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with Cardiac Disorders
LEARNING OUTCOMES
1. Compare and contrast the etiology, pathophysiology, and 3. Discuss indications for and management of patients with
manifestations of common cardiac disorders, including heart hemodynamic monitoring.
failure, structural disorders, and inflammatory disorders. 4. Discuss the effects and nursing implications for medications
2. Explain risk factors and preventive measures for cardiac commonly prescribed for patients with cardiac disorders.
disorders such as heart failure, inflammatory disorders, and 5. Describe nursing care for the patient undergoing cardiac
valve disorders. surgery or cardiac transplant.
CLINICAL COMPETENCIES
1. Apply knowledge of normal cardiac anatomy and physiology 5. Safely and knowledgeably administer prescribed medica-
and assessment techniques in caring for patients with car- tions and treatments to patients with cardiac disorders.
diac disorders. 6. Actively participate in planning and coordinating interprofes-
2. Assess the functional health status of patients with cardiac sional care for patients with cardiac disorders.
disorders, documenting and reporting deviations for ex- 7. Provide appropriate teaching and community-based care for
pected findings. patients with cardiac disorders and their families.
3. Based on patient assessment and knowledge of the disorder, 8. Evaluate the effectiveness of nursing care, revising the plan
determine priority nursing diagnoses. of care as needed to promote, maintain, or restore the func-
4. Plan, prioritize, and provide evidence-based, individualized tional health status of patients with cardiac disorders.
care for patients with cardiac disorders.
KEY TERMS
aortic valve, 950 mean arterial pressure paroxysmal nocturnal dyspnea rheumatic fever, 939
cardiac tamponade, 947 (MAP), 927 (PND), 924 rheumatic heart disease
cardiomyopathy, 959 mitral valve, 950 pericarditis, 946 (RHD), 939
endocarditis, 941 murmur, 951 pulmonary edema, 935 stenosis, 939
heart failure, 920 myocarditis, 945 pulmonic valve, 950 tricuspid valve, 950
hemodynamics, 926 orthopnea, 924 regurgitation, 939 valvular heart disease, 950
Cardiac disorders affect the structure and/or function of the heart. failure and death. Emergence of symptoms (fatigue, dyspnea, chest
These disorders interfere with the heart’s primary purpose: to pain) is common with the progression of cardiac disorders. The
pump enough blood to meet the body’s demand for oxygen and New York Heart Association (NYHA) classification is commonly
nutrients. Disruptions in cardiac function affect the functioning used to describe the severity of exertional symptoms observed
of other organs and tissues, potentially leading to organ system (see Table 31–1).
919
920 Unit 8 • Responses to Altered Cardiovascular Function
New York Heart Association Heart failure is the most common cardiac disorder. Other
TABLE 31–1 Classification cardiac disorders discussed in this chapter include structural car-
diac disorders, such as valve disorders and cardiomyopathy, and
Class Severity of Symptoms
inflammatory cardiac disorders, such as endocarditis and pericar-
I No limitation in physical activity/asymptomatic ditis. B
efore continuing with this chapter, please review the heart’s
II Symptoms with strenuous activity anatomy and physiology, nursing assessment, and diagnostic tests
III Symptoms with mild activity in Chapter 29.
IV Symptoms at rest
Heart Failure
Heart failure is a complex syndrome resulting from cardiac disor- prevalence of hypertension in African Americans contributes signifi-
ders that impair the ventricles’ ability to fill with and effectively pump cantly to their risk for and incidence of heart failure.
blood. In heart failure, the heart is unable to pump enough blood to
meet the metabolic demands of the body. It is the end result of many Incidence, Prevalence, and Risk Factors
conditions. Frequently, it is a long-term effect of coronary heart dis- More than 6.6 million people in the United States are currently living
ease and myocardial infarction (MI) when left ventricular damage with heart failure; approximately 550,000 new cases of heart failure
is extensive enough to impair cardiac output (refer to Chapter 29). are diagnosed annually (American Heart Association [AHA], 2013).
Other diseases of the heart also may cause heart failure, including Estimates predict an additional 3 million people will have heart fail-
structural and inflammatory disorders. In normal hearts, failure can ure by 2030. Its incidence and prevalence increase with age: Fewer
result from excessive demands placed on the heart. Heart failure may than 5% of people between ages 55 and 64 have heart failure, whereas
be acute or chronic. 6% to 10% of people ages 65 to 74 are affected. There is a rapid rise in
heart failure prevalence after age 65. Those ages 75 to 84 have a 14.8
The Patient with Heart Failure to 22.3/1000 person (per) years incidence, while those older than
As mentioned, heart failure develops when the heart cannot effec- 85 years have a 32.7 to 41.9/1000 person-years incidence (see Nurs-
tively fill or contract with adequate strength to function as a pump to ing Care of the Older Adult box). At age 40, the lifetime risk of devel-
meet the needs of the body. As a result, cardiac output falls, leading oping heart failure is one in five (AHA, 2013). The estimated direct
to decreased tissue perfusion. The body initially adjusts to reduced and indirect cost of heart failure in the United States in 2011 was
cardiac output by activating inherent compensatory mechanisms $34.4 billion. The prevalence and mortality rate for heart failure is
to restore tissue perfusion. These normal mechanisms may result higher in African Americans than in Whites. See the accompanying
in vascular congestion—hence, the commonly used term congestive Focus on Cultural Diversity box.
