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CARDIAC CONDITIONS,
INTERVENTIONS & REHABILITATION
Jassin M. Jouria, MD
Dr. Jassin M. Jouria is a medical doctor, professor of
academic medicine, and medical author. He graduated from
Ross University School of Medicine and has completed his
clinical clerkship training in various teaching hospitals
throughout New York, including King’s County Hospital
Center and Brookdale Medical Center, among others. Dr. Jouria has passed all
USMLE medical board exams, and has served as a test prep tutor and instructor for
Kaplan. He has developed several medical courses and curricula for a variety of
educational institutions. Dr. Jouria has also served on multiple levels in the academic
field including faculty member and Department Chair. Dr. Jouria continues to serves
as a Subject Matter Expert for several continuing education organizations covering
multiple basic medical sciences. He has also developed several continuing medical
education courses covering various topics in clinical medicine. Recently, Dr. Jouria
has been contracted by the University of Miami/Jackson Memorial Hospital’s
Department of Surgery to develop an e-module training series for trauma patient
management. Dr. Jouria is currently authoring an academic textbook on Human
Anatomy & Physiology.
Abstract
Just as a serious limb injury requires rehabilitation to return to optimal
performance, the heart also requires serious rehab in order to function
at its best after a trauma. When a cardiac event occurs, the patient
may suffer emotional difficulties and challenges to accept and
overcome events that caused the condition. Cardiac rehabilitation is a
whole-body approach to restore health that incorporates a multidimensional methodology to address body, mind, and spirit. Exercise,
counseling, and physical therapy combine with medical management
to ensure that as much normal function as possible is restored, and
that every patient is able to adapt to lifestyle changes that reduce the
risk of a repeat occurrence. The cardiac rehabilitation team and
program goals for various cardiac diagnoses and interventions are
discussed to support further studies and to increase knowledge in
everyday practice.
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Continuing Nursing Education Course Planners
William A. Cook, PhD, Director, Douglas Lawrence, MA, Webmaster,
Susan DePasquale, MSN, FPMHNP-BC, Lead Nurse Planner
Policy Statement
This activity has been planned and implemented in accordance with
the policies of NurseCe4Less.com and the continuing nursing education
requirements of the American Nurses Credentialing Center's
Commission on Accreditation for registered nurses. It is the policy of
NurseCe4Less.com to ensure objectivity, transparency, and best
practice in clinical education for all continuing nursing education (CNE)
activities.
Continuing Education Credit Designation
This educational activity is credited for 4 hours. Nurses may only claim
credit commensurate with the credit awarded for completion of this
course activity.
Statement of Learning Need
Assisting patients to lower their risk of heart disease following a new
cardiac diagnosis often involves specialized health professionals to
encourage and educate them on best practice exercise programs and
healthy lifestyle choices. Nurses are key partners within the health
team to support the patient with heart disease in their progress to heal
and to lead a healthy life.
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Course Purpose
To provide nursing professionals with knowledge of a holistic approach
for cardiac rehabilitation to support the patient with heart disease to
recover and heal.
Target Audience
Advanced Practice Registered Nurses and Registered Nurses
(Interdisciplinary Health Team Members, including Vocational Nurses
and Medical Assistants may obtain a Certificate of Completion)
Course Author & Planning Team Conflict of Interest Disclosures
Jassin M. Jouria, MD, William S. Cook, PhD, Douglas Lawrence, MA,
Susan DePasquale, MSN, FPMHNP-BC – all have no disclosures
Acknowledgement of Commercial Support
There is no commercial support for this course.
Activity Review Information
Reviewed by Susan DePasquale, MSN, FPMHNP-BC
Release Date: 3/1/2016
Termination Date: 3/17/2018
Please take time to complete a self-assessment of knowledge,
on page 4, sample questions before reading the article.
Opportunity to complete a self-assessment of knowledge
learned will be provided at the end of the course.
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1. Which of the following is a modifiable risk factor for
atherosclerosis:
a. Diabetes mellitus
b. Age
c. Family history of premature coronary heart disease
d. Male-pattern baldness
2. True or False: Angina is the term used to describe the pain
and discomfort that occurs when the heart is deprived of
blood.
a. True.
b. False.
3. Patients with typical myocardial infarction may have the
following prodromal symptoms in the days preceding the
event:
a. fatigue.
b. intense and unremitting for 30-60 minutes.
c. a feeling of indigestion or of fullness and gas.
d. All of the above.
4. There is evidence to show that comprehensive cardiac
rehabilitation programs, including exercise training, can do
the following:
a. Reduce smoking
b. Alter lipid profiles
c. Reduce blood pressure
d. All of the above.
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Introduction
There are a number of conditions that require cardiac rehabilitation.
However, each patient must be assessed regardless of the condition to
ensure that he or she is a candidate for the program. If the patient
presents with a cardiac condition, and is determined to be a candidate,
cardiac rehabilitation will be initiated.
Cardiac Conditions And Rehabilitation
The conditions that require cardiac rehabilitation and program
selection are unique to the patient’s health history, health resources
and individual choices. Specific cardiac conditions in patients who
would benefit from enrollment in a cardiac rehabilitation program are
highlighted in this course. Its necessary for trained health
professionals to ensure that the patient with a cardiac condition, and
undergoing specific treatments and procedures, as well as their family
are educated on options for recovery and healing.
Myocardial Infarction (Heart Attack)
Myocardial infarction, commonly known as a heart attack, “is the
irreversible necrosis of heart muscle secondary to prolonged ischemia.
This usually results from an imbalance in oxygen supply and demand,
which is most often caused by plaque rupture with thrombus formation
in a coronary vessel, resulting in an acute reduction of blood supply to
a portion of the myocardium.”15
Myocardial infarctions occur when blood flow to a section of the heart
is blocked. This blockage prevents the heart from receiving the oxygen
that is required to function properly. Without sufficient oxygen, the
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section of the heart will die. Myocardial infarctions are the leading
killer of men and women in the United States. However, with proper
treatment and long-term management, these effects can be
minimized. Cardiac rehabilitation is especially useful in treating
patients who have experienced myocardial infarctions.16
The following is a basic description of what occurs during a heart
attack:17

Heart attacks most often occur as a result of coronary heart
disease (CHD), also called coronary artery disease. CHD is a
condition in which a waxy substance called plaque builds up
inside the coronary arteries. The buildup of plaque occurs over
many years.

Eventually, an area of plaque can rupture (break open) inside of
an artery. This causes a blood clot to form on the plaque's
surface. If the clot becomes large enough, it can mostly or
completely block blood flow through a coronary artery.

If the blockage isn't treated quickly, the portion of heart muscle
fed by the artery begins to die. Healthy heart tissue is replaced
with scar tissue. This heart damage may not be obvious, or it
may cause severe or long-lasting problems.

A less common cause of heart attack is a severe spasm
(tightening) of a coronary artery. The spasm cuts off blood flow
through the artery. Spasms can occur in coronary arteries that
aren't hardened due to plaque buildup (“atherosclerosis”).
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
Heart attacks can be associated with or lead to severe health
problems, such as heart failure and life-threatening arrhythmias.

Heart failure is a condition in which the heart can't pump enough
blood to meet the body's needs. Arrhythmias are irregular
heartbeats. Ventricular fibrillation is a life-threatening
arrhythmia that can cause death if not treated right away.
Etiology
The primary cause of myocardial infarctions is atherosclerosis.
Approximately 90% of myocardial infarctions result from an acute
thrombus that obstructs an atherosclerotic coronary artery. Plaque
rupture and erosion are considered to be the major triggers for
coronary thrombosis. Following plaque erosion or rupture, platelet
activation and aggregation, coagulation pathway activation, and
endothelial vasoconstriction occur, leading to coronary thrombosis and
occlusion.18
Non-modifiable risk factors for atherosclerosis include the following:

Age

Sex

Family history of premature coronary heart disease

Male-pattern baldness
Modifiable risk factors for atherosclerosis include the following:19

Smoking or other tobacco use

Diabetes mellitus

Hypertension
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
Hypercholesterolemia and hypertriglyceridemia, including
inherited lipoprotein disorders

Dyslipidemia

Obesity

Sedentary lifestyle and/or lack of exercise

Psychosocial stress

Poor oral hygiene

Type A personality

Elevated homocysteine levels and the presence of peripheral
vascular disease are also risk factors for atherosclerosis.
Causes of myocardial infarction other than atherosclerosis
Non-atherosclerotic causes of myocardial infarction include the
following conditions:20

Coronary occlusion secondary to vasculitis

Ventricular hypertrophy (i.e., left ventricular hypertrophy,
idiopathic hypertrophic subaortic stenosis [IHSS], underlying
valve disease)

Coronary artery emboli, secondary to cholesterol, air, or the
products of sepsis

Congenital coronary anomalies

Coronary trauma

Primary coronary vasospasm (variant angina)

Drug use (i.e., cocaine, amphetamines, ephedrine)

Arteritis

Coronary anomalies, including aneurysms of coronary arteries

Factors that increase oxygen requirement, such as heavy
exertion, fever, or hyperthyroidism
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
Factors that decrease oxygen delivery, such as hypoxemia of
severe anemia

Aortic dissection, with retrograde involvement of the coronary
arteries

Infected cardiac valve through a patent foramen ovale (PFO)

Significant gastrointestinal bleed

In addition, myocardial infarction can result from hypoxia due to
carbon monoxide poisoning or acute pulmonary disorders.
Infarcts due to pulmonary disease usually occur when demand
on the myocardium dramatically increases relative to the
available blood supply.

Myocardial infarction induced by chest trauma has also been
reported, usually following severe chest trauma such as motor
vehicle accidents and sports injuries.

Coronary Artery Spasm - A less common cause of heart attack is
a severe spasm (tightening) of a coronary artery. The spasm
cuts off blood flow through the artery. Spasms can occur in
coronary arteries that aren't affected by atherosclerosis. What
causes a coronary artery to spasm isn't always clear. A spasm
may be related to:
 Taking certain drugs, such as cocaine
 Emotional stress or pain
 Exposure to extreme cold
 Cigarette smoking
Signs and Symptoms
Patients with typical myocardial infarction may have the following
prodromal symptoms in the days preceding the event (although typical
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ST elevation myocardial infarction (STEMI) may occur suddenly,
without warning):

Fatigue

Chest discomfort

Malaise
Typical chest pain in acute myocardial infarction has the following
characteristics:15

Intense and unremitting for 30-60 minutes

Retrosternal and often radiates up to the neck, shoulder, and
jaw and down to the ulnar aspect of the left arm

Usually described as a substernal pressure sensation that also
may be characterized as squeezing, aching, burning, or even
sharp

In some patients, the symptom is epigastric, with a feeling of
indigestion or of fullness and gas
The patient’s vital signs may demonstrate the following in myocardial
infarction:17

The patient’s heart rate is often increased secondary to
sympathoadrenal discharge

The pulse may be irregular because of ventricular ectopy, an
accelerated idioventricular rhythm, ventricular tachycardia, atrial
fibrillation or flutter, or other supraventricular arrhythmias;
bradyarrhythmias may be present

In general, the patient's blood pressure is initially elevated
because of peripheral arterial vasoconstriction resulting from an
adrenergic response to pain and ventricular dysfunction
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
However, with right ventricular myocardial infarction or severe
left ventricular dysfunction, hypotension is seen

The respiratory rate may be increased in response to pulmonary
congestion or anxiety

Coughing, wheezing, and the production of frothy sputum may
occur

Fever is usually present within 24-48 hours, with the
temperature curve generally parallel to the time course of
elevations of creatine kinase (CK) levels in the blood. Body
temperature may occasionally exceed 102°F
Pathophysiology
The spectrum of myocardial injury depends not only on the intensity of
impaired myocardial perfusion but also on the duration and the level of
metabolic demand at the time of the event. “The damage in the
myocardium is essentially the result of a tissue response that includes
apoptosis (cell death) and inflammatory changes. Therefore, the
hearts of patients who suddenly die from an acute coronary event may
show little or no evidence of damage response to the myocardium at
autopsy. The typical myocardial infarction initially manifests as
coagulation necrosis that is ultimately followed by myocardial fibrosis.
Contraction-band necrosis is also seen in many patients with ischemia.
This is followed by reperfusion, or it is accompanied by massive
adrenergic stimulation, often with concomitant myocytolysis.”14
The following table provides an overview of the different outcomes
that can occur in the setting of a myocardial infarction.20
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Arrhythmogenesis
In addition to the direct effects of ischemia and tissue
hypoxia, decreased removal of noxious metabolites,
including potassium, calcium, amphophilic lipids, and
oxygen-centered free radicals, also impair ventricular
performance. These abnormalities promote potentially
lethal arrhythmias.
Pericarditis
Epicardial inflammation may initiate pericarditis, which is
seen in more than 20% of patients presenting with Q-wave
infarctions.
Reduced systolic
Lack of adequate oxygen and insufficient metabolite
function
delivery to the myocardium diminish the force of muscular
contraction and decrease systolic wall motion in the
affected territory.
Abnormal regional
Even brief deprivation of oxygen and the requisite
wall motion
metabolites to the myocardium diminishes diastolic
relaxation and causes abnormal regional systolic contractile
function, wall thickening, and abnormal wall motion. If the
area affected is extensive, diminished stroke volume and
cardiac output may result.
Hypokinesis and
In general, regions of hypokinesis and akinesis of the
akinesis
ventricular myocardium reflect the location and extent of
myocardial injury.
Myocardial
In general, expansion of infarcted myocardium and
infarction
resultant ventricular dilatation (i.e., ventricular remodeling)
expansion
ensues within a few hours after the onset of a myocardial
infarction. An expanding myocardial infarction leads to
thinning of the infarct zone and realignment of layers of
tissue in and adjacent to it, causing ventricular dilatation.
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Myocardial
Myocardial rupture was seen in as many as 10% of fatal
rupture
myocardial infarctions before the era of thrombolytics, but
it is now encountered much less often. When rupture
occurs, it may be associated with large infarctions;
indications include cardiogenic shock or hemodynamically
significant arrhythmia. Patients may have a history of
hypertension with ventricular hypertrophy.
Ventricular
A ventricular aneurysm is an outward bulging of a
aneurysm
noncontracting segment. In the early days of cardiac
imaging, ventricular aneurysms were seen in as many as
20% of patients with Q-wave myocardial infarction, but now
it is seen in less than 8%.
Cardiogenic shock
In patients with extensive myocardial injury, coronary blood
flow diminishes as cardiac output declines and heart rate
accelerates. Because coronary artery disease is usually
generalized or diffuse, ischemia that occurs at a distance
from the infracted segment may result in a vicious cycle in
which a stuttering and expanding myocardial infarction
ultimately leads to profound LV failure, hypotension, and
cardiogenic shock.
Effect on diastolic
Immediately after the onset of myocardial infarction, the
function
ability of ischemic myocardium to relax declines. Relaxation
is an active process that uses ATP. Impaired relaxation
increases LV end-diastolic volume (LVEDV) and LV enddiastolic pressure (LVEDP).
The increased LVEDP results in ventricular dilation,
increased pulmonary venous pressure, decreased
pulmonary compliance, and interstitial and (ultimately)
alveolar pulmonary edema. These effects lead to increased
hypoxemia, which may worsen ischemic injury to the
myocardium.
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Prognosis
Approximately thirty percent of patients who experience a myocardial
infarction die within twenty-four hours of onset. Those that survive the
initial event experience significant morbidity. An additional 5-10% of
survivors die within the first year after their myocardial infarction.
Approximately half of all patients with a myocardial infarction are
rehospitalized within 1 year of their index event.20
Better prognosis is associated with the following factors:

Successful early reperfusion (STEMI goals: patient arrival to
fibrinolysis infusion within 30 minutes or patient arrival to
percutaneous coronary intervention within 90 minutes)

Preserved left ventricular function

Short-term and long-term treatment with beta-blockers, aspirin,
and ACE inhibitors
Poorer prognosis is associated with the following factors:22

Increasing age

Diabetes

Previous vascular disease (i.e., cerebrovascular disease or
peripheral vascular disease)

Elevated Thrombolysis in Myocardial Infarction (TIMI) risk score
for unstable angina/NSTEMI (7 factors: Age ≥65 year, ≥3 risk
factors for cardiac disease, previous coronary disease, ST
segment deviation ≥0.5 mm, ≥2 episodes of angina in last 24
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hours, aspirin use within prior week, and elevated cardiac
enzyme levels)

Delayed or unsuccessful reperfusion

Poorly preserved left ventricular function (the strongest predictor
of outcome)

Evidence of congestive heart failure (Killip classification ≥II) or
frank pulmonary edema (Killip classification ≥III)

Elevated B-type natriuretic peptide (BNP) levels

Elevated high sensitive C-reactive protein (hs-CRP), a
nonspecific inflammatory marker

Secretory-associated phospholipase A2 activity is related to
atherosclerosis and predicts all-cause mortality in elderly
patients; it also predicts mortality or MI in post-MI patients.

The presence of ST deviation in ECG lead aVR indicates an
increased mortality risk. Data from the APEX-AMI (Pexelizumab
in Conjunction With Angioplasty in Acute Myocardial Infarction)
trial were examined to determine the incidence and prognostic
value of aVR ST deviation in STEMI patients undergoing primary
percutaneous coronary intervention within 6 hours of symptom
onset; the investigators determined that aVR ST deviation was
associated with a 50% relative increase in the risk of death
within 90 days in patients with noninferior MI, while aVR ST
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elevation in patients with inferior MI was associated with a
nearly 6-fold increase in such risk.

Blood glucose - elevated blood glucose level on admission is
associated with increased short-term mortality in nondiabetic
patients presenting with a first acute myocardial infarction.

Psychological depression - The combination of acute myocardial
infarction and psychological depression appears to worsen the
patient's prognosis. Acute myocardial infarction may precipitate
reactive depression whether or not beta-adrenergic blocking
agents or other CNS-active agents are administered.

Myocardial hibernation and stunning - After the occurrence of 1
or more ischemic insults, impaired wall motion is often transient
(myocardial stunning) or prolonged (myocardial hibernation).
These phenomena occur because of the loss of essential
metabolites such as adenosine, which is needed for adenosine
triphosphate (ATP)–dependent contraction. Hibernation, a
persisting wall-motion abnormality that is curable with
revascularization, must be differentiated from permanent,
irreversible damage or completed infarct.

