 2000 TCHP Education Consortium; 2014 edition
Page 13
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
Cardiovascular Critical Care Primer
© 2000 TCHP Education Consortium; 2014 edition
Page 14
Cardiovascular Critical
Care Primer Post-Test
Please print all information clearly and sign the
verification statement. If you wish to submit your
post-test electronically (preferred method), please
access it from www.tchpeducation.com under home
studies.
1. Name
8.
Baroreceptor stimulation from decreased BP will
cause:
a) increased heart rate
b) activation of the parasympathetic nervous
system
c) decreased blood pressure
d) stimulation of the vagus nerve
9.
A symptom of left sided heart failure is:
a) pitting edema
b) dysrhythmias
c) basilar rales
d) elevated CVP
(please print legal name above)
2. Birth date
(required)
Format: 01/03/1999
M
M
D
D
Y
Y
Y
Y
3. Email:
(Required to return your certificate of completion to you—TCHP
Hospitals must use work email)
4. Where do you work? (example: HCMC, MVAHCS,
etc.). Enter N/A if you are not employed
Hospital
Unit
5. 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
6.
7.
Which of the following can be a symptom of
angina?
a) chest pressure
b) jaw pain
c) GI distress
d) all of the above
The right coronary artery supplies:
a) the SA node, the LA and LV
b) the AV node, the LA and LV
c) the AV node, the RA, and RV
d) the bundle branches, the LA and RV
10. Arterial insufficiency refers to:
a) total occlusion of the artery
b) blood supply inadequate for tissue need
c) clot formation in the artery
d) arterial wall spasm
11. A bruit is caused by:
a) turbulent blood flow
b) arterial occlusion
c) carotid artery dysfunction
d) myocardial infarction
12. Which of the following is NOT a component of
Virchow’s triad?
a) hypercoagulability
b) intimal damage
c) arterial insufficiency
d) venous stasis
13. Symptoms of dilated cardiomyopathy are the
same as the symptoms of:
a) myocardial infarction
b) subaortic stenosis
c) congestive heart failure
d) hypertension
14. Which of the following disease may result in
gangrene and possible amputation of a digit?
a) Buerger’s Disease
b) Raynaud’s Syndrome
c) both of the above
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.
Cardiovascular Critical Care Primer
© 2000 TCHP Education Consortium; 2014 edition
Page 15
Evaluation: Cardiovascular Critical Care Primer
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:
1.
Identify the normal anatomy and physiology of the
cardiovascular system.
2.
Describe the pathophysiology of an acute myocardial
infarction.
3.
Describe the symptoms of heart failure.
4.
Describe the pathophysiology of tamponade.
5.
Identify the factors that favor the development of a venous
thrombosis.
6.
Differentiate between dilated, hypertrophic, and restrictive
cardiomyopathy.
7.
Differentiate between Buerger’s Disease and Raynaud’s
Syndrome.
Strongly
Agree
Agree
Neutral
Disagree
Strongly
Disagree
8. 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
9.
No
Notice of requirements for successful completion, including purpose and objectives
10. Conflicts of interest, if present
11. Expiration Date for Awarding Contact Hours
12. 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:
13. How long did it take you to read this home study and complete the post test and evaluation:
______hours and ______minutes.
14. 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
15. Describe how you plan to incorporate the knowledge gained in this home study into your practice (indicate all that
apply):
___This information has made me more knowledgeable about my practice.
___I feel that I will be more skilled at assessing and managing elderly patients.
___I have a better understanding of the normal aging process.
___I will use this information to educate my patients.
___I will use this information to educate my colleagues.
Cardiovascular Critical Care Primer
© 2000 TCHP Education Consortium; 2014 edition
Page 16
___I do not plan to integrate any of this information into my practice (please explain)
Other/answer explanation:______________________________________________
16. What best describes your reason for completing this home study? (select all that apply):
___I wanted to learn more about caring for elderly patients.
___I needed contact hours.
Other: ________________________________________________________________
17. Do you think there is a continued need to have this home study available?
___Yes, this information will continue to be relevant.
___No, this information is no longer relevant.
___Don’t know.
___It depends. (please specify):_____________________________________________
If you are an ANCC-certified nurse* or need contact hours based on a 60 min/contact hour formula, fill out the information
below. Please note that you will receive a follow up survey via email to track how you are using the information presented
in this packet in your professional practice 3-6 months from now.
Name:
Email:
*Certified nurses renew their certification (CCRN, PCCN, etc.) with the organization that manages their certification.
Most nurses are not certified and renew licensure with their state Board of Nursing.
Expiration date: March 27, 2015
Cardiovascular Critical Care Primer
© 2000 TCHP Education Consortium; 2014 edition
Page 17
TCHP
Education
Consortium
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.
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
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Shock and Infection in Critical Care Primer
© 2007 TCHP Education Consortium
Page 1
Contact Hour Information
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Planning Committee/Editors
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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.