heart failure (CHF). As these mechanisms are exhausted, heart failure Ischemic heart disease (coronary heart disease) is the leading
ensues, with increased morbidity and mortality. risk factor for heart failure. Up to 75% of individuals with heart failure
Heart failure is a disorder of cardiac function. It frequently is due have a history of hypertension.
to impaired myocardial contraction, which may result from coronary The prognosis for a patient with heart failure depends on its un-
heart disease and myocardial ischemia or infarct or from a primary derlying cause and how effectively precipitating factors can be treated.
cardiac muscle disorder such as cardiomyopathy or myocarditis. Most patients with heart failure die within 8 years of the diagnosis. The
Structural cardiac disorders, such as valve disorders or congenital risk for sudden cardiac death is dramatically increased, occurring at a
heart defects, and hypertension also can lead to heart failure when the rate six to nine times that of the general population. In 2009, one in
heart muscle is damaged by the long-standing excessive workload as- nine death certificates in the United States mentioned heart failure as
sociated with these conditions. Other patients without a primary ab- the primary or a contributing cause of death (AHA, 2013).
normality of myocardial function may present with manifestations of
heart failure due to acute excess demands placed on the myocardium, Physiology Review
such as volume overload, hyperthyroidism, and massive pulmonary The mechanical pumping action of cardiac muscle propels the blood
embolus (see Table 31–2). Hypertension and coronary heart disease it receives to the pulmonary and systemic vascular systems for reoxy-
are the leading causes of heart failure in the United States. The high genation and delivery to the tissues. Cardiac output (CO) is the amount
Heart Failure
Heart failure is common in older adults, affecting nearly 10% of peo- Discuss normal daily activities and assess sleep and rest patterns. It
ple over the age of 75 years. is also important to assess the environment for the following:
Aging affects cardiac function. Diastolic filling is impaired by • Safe roads or neighborhoods for walking
decreased ventricular compliance. With aging, the heart is less re- • Access to pharmacy, medical care, and assistive services
sponsive to SNS stimulation. As a result, maximal heart rate, car- such as a cardiac rehabilitation program or structured exercise
diac reserve, and exercise tolerance are reduced. Concurrent health programs designed for older adults.
problems such as arthritis that affect stamina or mobility often con-
tribute to a more sedentary lifestyle, further decreasing the heart’s Patient and Family Teaching
ability to respond to increased stress. Teaching for the older adult with heart failure focuses on maintain-
ing function and promptly identifying and treating episodes of heart
Assessing for Home Care failure. Teach patients how to adapt to changes in cardiovascular
The older adult with heart failure may not be dyspneic, instead pre- function associated with aging, such as the following:
senting with weakness and fatigue, somnolence, confusion, disori- • Allowing longer warm-up and cool-down periods during exercise
entation, or worsening dementia. Dependent edema and respiratory • Engaging in regular exercise such as walking five or more times
crackles may or may not indicate heart failure in older adults. a week
Assess the diet of the older adult. Decreased taste may lead to • Resting with feet elevated (e.g., in a recliner) when fatigued
increased use of salt to bring out food flavors. Limited mobility or • Maintaining adequate fluid intake
visual acuity may cause the older adult to rely on prepared foods • Preventing infection through pneumococcal and influenza
that are high in sodium such as canned soups and frozen meals. immunizations.
922 Unit 8 • Responses to Altered Cardiovascular Function
Neuroendocrine Decreased CO stimulates the • Increased HR, BP, and contractility • Tachycardia with decreased filling
response sympathetic nervous system • Increased vascular resistance time and decreased CO
and catecholamine release. • Increased venous return • Increased vascular resistance
• Increased myocardial work
and oxygen demand
Decreased CO and decreased • Vasoconstriction and increased BP • Increased myocardial work
renal perfusion stimulate renin– • Renal vasoconstriction and
angiotensin system. decreased renal perfusion
Angiotensin stimulates aldosterone • Salt and water retention by the kidneys • Increased preload and afterload
release from adrenal cortex. • Increased vascular volume • Pulmonary congestion
ADH is released from posterior • Water excretion inhibited • Fluid retention and increased
pituitary. • Increased sodium excretion preload and afterload
Atrial natriuretic factor is released. • Diuresis
Blood flow is redistributed to vital • Decreased perfusion of other organ • Renal failure
organs (heart and brain). systems • Anaerobic metabolism and lactic
• Decreased perfusion of skin acidosis
and muscles
Ventricular Increased cardiac workload • Increased contractile force to • Increased myocardial oxygen
hypertrophy causes myocardial muscle to hy- maintain CO demand
pertrophy and ventricles to dilate. • Cellular enlargement
Pathophysiology volume and venous return also increase atrial pressures, stimulat-
When the heart begins to fail, mechanisms are activated to com- ing the release of an additional hormone, atrial natriuretic factor
pensate for the impaired function and maintain the cardiac output. (ANF) or atriopeptin. ANF balances the effects of the other hor-
The primary compensatory mechanisms are (1) the Frank-Starling mones to a certain extent, promoting sodium and water excretion
mechanism, (2) neuroendocrine responses including activation of and inhibiting the release of norepinephrine, renin, and ADH. This
the sympathetic nervous system (SNS) and the renin–angiotensin– hormone is thought to be a natural preventive that delays severe
aldosterone system (RAAS), and (3) ventricular hypertrophy. These cardiac decompensation.