Scar tissue and prognosis - Scars involving less than one third of
the thickness of the wall, as shown on contrast-enhanced MRI,
likely correspond to a recovery of myocardial function, whereas
with scars measuring more than one third the thickness of the
wall, the potential for recovery with therapy is limited (except in
cases involving research cell therapies or surgical scar revision).
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Other findings associated with recovery are activity on 2[Fluorine 18]-fluoro-2-deoxy-D-glucose (FDG) positron emission
tomography (PET) scanning and a monophasic or biphasic
contractile response to dobutamine infusion, caused by the
induction of ischemia.
Heart Condition
Heart condition is a general term used to categorize a variety of
disorders that may occur within the cardiovascular system.
Coronary Artery Disease
Coronary artery disease (CAD) is a condition that is characterized by
the occurrence of atherosclerosis in the epicardial arteries. In this
condition, the plaque narrows the coronary artery lumen, thereby
impairing blood flow to the antegrade myocardial. Some patients may
exhibit symptoms of blood flow reduction, while others will be
asymptomatic. The reduction of coronary artery flow may occur during
instances of rest of exertion. There is no consistent presentation with
CAD. In many instances, the reduction in blood flow will culminate in a
myocardial infarction, but not in all instances. This will ultimately
depend on the severity of the obstruction and the rate or
progression.23
According to the American Heart Association:
“Patients with CAD can present with stable angina pectoris,
unstable angina pectoris, or an MI. They may seek medical
attention
with
their
first
symptomatic
episode
of
chest
discomfort. Many of these patients suffer from unrecognized
CAD and may experience an acute plaque rupture or acute
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myocardial infarction as their first coronary artery diagnostic
presentation.
Electrical
instability
can
ensue,
including
potentially lethal cardiac dysrhythmias.
Identifying high-risk persons before their first myocardial event
is a multifaceted process that involves both patient and
physician education efforts. Screening for coronary artery
disease is not sufficient. Risk factor modification, from an early
age,
initiates
primary
prevention
efforts,
forestalling
the
development of symptomatic CAD. Severe CAD can be detected
before a patient develops symptoms, especially in a high-risk
patient subpopulation where pre-test probability of flow limiting
coronary artery disease is higher than average.
CAD is the most common type of heart disease and in 2008,
405,309 individuals died in the U.S. from this specific etiology.
Every year, approximately 785,000 Americans suffer a first
heart attack and another 470,000 will suffer an additional
myocardial infarction (MI). In 2010, CAD alone was projected to
cost the U.S. $108.9 billion including the cost of health care
services, medications, and lost productivity.”24
Coronary artery disease typically begins during adolescence and
progresses throughout the patient’s life. The rate of progression is
very slow, and most patients will be unaware of their medical status.
Although CAD typically progresses slowly, there are a number of risk
factors that can accelerate or modify the progression of the condition.
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The most common risk factors include:25

Family history of premature CAD

Cigarette smoking

Diabetes mellitus

Hypertension

Hyperlipidemia

Sedentary lifestyle
Diagnosis
The diagnostic process for coronary artery disease includes a thorough
assessment and physical examination. Since the illness typically begins
in adolescence, the physician will need to conduct a thorough medical
history for the patient. In addition to the detailed medical history and
physical examination, the physician may also require an
electrocardiogram, laboratory blood tests, stress testing, and a cardiac
catheterization.26 These additional assessments are often required
when the initial examination produces results that indicate CAD.
The following table provides a detailed overview of the various
components of the patient assessment.27
History
The history should include any current symptoms and a
complete inventory of comorbid conditions. An inventory
of cardiac risk factors, and a complete family history are
essential components. The history should also include
information about the character and location of
discomfort, radiation of discomfort, associated
symptoms, and precipitating, exacerbating, or
alleviating factors.
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The importance of the family history should not be
underestimated. A detailed assessment, particularly of
first-degree relatives for the presence of CAD and age of
diagnosis is imperative when evaluating a patient’s risk
factor profile.
Physical Examination
The results of the physical examination of a patient with
stable or unstable angina may be entirely normal. The
presence of multiple risk factors or atherosclerosis in
the carotid or peripheral arteries increases the likelihood
that a chest pain syndrome is related to myocardial
ischemia. Evaluation should include measurements of
blood pressure and the brachial index. Examination of
the carotid arteries should include auscultation for
bruits. Examination of the chest wall, neck, and
shoulders for deformities and tenderness may be helpful
in diagnosing musculoskeletal chest discomfort.
Cardiac auscultation may detect murmurs caused by
aortic stenosis or hypertrophic cardiomyopathy, either
of which can cause angina in the absence of epicardial
CAD.
Assessment of the abdominal aorta for an aneurysm or
bruits and palpation of lower extremity pulses is
necessary to evaluate for peripheral vascular disease.
Careful palpation of all peripheral pulses and
assessment of symmetry versus diminution are also
valuable noninvasive approaches for assessing the
integrity of the arterial circulation.
Finally, examination for xanthelasmas, tendon
xanthomas, retinal arterial abnormalities, and peripheral
neuropathy can be helpful.
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Electrocardiography
A resting 12-lead electrocardiogram should be obtained
on all patients with suspected CAD. Electrocardiographic
results are normal in approximately 50% of patients
with chronic stable angina, and they can remain normal
during an episode of chest discomfort. Importantly, a
normal electrocardiogram does not exclude coronary
artery disease.
When abnormal, especially when Q waves are present in
a regional myocardial territory of diagnostic duration
can signify the presence of a past MI with high
accuracy.
Chest Radiography
The usefulness of a routine chest radiograph in a patient
with chest discomfort has not been established.
Calcification of the aortic knob is a common finding in
older patients and is a nonspecific indicator of flowlimiting obstructive coronary disease. Coronary
calcification may also be present. A widened
mediastinum may signify an aortic aneurysm and
represent the first clue of unstable aortic disease as the
cause of chest discomfort.
Cardiac Computed
A noninvasive imaging assessment of coronary
Tomography
atherosclerosis is now possible in the form of cardiac
Angiography
computed tomography angiography. When negative,
this test possesses a high negative predictive value. The
positive predictive value is also high, but exact stenosis
quantification can be complicated. Associated
calcification can cause a blooming artifact, resulting in
an overestimation of stenosis severity. Additionally,
previous coronary artery intervention in the form of
coronary artery stent placement can create a blooming
shadowing artifact rendering stenosis severity
assessment within the stent challenging.
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Echocardiography
Echocardiography is recommended for patients with
stable angina and physical findings suggesting
concomitant valvular heart disease. It is invaluable for
assessing the patient with suspected hypertrophic
cardiomyopathy. It is also recommended for the
assessment of global and regional left ventricular
systolic function in patients who have been diagnosed
with congestive heart failure, complex ventricular
arrhythmias, or a history of MI.
The echocardiogram is in many ways an ideal test when
assessing a patient with known CAD. It is painless,
carries no known risk, and the results are available
within approximately 30 minutes. An experienced
echocardiographer can identify 1 or more MIs, localize
the infarct to a coronary artery distribution, and assess
for associated ischemic structural complications such as
a left ventricular aneurysm, left ventricular
pseudoaneurysm, and ventricular thrombus.
Laboratory Studies
Routine laboratory measurements recommended, as a
part of the initial evaluation of patients with CAD,
should include determination of fasting glucose and
fasting lipid levels (total cholesterol, high-density
lipoprotein [HDL] cholesterol, triglycerides, and
calculated low-density lipoprotein [LDL] levels). Other
markers such as lipoprotein(a) (Lp[a]) and highsensitivity C-reactive protein may be useful in assessing
cardiac risk.
High-sensitivity C-reactive protein is gaining greater
prominence in assessing the inflammatory level of
vascular disease and predicting future risk of vascular
events, such as MIs and cerebrovascular accidents.
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This was most recently highlighted in the Jupiter Trial
where patients with a LDL cholesterol level <130 mg/dL
and a high-sensitivity C-reactive protein >2.0 mg/L
were randomized to rosuvastatin 20 mg/d or placebo.
Those with a high-sensitivity C-reactive protein >2.0
were shown to derive benefit from rosuvastatin based
on a statistically significant reduction in myocardial
event rates, cardiovascular mortality, and rates of death
from any cause compared to those patients who were
administered placebo.
When working with patients who are diagnosed with coronary artery
disease, there are a number of key points to remember:28

The diagnostic and treatment options for CAD are changing
rapidly.

New pharmaceuticals are being developed and introduced into
the treatment armamentarium, particularly novel anti-platelet
agents.

Biologic markers are now used to track coronary artery disease
activity at the vascular level, guiding medication selection and
dose titration.

Procedures are less invasive and offer percutaneous treatment
options, such as drug-eluting stents, that were previously
unavailable.

Despite these advances, CAD and its deleterious manifestations
represent the primary cause of mortality in the U.S. This is
largely caused by poor dietary choices, sedentary lifestyles,
suboptimal control of serum triglyceride, cholesterol, and glucose
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levels, inadequate prescription medication administration and
delayed dose titration, and ongoing tobacco use.

Efforts at primary and secondary prevention of obstructive CAD
among the general public are still lacking.

Public awareness campaigns are a partial success.

It is imperative for the physician to allocate time to address the
importance of lifestyle modification efforts.

The genetic basis of CAD is being unraveled at an accelerated
pace.

The future genetic assessment of a person’s lifetime risk for
developing atherosclerotic vascular disease, formerly an idea is
now emerging as a reality.

These findings can guide lifestyle modification prescription and
the choice and dosage of specific pharmaceuticals.

A preemptive approach is the best way to tackle the immensity
of CAD.

Medications, stenting, and bypass surgery are only curative
approaches. In addition to these methods, the patient must
meet the health care team at least halfway to achieve a
successful health outcome.
Angina
Angina is the term used to describe the pain and discomfort that
occurs when the heart is deprived of blood. Many patients describe the
feeling as a pressure or squeezing sensation in the chest. Some
patients will also experience discomfort in the shoulders, arm, neck,
jaw, or back. In some patients, the feeling will present as
indigestion.29 Angina is not a stand-alone heart condition. Instead, it is
a symptom of another heart problem. It is especially common in
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instances of coronary heart disease. There are a number of different
types of angina, all producing a specific set of conditions.30 The
following section outlines the most common types of angina.
Stable Angina
Angina pectoris is said to be stable when its pattern of frequency,
intensity, ease of provocation, or duration does not change over a
period of several weeks. Identification of activities that provoke angina
and the amount of sublingual nitroglycerin required to relieve
symptoms are helpful indicators of stability versus progression. A
decrease in exercise tolerance or an increase in the need for
nitroglycerin suggests that the angina is progressing in severity or
transitioning to an accelerating pattern.
Symptoms of stable angina involves pain or discomfort that:31

Occurs when the heart must work harder, usually during physical
exertion

Doesn't come as a surprise, and episodes of pain tend to be alike

Usually lasts a short time (5 minutes or less)

Is relieved by rest or medicine

May feel like gas or indigestion

May feel like chest pain that spreads to the arms, back, or other
areas
Possible triggers of stable angina include:

Emotional stress – learn stress management

Exposure to very hot or cold temperatures – learn how cold and
hot weather affect the heart.

Heavy meals
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
Smoking – learn more about quitting smoking
Accelerating Angina
Angina pectoris is said to be accelerating when there is a change in the
pattern of stable angina. This may include a greater ease of
provocation, more prolonged episodes, and episodes of greater
severity, requiring a longer recovery period or more frequent use of
sublingual nitroglycerin. This suggests a transition and most likely
reflects a change in coronary artery blood flow and perfusion of the
myocardium. This frequently portends unstable angina or an acute
coronary syndrome, such as an acute MI; should a patient transition
from a stable to an accelerating pattern of angina then acute medical
attention is warranted.32
Unstable Angina
Unstable angina pectoris occurs when the pattern of chest discomfort
changes abruptly. Signs of unstable angina are: symptoms at rest, a
marked increase in the frequency of attacks, discomfort that occurs
with minimal activity, and new-onset angina of incapacitating severity.
Unstable angina usually is related to the rupture of an atherosclerotic
plaque and the abrupt narrowing or occlusion of a coronary artery,
representing a medical emergency with an incipient acute coronary
syndrome and an MI to follow. Immediate medical attention is
mandatory.
Unstable angina or sometimes referred to as acute coronary syndrome
causes unexpected chest pain, and usually occurs while resting. The
most common cause is reduced blood flow to the heart muscle
because the coronary arteries are narrowed by fatty buildups
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(atherosclerosis) which can rupture causing injury to the coronary
blood vessel resulting in blood clotting which blocks the flow of blood
to the heart muscle. Unstable angina should be treated as an
emergency. If the patient has new, worsening or persistent chest
discomfort, he or she must receive care immediately. Symptoms of
unstable angina involves pain or discomfort that:33

Often occurs while the person may be resting, sleeping, or with
little physical exertion

Comes as a surprise

May last longer than stable angina

Rest or medicine usually do not help relieve it

May get worse over time

Can lead to a heart attack
Variant Angina
Unlike typical angina – which is often triggered by exertion or
emotional stress - variant angina almost always occurs when a person
is at rest, usually between midnight and early morning. These attacks
can be very painful.
Causes of Variant (Prinzmetal) Angina: The pain from variant angina is
caused by a spasm in the coronary arteries (which supply blood to the
heart muscle). The coronary arteries can spasm as a result of:

Exposure to cold weather

Stress

Medicines that tighten or narrow blood vessels

Smoking

Cocaine use
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Symptoms of variant (Prinzmetal) angina include pain or discomfort
that:34

Usually occurs while resting and during the night or early
morning hours

Are usually severe

Can be relieved by taking medication
Microvascular Angina
This type of angina may be a symptom of coronary microvascular
disease (MVD). Coronary MVD is heart disease that affects the heart’s
smallest coronary artery blood vessels.
Causes of microvascular angina involve spasms within the walls of
these very small arterial blood vessels causes reduced blood flow to
the heart muscle leading to a type of chest pain referred to as
microvascular angina. The symptoms of microvascular angina involves
angina that occurs in coronary MVD, which may differ from the typical
angina that occurs in heart disease in that the chest pain usually lasts
longer than 10 minutes, and it can last longer than 30 minutes.
The pain or discomfort:35

May be more severe and last longer than other types of angina
pain;

May occur with shortness of breath, sleep problems, fatigue, and
lack of energy;

Often is first noticed during routine daily activities and times of
mental stress.
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Heart Failure
Heart failure occurs when the heart is unable to pump blood at a rate
that is not adequate enough to maintain the requirements of tissue
metabolization, or at a rate that requires an elevated diastolic filling
pressure. According to the American Heart Association:
“heart failure affects nearly 5.7 million Americans of all ages and
is responsible for more hospitalizations than all forms of cancer
combined. It is the number 1 cause of hospitalization for
Medicare patients. With improved survival of patients with acute
myocardial infarction and with a population that continues to
age, heart failure will continue to increase in prominence as a
major health problem in the United States.”36
Heart failure statistics for the United States are as follows:

Heart failure is the fastest-growing clinical cardiac disease entity
in the United States, affecting 2% of the population

Heart failure accounts for 34% of cardiovascular-related deaths

Approximately 670,000 new cases of heart failure are diagnosed
each year

About 277,000 deaths are caused by heart failure each year

Heart failure is the most frequent cause of hospitalization in
patients older than 65 years, with an annual incidence of 10 per
1,000

Rehospitalization rates during the 6 months following discharge
are as much as 50%

Nearly 2% of all hospital admissions in the United States are for
decompensated heart failure, and the average duration of
hospitalization is about 6 days
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
In 2010, the estimated total cost of heart failure in the United
States was $39.2 billion, representing 1-2% of all health care
expenditures

The incidence and prevalence of heart failure are higher in
blacks, Hispanics, Native Americans, and recent immigrants from
developing nations, Russia, and the former Soviet republics. The
higher prevalence of heart failure in blacks, Hispanics, and
Native Americans is directly related to the higher incidence and
prevalence of hypertension and diabetes. This problem is
particularly exacerbated by a lack of access to health care and
by substandard preventive health care available to the most
indigent of individuals in these and other groups; in addition,
many persons in these groups do not have adequate health
insurance.

The higher incidence and prevalence of heart failure in recent
immigrants from developing nations are largely due to a lack of
prior preventive health care, a lack of treatment, or substandard
treatment for common conditions, such as hypertension,
diabetes, rheumatic fever, and ischemic heart disease.

Men and women have the same incidence and the same
prevalence of heart failure. However, there are still many
differences between men and women with heart failure, such as
the following:
o Women tend to develop heart failure later in life than
men
o Women are more likely than men to have preserved
systolic function
o Women develop depression more commonly than men
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o Women have signs and symptoms of heart failure
similar to those of men, but they are more pronounced
in women
o Women survive longer with heart failure than men

The prevalence of heart failure increases with age. The
prevalence is 1-2% of the population younger than 55 years and
increases to a rate of 10% for persons older than 75 years.37
Causes
The causes of heart failure can be broken into four main categories:38
1) Underlying causes:
Underlying causes of heart failure include structural
abnormalities (congenital or acquired) that affect the peripheral
and coronary arterial circulation, pericardium, myocardium, or
cardiac valves, thus leading to increased hemodynamic burden
or myocardial or coronary insufficiency.
Underlying causes of systolic heart failure include the following:

Coronary artery disease

Diabetes mellitus

Hypertension

Valvular heart disease (stenosis or regurgitant lesions)

Arrhythmia (supraventricular or ventricular)

Infections and inflammation (myocarditis)

Peripartum cardiomyopathy

Congenital heart disease

Drugs (either recreational, such as alcohol and cocaine,
or therapeutic drugs with cardiac side effects, such as
doxorubicin)
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
Idiopathic cardiomyopathy

Rare conditions (endocrine abnormalities, rheumatologic
disease, neuromuscular conditions)
Underlying causes of diastolic heart failure include the following:

Coronary artery disease

Diabetes mellitus

Hypertension

Valvular heart disease (aortic stenosis)

Hypertrophic cardiomyopathy

Restrictive cardiomyopathy (amyloidosis, sarcoidosis)

Constrictive pericarditis
Underlying causes of acute heart failure include the following:

Acute valvular (mitral or aortic) regurgitation

Myocardial infarction

Myocarditis

Arrhythmia

Drugs (i.e., cocaine, calcium channel blockers, or betablocker overdose)

Sepsis
Underlying causes of high-output heart failure include the
following:

Anemia

Systemic arteriovenous fistulas

Hyperthyroidism

Beriberi heart disease

Paget disease of bone
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
Albright syndrome (fibrous dysplasia)

Multiple myeloma

Pregnancy

Glomerulonephritis

Polycythemia vera

Carcinoid syndrome
Underlying causes of right heart failure include the following:

Left ventricular failure

Coronary artery disease (ischemia)