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Shock and Infection in Critical Care Primer
© 2007 TCHP Education Consortium
Page 2
An Overview of Shock
Definition
Shock is a state of inadequate perfusion relative to
tissue demands.
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.
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.
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
Shock and Infection in Critical Care Primer
© 2007 TCHP Education Consortium
Page 3
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.
2.
3.
4.
5.
6.
Constrict the blood vessels in the skin, GI tract
and kidneys
Dilate the blood vessels in the skeletal muscles
and coronary arteries
Sweat
Increase the heart rate and contractility
Increase the rate and depth of breathing
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
Shock and Infection in Critical Care Primer
© 2007 TCHP Education Consortium
Page 4
•
•
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
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 reninangiotensin-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
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.”
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.
Shock and Infection in Critical Care Primer
© 2007 TCHP Education Consortium
Page 5
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.
Impaired pumping ability
of the left ventricle
Decreased S.V .
Inadequate systolic emptying
Decreased C.O
Elevated left ventricular
filling pressure
Decreased BP
IncreasedLAP
Decreased tissue perfusion
Increased pulmonary
venous pressure
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.
Increased pulmonary
capillary pressure
Pulmonary interstitial edema
Intra-alveolar edema
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.
Shock and Infection in Critical Care Primer
© 2007 TCHP Education Consortium
Page 6
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.
Pathophysiology of Neurogenic Shock
Loss of sympathetic tone
Massive vasodilation
Decreased intravascular volume
Venous dilation
Arteriolar dilation
Venous return
Peripheral vascular
resistance
Decreased venous return
Decreased ventricular filling
Stroke volume
Decreased stroke volume
Cardiac output
Decreased cardiac output
Tissue perfusion
Inadequate tissue perfusion
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.
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.
Shock and Infection in Critical Care Primer
© 2007 TCHP Education Consortium
Page 7
Anaphylactic Shock
Septic 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.
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 Anaphylactic Shock
Exposure to antigen
Activation of
sensitized antibodies
Antigen-antibody reaction
Release of vasoactive mediators
Massive
vasodilation
 Capillary
permeability
Venous & arterial dilation
Interstitial edema
Relative hypovolemia
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.
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.
Shock and Infection in Critical Care Primer
© 2007 TCHP Education Consortium
Page 8
Resources
1.
2.
3.
4.
5.
Barone, J., and Snyder, A. (1991). Treatment
strategies in shock:
Use of oxygen transport
measurements. Heart and Lung, 20(1), 81-86.
Rice, V. (1992). Shock, a clinical syndrome: An
update. Part 1: An overview of shock. Critical Care
Nurse, 11(4), 20-27.
Rice, V. (1992). Shock, a clinical syndrome: An
update. Part 2: The stages of shock. Critical Care
Nurse, 11(5), 74-82.
Rice, V. (1992). Shock, a clinical syndrome: An
update. Part 3: Therapeutic Management. Critical
Care Nurse, 11(6), 34-39.
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.
2.
3.
4.
5.
6.
Brozenee S, Russell SS. (1999). Core
Curriculum for Medical-Surgical Nursing, 2nd
ed. Academy of Medical-Surgical Nurses, Janetti
NJ.
Phipps WJ, Sands JK, Marek JF, eds.
(1999)..Medical-Surgical Nursing: Concepts &
Clinical Practice, 6th ed. St. Louis: Mosby, Inc.
Seidel HM, Ball JW, Dains JE et al, eds.(2002)
Mosby's Guide to Physical Examination, 5th ed.
St. Louis: Mosby, Inc.
Stillwell, S. (2002). Mosby’s Critical Care
Nursing Reference. 3rd ed. St. Louis, Mo:
Mosby/Elsevier.
Smeltzer SC, Bare BG, eds. (2002) Brunner &
Suddarth's Textbook of Medical-Surgical
Nursing, 10th ed. Philadelphia: Lippincott
William and Wilkins.
Wiegand, D.J.L. & Carlson, K.K. (eds.) (2005).
AACN Procedure Manual fro Critical Care. 5th
ed. Philadelphia: Elsevier.
Directions for Submitting
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You have received this packet as pre-reading to
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Shock and Infection in Critical Care Primer
© 2007 TCHP Education Consortium
Page 9
Shock & Infection
Critical Care Primer
Post-Test
in
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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
neurogenic shock results in:
a) venous dilation
b) arteriolar dilation
c) decreased cardiac output
d) all of the above
that
occurs
in
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.
Primer completed with Class
Shock and Infection in Critical Care Primer
© 2007 TCHP Education Consortium
Page 10
Evaluation: Shock and Infection Critical Care Primer
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:
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.
Define terms related to shock.
5.
Strongly
Agree
Agree
Neutral
Disagree
Strongly
Disagree
6. 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).
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7.
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8.
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10. Sponsorship or commercial support
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15. How long did it take you to read this home study and complete the post test and evaluation:
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Expiration date: March 27, 2015
Shock and Infection in Critical Care Primer
© 2007 TCHP Education Consortium
Page 11