mechanisms and their effects are summarized in Table 31–3. Ventricular remodeling occurs as the heart chambers and
Decreased cardiac output initially stimulates aortic barorecep- myocardium adapt to fluid volume and pressure increases. The
tors, which in turn stimulate the SNS. SNS stimulation produces both chambers dilate to accommodate excess fluid resulting from in-
cardiac and vascular responses through the release of norepineph- creased vascular volume and incomplete emptying. Initially, this
rine. Norepinephrine increases heart rate and contractility by stimu- additional stretch causes more effective contractions. Ventricular
lating cardiac beta-receptors. Cardiac output improves as both heart hypertrophy occurs as existing cardiac muscle cells enlarge, in-
rate and stroke volume increase. Norepinephrine also causes arterial creasing their contractile elements (actin and myosin) and force
and venous vasoconstriction, increasing venous return to the heart. of contraction.
Increased venous return increases ventricular filling and myocardial Although these responses may help in the short-term regulation
stretch, increasing the force of contraction (the Frank-Starling mech- of cardiac output, it is now recognized that they hasten the deterio-
anism). Overstretching the muscle fibers past their physiologic limit ration of cardiac function. The onset of heart failure is heralded by
results in an ineffective contraction. decompensation, the loss of effective compensation. Heart failure pro-
Blood flow is redistributed to the brain and the heart to main- gresses due to the very mechanisms that initially maintained circula-
tain perfusion of these vital organs. Decreased renal perfusion tory stability.
causes renin to be released from the kidneys. Activation of the The rapid heart rate shortens diastolic filling time, compro-
RAAS produces additional vasoconstriction and stimulates the mises coronary artery perfusion, and increases myocardial oxy-
adrenal cortex to produce aldosterone and the posterior pituitary gen demand. Resulting ischemia further impairs cardiac output.
to release antidiuretic hormone (ADH). Aldosterone stimulates Beta-receptors in the heart become less sensitive to continued
sodium reabsorption in renal tubules, promoting water retention. SNS stimulation, decreasing heart rate and contractility. As the
ADH acts on the distal tubule to inhibit water excretion and causes beta-receptors become less sensitive, norepinephrine stores in the
vasoconstriction. The effect of these hormones is significant vaso- cardiac muscle become depleted. In contrast, alpha-receptors on
constriction and salt and water retention, with a resulting increase peripheral blood vessels become increasingly sensitive to persis-
in vascular volume. Increased ventricular filling increases the force tent stimulation, promoting vasoconstriction and increasing after-
of contraction, improving cardiac output. The increased vascular load and cardiac work.
Chapter 31 • Nursing Care of Patients with Cardiac Disorders 923
Initially, ventricular hypertrophy and dilation increase cardiac affected. Many patients have components of both systolic and dia-
output, but chronic distention causes the ventricular wall eventually stolic failure.
to thin and degenerate. The purpose of hypertrophy is thus defeated.
In addition, chronic overloading of the dilated ventricle eventually Left-Sided versus Right-Sided Failure
stretches the fibers beyond the optimal point for effective contrac- Depending on the pathophysiology involved, either the left or the
tion. The ventricles continue to dilate to accommodate the excess right ventricle may be primarily affected. In chronic heart failure,
fluid, but the heart loses the ability to contract forcefully. The heart however, both ventricles typically are impaired to some degree. Coro-
muscle may eventually become so large that the coronary blood sup- nary heart disease and hypertension are common causes of left-sided
ply is inadequate, causing ischemia. heart failure, whereas right-sided heart failure often is caused by condi-
Chronic distention exhausts atrial stores of ANF. The effects of tions that restrict blood flow to the lungs, such as acute or chronic
norepinephrine, renin, and ADH prevail, and the renin–angiotensin pulmonary disease. Left-sided heart failure also can lead to right-
pathway is continually stimulated. This mechanism ultimately raises sided failure as pressures in the pulmonary vascular system increase
the hemodynamic stress on the heart by increasing both preload with congestion behind the failing left ventricle.