Pulmonary hypertension

Pulmonary valve stenosis

Pulmonary embolism

Chronic pulmonary disease

Neuromuscular disease
2) Fundamental causes
Fundamental causes include the biochemical and physiologic
mechanisms, through which either an increased hemodynamic
burden or a reduction in oxygen delivery to the myocardium
results in impairment of myocardial contraction.39
3) Precipitating causes
Overt heart failure may be precipitated by progression of the
underlying heart disease (i.e., further narrowing of a stenotic
aortic valve or mitral valve) or various conditions (fever, anemia,
infection) or medications (chemotherapy, NSAIDs) that alter the
homeostasis of heart failure patients.36
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4) Genetics of cardiomyopathy
Dilated, arrhythmic right ventricular and restrictive
cardiomyopathies are known genetic causes of heart failure.40
Prognosis
In general, the mortality following hospitalization for patients with
heart failure is 10.4% at 30 days, 22% at 1 year, and 42.3% at 5
years, despite marked improvement in medical and device therapy.
Each rehospitalization increases mortality by about 20-22%.
Mortality is greater than 50% for patients with NYHA class IV,
ACC/AHA stage D heart failure. Heart failure associated with acute MI
has an inpatient mortality of 20-40%; mortality approaches 80% in
patients who are also hypotensive (i.e., cardiogenic shock).41
Pathophysiology
Heart failure can occur from a variety of conditions and will present
differently depending on the cause and severity of the condition. In
addition, the condition will have a different impact on the patient
depending on the causes and severity. The following table provides a
comprehensive overview of the different effects of heart failure.42
Systolic
In systolic dysfunction (also called heart failure (HF) with
dysfunction
reduced ejection fraction (EF)), the ventricle contracts poorly
and empties inadequately, leading initially to increased
diastolic volume and pressure and decreased EF. Many
defects in energy utilization, energy supply,
electrophysiologic functions, and contractile element
interaction occur, with abnormalities in intracellular Ca
modulation and cAMP production.
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Predominant systolic dysfunction is common in HF due to MI,
myocarditis, and dilated cardiomyopathy. Systolic dysfunction
may affect primarily the left ventricle (LV) or the right
ventricle (RV); LV failure often leads to RV failure.
Diastolic
In diastolic dysfunction, also called HF with preserved EF,
dysfunction
ventricular filling is impaired, resulting in reduced ventricular
end-diastolic volume, increased end-diastolic pressure, or
both. Contractility and hence EF remain normal; EF may even
increase as the poorly filled LV empties more completely to
maintain cardiac output (CO). Markedly reduced LV filling can
cause low CO and systemic symptoms.
Elevated left atrial pressures can cause pulmonary
hypertension and pulmonary congestion. Diastolic dysfunction
usually results from impaired ventricular relaxation (an active
process), increased ventricular stiffness, valvular disease, or
constrictive pericarditis. Acute myocardial ischemia is also a
cause of diastolic dysfunction. Resistance to filling increases
with age, probably reflecting myocyte loss and increased
interstitial collagen deposition; thus, diastolic dysfunction is
particularly common among the elderly.
Diastolic dysfunction predominates in hypertrophic
cardiomyopathy, disorders with ventricular hypertrophy (i.e.,
hypertension, significant aortic stenosis), and amyloid
infiltration of the myocardium.
LV filling and function may also be impaired if marked
increases in RV pressure shift the interventricular septum to
the left. Diastolic dysfunction has increasingly been
recognized as a cause of HF. Estimates vary, but about 50%
of patients with HF have diastolic dysfunction and a normal
EF; the prevalence increases with age and with diabetes.
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LV failure
In failure due to LV dysfunction, CO decreases and pulmonary
venous pressure increases. When pulmonary capillary
pressure exceeds the oncotic pressure of plasma proteins
(about 24 mm Hg), fluid extravasates from the capillaries into
the interstitial space and alveoli, reducing pulmonary
compliance and increasing the work of breathing. Lymphatic
drainage increases but cannot compensate for the increase in
pulmonary fluid.
Marked fluid accumulation in alveoli (pulmonary edema)
significantly alters ventilation/perfusion (V/Q) relationships:
Deoxygenated pulmonary arterial blood passes through
poorly ventilated alveoli, decreasing systemic arterial
oxygenation (Pao2) and causing dyspnea. However, dyspnea
may occur before V/Q abnormalities, probably because of
elevated pulmonary venous pressure and increased work of
breathing; the precise mechanism is unclear.
In severe or chronic LV failure, pleural effusions
characteristically develop in the right hemithorax and later
bilaterally, further aggravating dyspnea. Minute ventilation
increases; thus, Paco2 decreases and blood pH increases
(respiratory alkalosis). Marked interstitial edema of the small
airways may interfere with ventilation, elevating Paco2 — a
sign of impending respiratory failure.
RV failure
In failure due to RV dysfunction, systemic venous pressure
increases, causing fluid extravasation and consequent edema,
primarily in dependent tissues (feet and ankles of ambulatory
patients) and abdominal viscera. The liver is most severely
affected, but the stomach and intestine also become
congested; fluid accumulation in the peritoneal cavity
(ascites) can occur.
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RV failure commonly causes moderate hepatic dysfunction,
with usually modest increases in conjugated and
unconjugated bilirubin, PT, and hepatic enzymes (i.e.,
alkaline phosphatase, AST, ALT, gamma-glutamyl
transpeptidase [GGT]). The impaired liver breaks down less
aldosterone, further contributing to fluid accumulation.
Chronic venous congestion in the viscera can cause anorexia,
malabsorption of nutrients and drugs, protein-losing
enteropathy (characterized by diarrhea and marked
hypoalbuminemia), chronic GI blood loss, and rarely ischemic
bowel infarction.
Cardiac
If ventricular function is impaired, a higher preload is
response
required to maintain CO. As a result, the ventricles are
remodeled over time: the LV becomes less ovoid and more
spherical, dilates, and hypertrophies; the RV dilates and may
hypertrophy. Initially compensatory, these changes
eventually increase diastolic stiffness and wall tension (i.e.,
diastolic dysfunction develops), compromising cardiac
performance, especially during physical stress. Increased wall
stress raises O2 demand and accelerates apoptosis
(programmed cell death) of myocardial cells. Dilation of the
ventricles can also cause mitral or tricuspid valve
regurgitation with further increases in end-diastolic volumes.
Hemodynamic
With reduced CO, O2 delivery to the tissues is maintained by
responses
increasing O2 extraction and sometimes shifting the
oxyhemoglobin dissociation curve to the right to favor O2
release. Reduced CO with lower systemic BP activates arterial
baroreflexes, increasing sympathetic tone and decreasing
parasympathetic tone. As a result, heart rate and myocardial
contractility increase, arterioles in selected vascular beds
constrict, venoconstriction occurs, and Na and water are
retained.
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These changes compensate for reduced ventricular
performance and help maintain hemodynamic homeostasis in
the early stages of HF. However, these compensatory
changes increase cardiac work, preload, and afterload;
reduce coronary and renal perfusion; cause fluid
accumulation resulting in congestion; increase K excretion;
and may cause myocyte necrosis and arrhythmias.
Renal
As cardiac function deteriorates, renal blood flow and GFR
responses
decrease, and blood flow within the kidneys is redistributed.
The filtration fraction and filtered Na decrease, but tubular
resorption increases, leading to Na and water retention. Blood
flow is further redistributed away from the kidneys during
exercise, but renal blood flow improves during rest, possibly
contributing to nocturia.
Decreased perfusion of the kidneys (and possibly decreased
arterial systolic stretch secondary to declining ventricular
function) activates the renin-angiotensin-aldosterone system,
increasing Na and water retention and renal and peripheral
vascular tone. These effects are amplified by the intense
sympathetic activation accompanying HF.
The renin-angiotensin-aldosterone-vasopressin (antidiuretic
hormone [ADH]) system causes a cascade of potentially
deleterious long-term effects. Angiotensin II worsens HF by
causing vasoconstriction, including efferent renal
vasoconstriction, and by increasing aldosterone production,
which not only enhances Na reabsorption in the distal
nephron but also causes myocardial and vascular collagen
deposition and fibrosis.
Angiotensin II increases norepinephrine release, stimulates
release of vasopressin, and triggers apoptosis.
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Angiotensin II may be involved in vascular and myocardial
hypertrophy, thus contributing to the remodeling of the heart
and peripheral vasculature, potentially worsening HF.
Aldosterone can be synthesized in the heart and vasculature
independently of angiotensin II (perhaps mediated by
corticotropin, nitric oxide, free radicals, and other stimuli)
and may have deleterious effects in these organs. HF that
causes progressive renal dysfunction (including that renal
dysfunction caused by drugs used to treat HF) contributes to
worsening HF and has been termed the cardiorenal
syndrome.
Neurohumoral
In conditions of stress, neurohumoral responses help increase
responses
heart function and maintain BP and organ perfusion, but
chronic activation of these responses is detrimental to the
normal balance between myocardial-stimulating and
vasoconstricting hormones and between myocardial-relaxing
and vasodilating hormones. The heart contains many
neurohumoral receptors (α1, β1, β2, β3, angiotensin II type 1
[AT1] and type 2 [AT2], muscarinic, endothelin, serotonin,
adenosine, cytokine, natriuretic peptides); the roles of all of
these receptors are not yet fully defined.
In patients with HF, β1 receptors (which constitute 70% of
cardiac β receptors) are downregulated, probably in response
to intense sympathetic activation. The result of
downregulation is impaired myocyte contractility and
increased heart rate. Plasma norepinephrine levels are
increased, largely reflecting sympathetic nerve stimulation, as
plasma epinephrine levels are not increased. Detrimental
effects include vasoconstriction with increased preload and
afterload, direct myocardial damage including apoptosis,
reduced renal blood flow, and activation of other
neurohumoral systems, including the renin-angiotensinaldosterone-vasopressin system.
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Vasopressin is released in response to a fall in BP via various
neurohormonal stimuli. Increased vasopressin decreases
renal excretion of free water; possibly contributing to
hyponatremia in HF. Vasopressin levels in patients with HF
and normal BP vary.
Atrial natriuretic peptide is released in response to increased
atrial volume and pressure; brain (B-type) natriuretic peptide
(BNP) is released from the ventricle in response to ventricular
stretching. These peptides enhance renal excretion of Na, but
in patients with HF, the effect is blunted by decreased renal
perfusion pressure, receptor downregulation, and perhaps
enhanced enzymatic degradation. Because endothelial
dysfunction occurs in HF, fewer endogenous vasodilators
(i.e., nitric oxide, prostaglandins) are produced, and more
endogenous vasoconstrictors (i.e., endothelin) are produced,
thus increasing afterload.
The failing heart and other organs produce tumor necrosis
factor (TNF)-α. This cytokine increases catabolism and is
possibly responsible for cardiac cachexia (loss of lean tissue
≥ 10%), which may accompany severely symptomatic HF,
and for other detrimental changes.
The failing heart also undergoes metabolic changes with
increased free fatty acid utilization and decreased glucose
utilization; these changes may become therapeutic targets.
Changes with
Age-related changes in the heart and cardiovascular system
aging
lower the threshold for expression of HF. Interstitial collagen
within the myocardium increases, the myocardium stiffens,
and myocardial relaxation is prolonged. These changes lead
to a significant reduction in diastolic LV function, even in
healthy elderly people.
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Modest decline in systolic function also occurs with aging. An
age-related decrease in myocardial and vascular
responsiveness to β-adrenergic stimulation further impairs
the ability of the cardiovascular system to respond to
increased work demands.
As a result of these changes, peak exercise capacity
decreases significantly (about 8%/decade after age 30), and
CO at peak exercise decreases more modestly. This decline
can be slowed by regular physical exercise. Thus, elderly
patients are more prone than are younger ones to develop HF
symptoms in response to the stress of systemic disorders or
relatively modest cardiovascular insults.
Stressors include infections (particularly pneumonia),
hyperthyroidism, anemia, hypertension, myocardial ischemia,
hypoxia, hyperthermia, renal failure, perioperative IV fluid
loads, nonadherence to drug regimens or to low-salt diets,
and use of certain drugs (including NSAIDs, β-blockers, and
certain Ca channel blockers).
Signs and Symptoms
Signs and symptoms of heart failure include the following:43

Exertional dyspnea and/or dyspnea at rest

Orthopnea

Acute pulmonary edema

Chest pain/pressure and palpitations

Tachycardia

Fatigue and weakness

Nocturia and oliguria
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
Anorexia, weight loss, nausea

Exophthalmos and/or visible pulsation of eyes

Distention of neck veins

Weak, rapid, and thready pulse

Rales, wheezing

S3 gallop and/or pulsus alternans

Increased intensity of P2 heart sound

Hepatojugular reflux

Ascites, hepatomegaly, and/or anasarca

Central or peripheral cyanosis, pallor
Diagnosis
Heart failure is diagnosed using a set of criteria and a classification and
staging process. There are a number of classification systems that can
be used to diagnose heart failure. The most widely used systems
include those outlined below.
Framingham:
The Framingham criteria for the diagnosis of heart failure consist of
the concurrent presence of either 2 major criteria or 1 major and 2
minor criteria. Major criteria include the following:44

Paroxysmal nocturnal dyspnea

Weight loss of 4.5 kg in 5 days in response to treatment

Neck vein distention

Rales

Acute pulmonary edema

Hepatojugular reflux

S3 gallop

Central venous pressure greater than 16 cm water
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
Circulation time of 25 seconds

Radiographic cardiomegaly

Pulmonary edema, visceral congestion, or cardiomegaly at
autopsy
Minor criteria are as follows:

Nocturnal cough

Dyspnea on ordinary exertion

A decrease in vital capacity by one third the maximal value
recorded

Pleural effusion

Tachycardia (rate of 120 bpm)

Bilateral ankle edema
The New York Heart Association (NYHA):
The New York Heart Association (NYHA) classification system
categorizes heart failure on a scale of I to IV are listed below.45

Class I: No limitation of physical activity

Class II: Slight limitation of physical activity

Class III: Marked limitation of physical activity

Class IV: Symptoms occur even at rest; discomfort with any
physical activity
The American College of Cardiology/American Heart Association
(ACC/AHA):
The American College of Cardiology/American Heart Association
(ACC/AHA) staging system is defined by the following 4 stages.46
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
Stage A: High risk of heart failure but no structural heart disease
or symptoms of heart failure

Stage B: Structural heart disease but no symptoms of heart
failure

Stage C: Structural heart disease and symptoms of heart failure

Stage D: Refractory heart failure requiring specialized
interventions

Testing
Diagnostic Testing
The following tests may be used as part of the initial evaluation for
suspected heart failure:47

Complete blood count (CBC)

Urinalysis

Electrolyte levels

Renal and liver function studies

Fasting blood glucose levels

Lipid profile

Thyroid stimulating hormone (TSH) levels

B-type natriuretic peptide levels

N-terminal pro-B-type natriuretic peptide

Electrocardiography

Chest radiography

2-dimensional (2-D) echocardiography

Nuclear imaging

Maximal exercise testing

Pulse oximetry or arterial blood gas
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Heart Procedure or Surgery
Many patients who undergo heart procedures or surgery will benefit
from cardiac rehabilitation. In these instances, a rehabilitation
program will help the patient return to normal cardiac performance
levels. There are a number of cardiac procedures that can benefit from
post-procedure cardiac rehabilitation.
Coronary Artery Bypass Graft
Coronary artery bypass grafts are the most common cardiac surgeries
performed in the United States. The procedure is used to treat patients
who have significant narrowings and blockages of their coronary
arteries. It is most used to treat patients with coronary artery disease.
The buildup of fatty material in the arterial walls causes significant
narrowing which reduces blood flow. The procedure creates new,
unblocked routes around the blocked (narrowed) arteries. Once the
new routes are created, adequate blood flow will return to the heart,
thereby delivering the appropriate amounts of oxygen and nutrients to
the heart.48
One way to treat the blocked or narrowed arteries is to:
“bypass the blocked portion of the coronary artery with another
piece of blood vessel. Blood vessels, or grafts, used for the
bypass procedure may be pieces of a vein taken from the legs or
an artery in the chest. At times, an artery from the wrist may
also be used. One end of the graft is attached above the
blockage and the other end is attached below the blockage.
Thus, the blood is rerouted around, or bypasses, the blockage
through the new graft to reach the heart muscle. This bypass of
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the blocked coronary artery can be done by performing coronary
artery bypass surgery.”49
The standard procedure for performing a bypass involves opening the
chest fully and stopping the heart. This requires an intensive
procedure in a standard hospital operating room.
“In order to open the chest, the breastbone (sternum) is cut in
half and spread apart. Once the heart is exposed, tubes are
inserted into the heart so that the blood can be pumped through
the body during the surgery by a cardiopulmonary bypass
machine (heart-lung machine). The bypass machine is necessary
to pump blood while the heart is stopped and kept still in order
for the surgeon to perform the bypass operation.”23
The following is a fact sheet that provides a thorough overview of the
standard bypass procedure, which the cardiac rehab team nurse may
share with patients and their families.48
When atherosclerosis develops in the coronary arteries, flow of blood through
these vessels is blocked, and the blood supply to heart muscle is jeopardized. If
the blockages are significant enough, the end result will be a heart attack or
sudden death. CABG is an operation that is designed to re-route the blood
around these blockages to prevent a heart attack or sudden death.
Conventionally an artery from behind the breastbone, and veins from the legs
are used to "bypass" the blood around the coronary artery blockages.
The operation takes 2-3 hours to perform, and begins after general anesthesia is
induced. Patients are completely asleep during the entire course of the operation.
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The saphenous vein is removed through incisions in the legs. The length of the
incision is dependent upon the amount of vein required to complete the
necessary number of "bypasses" (i.e., 5 bypasses will require more vein than 2
bypasses). There are many "redundant" veins in the leg ... once some vein is
removed, the other veins in the leg take over for the missing vein. Once the vein
has been removed from the leg, it has the appearance of a long tube or
"conduit". The vein will be divided into separate shorter segments, each of which
will be used for individual bypasses. As vein is removed from the leg by a
physician assistant, the surgeon simultaneously opens the chest by dividing the
breast bone or sternum, affording excellent exposure of the heart. An artery
behind the sternum, the left internal mammary artery (LIMA) is taken down and
one end prepared for bypass grafting. Tubes or cannulae are inserted into the
heart and major blood vessels surrounding the heart in preparation for
cardiopulmonary bypass with the heart-lung machine.
At this point, the patient is placed on the heart-lung machine. Blood is redirected from the heart into the heart-lung machine. This permits the surgeon to
safely operate on the heart without blood pumping through it. The heart is then
stopped, and the heart-lung machine continues to pump freshly oxygenated
blood to the rest of the body, in effect, taking over the roles of the heart and
lungs. The diseased coronary arteries are now identified and opened beyond the
level of the blockages. The open ends of the saphenous veins and LIMA are now
sewn to the openings in the coronary arteries using very fine non-absorbable
suture material; these are called the "distal" anastamoses. Surgeons wear
special magnifying lenses in order to see the delicate suture and small vessels.
Because the "inflow" through the LIMA is left intact, as soon as the LIMA
anastamosis is completed, blood flow is established to that region of the heart. A
vein graft however, is harvested as a "free graft" and has no "inflow"; therefore,
after the "distal" vein graft anastamosis is constructed, the other end of the vein
graft is sewn to the aorta (the main artery leaving the heart) in order to
establish "inflow". These are called the "proximal" anastamoses. After this stage,
blood flow has now been established beyond all the blocked arteries, and the
heart has effectively been "bypassed"
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The heart-lung machine is then gradually weaned off, and the patient's heart and
lungs resume their normal functions. The cannulae are removed from in and
around the heart, and the sternum and incisions are closed.
Drainage catheters are placed around the heart ... these are usually removed
after 24 hours. Temporary pacing wires to regulate the patient's heart rate are
sewn to the surface of the heart ... these are removed before the patient goes
home.
Following the operation, patients are transported to the Cardiac Post-Anesthesia
Care Unit, a specialized unit caring exclusively for open-heart surgery patients.
Patients generally awaken from anesthesia 4-6 hr after the operation. The
following morning all drainage catheters and monitoring lines are usually
removed, and patients are transferred to a standard hospital room in the cardiac
recovery wing of the hospital. Patients undergoing a CABG operation are usually
hospitalized for 4-5 days following the surgery.
Patients will receive the following detailed instructions prior to the
procedure(s):

You will be asked to empty your bladder prior to the procedure.