and afterload. As heart function deteriorates, less blood is delivered As left ventricular function fails, cardiac output falls. Pressures
to the tissues and to the heart itself. Ischemia and necrosis of the in the left ventricle and atrium increase as the amount of blood re-
myocardium further weaken the already failing heart, and the cycle maining in the ventricle after systole increases. These increased pres-
repeats. sures impair filling, causing congestion and increased pressures in
In normal hearts, the cardiac reserve allows the heart to adjust the pulmonary vascular system. Increased pressures in this normally
its output to meet metabolic needs of the body, increasing the cardiac low-pressure system increase fluid movement from the blood vessels
output by up to five times the basal level during exercise. Patients with into interstitial tissues and the alveoli (Figure 31–1 •).
heart failure have minimal to no cardiac reserve. At rest, they may The manifestations of left-sided heart failure result from pul-
be unaffected; however, any stressor (e.g., exercise, illness) taxes their monary congestion (backward effects) and decreased cardiac output
ability to meet the demand for oxygen and nutrients. Manifestations (forward effects). Fatigue and activity intolerance are common early
of activity intolerance when the person is at rest indicate a critical manifestations. Dizziness and syncope also may result from decreased
level of cardiac decompensation. cardiac output. Pulmonary congestion causes dyspnea, shortness of
FAST FACTS
Diminished
Terms used to describe or classify heart failure are as follows: cardiac
• Systolic or diastolic failure output
• Left ventricular (or sided) or right ventricular (or sided) failure
• Low-output or high-output failure
• Acute or chronic failure
• Forward or backward effects
Heart
breath, and a cough. The patient may develop orthopnea (difficulty described. Patients in hypermetabolic states (e.g., hyperthyroidism,
breathing while lying down), prompting use of two or three pillows infection, anemia, or pregnancy) require increased cardiac output to
or a recliner for sleeping. Cyanosis from impaired gas exchange may maintain blood flow and oxygen to the tissues. If the increased blood
be noted. On auscultation of the lungs, inspiratory crackles (rales) flow cannot meet the oxygen demands of the tissues, compensatory
and wheezes may be heard in lung bases. An S3 gallop may be present, mechanisms are activated to further increase cardiac output, which
reflecting the heart’s attempts to fill an already distended ventricle. in turn further increases oxygen demand. Thus, even though cardiac
In right-sided heart failure, increased pressures in the pulmo- output is high, the heart is unable to meet increased oxygen demands.
nary vasculature or right ventricular muscle damage impair the right This condition is known as high-output failure.
ventricle’s ability to pump blood into the pulmonary circulation. The
right ventricle and atrium become distended, and blood accumulates Acute versus Chronic Failure
in the systemic venous system. Increased venous pressures cause ab- Acute failure is the abrupt onset of a myocardial injury (such as a mas-
dominal organs to become congested and peripheral tissue edema to sive MI) resulting in suddenly decreased cardiac function and signs
develop (Figure 31–2 •). of decreased cardiac output. Chronic failure is a progressive deteriora-
Dependent tissues tend to be affected because of the effects of tion of the heart muscle due to cardiomyopathies, valvular disease, or
gravity; edema develops in the feet and legs, or if the patient is bedrid- coronary heart disease (CHD).
den, in the sacrum. Congestion of gastrointestinal tract vessels causes
Other Manifestations
anorexia and nausea. Right upper quadrant pain may result from
In addition to the previous manifestations for the various classifica-
liver engorgement. Neck veins distend and become visible even when
tions of heart failure, other signs and symptoms commonly are seen.
the patient is upright due to increased venous pressure.
A fall in cardiac output activates mechanisms that cause in-
Low-Output versus High-Output Failure creased salt and water retention. This causes weight gain and further
Patients with heart failure due to coronary heart disease, hyperten- increases pressures in the capillaries, resulting in edema. Noctu-
sion, cardiomyopathy, and other primary cardiac disorders develop ria, voiding more than one time at night, develops as edema fluid
low-output failure and manifestations such as those previously from dependent tissues is reabsorbed when the patient is supine.
aroxysmal nocturnal dyspnea (PND), a frightening condition
P
in which the patient awakens at night acutely short of breath, also may
Pulmonary develop. PND occurs when edema fluid that has accumulated dur-
circulation
ing the day is reabsorbed into the circulation at night, causing fluid
overload and pulmonary congestion. Severe heart failure may cause
Pulmonary Pulmonary dyspnea at rest as well as with activity, signifying little or no cardiac
artery veins
reserve. Both an S3 and an S4 gallop may be heard on auscultation.
See the Multisystem Effects of Heart Failure feature on page 925.
Complications
The compensatory mechanisms initiated in heart failure can lead to
complications in other body systems. Congestive hepatomegaly and
splenomegaly caused by engorgement of the portal venous system re-
sult in increased abdominal pressure, ascites, and gastrointestinal prob-
lems. With prolonged right-sided heart failure, liver function may be
Heart
impaired. Myocardial distention can precipitate dysrhythmias, further
impairing cardiac output. Pleural effusions and other pulmonary prob-
lems may develop. Major complications of severe heart failure are car-
diogenic shock (described in Chapter 11) and acute pulmonary edema,
a medical emergency described in the next section of this chapter.