An intravenous (IV) line will be started in your arm or hand. Additional
catheters will be inserted in your neck and wrist to monitor the status of
your heart and blood pressure, as well as for obtaining blood samples.
Alternate sites for the additional catheters include the subclavian (under
the collarbone) area and the groin.

You will be positioned on the operating table, lying on your back.

The anesthesiologist will continuously monitor your heart rate, blood
pressure, breathing, and blood oxygen level during the surgery. Once you
are sedated, a breathing tube will be inserted into your throat and into
your trachea (breathing tube) to provide oxygen to your lungs, and you
will be connected to a ventilator, which will breathe for you during the
surgery.

A catheter will be inserted into your bladder to drain urine.

The skin over the surgical site will be cleansed with an antiseptic solution.
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
Once all the tubes and monitors are in place, incisions may be made in
one or both of your legs or one of your wrists to obtain a section of vein
to be used for grafts.

The doctor will make an incision (cut) down the center of the chest from
just below the Adam's apple to just above the navel.

The sternum (breastbone) will be divided in half with a special operating
instrument. The doctor will separate the two halves of the breastbone and
spread them apart to expose the heart.
Coronary artery bypass graft surgery--on-pump procedure:

In order to sew the grafts onto the very small coronary arteries, the heart
must be stopped to allow the doctor to perform the very delicate
procedure. Tubes will be inserted into the heart so that the blood can be
pumped through your body by a cardiopulmonary bypass machine.

Once the blood has been diverted into the bypass machine for pumping,
the heart will be stopped by injecting it with a cold solution.

When the heart has been stopped, the doctor will perform the bypass
graft procedure by sewing one end of a section of vein over a tiny opening
made in the aorta, and the other end over a tiny opening made in the
coronary artery just below the blockage. If the internal mammary artery
inside your chest is being used as a bypass graft, the lower end of the
artery will be cut from inside the chest and sewn over an opening made in
the coronary artery below the blockage.

You may have more than one bypass graft performed, depending on how
many blockages you have and where they are located. After all the grafts
have been completed, the doctor will examine them to make sure they
are working.

Once the bypass grafts have been completed, the blood circulating
through the bypass machine will be allowed back into your heart and the
tubes to the machine will be removed. Your heart will be restarted.

Temporary wires for pacing may be inserted into the heart. These wires
can be attached to a pacemaker and your heart can be paced, if needed,
during the initial recovery period.
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Coronary artery bypass surgery--off-pump procedure:

Once the chest has been opened, the area around the artery to be
bypassed will be stabilized with a special type of instrument.

The rest of the heart will continue to function and pump blood through the
body.

The cardiopulmonary bypass machine and the perfusionist who runs it
may be kept on stand-by should the procedure need to be completed on
bypass.

The doctor will perform the bypass graft procedure by sewing one end of
a section of vein over a tiny opening made in the aorta, and the other end
over a tiny opening made in the coronary artery or internal mammary
artery just below the blockage.

You may have more than one bypass graft performed, depending on how
many blockages you have and where they are located.

Before the chest is closed, the doctor will examine the grafts to make sure
they are working.
Possible risks associated with coronary artery bypass graft surgery
include, but are not limited to, the following:50

Bleeding during or after the surgery

Blood clots that can cause heart attack, stroke, or lung problems

Infection at the incision site

Pneumonia

Breathing problems

Cardiac dysrhythmias/arrhythmias (abnormal heart rhythms)
Indications
Class I indications for CABG from the American College of Cardiology
(ACC) and the American Heart Association (AHA) are as follows:46

Left main coronary artery stenosis >50%
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
Stenosis of proximal LAD and proximal circumflex >70%

3-vessel disease in asymptomatic patients or those with mild or
stable angina

3-vessel disease with proximal LAD stenosis in patients with poor
left ventricular (LV) function

or 2-vessel disease and a large area of viable myocardium in
high-risk area in patients with stable angina

>70% proximal LAD stenosis with either ejection fraction < 50%
or demonstrable ischemia on noninvasive testing
Other indications for CABG include the following:51

Disabling angina (Class I)

Ongoing ischemia in the setting of a non–ST segment elevation
MI that is unresponsive to medical therapy (Class I)

Poor left ventricular function but with viable, nonfunctioning
myocardium above the anatomic defect that can be
revascularized

CABG may be performed as an emergency procedure in the
context of an ST-segment elevation MI (STEMI) in cases where it
has not been possible to perform percutaneous coronary
intervention (PCI) or where PCI has failed and there is persistent
pain and ischemia threatening a significant area of myocardium
despite medical therapy.
Contraindications

CABG is not considered appropriate in asymptomatic patients
who are at a low risk of MI or death. Patients who will experience
little benefit from coronary revascularization are also excluded.
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
Although advanced age is not a contraindication, CABG is less
commonly performed in the elderly. Because elderly patients
have a shorter life expectancy, CABG may not necessarily
prolong survival. These patients are also more likely to
experience perioperative complications after CABG.52
Many patients still undergo traditional bypass procedures. However, in
some instances, less invasive procedures may be used. "Off-pump"
procedures, in which the heart does not have to be stopped, were
developed in the 1990's. Other minimally-invasive procedures, such as
key-hole surgery (performed through very small incisions) and robotic
procedures (performed with the aid of a moving mechanical device),
increasingly are being used.53
The following table provides information on the different types of
bypass procedures:51, 54-60
Off-Pump
Coronary artery bypass grafting (CABG) has conventionally been
Coronary
an operation that requires the use of the heart lung machine. For
Artery
selected patients, surgeons have designed an innovative way to
Bypass
bypass blocked arteries on the heart without the use of the heart-
Grafting
lung machine ... this operation is called "off-pump coronary artery
bypass grafting" or "OPCAB". Although indications for performing
this procedure are more limited, and long-term results compared
with conventional CABG are unknown, there are some patients
who may benefit from this procedure.
The principals of OPCAB are in some ways similar to that of CABG,
namely, that an artery from behind the breast bone and/or veins
from the legs are used to "bypass" blood around coronary artery
blockages.
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OPCAB is different from CABG in that the heart-lung machine is
not used. This means that the special catheters and "cannulae"
that are placed in and around the heart for a conventional CABG
operation are not used. The heart continues to pump blood to the
rest of the body, and surgeons must operate on a "beating heart".
An advantage of OPCAB over conventional CABG is that it may
eliminate some of the risks associated with using the heart-lung
machine. In most patients these risks are very, very small ... but
in some older patients with significant atherosclerotic disease of
their aorta, poor kidney function, or significant lung disease ...
these risks may be more considerable, and OPCAB might be a
reasonable and safer approach than conventional CABG. There are
many more variables that determine whether or not a patient
would be an acceptable candidate for OPCAB ... these issues are
best discussed with your surgeon.
A disadvantage of OPCAB is that because the heart is not stopped,
surgeons must perform delicate suturing on a "beating heart".
Consequently, stabilizing devices have been developed to help
limit the motion of the heart as surgeons operate. The operation
itself is similar to the CABG operation described above.
General anesthesia is induced, and the patient is asleep for the
entire course of the operation. The surgeon opens the chest by
dividing the breastbone or sternum. An artery behind the sternum,
the left internal mammary artery (LIMA), is taken down and one
end prepared for bypass grafting. If more than one coronary artery
will be bypassed, saphenous vein from the leg is removed and
prepared for the additional bypasses. A stabilizing device is now
placed on the surface of the heart, limiting the motion of the
beating heart. The coronary arteries are opened beyond the sites
of the blockage, and the open ends of the LIMA and vein grafts are
sewn to the openings in the coronary arteries. These are called the
"distal" anastamoses.
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Because the "inflow" through the LIMA is left intact, as soon as the
LIMA anastamosis is completed, blood flow is established to that
region of the heart. A vein graft however, is harvested as a "free
graft" and has no "inflow" ... therefore, after the "distal" vein graft
anastamosis is constructed, the other end of the vein graft is sewn
to the aorta (the main artery leaving the heart) in order to
establish "inflow". These are called the "proximal" anastamoses.
At this point in the operation, blood flow has now been established
beyond all the blocked arteries, and the heart has effectively been
"bypassed".
Drainage catheters are placed around the heart ... these are
usually removed after 24hr. Temporary pacing wires to regulate
the patient's heart rate, are sewn to the surface of the heart ...
these are removed before the patient goes home.
The sternum and incisions are closed, and the patient is
transported to the Cardiac Post-Anesthesia Care Unit, a specialized
unit caring exclusively for open-heart surgery patients. Patients
generally awaken from anesthesia 4-6 hr after the operation. The
following morning all drainage catheters and monitoring lines are
usually removed, and patients are transferred to a standard
hospital room in the cardiac recovery wing of the hospital. Patients
undergoing an OPCAB are usually hospitalized for 3-4 days
following surgery. To see what to expect during the recovery of
this operation, please refer to our education section.
Robotic-
The daVinci surgical robotic system is used to perform minimally
assisted
invasive heart surgery. Surgeons are pioneering new robotic
Coronary
surgical approaches. Coronary Artery Bypass Grafting, or CABG, is
Artery
a surgical procedure to bypass the clogged coronary blood vessel,
Bypass
and restore blood flow to the heart. The surgeon uses a section of
Grafting
a healthy artery from the patient's left chest, known as the left
internal mammary artery (LIMA), to "bypass" the diseased section
of the patient's own coronary artery.
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Traditional bypass surgery requires the chest to be cut open, the
patient's breastbone to be split, and the function of the heart to be
taken over by a heart-lung bypass machine. Skilled surgeons are
able to use the daVinci robot to carefully prepare the LIMA for use
as a single bypass to the heart without the use of the heart-lung
machine and with no incisions over the breastbone. With only
small incisions over the patient's left chest, smaller surgical
instruments, and greater precision in robotic surgery, patients
experience less pain and have more rapid recovery times.
Robotic-assisted coronary artery bypass grafting is a minimally
invasive procedure. The surgeon makes several small incisions
between the ribs, and then inserts a small camera and small
robotic arms through the incisions.
During the procedure, the surgeon sits at a console and controls
the robotic instruments. The camera that was inserted provides
images of the heart at a high magnification. Using robotic-assisted
coronary artery bypass grafting, patients can typically undergo a
single bypass using the LIMA to the main artery of the heart,
known as the left anterior descending artery, or LAD. If the patient
has disease in more than one vessel in the heart, this procedure
can at times be combined with coronary stents in the other
vessels, performed by cardiologists, to achieve repairs or bypasses
to each of the diseased vessels. In this way, for selected patients,
surgeons have designed an innovative way to bypass the main
blocked LAD artery with minimally invasive robotic surgery,
combined with stents to other vessels.
Although indications for performing this procedure are more
limited, and long-term results compared with conventional CABG
are unknown, there are some patients who may benefit from this
procedure.
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Minimally
Coronary Artery Bypass Grafting, or CABG, is a surgical procedure
Invasive
to bypass the clogged coronary blood vessel, and restore blood
Coronary
flow to the heart. The surgeon uses a section of a healthy artery
Artery
from the patient's left chest, known as the left internal mammary
Bypass
artery (LIMA), to "bypass" the diseased section of the patient's
Grafting
own coronary artery.
Traditional bypass surgery required the chest to be cut open, the
patient's breastbone to be split, and the function of the heart to be
taken over by a heart-lung bypass machine. A minimally invasive
CABG is an "off-pump" procedure. Only a single 3-inch incision is
typically used over the patient's left chest between the ribs and no
incisions over the breastbone. The beating heart is held in place
with "stabilizers", which are instruments that immobilize the area
of the heart where the bypass is being done.
With only a single, small incision over the patient's left chest,
patients experience less pain and have more rapid recovery times.
Skilled surgeons are able to use a minimally invasive incision to
carefully prepare the LIMA for use as a single bypass to the heart
without the use of the heart-lung machine and with no incisions
over the breastbone. With a minimally invasive coronary artery
bypass procedure, the surgeon can typically perform a single
bypass using the LIMA to the main artery of the heart, known as
the left anterior descending artery, or LAD.
If the patient has disease in more than one vessel in the heart,
this procedure can at times be combined with coronary stents in
the other vessels, performed by cardiologists, to achieve repairs or
bypasses to each of the diseased vessels. In this way, for selected
patients, surgeons have designed an innovative way to bypass the
main blocked LAD artery with minimally coronary artery bypass
grafting, combined with stents to other vessels.
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Although indications for performing this procedure are more
limited, and long-term results compared with conventional CABG
are unknown, there are some patients who may benefit from this
procedure.
Endoscopic
Standard incisions for harvesting saphenous vein for bypass
Vein
operations historically have been long incisions that run the length
Harvesting
of a patient’s leg. Alternatively several smaller “skip” incisions can
be made to provide a more cosmetic and less painful result.
Surgeons now utilize a new technology called Endoscopic Vein
Harvesting that permits them to harvest a complete leg’s length of
vein through a 1 or 2 small (1 cm) incisions. The incision can be
made anywhere along the leg, and vein is removed using specially
designed telescoping surgical and video equipment.
In addition to reducing the size of the surgical scar, Endoscopic
Vein Harvesting significantly reduces leg discomfort in the postoperative period, and is associated with fewer complications such
as infection and hematoma formation.
Percutaneous Coronary Intervention
Percutaneous coronary intervention (PCI) is a non-surgical procedure
that is performed on patients who have narrowed arteries. The
procedure opens the narrowed arteries so that blood can flow more
easily to the heart.61 With this procedure, a catheter is inserted
through the skin in the groin or the arm. The catheter is inserted
directly into an artery. Once the catheter is secure in the artery,
several devices can be used to help expand the artery. The most
common devices include a balloon, stent, or an artherectomy device.
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The catheter and its devices are threaded through the inside of the
artery back into an area of coronary artery narrowing or blockage.62
This procedure can be used on patients who are actively experiencing
a myocardial infarction. In these instances, the percutaneous coronary
intervention will be used as a method of intervening and stopping the
infarction by opening the blocked artery. This will reinstate blood flow
to the heart, thereby stopping the acute infarction. “Although
treatment of acute heart attack is a very important use of
percutaneous coronary intervention, it has several other uses.
Percutaneous coronary intervention can be used to relieve or reduce
angina, prevent heart attacks, alleviate congestive heart failure, and
allows some patients to avoid surgical treatment (coronary artery
bypass graft or CABG) that involves extensive surgery and often long
rehabilitation time.”63
Indications and Contraindications
Clinical indications for Percutaneous Coronary Intervention include the
following:

Acute ST-elevation myocardial infarction (STEMI)

Non–ST-elevation acute coronary syndrome (NSTE-ACS)

Unstable angina

Stable angina

Anginal equivalent (i.e., dyspnea, arrhythmia, or dizziness or
syncope)

High risk stress test findings

In an asymptomatic or mildly symptomatic patient, objective
evidence of a moderate to large area of viable myocardium or
moderate to severe ischemia on noninvasive testing is an
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indication for PCI. Angiographic indications include
hemodynamically significant lesions in vessels serving viable
myocardium (vessel diameter >1.5 mm).64
Clinical contraindications for Percutaneous Coronary Intervention
include the following:65

Intolerance of long-term antiplatelet therapy or the presence of
any significant comorbid conditions that severely limit the
lifespan of the patient (this is a relative contraindication).