Diagnosis
Diagnosis of heart failure is based on the history, physical examina-
Congested tion, and diagnostic findings.
systemic
circulation • Atrial natriuretic factor (ANF), also called atrial natriuretic hormone
Figure 31–2 • The hemodynamic effects of right-sided heart (ANH), and brain natriuretic peptide (BNP) are hormones released
failure. by the heart muscle in response to changes in blood volume.
Chapter 31 • Nursing Care of Patients with Cardiac Disorders 925
MULTISYSTEM EFFECTS OF
Heart Failure
Neurologic
• Confusion
• Impaired memory
• Anxiety, restlessness
• Insomnia
Respiratory
• Dyspnea on exertion
• Shortness of breath
• Tachypnea
• Orthopnea Cardiovascular
• Dry cough • Activity intolerance
• Crackles (rales) in lung bases • Tachycardia
Potential Complications • Palpitations
• Pulmonary edema • S3, S4 heart sounds
• Pneumonia • Elevated central venous
• Cardiac asthma pressure
• Pleural effusion • Neck vein distention
• Cheyne-Stokes respirations • Hepatojugular reflux
• Respiratory acidosis • Splenomegaly
Potential Complications
• Angina
Gastrointestinal • Dysrhythmias
• Anorexia, nausea • Sudden cardiac death
• Abdominal distention • Cardiogenic shock
• Liver enlargement
• Right upper quadrant pain
Potential Complications
• Malnutrition
• Ascites
• Liver dysfunction
Genitourinary
• Decreased urine output
• Nocturia
Integumentary
• Pallor or cyanosis
Musculoskeletal • Cool, clammy skin
• Fatigue • Diaphoresis
• Weakness Potential Complications
• Increased risk for tissue
breakdown
Metabolic Processes
• Peripheral edema
• Weight gain
Potential Complication
• Metabolic acidosis
926 Unit 8 • Responses to Altered Cardiovascular Function
N-terminal prohormone of brain natriuretic peptide (NT-proBNP) • Radionuclide imaging is used to evaluate ventricular function
is a rapid test (readable in 15 minutes) for BNP (Kee, 2014). Blood and size.
levels of these hormones increase in heart failure, however, it is im-
Refer to Chapter 29 for more information and the nursing im-
portant to remember that BNP levels may be elevated in women
plications of these tests.
and in people over age 60 who do not have heart failure. Therefore,
an elevated BNP cannot be used alone to diagnose heart failure. Hemodynamic Monitoring
• Serum electrolytes are measured to evaluate fluid and electro- Hemodynamics is the study of forces involved in blood circulation.
lyte status. Serum osmolality may be low due to fluid retention. Hemodynamic monitoring is used to assess cardiovascular function
Sodium, potassium, and chloride levels provide a baseline for in patients who are critically ill or unstable. The main goals of inva-
evaluating the effects of treatment; serum calcium and magne- sive hemodynamic monitoring are to evaluate cardiac and circula-
sium are measured as well. tory function and the response to interventions.
• Urinalysis, blood urea nitrogen (BUN), and serum creatinine are Hemodynamic parameters include heart rate, arterial blood
obtained to evaluate renal function. pressure, central venous or right atrial pressure, pulmonary pres-
• Liver function tests, including ALT, AST, LDH, serum bilirubin, sures, and cardiac output. Direct hemodynamic parameters are ob-
and total protein and albumin levels, are obtained to evaluate pos- tained straight from the monitoring device (e.g., heart rate, arterial
sible effects of heart failure on liver function. and venous pressures). Indirect or derived measurements are calcu-
• Thyroid function tests, including TSH and TH levels, are obtained lated using the direct data (e.g., the cardiac index, mean arterial blood
because both hyperthyroidism and hypothyroidism can be either pressure, and stroke volume). Invasive hemodynamic monitoring is
a primary or a contributing cause of heart failure. routinely used in critical care units.
• In acute heart failure, arterial blood gases (ABGs) are drawn to Hemodynamic monitoring systems measure the pressure
evaluate gas exchange in the lungs and tissues. within a vessel and convert this signal into an electrical waveform
• Chest x-ray may show pulmonary vascular congestion and cardio- that is amplified and displayed. The electrical signal may be graphi-
megaly in heart failure. cally recorded on graph paper and displayed digitally on the monitor.