A Heart Team approach (involving interventional cardiologists
and cardiac surgeons) should be used in patients with diabetes
and multivessel coronary artery disease and in patients with
severe left main disease and a high Syntax score.
Relative angiographic contraindications include the following:66

Arteries < 1.5 mm in diameter

Diffusely diseased saphenous vein grafts

Other coronary anatomy not amenable to PCI
In patients with stable angina, medical therapy is recommended as
first-line therapy unless one or more of the following indications for
cardiac catheterization and PCI or coronary artery bypass grafting
(CABG) are present:67

Severe symptoms

A change in symptom severity

Failed medical therapy

High-risk coronary anatomy

Worsening left ventricular (LV) dysfunction
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
For patients with STEMI, immediate coronary angiography with
PCI is recommended (primary PCI).
For patients with NSTE-ACS, the American College of Cardiology
Foundation (ACCF)/American Heart Association (AHA) guidelines on
the management of NSTE-ACS (updated in 2014) recommend an early
invasive strategy in most cases, with timing as follows:68

Immediate (within 2 hours) - Patients with refractory or
recurrent angina with initial treatment, signs/symptoms of heart
failure, new/worsening mitral regurgitation, hemodynamic
instability, sustained ventricular tachycardia, or ventricular
fibrillation

Early (within 24 hours) - None of the immediate characteristics
but new ST-segment depression, a GRACE risk score >140, or
temporal change in troponin

Delayed invasive (within 25-72 hours) - None of the immediate
or early characteristics but renal insufficiency (glomerular
filtration rate [GFR] < 60 mL/min/1.73 m2), left ventricular
ejection fraction (LVEF) < 40%, early postinfarct angina, history
of PCI within the preceding 6 months, prior CABG, GRACE risk
score of 109-140, or TIMI score of 2 or higher

Ischemia-guided approach is recommended for patients with a
low-risk score (TIMI 0 or 1, GRACE < 1).
Equipment for a PCI Procedure
Balloon catheters for PCI have the following features:64

A steerable guide wire precedes the balloon into the artery and
permits navigation through the coronary tree
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
Inflation of the balloon compresses and axially redistributes
atheromatous plaque and stretches the vessel wall

The balloon catheter also serves as an adjunctive device for
many other interventional therapies
Atherectomy devices have the following features:69

These devices are designed to physically remove coronary
atheroma, calcium, and excess cellular material

Rotational or orbital atherectomy, which relies on plaque
abrasion and pulverization, is used mostly for fibrotic or heavily
calcified lesions that can be wired but not crossed or dilated by a
balloon catheter

Atherectomy devices may be used to facilitate stent delivery in
complex lesions

Directional coronary atherectomy (DCA) has been used to debulk
coronary plaques

Laser atherectomy is not widely used at present

Atherectomy is typically followed by balloon dilation and
stenting.
Intracoronary stents have the following features:67

Stents differ with respect to composition (i.e., cobalt chromium
or platinum chromium), architectural design, delivery system
and the drug delivered

Drug-eluting stents (DESs) have demonstrated significant
reductions in restenosis and target-lesion revascularization rates,
with further reduction with the second-generation DESs
(compared with first-generation DESs or bare-metal stents)
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
In the United States, the commercially available DESs are
second-generation models that elute everolimus and zotarolimus

The stents with bioabsorbable polymer, polymer-free systems or
fully bioresorbable scaffolds are still investigational and not
available for commercial use in the United States

Stents are conventionally placed after balloon predilation, but in
selected coronary lesions, direct stenting may lead to better
outcomes
Other devices used for PCI include the following:69

Thrombus aspiration is reasonable in selected patients
undergoing primary PCI; however, one trial showed no reduction
in the rate of death from any cause or the composite of death
from any cause, rehospitalization for myocardial infarction, or
stent thrombosis

Distal embolic protection during saphenous vein graft
intervention can be considered when technically feasible
Technique:
Intravascular ultrasonography (IVUS) and optical coherence
tomography (OCT) are used in PCI for the following purposes:64

Provision of information about atherosclerotic plaque
composition and burden, the vessel wall, vessel size, degree of
calcium, and degree of luminal narrowing

Assessment of indeterminate lesions

Evaluation of adequate stent deployment
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Intracoronary Doppler pressure wires are used in PCI as follows:70

Characterization of coronary lesion physiology and estimation of
lesion severity

Comparison of pressure distal to a lesion with aortic pressure
enables determination of fractional flow reserve (FFR); FFR <
0.80 during maximal hyperemia (induced via administration of
adenosine) is consistent with a hemodynamically significant
lesion
Antithrombotic therapy includes the following:71

Aspirin 162-325 mg is given to all patients on the day of PCI

Unfractionated heparin, low-molecular-weight heparin (LMWHs)
or bivalirudin is used at the time of balloon angioplasty or PCI;
fondaparinux can be used but needs another agent along with it
to prevent catheter thrombosis and therefore is less commonly
preferred
Antiplatelet therapy:72
Patients receiving stents are treated with a combination of aspirin and
a P2Y12 receptor inhibitor (clopidogrel, prasugrel, or ticagrelor). The
minimum duration of P2Y12 receptor inhibitor therapy, according to
the current ACCF/AHA guidelines, is as follows:

Bare-metal stents - Minimum of 4 weeks

DESs - Minimum of 12 months

Use of proton pump inhibitors (PPIs) is appropriate in patients
with multiple risk factors for gastrointestinal bleeding who
require antiplatelet therapy.
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Glycoprotein inhibitor therapy:73

Abciximab, tirofiban, and eptifibatide have all been shown to
reduce ischemic complications in patients undergoing balloon
angioplasty and coronary stenting; however, evidence
supporting their use was established largely before the use of
oral P2Y12 inhibitors

Several studies have failed to show the benefit of “upstream”
administration of GPIIb/IIIa inhibitors in the era of dual
antiplatelet therapy (DAPT); because GPIIb/IIIa inhibitors
increase the risk of bleeding, their routine use is no longer
recommended

GPIIb/IIIa inhibitors can be used as an adjunctive therapy at the
time of PCI, on an individual basis, for large thrombus burden or
inadequate P2Y12 receptor antagonist loading.
Coronary Angioplasty
Percutaneous coronary intervention (PCI) is performed to open blocked
coronary arteries caused by coronary artery disease (CAD) and to
restore arterial blood flow to the heart tissue without open-heart
surgery. Using a guidewire, a special catheter (long hollow tube) is
inserted into the coronary artery and past the blockage in the
blockage. The catheter contains a tiny balloon. When the catheter is in
place, the balloon is inflated.
The inflation of the balloon compresses the fatty tissue in the artery
and makes a larger opening inside the artery for improved blood
flow.74 The following procedural steps are involved during the PCI.
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
The use of fluoroscopy (a special type of X-ray, similar to an Xray "movie") assists the doctor in the location of blockages in the
coronary arteries as the contrast dye moves through the
arteries.

A technique called intravascular ultrasound (IVUS), a technique
that uses a computer and a transducer that sends out sound
waves to create images of the blood vessels, may be used during
PCI. The use of IVUS provides direct visualization and
measurement of the inside of the blood vessels and may assist
the doctor in selecting the appropriate size of balloons and/or
stents, to ensure that a stent, if used, is properly opened, or to
evaluate the use of other angioplasty instruments. A technique
called fractional flow reserve (FFR) assessment is often used
during a catheterization to assist in determining the significance
of a moderate coronary narrowing.
The technique involves placing a pressure-transducing wire
across the narrowing, and after a brief infusion of medication,
measuring the pressure change in the coronary artery. This may
assist the physician in deciding whether PCI or stenting is
appropriate.

The physician may determine that another type of procedure is
necessary. This may include the use of atherectomy (removal of
plaque) at the site of the narrowing of the artery. In
atherectomy, there may be tiny blades on a balloon or a rotating
tip at the end of the catheter. When the catheter reaches the
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narrowed spot in the artery, the plaque is broken up or cut away
to open the artery.
Coronary Stenting
Coronary stents are now almost universally used in PCI procedures,
often following balloon angioplasty, which opens the narrowed artery
and facilitates stent placement. A stent is a tiny, expandable metal coil
that is inserted into the newly-opened area of the artery to help keep
the artery from narrowing or closing again.67 The following are
procedural steps used during stent placement.

Once the stent has been placed, tissue will begin to form over it
within a few days after the procedure. The stent will be
completely covered by tissue within a month or so. It is
necessary to take medications, such as aspirin, clopidogrel
(Plavix), prasugrel (Effient), or ticagrelor (Brilinta), which
decrease the "stickiness" of platelets (special blood cells that
clump together to stop bleeding), in order to prevent blood clots
from forming inside the stent. The physician will provide specific
instructions regarding which medications need to be taken and
for how long.

Newer stents (drug-eluting stents, or DES) are coated with
medication to prevent the formation of scar tissue inside the
stent. These drug-eluting stents release medication within the
blood vessel itself. This medication inhibits the overgrowth of
tissue that can occur within the stent. The effect of this
medication is to deter the narrowing of the newly stented blood
vessel. Because stents can become blocked, it is important for
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the patient to talk with their physician about what is needed if
the patient experiences chest pain after a stent placement.

If scar tissue does form inside the stent, a repeat procedure may
be performed, either with balloon angioplasty or with a second
stent, or occasionally with local radiation therapy (called
brachytherapy) may be used to clear the scarred area and open
up the vessel.
Stents are most useful for:75

Short lesions in large native coronary arteries not previously
treated with PTCA

Focal lesions in saphenous vein grafts

Treatment of abrupt closure during PTCA
Other Procedures
Other related procedures that may be used to assess the heart
include:76

Resting or exercise electrocardiogram (ECG or EKG)

Holter monitor

Signal-averaged ECG

Cardiac catheterization
chest X-ray

Computed tomography (CT scan) of the chest

Echocardiography

Electrophysiological studies
magnetic resonance imaging (MRI) of the heart

Myocardial perfusion scans

Radionuclide angiography
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
Cardiac CT scan.

Rotational atherectomy - This is sometimes used to aid stent
placement when the plaque is hardened and calcified.
Valve Replacement
Heart valve replacement (or repair) is used to treat valvular heart
disease. It is especially common in patients with valvular stenosis and
valvular insufficiency.77 Heart valve repair or replacement surgery is a
treatment option for valvular heart disease. When heart valves
become damaged or diseased, they may not function properly.
Conditions which may cause heart valve dysfunction are valvular
stenosis and valvular insufficiency (regurgitation).78 When one (or
more) valve(s) becomes stenotic, it becomes more difficult for the
heart to pump blood through the valve. Valvular stenosis “may be the
result of infection or aging, and the effects on the patient will vary. In
some instances, such as when one or more valves become insufficient
(leaky), blood leaks backwards. Based on the symptoms and overall
condition of the heart, the physician may determine that the diseased
valve(s) needs to be surgically repaired or replaced.”79
The following describes the traditional procedure for repairing or
replacing a valve:
“Traditionally, repair or replacement of heart valves has
involved open-heart surgery, which means that the chest is
opened in the operating room and the heart stopped for a
time so that the surgeon may repair or replace the valve(s).
In order to open the chest, the breastbone, or sternum, is
cut in half and spread apart. Once the heart is exposed, large
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tubes are inserted into the heart so that the blood can be
pumped
through
the
body
during
the
surgery
by
a
cardiopulmonary bypass machine (heart-lung machine). The
bypass machine is necessary to pump blood because the
heart is stopped and kept still while the surgeon performs the
valve repair or replacement procedure.”80
The detailed process is described below.81

An intravenous (IV) line will be started in the arm or hand.
Additional catheters will be inserted in the neck and wrist to
monitor the status of the heart and blood pressure, as well as for
obtaining blood samples. Alternate sites for the additional
catheters include the subclavian (under the collarbone) area and
the groin.

The patient will be positioned on the operating table, lying on his
or her back.

The anesthesiologist will continuously monitor heart rate, blood
pressure, breathing, and blood oxygen level during the surgery.
Once the patient is sedated, a breathing tube will be inserted
through the throat into the lungs. The patient will be connected
to a ventilator.

A catheter will be inserted into the bladder to drain urine.

The skin over the surgical site will be cleansed with an antiseptic
solution.
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
The physician will make an incision (cut) down the center of the
chest from just below the Adam's apple to just above the navel.

The sternum (breastbone) will be divided in half and spread
them apart to expose the heart.

In order to perform the valve repair or replacement, the heart
must be stopped to allow the doctor to perform the very delicate
procedure. Tubes will be inserted into the heart so that the blood
can be pumped through the body by a cardiopulmonary bypass
machine.

Once the blood has been completely diverted into the bypass
machine for pumping, injecting the heart with a cold solution will
stop it from beating.

When the heart has stopped, the doctor will perform the
procedure by removing the diseased valve and putting in the
artificial valve, in the case of a valve replacement. For a valve
repair, the procedure performed will depend on the type of valve
problem that exists, for example, separation of fused valve
leaflets, repair of torn leaflets, and/or the reshaping of valve
parts to ensure better function.

Once the procedure has been completed, the blood circulating
through the bypass machine will be allowed to reenter the heart,
and the heart will be shocked with small paddles to restart its
electrical activity.
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
Once the heart is beating again, the physician will observe the
heart to assess the function of the heart and the valves.

Temporary wires for pacing may be inserted into the heart.
These wires can be attached to a pacemaker and the heart can
be paced, if needed, during the initial recovery period.

The sternum will be rejoined and sewn together with small wires.

The skin over the sternum will be sewn back together. The
incision will be closed with sutures or surgical staples.

Tubes will be inserted into the chest to drain blood and other
fluids from around the heart. These tubes will be connected to a
suction device to drain fluids away from the heart.

A tube will be inserted through the mouth or nose into the
stomach to drain stomach fluids.
In recent years, more advanced techniques have been developed,
which require smaller incisions and less recovery time. One such
procedure is the transcatheter aortic valve replacement (TAVR).82 The
TAVR is a new alternative for some cases of aortic valve stenosis. A
cardiac surgeon and an interventional cardiologist typically do this
hybrid procedure. The diseased valve may be repaired using a ring to
support a person's own valve, or the entire valve may be removed and
replaced by an artificial valve. Artificial valves may be mechanical
(made of metal or plastic) or tissue (made from animal valves or
human valves taken from cadavers).
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Cardiac Pacemakers
Artificial cardiac pacemakers are electronic devices that stimulate the
heart with electrical impulses to maintain or restore a normal rhythm
in people with slow heart rhythms. There are many situations in which
an artificial pacemaker may be recommended. Most commonly, a
pacemaker is used to treat arrhythmias.83 A pacemaker can relieve
some arrhythmia symptoms, such as fatigue and fainting. A
pacemaker also can help a person who has abnormal heart rhythms
resume a more active lifestyle. Faulty electrical signaling in the heart
causes arrhythmias.
Pacemakers use low-energy electrical pulses to overcome this faulty
electrical signaling. Pacemakers can:84

Speed up a slow heart rhythm.

Help control an abnormal or fast heart rhythm.

Make sure the ventricles contract normally if the atria are
quivering instead of beating with a normal rhythm (a condition
called atrial fibrillation).

Coordinate electrical signaling between the upper and lower
chambers of the heart.

Coordinate electrical signaling between the ventricles.
Pacemakers that do this are called cardiac resynchronization
therapy (CRT) devices. CRT devices are used to treat heart
failure.

Prevent dangerous arrhythmias caused by a disorder called long
QT syndrome.

Pacemakers also can monitor and record the heart's electrical
activity and heart rhythm. Newer pacemakers can monitor blood
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temperature, breathing rate, and other factors. They also can
adjust the heart rate to changes in activity.
The decision to use such a device, as well as which specific type, will
depend upon multiple factors, including:85

The exact nature and underlying cause of the arrhythmia

Whether the condition is temporary or permanent

The presence or absence of symptoms as described above

The potential risk of complications from a pacemaker
An artificial pacemaker provides an electrical impulse (or "discharge")
that can stimulate the heart, thus restoring or maintaining a regular
heartbeat. Although various types of artificial pacemaker devices are
available, they generally include the following components:86

A thin metal box or case called a pulse generator, which contains
the power source producing the electrical impulses of the
pacemaker. In addition, the pulse generator contains a small
computer processor that can be programmed to set the rate of
the pacemaker, the pattern of pacing, the energy output, and
various other parameters. The pulse generator for most modern
permanent pacemakers weighs one to two ounces.

Flexible insulated wires or leads carry electrical impulses from
the generator to the heart muscle and relay information
concerning the heart's natural activities back to the pacemaker.
There may be several such wires, or leads, placed within the
heart, most commonly in the right atrium and right ventricle.
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
One or more electrodes at the tips of the leads transmit electrical
impulses to the heart muscle when needed and also sense the
heart's own electrical activity.
Arrhythmias
Pacemakers are used to treat arrhythmias, which are complications
with the rate or rhythm of the heartbeat. During an arrhythmia, the
heart can beat too fast, too slow, or with an irregular rhythm. “The
heart's conduction system must function normally for the heart to beat
properly and to pump blood effectively to meet the body's needs.
Problems with the flow of electrical impulses in the heart are called
arrhythmias, which is a general term meaning that there is an
abnormality in the pattern of electrical conduction or electrical
rhythm.”87
The decision to treat an arrhythmia with a pacemaker (or any other
treatment) depends in part upon whether the person has symptoms or
not as well as the severity of the symptoms. There are two primary
types of arrhythmias, bradyarrythmias and tachyarrythmias, which are
discussed below.
Bradyarrhythmias:
Bradyarrhythmias are heart rhythm abnormalities that cause an
abnormally slow heartbeat. Most bradyarrhythmias are due to one of
two kinds of problems: sinus bradycardia or heart block. Sinus
bradycardia occurs when the heartbeat is too slow because the heart's
"natural pacemaker" is operating too slowly. Although some people
(for example, competitive athletes) may have a slow heartbeat as a
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result of good health, in others sinus bradycardia is an abnormal
condition that requires treatment.
Heart block is a term for a delay or interruption in the heart's
conduction system, causing the electrical impulses to travel too slowly
or to be stopped. There are several kinds of heart block, classified
according to location (where in the conduction system the block
occurs) and degree (whether the block is mild, causing delayed
conduction, or severe, causing conduction to stop).
In first-degree atrioventricular (AV) block, all electrical impulses reach
the ventricles from the atria, but are abnormally slowed as they pass
through the AV node. In second-degree AV block, some atrial impulses
fail to reach the ventricles ("dropped beats"), resulting in a slow or an
irregular heart rate. In third-degree AV block, the most serious form,
no atrial impulses are conducted to the ventricles. This condition is
sometimes called complete heart block. For the heart to continue to
beat, a separate electrical impulse (called an escape rhythm) may be
generated in the ventricles. Without an escape rhythm, the ventricles
(the chambers that pump blood throughout the body) stop beating.
In right bundle branch block (RBBB), the right bundle branch does not
conduct impulses; the electrical impulses reach the right ventricle only
by traveling through the heart muscle from the left ventricle. As a
result, activation of the right ventricle is delayed. In left bundle branch
block (LBBB), the left bundle branch does not conduct impulses;
electrical impulses reach the left ventricle only by traveling through
the heart muscle from the right ventricle. As a result, activation of the
left ventricle is delayed.87-90
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Tachyarrhythmias:
Tachyarrhythmias are heart rhythm abnormalities that cause an
abnormally fast heartbeat. Two tachyarrhythmias that are sometimes
treated with a pacemaker are atrial fibrillation and ventricular
tachycardia.
Atrial fibrillation (AF) is a tachyarrhythmia originating in the atria.
Electrical impulses appear at random in the atria and spread through
the atrial muscle in an irregular, uncoordinated way. The atria "quiver"
rather than contract normally. As a result, blood is not pumped
effectively or regularly into the ventricles. Impulses to the ventricles
may be conducted very rapidly, resulting in a rapid and irregular heart
rate.
Ventricular tachycardia (VT) is a tachyarrhythmia originating in the
ventricles. A repetitive electrical impulse appears somewhere in the
ventricles and spreads through the ventricular muscle. Usually, VT
produces some effective ventricular contractions, but at a rapid rate.
With very rapid VT, blood may not be pumped effectively, and cardiac
arrest may result. Therefore, VT is a potentially dangerous
tachyarrhythmia.91-94
Arrhythmia Symptoms
The symptoms of arrhythmias vary, depending upon the specific
arrhythmia and other factors, especially if there is underlying heart
disease. While some people may have no symptoms, others may have
various symptoms and signs. Symptoms may include:88

Fainting episodes (syncope)

Dizziness or lightheadedness (presyncope)
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
Palpitations (a sensation of the heart pounding)

Confusion

Extreme fatigue

Shortness of breath

Impaired ability of the heart to pump enough blood to meet the
body's needs (heart failure)
Diagnostic Tests:
The following tests will be used to determine the type of arrhythmia:95

EKG (Electrocardiogram)

Holter and Event Monitors

Echocardiography

Electrophysiology Study

Stress Test
Underlying Causes:
A variety of conditions can lead to the development of cardiac
arrhythmias. Some of the more common causes are included below.96

Coronary artery disease, where there is a malfunction or damage
of the heart due to narrowing or blockage of arteries supplying
blood to heart muscle

Damage from a heart attack and the development of scar tissue
in the muscle of the heart

Certain structural heart malformations present at birth
(congenital heart defects)

Inherited genetic abnormalities that are not necessarily
associated with a structural problem of the heart, but may result
in an arrhythmia (such as the long QT syndrome)
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
Abnormalities in the control and regulation of the heartbeat by
the nervous system, leading to fainting (called neurocardiogenic
syncope)

Diseases of heart muscle tissue, called cardiomyopathies

Therapy with certain medications that may alter the heart's
normal rhythm

Normal aging of heart muscle
Types of Pacemakers
A variety of types of pacemakers have been developed to restore or
sustain a regular heartbeat in different ways.97

Demand pacemakers monitor the heart's natural electrical
activity and discharge only when the heart's own rate is too slow
or the heart misses a beat.