• Electrocardiography is used to identify ECG changes associated System components include an invasive catheter threaded into an ar-
with ventricular enlargement and to detect dysrhythmias, myo- tery or vein connected to a transducer by stiff, high-pressure tubing.
cardial ischemia, or infarction. The pressure transducer translates pressures into an electrical signal
• Echocardiography with Doppler flow studies are performed to eval- that is relayed to the monitor. Additional components of the system
uate left ventricular function. Either transthoracic echocardiogra- include stopcocks and a continuous flush system with normal saline
phy or transesophageal echocardiography may be used. or heparinized saline and an infusion pressure bag to prevent clots
Chapter 31 • Nursing Care of Patients with Cardiac Disorders 927
Pressure bag
around bag
of flush Pressure monitor
Hand bulb for
solution pressurizing
bag
Manometer
for bag
Intravenous
solution
tubing Two-way
Pressure stopcock
transducer
Flush Nondistensible
device tubing Three-way Catheter
stopcock for
blood samples
Figure 31–3 • A hemodynamic monitoring setup.
from forming in the catheter. Figure 31–3 • illustrates a pressure determinations. Because the invasive catheter is inserted directly into
transducer and typical hemodynamic monitoring system. the artery, it offers immediate access for blood gas measurements and
Hemodynamic pressure monitoring may be used to measure pe- blood testing.
ripheral arterial pressures, or central pressures, such as central venous The arterial blood pressure reflects the cardiac output and the
pressure (CVP) or right atrial pressure (RAP) and pulmonary artery resistance to blood flow created by the elastic arterial walls (systemic
pressure (PAP). Although the information obtained from invasive vascular resistance, SVR). Cardiac output is determined by the blood
monitoring is valuable, the procedure is not without risk. Nursing volume and the ability of the ventricles to fill and effectively pump
care of the patient undergoing hemodynamic monitoring is outlined that blood. SVR is primarily determined by vessel diameter and dis-
on page 928. Box 31–2 lists potential complications of central pres- tensibility (compliance). Factors such as SNS input, circulating hor-
sure monitoring. Pressure monitoring systems require calibration, mones (e.g., epinephrine, norepinephrine, atrial natriuretic factor,
leveling, and zeroing of the transducer to the level of the patient’s left and vasopressin), and the RAAS affect SVR.
atrium. This is called the phlebostatic axis. The systolic blood pressure, normally about 120 mmHg in
healthy adults, reflects the pressure generated during ventricular sys-
Intra-Arterial Pressure Monitoring Intra-arterial tole. During diastole, elastic arterial walls keep a minimum pressure
pressure monitoring is commonly used in intensive and coronary care within the vessel (diastolic blood pressure) to maintain blood flow
units. An indwelling arterial line, commonly called an art line or an through the capillary beds. The average diastolic pressure in a healthy
A line, allows direct and continuous monitoring of systolic, diastolic, adult is 80 mmHg. The mean arterial pressure (MAP) is the aver-
and mean arterial blood pressure and provides easy access for arterial age pressure in the arterial circulation throughout the cardiac cycle.
blood sampling. Arterial lines are used to assess blood volume, It reflects the driving pressure, or perfusion pressure, an indicator of
monitor the effects of vasoactive drugs, and obtain frequent ABG tissue perfusion. The formula MAP = CO × SVR often is used to
show the relationships between factors determining the blood pres-
sure. Mean arterial pressure can be calculated by adding one-third
Potential Complications of the pulse pressure (PP) to the diastolic blood pressure (DBP):
BOX 31–2 of Central Catheters MAP = DBP + PP/3. For example, a blood pressure of 120/80 re-
• Bleeding sults in a mean arterial pressure of 93. Mean arterial pressures of
• Hematoma 70 to 90 mmHg are desirable. Perfusion to vital organs is severely
• Pneumothorax jeopardized at MAPs of 50 mmHg or less; MAPs greater than
• Hemothorax 105 mmHg may indicate hypertension or vasoconstriction.
• Arterial puncture
• Dysrhythmias
• Venospasm Venous Pressure Monitoring Central venous pressure
• Infection (CVP) and right atrial pressure (RAP) are measures of blood volume
• Air embolism and venous return. They also reflect right heart filling pressures.
• Thromboembolism Pressures are elevated in right-sided heart failure. CVP and RAP are
• Brachial nerve injury primarily used to monitor fluid volume status. To measure venous
• Thoracic duct injury
and atrial pressures, a catheter is inserted in the internal jugular or
928 Unit 8 • Responses to Altered Cardiovascular Function
Pulmonary Artery Pressure (PAP) slow its progression, reduce manifestations, and prevent cardiac
complications.
Beta-blockers improve cardiac function in heart failure by in-
hibiting SNS activity. This prevents the long-term deleterious effects
of sympathetic stimulation. Because beta-blockers reduce the force
of myocardial contraction and may actually worsen symptoms, they
are used in low doses. Beta-blockers are indicated for all classes of
patients with heart failure. The combination of ACE inhibitors and
beta-blockers improves patient outcomes. Beta-blockers are dis-
A cussed further in Chapter 30.