Fixed-rate pacemakers (which are rarely used today) discharge
impulses at a single, steady rate, regardless of the heart's own
electrical activity.

Rate-responsive pacemakers are designed to raise or lower the
heart rate to help meet the body's needs during physical activity
or rest. These devices also work on "demand."

Temporary pacemakers — Temporary pacemakers are intended
for short-term use during hospitalization. They are used because
the arrhythmia is expected to be temporary and eventually
resolve, or because the person requires temporary treatment
until a permanent pacemaker can be placed. The pulse generator
of a temporary pacemaker is located outside the body, and may
be taped to the skin or attached to a belt or to the patient's bed.
Patients with temporary pacemakers are hospitalized and
continuously monitored. Members of the healthcare team will
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perform regular examinations to monitor for any possible
complications.

Permanent pacemakers — Permanent pacemakers are
pacemakers that are intended for long-term use.
Pacemakers may be single, dual, or triple chambered:98

Single-chamber pacemakers have one lead to carry impulses to
and from either the right atrium or right ventricle.

A dual-chamber pacemaker usually has two leads, one to the
right atrium and one to the right ventricle, which can allow a
heart rhythm that more naturally resembles the normal activities
of the heart.

Triple-chambered pacemakers typically have one lead in the
right atrium, one to stimulate the right ventricle, and one to
stimulate the left ventricle. These devices are inserted in
patients who have weakened heart muscle (which results in
heart failure). These pacemakers "resynchronize" the ventricles
and may improve the efficiency of the contraction of the heart,
improving its blood flow.
Indications for Permanent Pacemakers
The following is an explanation of the specific guidelines used when
determining if a permanent pacemaker is appropriate:
“Specific guidelines have been established concerning the
conditions when a permanent pacemaker is (1) definitely
beneficial, useful, and effective, (2) may be indicated, or (3)
is not useful or effective and, in some cases, may be harmful.
Patients should speak with their healthcare provider
concerning these guidelines and how they apply to their
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specific case. As a general rule, permanent pacing is
recommended for certain conditions that are chronic or
recurrent and not due to a transient cause. Permanent pacing
may be considered necessary or appropriate for certain
people with symptomatic bradyarrhythmia or, less
commonly, to help prevent or terminate tachyarrhythmia.”83
Absolute indications for pacemaker placement include the following:99

Sick sinus syndrome

Symptomatic sinus bradycardia

Tachycardia-bradycardia syndrome

Atrial fibrillation with sinus node dysfunction

Complete atrioventricular block (third-degree block)

Chronotropic incompetence (inability to increase the heart rate
to match a level of exercise)

Prolonged QT syndrome

Cardiac resynchronization therapy with biventricular pacing
Relative indications include the following:100

Cardiomyopathy (hypertrophic or dilated)

Severe refractory neurocardiogenic syncope

Temporary emergency pacing is indicated for therapy of
significant and hemodynamically unstable bradydysrhythmias
and for prevention of bradycardia-dependent malignant
dysrhythmias.
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Implantation Procedure/Guidelines:101

The pacemaker is most commonly implanted into soft tissue
beneath the skin in an area below the clavicle, which is known as
prepectoral implantation; this is located under the skin and fat
tissue but above the pectoral or breast muscle.

The pacemaker leads are typically inserted into a major vein
(transvenously) and advanced until the electrodes are secured
within the proper region(s) of heart muscle. The other ends of
the leads are attached to the pulse generator. Less commonly,
the pulse generator is placed under the skin of the upper
abdomen.

Generally the pacemaker is implanted in a sterile laboratory or
operating room by a specialist (cardiologist, surgeon, or cardiac
electrophysiologist) with experience in this procedure. Local
anesthesia is used to make the procedure as pain-free as
possible. In some cases, sedation or even general anesthesia
may be used. The position of the pacemaker leads is usually
checked using X-ray imaging (called fluoroscopy). The length of
the procedure depends upon the type of device being placed.

Recovery from the procedure is rapid, but there may be some
restrictions on arm movement and activities for the first few
weeks. Lead dislodgement is more common in the first few
weeks after implantation. The hospital stay is usually brief, and
in some cases the procedure can be done as a day surgery.
Uncommon but possible risks associated with permanent
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pacemaker implantation include collapsed lung (pneumothorax),
infection, and bleeding.

Once implanted, pacemakers can be programmed to change the
baseline heart rate, the upper heart rate at which the pacemaker
will pace, and heart rate changes that should occur with
exercise.
Although pacemakers are most commonly used for arrhythmia, a
physician may also recommend a pacemaker in instances of:102

Atrial fibrillation – a common heart rhythm disorder in which the
upper chambers of the heart beat rapidly and chaotically.
Sometimes people with atrial fibrillation can also have slow
rhythms. Medicines used to control atrial fibrillation may result in
slow rhythms, which are treated by pacemakers.

Heart failure – a condition in which the heartbeat is not sufficient
to supply a normal volume of blood and oxygen to the brain and
other parts of the body. A special pacemaker can be carefully
programmed to increase the force of muscle contractions in the
heart. This is called “biventricular pacing” or “resynchronization”
therapy.

Syncope – a condition best known as the common faint, is
usually not serious. Some patients faint when their heart rhythm
becomes very slow. For a small percentage of people who
experience severe and frequent fainting spells, a pacemaker may
prevent the heart rate from slowing to the point of fainting.
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
Aging or heart disease damages the sinus node's ability to set
the correct pace for the heartbeat. Such damage can cause
slower than normal heartbeats or long pauses between
heartbeats. The damage also can cause the heart to switch
between slow and fast rhythms. This condition is called sick
sinus syndrome.

The patient has had an atrial fibrillation. A pacemaker can help
regulate the heartbeat after the procedure.

The patient is required to take certain heart medicines, such as
beta-blockers, which can slow the heartbeat too much.

The patient faints or has other symptoms of a slow heartbeat.

The patient has heart muscle problems that cause electrical
signals to travel too slowly through the heart muscle. The
pacemaker may provide cardiac resynchronization therapy (CRT)
for this problem. CRT devices coordinate electrical signaling
between the heart's lower chambers.

The patient has long QT syndrome, which puts him or her at risk
for dangerous arrhythmias.

Physicians also may recommend pacemakers for people who
have certain types of congenital heart disease or for people who
have had heart transplants. Children, teens, and adults can use
pacemakers.
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Types of Pacemaker Programming
The two main types of programming for pacemakers are:103

Demand Pacing
A demand pacemaker monitors a person’s heart rhythm. It only
sends electrical pulses to the heart if the heart is beating too
slow or if it misses a beat.

Rate-responsive
A rate-responsive pacemaker will speed up or slow down the
heart rate depending on how active the patient may be. To do
this, the device monitors the sinus node rate, breathing, blood
temperature, and other factors to determine a person’s activity
level.
Procedure:
Placing a pacemaker requires minor surgery. The surgery usually is
done in a hospital or special heart treatment laboratory.99

Before the surgery, an intravenous (IV) line will be inserted into
one of the veins. The patient will receive medicine through the
IV line to help him or her relax.

The surgeon will numb the area where he or she will put the
pacemaker so the patient doesn’t feel any pain. The surgeon
may also give antibiotics to prevent infection.

A needle will be inserted into a large vein, usually near the
shoulder opposite the dominant hand. The needle will be used to
thread the pacemaker wires into the vein and to correctly place
them in the heart.

An x-ray will track the wires as they pass through the vein and
into the heart will so that they can be placed properly. Once the
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wires are in place, the doctor will make a small cut into the skin
of the chest or abdomen.

The pacemaker's small metal box will be inserted through the
cut, placed just under the skin, and connected it to the wires
leading to the heart. The box contains the pacemaker's battery
and generator.
Three basic types exist to serve different purposes, which are
described below.101

Single-Chamber Pacemakers
In a single-chamber pacemaker, only one wire (pacing lead) is
placed into a chamber of the heart. Sometimes it is the upper
chamber, or atrium. Other times it is the lower chamber, or
ventricle.

Dual-Chamber Pacemakers
In dual chamber pacemakers, wires are placed in two chambers
of the heart. One lead paces the atrium and one paces the
ventricle. This approach more closely matches the natural pacing
of the heart. This type of pacemaker can coordinate function
between the atria and ventricles.

Rate-Responsive Pacemakers
These have sensors that automatically adjust to changes in a
person's physical activity.
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
Other devices
Some devices, such as implantable cardioverter defibrillators
(ICDs), designed primarily for other purposes, can function as
pacemakers in certain situations.
Guidelines for Pacemaker Use
Patients with pacemakers are advised to avoid electromagnetic
interference. Although contemporary pacemakers are less susceptible
to interference than older models, electromagnetic energy can
interfere in some cases. Thus, experts advise that individuals with
pacemakers be aware of the following:85

Household appliances
Pacemaker manufacturers do not recommend any special
precautions when using normally functioning common household
appliances such as microwave ovens, televisions, radios,
toasters, and electric blankets.

Cellular phones
Due to the growing use of hand-held cellular phones, patients
must be aware of their potential adverse effects. As examples,
evidence suggests that cellular phones do not cause interference
with permanent pacemakers. While some older generation
pacemakers and implantable cardioverter-defibrillators (ICDs)
did occasionally experience interference from cellular telephones,
clinical experience suggests that there is no significant
interference between pacemakers or ICDs and modern wireless
communication devices or portable media players.
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
Anti-theft systems
Electromagnetic anti-theft security systems are often found in or
near the workplace, at airports, in stores, at courthouses, or in
other high-security areas. Although interference with a
pacemaker is possible, it is unlikely that any clinically significant
interference would occur with the transient exposure associated
with walking through such a field. Based upon several studies
and observations, experts advise that patients with pacemakers
should:
o Be aware of the location of anti-theft systems and move
through them at a normal pace
o Avoid sitting or standing close to an anti-theft system

Metal detectors at airports
Similar to antitheft systems, metal detectors at airports can
potentially interfere with pacemakers, although this is unlikely.
Such exposure has been shown to cause interference in some
cases and may be related to the duration of exposure and/or
distance between the security system and the pacemaker. Metal
detectors will likely be triggered by the presence of a pacemaker
and therefore at places such as airports, it will be important for
individuals with pacemakers to carry an identification card for
their pacemaker, and airport personnel will likely prefer to do a
manual search.

External electrical equipment
External electrical fields do not seem to cause a problem for
most people with a pacemaker. However, in workplaces that
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contain welding equipment or strong motor-generator systems,
because interference can inhibit pacing, it is recommended that
a person with an implanted cardiac device remain at least two
feet from external electrical equipment, verify that the
equipment is properly grounded, and leave the immediate locale
if lightheadedness or other symptoms develop.

Diagnostic or therapeutic procedures
Certain types of surgery and procedures may interfere with
pacemakers. Most importantly, the use of electrocautery can
inhibit pacemaker function. It is not uncommon therefore that a
pulse generator may require specific reprogramming before the
procedure and programming back to its baseline condition after
the procedure. In some instances, a magnet is all that is
required on the device to make sure that there is no problem
with the device during the procedure. Such procedures include:
o Magnetic resonance imaging (MRI), which uses a strong
magnetic field that is pulsed on and off at a rapid rate. For
most patients with a pacemaker, this procedure is
contraindicated.
o Transcutaneous electrical nerve/muscle stimulators
(TENS), which is a method of pain control.
o Diathermy, which heats body tissues with high-frequency
electromagnetic radiation or microwaves.
o Extracorporeal shock wave lithotripsy, the use of sound
waves to break up gallstones and kidney stones.
o Therapeutic radiation for cancer or tumors, which can
cause permanent pacemaker damage.
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o Any surgery in which electrocautery is being used. The
risks are greatest when the electrocautery is being
performed close to the pulse generator.
Pacemaker complications include the following:104

Pneumothorax

Pericarditis

Infection

Skin erosion- Erosion of the pacer through the skin, while rare,
requires device replacement and systemic antibiotics.
Hematomas may be treated with direct pressure and
observation, rarely requiring surgical drainage.

Hematoma

Lead dislodgment - Lead dislodgment generally occurs within 2
days of device implantation pacer and may be seen on chest
radiography. Alternatively, fluctuating impedance may be a
subtle clue, as the patient may have normal impedance when
the lead is in contact with the endocardium, but infinite (or very
high) impedance when the lead is dislodged.

Venous thrombosis

Free-floating ventricular leads may trigger malignant
arrhythmias. Device-associated venous thrombosis is rare but
generally presents as unilateral arm edema. Treatment includes
extremity elevation and anticoagulation.
Major pacemaker malfunctions include the following:83

Failure to output

Failure to capture

Failure to sense
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
Pacemaker-mediated tachycardia

Runaway pacemaker

Pacemaker syndrome

Twiddler's syndrome

Cardiac monitor pseudomalfunction

Pacemaker pseudomalfunction
Implantable Cardioverter Defibrillator
An implantable cardioverter-defibrillator (ICD) is a device that is used
to treat a cardiac tachydysrhythmia. It is a type of permanent
pacemaker that is used to provide electrical stimuli, which causes
cardiac contraction when intrinsic myocardial electrical activity is
inappropriately slow or absent.105
Indications for Use
Indications for implantable cardioverter-defibrillator (ICD) implant can
be divided into two broad categories:106

Secondary prophylaxis against sudden cardiac death:
Multiple studies have shown the ICD to be superior to
antiarrhythmic drug therapy in patients with a history of lifethreatening VT and VF. Therefore, the indications for secondary
prophylaxis are well supported by clinical evidence gained from
randomized clinical trials. An ICD is recommended as initial
therapy in survivors of cardiac arrest due to VF or
hemodynamically unstable VT.
Published guidelines exclude cases in which there are
“completely reversible causes.” The exclusion for completely
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reversible causes is somewhat controversial. As an example, an
acute MI predisposes to polymorphic VT, and the culprit lesion
may be reversed with intracoronary stenting. However, we know
that any patient who presents with an MI is at increased risk of
recurrent MI, which may again precipitate an unstable
ventricular arrhythmia.
One school of thought suggests that such patients should
undergo ICD implant, even though the cause of cardiac arrest is
completely reversible, because the risk of recurrence is
increased. In another example, consider cardiac arrest
secondary to transient prolongation of the QT interval, perhaps
secondary to drug therapy. QT interval prolongation increases
the risk of torsades de pointes, a potentially life-threatening
arrhythmia.
Withdrawal of the offending agent may normalize the QT
interval, thereby reversing the cause of cardiac arrest. However,
such a patient remains at risk of recurrent QT prolongation and
subsequent cardiac arrest, perhaps from an electrolyte
disturbance or as a result of ingestion of a different QTprolonging agent.

Primary prophylaxis:
Indications for primary prophylaxis account for most of ICD
implants, even though the evidence for such implants is often
less well established. Indications for an ICD implant as primary
prophylaxis against sudden cardiac death are listed below. The
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indications are listed as Class I or Class IIa, as classified by the
ACC/AHA 2008 guidelines.
Class I means that the treatment is useful, that its benefit
greatly outweighs the risk, and that it should be administered.
Class IIa means that the benefit outweighs the risk and it is
reasonable to administer the treatment. Class IIb means that the
benefit probably outweighs the risk and that the treatment may
be considered. Class III means that the risk outweighs the
benefit, and the treatment should not be performed. Only Class I
and Class IIa indications are included in the table. For a
complete list, the reader is referred to the American College of
Cardiology (ACC)/American Heart Association (AHA) 2008
guidelines.
The greatest predictors of risk for sudden cardiac death include
left ventricular systolic function and heart failure symptoms. The
vast majority of investigational studies have quantified left
ventricular systolic function using the measure of left ventricular
ejection fraction (LVEF). The most widely used form of heart
failure symptom classification is the New York Heart Association
(NYHA) functional class classification system, which classifies
mild to no symptoms as Class I, and the most severe symptoms
as Class IV.107
Indications for ICD placement
Currently, indications for primary prophylaxis account for most of ICD
implants, even though the evidence for such implants is often less well
established. Class I indications (i.e., the benefit greatly outweighs the
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risk, and the treatment should be administered) are listed below and
outlined in the following table:108,109

Structural heart disease, sustained VT

Syncope of undetermined origin, inducible VT or VF at
electrophysiologic study (EPS)

Left ventricular ejection fraction (LVEF) < 35% due to prior MI,
at least 40 days post-MI, NYHA class II or III

LVEF ≤35%, NYHA class II or III

LVEF ≤30% due to prior MI, at least 40 days post-MI

LVEF < 40% due to prior MI, inducible VT or VF at EPS

Class IIa indications (i.e., the benefit outweighs the risk and it is
reasonable to administer the treatment) are as follows:

Unexplained syncope, significant LV dysfunction, nonischemic
cardiomyopathy

Sustained VT, normal or near-normal ventricular function

Hypertrophic cardiomyopathy with 1 or more major risk factors

Arrhythmogenic right ventricular dysplasia/cardiomyopathy
(ARVD/C) with 1 or more risk factors for sudden cardiac death
(SCD)

Long QT syndrome, syncope or VT while receiving beta-blockers

Nonhospitalized patients awaiting heart transplant

Brugada syndrome, syncope or VT

Catecholaminergic polymorphic VT, syncope or VT while
receiving beta-blockers

Cardiac sarcoidosis, giant cell myocarditis, or Chagas disease
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Indication
Classification Supporting Studies
Structural heart disease, sustained VT
Class I
AVID, CASH, CIDS
Syncope of undetermined origin,
Class I
CIDS
Class I
SCD-HeFT
LVEF ≤35%, NYHA Class II or III
Class I
SCD-HeFT
LVEF ≤30% due to prior MI, at least
Class I
MADIT II
Class I
MADIT, MUSTT
Class IIa
Expert opinion
Class IIa
Expert opinion
Class IIa
Expert opinion
Class IIa
Expert opinion
Class IIa
Zareba et al, Viskin et
inducible VT or VF at EPS
LVEF < 35% due to prior MI, at least
40 days post-MI, NYHA Class II or III
40 days post-MI
LVEF < 40% due to prior MI, inducible
VT or VF at EPS
Unexplained syncope, significant LV
dysfunction, nonischemic CM
Sustained VT, normal or near-normal
ventricular function
Hypertrophic CM with 1 or more major
risk factors
Arrhythmogenic right ventricular
dysplasia/cardiomyopathy (ARVD/C)
with 1 or more risk factors for sudden
cardiac death (SCD)
Long QT syndrome, syncope or VT
while receiving beta blockers
al., Goel et al., Monnig
et al., Goldenberg et al.,
Hobbs et al.
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Nonhospitalized patients awaiting
Class IIa
Expert opinion
Brugada syndrome, syncope
Class IIa
Expert opinion
Brugada syndrome, VT
Class IIa
Expert opinion
Catecholaminergic polymorphic VT,
Class IIa
Expert opinion
Class IIa
Expert opinion
heart transplant
syncope or VT while receiving beta
blockers
Cardiac sarcoidosis, giant cell
myocarditis, or Chagas disease
ICD Complications and Malfunctions:
Several complications of implantable cardioverter-defibrillators (ICD)
implant have been described, some of which are currently tracked in a
national database of ICD implants.
Acute surgical complications include the following:

Pain

Bleeding

Pneumothorax

Hemothorax

Cardiac perforation with or without pericardial effusion and
tamponade (sometimes requiring urgent drainage)

Pulseless electrical activity following intraoperative defibrillation
threshold testing111
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An analysis of more than 350,000 ICD implantations included in the
National Cardiovascular Data Registry – ICD Registry revealed 3.1% of
patients experienced in-hospital adverse events, 1.2% experienced
major adverse events, and 0.4% died. Adverse events were lower
(1.9%) with single-chamber ICD implants than with dual-chamber ICD
implants (2.9%) or with biventricular ICD implants (4.1%). Specific
adverse event rates included lead dislodgement (1%), hematoma
(0.9%), pneumothorax (0.4%), and cardiac arrest (0.3%).112
Physician level of training and level of specialty certification have been
shown to affect the risk of adverse events associated with ICD implant.
An ICD Registry analysis found that physicians who implant more ICDs
have lower rates of procedural complications and in hospital mortality.
Implant volume may partially explain the difference in adverse events
among physicians with different specialty certifications. However, no
inverse relationship was found between procedure volume and adverse
event rate observed within the board certified category.105
Subacute and chronic complications
Subacute ICD complications include the following:

Pain

Infection

Pocket hematoma

Wound dehiscence

Lead dislodgment

Deep venous thrombosis

Upper extremity edema

Degradation of lead function
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Chronic complications include the following:113

Device-related pain

Lead fracture

Inappropriate shocks

Erosion of device through skin

Immunologic rejection – Rare
Other complications include the following:

Infection - ICD infection rates are higher in patients undergoing
generator replacement compared with de novo implant. A
prospective study revealed an infection rate of 1.3% in patients
undergoing device replacement. In this study, postoperative
hematoma significantly increased the risk of infection (22.7% vs.
0.98%).108

Inappropriate shocks - One of the risks of ICD implant is that of
inappropriate ICD shocks. An inappropriate ICD shock is one that
is not precipitated by accurate detection of a malignant
ventricular arrhythmia, VT, or VF. Typically, inappropriate ICD
shocks result when atrial arrhythmias, such as atrial fibrillation,
atrial tachycardia, or atrial flutter, accelerate the ventricular rate
beyond the set limit for delivery of ICD shock therapy. However,
inappropriate shocks may also result from sinus tachycardia,
supraventricular tachycardia (SVT), illicit drug use (as with
cocaine and methamphetamine), and ventricular oversensing.
Ventricular oversensing may occur due to T-wave oversensing,
electromagnetic interference (EMI), a loose setscrew in the ICD
header, or ICD lead fracture. Analysis of the MADIT II trial data
revealed that 11.5% of the ICD patients received inappropriate
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ICD shocks and that 31.2% of all ICD shocks were deemed
inappropriate.
Inappropriate ICD shocks were attributed to atrial fibrillation
(44%), supraventricular tachycardia (36%), and abnormal
sensing (20%). Patients with inappropriate shocks had greater
all-cause mortality. Drug therapy with hydroxymethylglutarylcoenzyme A reductase inhibitors, or so-called statins, has been
shown to reduce, by more than half, the frequency of
inappropriate ICD shocks secondary to occurrence of atrial
fibrillation and atrial flutter. There is some indirect evidence that
the incidence of inappropriate shocks may be lower in patients
with dual-chamber devices compared with patients who receive
single-chamber devices.114

Failure to shock and ineffective cardioversion - Failure to deliver
a shock may be caused by failure to sense, lead fracture, EMI,
and inadvertent ICD deactivation. Management includes external
defibrillation or cardioversion and antidysrhythmic medications.
Ineffective cardioversion may result from inadequate energy
output, rise in defibrillation threshold (possibly due to an
antiarrhythmic medication, such as amiodarone, flecainide, or
phenytoin), myocardial infarction at the lead site, lead fracture,
insulation breakage, scarring at the lead implantation site, and
lead dislodgment.
Many ICDs deliver a programmed set of therapies per
dysrhythmic episode. The number of therapies per episode is
programming specific. If a delivered therapy does not terminate
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the arrhythmia, the device proceeds to the next programmed
therapy. For example, a total of 6 attempts at defibrillation are
attempted per episode of ventricular fibrillation. The device
attempts defibrillation and then reevaluates the cardiac rhythm.
If the arrhythmia persists, it delivers therapy number 2 and so
on until all 6 attempts have been delivered. Once this occurs,
the device does not deliver therapy until a new episode is
declared.
Initial therapy for ventricular tachycardia (VT) may be
antitachycardia pacing (also known as overdrive pacing) rather
than cardioversion. ICDs do not prevent all sudden deaths, and
acknowledging that cardiac arrest is not necessarily an ICD
malfunction is important. The device may have properly
delivered the required shocks for the triggering rhythm but still
have been ineffective in resolving it.106

Sprint Fidelis lead fracture - In July 2007, a higher than
expected rate of Sprint Fidelis model 6949 ICD lead fractures
were reported. Six patients presented with lead failure 4-23
months after implant. A subsequent database search for similar
reports revealed that 33% of affected patients had inappropriate
ICD shocks. Analysis of affected leads revealed 33% with high
lead impedance and a 35% rate of pace-sense and high-voltage
conductor fracture.110
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Implantation risk evaluation
The acute risk of ICD implantation is small but is increased by multiple
factors. The following are risk factors established by an ICD registry
risk score model:108

Age greater than 70 years - 1 point

Female - 2 points

NYHA class III - 1 point

NYHA class IV - 3 points

Atrial fibrillation - 1 point

Prior valve surgery - 3 points

Chronic lung disease - 2 points

Blood urea nitrogen (BUN) > 30 mg/dL - 2 points

Reimplantation for reasons other than battery change - 6 points

Dual chamber ICD type - 2 points

Biventricular ICD type - 4 points

Nonelective ICD implant -3 points

The risk of any inhospital complication increases from 0.6%
among patients with a score of less than 5 to 8.4% among the
patients with greater than 19 risk points.
Goals Of Cardiac Rehabilitation
There are a number of different goals associated with cardiac
rehabilitation. The specific goals will depend on the cardiac condition,
the status of the patient, and the lifestyle goals of the patient (i.e.,
return to work). The rehabilitation team will work with each patient to
determine his or her goals and develop a concrete set of attainable
goals.
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General Goals or Indications
The following bullets provide information regarding the main uses and
indications for cardiac rehabilitation. Cardiac rehabilitation is now a
Class I Indication in clinical guidelines for:7

Myocardial infarction (MI)

Percutaneous Coronary Intervention (PCI)

Coronary artery bypass grafting (CABG)

Angina

Heart failure

Valvular heart disease

Peripheral arterial disease (PAD)

The Performance Measures Set 1 (referral to CR from both an
inpatient and outpatient setting) has been endorsed by the
National Quality Forum (NQF).
The demonstrated evidence-based benefits of Cardiac Rehabilitation
include the following:10

20-30% reduction in all-cause mortality rates

Decreases mortality at up to 5 years post participation

Reduced symptoms (angina, dyspnea, fatigue)

Reduction in nonfatal recurrent myocardial infarction over
median follow-up of 12 months

Improves adherence with preventive medications

Increased exercise performance

Improved lipid panel (total cholesterol, HDL [good cholesterol],
LDL [bad cholesterol], and triglycerides)

Increased knowledge about cardiac disease and its management

Enhanced ability to perform activities of daily living

Improved health-related quality of life
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
Improved psychosocial symptoms (reversal of anxiety and
depression, increased self-efficacy)

Reduced hospitalizations and use of medical resources

Return to work or leisure activities
Increase Physical Fitness
An increase in physical fitness can benefit most individuals with
cardiovascular disease, including those who have been diagnosed with
heart failure. The specific exercise regimen will vary depending on the
needs and abilities of the individual, but all regimens will provide
additional benefits during the recovery or maintenance stage. One of
the primary benefits that occurs during an increase in physical fitness
is that the patient will experience an increased ability to use oxygen to
derive energy for work.115
Exercise training increases maximum ventilatory oxygen uptake by
increasing both maximum cardiac output (the volume of blood ejected
by the heart per minute, which determines the amount of blood
delivered to the exercising muscles) and the ability of muscles to
extract and use oxygen from blood. Beneficial changes in
hemodynamic, hormonal, metabolic, neurological, and respiratory
function also occur with increased exercise capacity. These changes
can also benefit persons with impaired left ventricular function, in
whom most adaptations to exercise training appear to be peripheral
and may occur with low-intensity exercise.116
An increase in physical fitness also produces decreased myocardial
oxygen demands for the same level of external work performed. This
is demonstrated by a decrease in the product of heart rate × systolic
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arterial blood pressure (an index of myocardial oxygen demand).
These changes are also beneficial in persons with coronary artery
disease, who after exercise training may attain a higher level of
physical work before reaching the level of myocardial oxygen
requirement that results in myocardial ischemia.117
Another benefit that occurs when patients increase their physical
fitness through regular exercise training is a favorable alteration in
lipid and carbohydrate metabolism. The exercise-induced increase in
high-density lipoproteins is strongly associated with changes in body
weight, and greater increases in high-density lipoproteins have been
found in women who exercise at higher levels of recreational
running.118 Increased physical fitness in overweight women and men
enhances the beneficial effect of a low-saturated fat and lowcholesterol diet on blood lipoprotein levels. Increased endurance
training in those who can tolerate it, will have a positive effect on
adipose tissue distribution.
This effect on adipose tissue distribution is likely to be important in
reducing cardiovascular risk. Exercise training and an increase in
general physical fitness is also shown to have a significant impact on
insulin sensitivity.12 In addition, intense endurance training has been
shown to initiate a highly significant salutary effect on fibrinogen levels
of healthy older men. Recent studies have shown that physical activity
plays an important role in the prevention and treatment of
osteoporosis and certain neoplastic diseases, especially colon cancer.
The following is a list of important points to consider regarding
physical fitness programs:119
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
Developing and maintaining aerobic endurance, joint flexibility,
and muscle strength is important in a comprehensive exercise
program, especially as people age.

Elderly women and men show comparable improvement in
exercise training, and adherence to training in the elderly is
high.

Resistance training exercise alone has only a modest effect on
risk factors compared with aerobic endurance training, but it
does aid carbohydrate metabolism through the development or
maintenance of muscle mass and effects on basal metabolism.
Furthermore, resistance training is currently recommended by
most health promotion organizations for its effects on
maintenance of strength, muscle mass, bone mineral density,
functional capacity, and prevention and/or rehabilitation of
musculoskeletal problems (i.e., low back pain).

In the elderly, resistance training is both safe and beneficial in
improving flexibility and quality of life. Persons with
cardiovascular disease are usually asked to refrain from heavy
lifting and forceful isometric exercises, but moderate-intensity
dynamic strength training is safe and beneficial in persons at low
risk.

Many activities of daily living require more arm work than leg
work. Therefore, persons with coronary artery disease are
advised to use their arms as well as their legs in exercise
training. The arms respond like the legs to exercise training both
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quantitatively and qualitatively, although ventilatory oxygen
uptake is less with arm ergometry.
Although peak heart rates are similar with arm and leg exercise,
heart rate and blood pressure response during arm exercise is
higher than leg exercise at any submaximal work rate.
Therefore, target heart rates are designated 10 beats per minute
lower for arm training than for leg training. Dynamic arm
ergometry is usually well tolerated by persons with coronary
artery disease; however, there may be an increase in blood
pressure that may be of concern in certain persons.

Maximum ventilatory oxygen uptake drops 5% to 15% per
decade between the ages of 20 and 80, and a lifetime of
dynamic exercise maintains an individual's ventilatory oxygen
uptake at a level higher than that expected for any given age.
The rate of decline in oxygen uptake is directly related to
maintenance of physical activity level, emphasizing the
importance of physical activity.

Middle-aged men and women who work in physically demanding
jobs or perform moderate to strenuous recreational activities
have fewer manifestations of coronary artery disease than their
less active peers. Meta-analysis studies of clinical trials reveal
that medically prescribed and supervised exercise can reduce
mortality rates of persons with coronary artery disease.

In addition to the physical benefits of exercise, both short-term
exercise and long-term aerobic exercise training are associated
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with improvements in various indexes of psychological
functioning. Cross-sectional studies reveal that, compared with
sedentary individuals, active persons are more likely to be better
adjusted, to perform better on tests of cognitive functioning, to
exhibit reduced cardiovascular responses to stress, and to report
fewer symptoms of anxiety and depression.

Exercise training reduces depression in healthy older men and in
persons with cardiac disease or major depression. Exercise also
improves self-confidence and self-esteem, attenuates
cardiovascular and neurohumoral responses to mental stress,
and reduces some type A behaviors.

Although exercise training generally has not been found to
improve cognitive performance, short bouts of exercise may
have short-term facilitative effects.

It is estimated that only 50% of all persons who initiate an
exercise program will continue the habit for more than 6
months. The issue of nonadherence is particularly important
because exercise is only beneficial if it is maintained for
extended periods of time. Thus, it is important to develop
strategies to improve exercise initiation and adherence,
especially for persons who are among the least active—some
African-American women, the less educated, the obese, and the
elderly.

Persons of all ages should include physical activity in a
comprehensive program of health promotion and disease
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prevention and should increase their habitual physical activity to
a level appropriate to their capacities, needs, and interest.

Activities such as walking, hiking, stair-climbing, aerobic
exercise, calisthenics, resistance training, jogging, running,
bicycling, rowing, swimming, and sports such as tennis,
racquetball, soccer, basketball, and “touch” football are
especially beneficial when performed regularly. Brisk walking is
also an excellent choice. The training effect of such activities is
most apparent at exercise intensities exceeding 40% to 50% of
exercise capacity. (Exercise capacity is defined as the point of
maximum ventilatory oxygen uptake or the highest work
intensity that can be achieved).

Evidence supports that even low- to moderate-intensity activities
performed daily can have some long-term health benefits and
lower the risk of cardiovascular disease.

Low-intensity activities generally range from 40% to 60% of
maximum capacity. The 40% to 60% of maximum capacity
range is similar for young, middle-aged, and elderly persons.
Such activities include walking for pleasure, gardening, yard
work, housework, dancing, and prescribed home exercise.

For health promotion, dynamic exercise of the large muscles for
extended periods of time (30 to 60 minutes, three to six times
weekly) is recommended. This may include short periods of
moderate intensity (60% to 75% of maximal capacity) activity
(approximately 5 to 10 minutes) that total 30 minutes on most
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days. Resistance training using eight to 10 different exercise sets
with 10 to 15 repetitions each (arms, shoulders, chest, trunk,
back, hips, and legs) performed at a moderate to high intensity
(for example, 10 to 15 pounds of free weight) for a minimum of
2 days per week is recommended.