Pulmonary Capillary Wedge Pressure (PCWP) Patients with symptomatic heart failure often are treated with
diuretics as well. Diuretics relieve symptoms related to fluid reten-
tion. They may, however, cause significant electrolyte imbalances
and rapid fluid loss. Patients with severe heart failure are often
treated with a loop, or high-ceiling, diuretic such as furosemide
(Lasix), bumetanide (Bumex), torsemide (Demadex), or ethacrynic
acid (Edecrin). These drugs have a rapid onset of action, inhibit-
ing chloride reabsorption in the ascending loop of Henle, which
prompts sodium and water excretion. Their major drawback is their
B
efficacy in promoting diuresis; loss of vascular volume can stimulate
Figure 31–5 • Typical waveforms seen when measuring the SNS. Thiazide diuretics may be used for patients with less severe
A, pulmonary artery pressure, and B, pulmonary wedge pressure. manifestations of heart failure. These agents promote fluid excretion
by blocking sodium reabsorption in the terminal loop of Henle and
Cardiac output also can be measured with the PA catheter using the distal tubule.
a technique called thermodilution. Cardiac output and the cardiac Vasodilators relax smooth muscle in blood vessels, causing dila-
index are used to assess the heart’s ability to meet the body’s oxygen tion. Arterial dilation reduces peripheral vascular resistance and af-
demands. Because body size affects overall cardiac output, the car- terload, reducing myocardial work. Venous dilation reduces venous
diac index is a more precise measure of heart function. The cardiac in- return and preload. Pulmonary vascular relaxation reduces pulmo-
dex is a calculation of cardiac output per square meter of body surface nary capillary pressure, allowing reabsorption of fluid from intersti-
area. The normal cardiac index is 2.8 to 4.2 L/min/m2. tial tissues and the alveoli. Vasodilators include nitrates, hydralazine,
and prazosin, an alpha-adrenergic blocker. See Chapter 32 for more
Medications information about vasodilators.
Patients with heart failure often receive multiple medications to re- Nitrates produce both arterial and venous vasodilation. They
duce cardiac work and improve cardiac function. The main drug may be given by nasal spray or by a sublingual, oral, or intravenous
classes used to treat heart failure are the angiotensin-converting route. Sodium nitroprusside is a potent vasodilator that may be used
enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), to treat acute heart failure. It can cause excessive hypotension, so it
beta-blockers, diuretics, inotropic medications (including digitalis, is often given along with dopamine or dobutamine to maintain the
sympathomimetic agents, and phosphodiesterase inhibitors), direct blood pressure. Isosorbide or nitroglycerin ointment may be used in
vasodilators, and antidysrhythmic drugs. Nursing implications for long-term management of heart failure (refer to Chapter 30, page 876).
ACE inhibitors and ARBs, diuretics, and inotropic medications are BiDil, a combination of two vasodilators, hydralazine and iso-
found in the Medication Administration box on page 930. sorbide, in fixed doses is an option for treatment of heart failure in
ACE inhibitors, ARBs, and beta-blockers interfere with the African Americans. In African Americans with severe heart failure,
neurohormonal mechanisms of sympathetic activation and the BiDil improved symptoms and significantly reduced the number
RAAS. ACE inhibitors interrupt the conversion of angiotensin I to of hospitalizations and deaths attributed to heart failure. The accom-
angiotensin II by inhibiting the enzyme that mediates the conversion panying box on cultural diversity discusses the nursing implications
(angiotensin-converting enzyme). Angiotensin II causes intense va- for BiDil.
soconstriction, increasing afterload and ventricular wall stress and Digitalis glycosides are used judiciously in symptomatic heart
increasing preload and ventricular dilation. It also stimulates aldo- failure. Digitalis has a positive inotropic effect on the heart, increasing
sterone and ADH production, causing fluid retention. ACE inhibi- the strength of myocardial contraction by increasing the intracellular
tors block this RAAS activity, decreasing cardiac work and increasing calcium concentrations. Digitalis also decreases SA node automatic-
cardiac output. They reduce the progression and manifestations of ity and slows conduction through the AV node, increasing ventricu-
heart failure, thus reducing the number and frequency of hospital lar filling time.
admissions, decreasing mortality rates, and preventing cardiac com- Digitalis has a narrow therapeutic index; in other words, thera-
plications. However, ACE inhibitors should be used with caution in peutic levels are very close to toxic levels. Early manifestations of
African Americans due to increased risk for developing angioedema. digitalis toxicity include anorexia, nausea and vomiting, headache,
In contrast to ACE inhibitors, ARBs do not block the produc- altered vision, and confusion. A number of cardiac dysrhythmias are
tion of angiotensin II; instead, they block its action. The pharma- also associated with digitalis toxicity, including sinus arrest, supra-
cologic effect is similar, and they also are used in heart failure to ventricular and ventricular tachycardias, and high levels of AV block.