Physical activity may have risks as well as benefits, although
risks are relatively infrequent. Estimates of sudden cardiac death
rates per 100 000 hours of exercise range from 0 to 2 per
100 000 in general populations and from 0.13 per 100 000 to
0.61 per 100 000 in cardiac rehabilitation programs. Studies
have also demonstrated the cardiovascular safety of maximum
strength testing and training in healthy adults and low-risk
cardiac patients. Falls and joint injuries are additional risks
associated with physical activity (especially in older women), but
most of these injuries do not require medical treatment. The
incidence of such complications is less in those participating in
low-impact activities such as walking.
Improve Physical and Mental Health
There is evidence to show that comprehensive cardiac rehabilitation
programs, including exercise training, can reduce smoking, alter lipid
profiles, reduce blood pressure, favorably alter body weight and
increase physical activity. Improvements in psychosocial outcomes
have also been shown. The following table provides an overview on the
goals and benefits in each of these areas:5.14.116.121-129
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Smoking
Strong advice from physicians to stop smoking, especially in
hospital, has been shown to be important. In one uncontrolled
study, such physician recommendations, coupled with follow-up
advice from nurses, were associated with a one-year self-reported
quit rate of 62%.
In another study of patients who had undergone coronary bypass
surgery, reduced smoking rates were found at one year in the
group randomly allocated to a program of exercise training and
education, coupled with physician advice to stop smoking,
compared with the control group.
Spousal support has been shown to facilitate smoking cessation in
cardiac patients. In a randomized controlled study of inpatient
group education followed by weekly telephone calls for six weeks
after discharge from hospital, results showed a significantly
greater decrease in smoking and unhealthy eating habits, and a
significantly greater increase in physical activity, among patients
whose partners also participated in the program.
While there were no overall differences at 12 months between the
intervention and control groups, a greater rate of smoking
cessation was found in the intervention group among patients
whose partners had participated. In general, evidence suggests
that interventions to reduce smoking are more likely to be
effective if they are initiated in hospital when patients are more
highly motivated rather than after discharge from hospital.
Further, a meta-analysis of controlled trials of cardiac patient
education concluded that while interventions, on average, showed
no significant impact on smoking behavior, behaviorally oriented
interventions generally produced better outcomes. Behavioral
strategies, such as regular reinforcement of advice to stop
smoking and continuing support, appear necessary.
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The positive studies described above indicate that follow-up
telephone contact by nurses is a convenient, inexpensive and
effective method of reinforcing physician advice to stop smoking.
Lapses tend to occur when interventions cease. Instructing
patients in relapse prevention methods before they lapse is
therefore of critical importance.
Lipids
Patients who participated in an educational program by mail and
telephone reported a significant decrease in dietary fat intake
after six months compared with a control group receiving usual
care, but no significant differences were found between groups in
cholesterol levels. Beneficial effects upon lipid levels have been
reported from interventions combining education and behavioral
strategies with the use of lipid lowering drugs. A large study of a
home-based multifactorial intervention combining education,
counseling and lipid lowering medication achieved a significant
mean reduction in total cholesterol and dietary fat intake in the
treatment group after four years, compared with the control
group.
Another multifactorial intervention, which included lipid-lowering
medication, also reported a significant reduction in serum
cholesterol levels in the intervention group compared with the
control group. A recent randomized controlled trial studied the
effects of diet alone, a combination of diet and exercise, exercise
alone and usual care in men and postmenopausal women with low
levels of HDL cholesterol and raised LDL cholesterol. This study
showed that the Step 2 diet of the US National Cholesterol
Education Program was ineffective in lowering LDL cholesterol
unless it was coupled with exercise training.
Similarly, a nonrandomized controlled study reported significant
improvements in lipid levels from a combination of education,
counseling and exercise compared with exercise alone.
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Blood
The effectiveness of antihypertensive drugs in lowering blood
pressure
pressure is well established. Further, beneficial effects upon blood
pressure in cardiac patients have been reported from two
multifactorial interventions including exercise training. One
randomized controlled trial of a multifactorial intervention
including lifestyle advice, which was reinforced during the four
year follow-up, produced significant benefits in reduction of blood
pressure in cardiac patients in the intervention group compared
with the control group. A significant reduction in blood pressure
was also reported in a multifactorial intervention involving
exercise, education and support. However, in another randomized
controlled trial of exercise training and education, there was no
impact upon blood pressure levels.
A further multifactorial intervention of stress management,
exercise, intensive dietary restriction and support produced no
significant impact on blood pressure levels, with both the
intervention and control groups showing a decrease in blood
pressure at one year.
Education and behavioral interventions for weight reduction,
physical activity and moderation of dietary sodium and alcohol
consumption are recommended as definitive or adjunctive therapy
for hypertension. They are important components of a
multifactorial approach to reduce hypertension in cardiac patients.
Body weight
Dietary education, counseling and behavioral interventions
designed to reduce body weight can help patients lose weight and
should be provided as part of comprehensive cardiac
rehabilitation. Education as a sole intervention is unlikely to
achieve and maintain weight loss. Several studies have reported a
reduction in body weight as a result of comprehensive cardiac
rehabilitation programs which include exercise, education,
counseling and behavioral interventions.
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A randomized controlled trial conducted over four years
demonstrated a statistically significant body weight reduction of 4
% in the intervention group compared with the control group.
Patients in the intervention group received individual advice
regarding lifestyle modification, which incorporated goal setting, a
monitored home exercise program, follow-up by mail, telephone
contact and regular visits to the clinic for follow-up.
Considerable weight loss occurred amongst the dedicated subjects
enrolled in a study of a one-year intervention including a low fat
vegetarian diet, group discussion for social support, stress
management and exercise. Significantly greater weight loss was
also reported in the treatment group in two further studies, and in
another study, a reduction in body fat was achieved in subjects
receiving the intervention.
In all three studies, however, the mean weight loss was less than
3 kg. A significant reduction in body mass index, percentage of
body fat and other measures was reported in one study and in
another, in percentage of body fat in women. Other studies
involving exercise reported no changes in body weight.
A randomized controlled study comparing exercise training alone,
exercise training plus group education and counseling, and a
control group found no significant differences between groups in
weight loss after three and six months. Positive results were
reported from three studies, which did not involve exercise.
Another randomized controlled trial reported a significant
reduction in mean body weight at one to 10 year follow-up in
patients in the intervention group receiving nutritional counseling
compared with the control group. In that study, the intervention
was intensive for the first three months, followed by a continued
intervention for three years.
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Psychosocial
Education, counseling and behavioral interventions, either alone
well-being
or as part of multifactorial interventions, improve psychological
wellbeing and improve quality of life. They should therefore be
integral parts of comprehensive cardiac rehabilitation programs.
Psychological disability has long been recognized as a greater
barrier to recovery than physical impairment. Thus, an important
aim of cardiac rehabilitation programs should be to improve the
psychological wellbeing of patients.
The psychological benefits of exercise training are widely
acknowledged. An important issue is whether specific education,
counseling or behavioral interventions enhance psychological
wellbeing, additional to those benefits achieved through exercise
training.
Stress
The aims of stress management programs are to assist the
patient to identify stressors, to recognize characteristic emotional
and physical responses to stress, to decrease levels of general
arousal and to develop effective coping strategies. Through the
use of various techniques including relaxation therapy,
meditation, cognitive therapy, anxiety management and
biofeedback, the patient is taught how to reduce stressful
reactions by altering stress-inducing perceptions of situations.
By acquiring more effective coping skills, maladaptive responses
to stress may be reduced.
Several studies have reported benefits from relaxation therapy. In
one study, patients who received cognitive training early after
myocardial infarction had greater confidence in their ability to
control their stress than those who received relaxation therapy.
In another, relaxation training was found to enhance the
psychological effects of exercise training.
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In a study involving monthly monitoring of stress levels of
patients and home nursing visits for those with high stress scores,
a significant reduction in stress scores was found as well as a
significantly reduced rate of long-term recurrence of acute
myocardial infarction and a marginal impact on cardiac mortality
during the first year after infarction. Little impact was observed
on those with low levels of stress in hospital. The authors
concluded that patients who can benefit from such an intervention
may be identified in hospital.
Summary
Patients with a cardiac condition must be assessed to ensure that he
or she is a candidate for a cardiac rehabilitation program. There are a
number of conditions require cardiac rehabilitation, and, likewise, a
number of different goals associated with cardiac rehabilitation. The
specific goals depend upon the cardiac condition, the status of and the
lifestyle goals of the patient. The cardiac rehabilitation team is trained
to work with each patient to determine his or her goals and to develop
a concrete set of individual attainable goals.
The primary goal of cardiac rehabilitation programs is to reduce
cardiac symptoms in patients. However, the specific goals will differ
depending on the type and severity of cardiac condition. In some
instances, the goal will be to eliminate the cardiac condition. In other
instances, the goal will be to maintain a level of health that prevents
further damage from the cardiac condition.116 Prior to initiating a
cardiac rehabilitation program, the medical provider will need to work
with the patient to determine the specific treatment goals. Throughout
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the course of treatment, the patient is assessed and monitored to
ensure goals are being met.120 This course addressed the cardiac
conditions that would benefit from patient participation in a cardiac
rehabilitation program. The history and role of cardiac rehabilitation is
a lengthy topic recommended for further reading by the interested
learner.
There are a number of different goals associated with cardiac
rehabilitation. The specific goals will depend on the cardiac condition,
the status of the patient, and the lifestyle goals of the patient (i.e.,
return to work). The rehabilitation team will work with each patient to
determine his or her goals and develop a concrete set of attainable
goals.
Please take time to help NurseCe4Less.com course planners
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1.
While men and women have the same incidence and the
same prevalence of heart failure, which of the following
states a difference noted between men and women with
heart failure:
a. Women tend to develop heart failure earlier in life than men
do.
b. Men are more likely than women to have preserved systolic
function.
c. Women develop depression more commonly than men do.
d. Women have signs and symptoms of heart failure similar to
those of men, but they are less pronounced in women.
2.
Cardiac rehabilitation is useful in treating heart patients so
long as the program is instituted before the patient has
experienced his or her first heart attack.
a. True.
b. False.
3.
Which of the following is a modifiable risk factor for
atherosclerosis:
a. Diabetes mellitus
b. Age
c. Family history of premature coronary heart disease
d. Male-pattern baldness
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4.
There are a number of different goals associated with
cardiac rehabilitation. Which statement best describes the
specific program for a patient?
a. the patient’s cardiac condition is not a factor because cardiac
rehabilitation is useful for patients with varied cardiac
conditions.
b. the lifestyle goals of the patient is not relevant because the
focus should be on cardiac rehabilitation.
c. The rehabilitation team will work with each patient to
determine his or her goals and develop a concrete set of
attainable goals.
d. None of the above.
5.
Patients with pacemakers are advised to avoid
electromagnetic interference. Which of the following
devices does the evidence suggest may interfere with
permanent pacemakers?
a. Properly operating household appliances such as microwave
ovens, televisions, radios, toasters, and electric blankets.
b. Cellular phones.
c. Electromagnetic anti-theft security systems.
d. Diagnostic or therapeutic procedures used in certain types of
surgery and procedures.
6.
True or False: Angina is the term used to describe the pain
and discomfort that occurs when the heart is deprived of
blood.
a. True.
b. False.
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7.
Patients with typical myocardial infarction may have the
following prodromal symptoms in the days preceding the
event:
a. Fatigue.
b. Intense and unremitting for 30-60 minutes.
c. A feeling of indigestion or of fullness and gas.
d. All of the above.
8.
The following is/are true when a patient increases his or
her physical fitness program:
a. Most individuals with cardiovascular disease will benefit from
increased physical fitness so long as they have NOT been
diagnosed with heart failure.
b. One of the primary benefits that occurs during an increase in
physical fitness is that the patient will experience an
increased ability to use oxygen to derive energy for work.
c. Exercise training decreases maximum ventilatory oxygen
because the muscles extract and use oxygen from blood.
d. Physical fitness program do not benefit persons with impaired
left ventricular function.
9.
There is evidence to show that comprehensive cardiac
rehabilitation programs, including exercise training, can do
the following:
a. Reduce smoking
b. Alter lipid profiles
c. Reduce blood pressure
d. All of the above.
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10. Intracoronary stents have the following features:
a. The commercially available second-generation DESs that elute
everolimus and zotarolimus are not approved for use in the
United States.
b. Bare-metal stents are used exclusively to target lesion
revascularization.
c. Drug-eluting stents (DESs) have demonstrated significant
reductions in restenosis.
d. Stents with bioabsorbable polymer, polymer-free systems or
fully bioresorbable scaffolds are approved and available for
commercial use in the United States.
11. Non-modifiable risk factors for atherosclerosis include the
following:
a. A person’s age and gender
b. Family history of premature coronary heart disease
c. Male-pattern baldness
d. *All of the above.
12. Immediately after the onset of myocardial infarction, the
ability of ischemic myocardium to relax declines. Impaired
relaxation ___________ LV end-diastolic volume (LVEDV)
and LV end-diastolic pressure (LVEDP).
a. decreases
b. *increases
c. does not interfere with
d. may both increase or decrease
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13. Studies have shown that _________________ helps to
reduce stress levels in patients after myocardial infarction.
a. massage therapy
b. *cognitive behavioral therapy
c. group therapy
d. desensitization therapy
14. Aging or heart disease damages the ______________
ability to set the correct pace for the heartbeat.
a. *sinus node’s
b. atrial node’s
c. ventricle’s
d. heart’s atrioventricular
15. Beneficial effects upon lipid levels have been reported from
interventions combining __________________________
with the use of lipid lowering drugs.
a. low fat diet alone
b. exercise alone
c. *education and behavioral strategies
d. cognitive behavioral therapy
16. The greatest predictors of risk for sudden cardiac death
include ________________and heart failure symptoms.
a. *left ventricular systolic function
b. right ventricular systolic and diastolic function
c. right ventricular filling pressure
d. answers b and c above
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17. Rate-responsive pacemakers have sensors that
automatically adjust to changes in a person's __________.
a. cardiac output
b. *physical activity
c. atrial rhythm
d. none of the above
18. Persons with cardiovascular disease may safely perform
a. heavy-lifting and forceful isometric exercises, under guidance
b. *moderate-intensity dynamic strength training, for person’s at
low risk
c. stretching and pilates exercises after completing cardiac rehab
d. hot yoga exercises, for no more than 30 minutes
19. A dual-chamber pacemaker usually has two leads, one to
the ______________ and one to the ________________.
a. *right atrium and right ventricle
b. right atrium and left atrium
c. left atrium and left ventricle
d. both ventricles
20. The following tests may be used to determine type of an
arrhythmia, EXCEPT:
a. EKG (Electrocardiogram)
b. Echocardiography
c. *Transesophageal electrocardiogram bubble study
d. Stress Test
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21. Patients needing a temporary pacemaker would be
a. *hospitalized.
b. not requiring hospitalization.
c. sent home with a 24-hour ambulatory EKG.
d. not expected to need a permanent pacemaker.
22. _____________________________ is gaining greater
prominence in assessing the inflammatory level of vascular
disease and predicting future risk of vascular events, such
as MIs and cerebrovascular accidents.
a. High-sensitivity CPK
b. *High-sensitivity C-reactive protein
c. High-sensitivity CK
d. High-sensitivity LDL and LDH
23. Abciximab, tirofiban, and eptifibatide are examples of
a. *Glycoprotein inhibitor therapy
b. Antianginals
c. Antibiotics that specifically treat pericarditis
d. Anticoagulant therapy
24. Medications shown to reduce ischemic complications in
patients undergoing balloon angioplasty and coronary
stenting belong to the following medication category:
a. Antianginals
b. Anticoagulants
c. *Glycoprotein inhibitor therapy
d. Antibiotic medication
25. True or False. Multiple studies have shown the ICD to be
superior to antiarrhythmic drug therapy in patients with a
history of life-threatening VT and VF.
a. *True.
b. False.
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26. While going through airports, individuals with pacemakers
should
a. not be concerned of metal detectors being triggered
b. *carry their pacemaker ID card
c. not expect airport personnel to request a manual search.
d. Both and c above.
27. Diastolic dysfunction predominates in conditions of
a. hypertrophic cardiomyopathy.
b. disorders with ventricular hypertrophy.
c. amyloid infiltration of the myocardium.
d. *All of the above.
28. For health promotion, dynamic exercise of the large
muscles for extended periods of time is recommended,
such as
a. a full hour seven days a week.
b. an hour every other day.
c. *30 to 60 minutes, three to six times weekly.
d. 15 to 20 minutes, every day of the week.
29. True or False. Increased physical fitness in overweight
women and men enhances the beneficial effect of a lowsaturated fat and low-cholesterol diet on blood lipoprotein
levels.
a. *True.
b. False.
30. Epicardial inflammation may initiate pericarditis, which is
seen in more than 20% of patients presenting with
_________________.
a. *Q-wave infarctions.
b. ST depression.
c. prolonged QT interval.
d. sudden death.
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31. Major pacemaker malfunctions include the following:
a. Failure to output.
b. Failure to capture.
c. Failure to sense.
d. *All of the above.
32. The failing heart and other organs produce
a. *tumor necrosis factor.
b. tumor cells.
c. cytokines.
d. None of the above.
33. Each rehospitalization for heart failure increases mortality
by about _________ percent.
a. 45 – 47
b. 33 – 35
c. *20 – 22
d. 15 - 17
34. The rate of decline in oxygen uptake is directly related to
a. geographic region.
b. *maintenance of physical activity level.
c. genetic factors.
d. Answers a and b above.
35. The TAVR is a new alternative for some cases of
a. coronary blockage.
b. pulmonary stenosis.
c. *aortic valve stenosis.
d. mitral valve prolapse.
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36. Artificial heart valves may be
a. mechanical metal.
b. mechanical plastic.
c. tissue made from animal valves or human valves taken from
cadavers.
d. *All of the above.
37. The demonstrated evidence-based benefits of Cardiac
Rehabilitation include all EXCEPT:
a. Reduced symptoms (angina, dyspnea, fatigue).
b. Increased exercise performance.
c. *Ability to no longer need to take heart medication and to
perform high intensity exercise and competitive sports.
d. Enhanced ability to perform activities of daily living.
Correct Answers:
1. c
6.
a
11. d
16. a
21. a
26. b
31. d
2. b
7.
d
12. b
17. b
22. b
27. d
32. a
3. a
8.
b
13. b
18. b
23. a
28. c
33. c
4. c
9.
d
14. a
19. a
24. c
29. a
34. b
5. d
10. c
15. c
20. c
25. a
30. a
35. c
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36. d
37. c
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Reference Section
The reference section of in-text citations include published works
intended as helpful material for further reading. Unpublished works
and personal communications are not included in this section, although
may appear within the study text.
The following citations pertain to the course series on cardiac
rehabilitation, which include: CARDIAC CONDITIONS, INTERVENTIONS
& REHABILITATION and THE CARDIAC REHAB TEAM: A HOLISTIC
APPROACH TO RECOVERY AND HEALING.
1.
Scarborough P, Bhatnagar P, Wickramasinghe K, Smolina K, Mitchell C.
Coronary heart disease statistics 2010 edition. Br Hear Found.
2010;21.
2.
Maganti K, Rigolin VH, Sarano ME, Bonow RO. Valvular Heart Disease:
Diagnosis and Management. Mayo Clinic Proceedings. 2010. p. 483–
500.
3.
Leon AS, Franklin B a, Costa F, Balady GJ, Berra K a, Stewart KJ, et al.
Cardiac rehabilitation and secondary prevention of coronary heart
disease. Circulation. 2005;111:369–76.
4.
Wenger NK. Current Status of Cardiac Rehabilitation. Journal of the
American College of Cardiology. 2008. p. 1619–31.
5.
Balady GJ, Williams MA, Ades PA, Bittner V, Comoss P, Foody JM, et al.
Core components of cardiac rehabilitation/secondary prevention
programs: 2007 update: a scientific statement from the American
Heart Association Exercise, Cardiac Rehabilitation, and Prevention
Committee, the Council on Clinical Cardiology; the Councils o.
Circulation. 2007 May 22;115(20):2675–82.
6.
Donker FJ. Cardiac rehabilitation. Clinical Psychology Review. 2000. p.
923–43.
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7.
Fernandez RS, Davidson P, Griffiths R, Salamonson Y. Improving
cardiac rehabilitation services - Challenges for cardiac rehabilitation
coordinators. Eur J Cardiovasc Nurs. 2011;10:37–43.
8.
Wofford JD, Wofford E, Beissel GF, Brumfield J. Cardiac rehabilitation. N
Engl J Med. 2002;2:379–80.
9.
Reeves GR, Whellan DJ. Recent advances in cardiac rehabilitation. Curr
Opin Cardiol. 2010;25:589–96.
10.
Lavie CJ, Milani R V. Benefits of cardiac rehabilitation and exercise
training. Chest. 2000;117:5–7.
11.
Lavie CJ, Berra K, Arena R. Formal cardiac rehabilitation and exercise
training programs in heart failure: evidence for substantial clinical
benefits. J Cardiopulm Rehabil Prev. 2013;33:209–11.
12.
Ades PA, Keteyian SJ, Balady GJ, Houston-Miller N, Kitzman DW,
Mancini DM, et al. Cardiac Rehabilitation Exercise and Self-Care for
Chronic Heart Failure. JACC: Heart Failure. 2013. p. 540–7.
13.
Eshah NF, Bond AE. Cardiac rehabilitation programme for coronary
heart disease patients: an integrative literature review. Int J Nurs
Pract. 2009;15:131–9.
14.
Piotrowicz R, Wolszakiewicz J. Cardiac rehabilitation following
myocardial infarction. Cardiol J. 2008;15:481–7.
15.
Myocardial Infarction [Internet]. [cited 2015 Jan 31]. Available from:
http://emedicine.medscape.com/article/155919overview#aw2aab6b2b8aa
16.
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