930 Unit 8 • Responses to Altered Cardiovascular Function
MEDICATION ADMINISTRATION
Heart Failure
Angiotensin-Converting Enzyme (ACE) Inhibitors torsemide (Demadex)
enalapril (Vasotec) hydrochlorothiazide (HydroDIURIL)
captopril (Capoten) spironolactone (Aldactone)
moexipril (Univasc) triamterene (Dyrenium)
quinapril (Accupril) amiloride (Midamor)
trandolapril (Mavik) acetazolamide (Diamox)
lisinopril (Prinivil, Zestril) metolazone (Zaroxolyn)
fosinopril (Monopril) Diuretics act on different portions of the kidney tubule to inhibit the
perindopril (Aceon) reabsorption of sodium and water and promote their excretion. With
ramipril (Altace) the exception of the potassium-sparing diuretics—spironolactone,
triamterene, and amiloride—diuretics also promote potassium ex-
Angiotensin II Receptor Blockers (ARBS) cretion, increasing the risk of hypokalemia. Spironolactone, an
candesartan (Atacand) aldosterone receptor blocker, reduces symptoms and slows the
losartan (Cozaar) progression of heart failure. Aldosterone receptors in the heart and
telmisartan (Micardis) blood vessels promote myocardial remodeling and fibrosis, activate
irbesartan (Avapro) the sympathetic nervous system, and promote vascular fibrosis
(which decreases compliance) and baroreceptor dysfunction.
nesiritide (Natrecor)
valsartan (Diovan) Nursing Responsibilities
• Obtain baseline weight and vital signs.
ACE inhibitors and ARBs prevent acute coronary events and reduce • Monitor blood pressure, intake and output, weight, skin turgor,
mortality in heart failure. ACE inhibitors interfere with production and edema as indicators of fluid volume status.
of angiotensin II, resulting in vasodilation, reduced blood volume, • Assess for volume depletion, particularly with loop diuretics
and prevention of its effects in the heart and blood vessels. In heart (furosemide, ethacrynic acid, and bumetanide): dizziness,
failure, ACE inhibitors reduce afterload and improve cardiac output
orthostatic hypotension, tachycardia, and muscle cramping.
and renal blood flow. They also reduce pulmonary congestion and • Report abnormal serum electrolyte levels to the physician.
peripheral edema. ACE inhibitors suppress myocyte growth and re- Replace electrolytes as indicated.
duce ventricular remodeling in heart failure. Although the pharmaco- • Do not administer potassium replacements to patients receiving
logic effect of ARBs is similar, they block the action of angiotensin II a potassium-sparing diuretic.
at the receptor rather than interfering with its production. • Evaluate renal function by assessing urine output, BUN,
Nursing Responsibilities and serum creatinine.
• Do not give these drugs to women in the second and third • Administer intravenous furosemide slowly, no faster than
trimesters of pregnancy. 20 mg/min. Evaluate for signs of ototoxicity. Do not administer
• Carefully monitor patients who are volume depleted or who this drug or ethacrynic acid concurrently with aminoglycoside
have impaired renal function (assess BUN and creatinine). antibiotics (e.g., gentamicin), which are also ototoxic.
• Use an infusion pump when administering ACE inhibitors
Health Education for the Patient and Family
intravenously. • Drink at least six to eight glasses of water per day.
• Monitor blood pressure closely for 2 hours following first dose
• Take your diuretic at times that will be the least disruptive to
and as indicated thereafter. your lifestyle, usually in the morning and early afternoon if a
• Monitor serum potassium levels; ACE inhibitors can cause
second dose is ordered. Take with meals to decrease gastric
hyperkalemia (this is less of a concern with ARBs). upset.
• Monitor white blood cell (WBC) count for potential neutropenia.
• Monitor your blood pressure, pulse, and weight weekly. Report
Report to the physician. significant weight changes to your doctor.
Health Education for the Patient and Family • Report any of the following to your doctor: severe abdominal
• Take the drug at the same time every day to ensure a stable pain, jaundice, dark urine, abnormal bleeding or bruising, flu-like
blood level. symptoms, signs of hypokalemia, hyponatremia, and dehydra-
• Monitor your blood pressure and weight weekly. Report signifi- tion (thirst, salt craving, dizziness, weakness, rapid pulse). See
cant changes to your doctor. Chapter 10 for manifestations of electrolyte imbalances.
• Avoid making sudden position changes; for example, rise from • Avoid sudden position changes. You may experience dizziness,
bed slowly. Lie down if you become dizzy or light-headed, par- light-headedness, or feelings of faintness.
ticularly after the first dose. • Unless you are taking a potassium-sparing diuretic, integrate
• Report any signs of easy bruising and bleeding, sore throat or foods rich in potassium into your diet. Limit sodium use.
fever, edema, or skin rash. Immediately report swelling of the
face, lips, or eyelids, and itching or breathing problems. Positive Inotropic Agents
• A persistent, dry cough may develop if you are taking an ACE Digitalis Glycosides
inhibitor. Contact your doctor if this becomes a problem. digoxin (Lanoxin)
• Take captopril or moexipril 1 hour before meals. Digitalis improves myocardial contractility by interfering with ATPase
in the myocardial cell membrane and increasing the amount of cal-
Diuretics cium available for contraction. The increased force of contraction
chlorothiazide (Diuril) causes the heart to empty more completely, increasing stroke vol-
furosemide (Lasix) ume and cardiac output. Improved cardiac output improves renal
ethacrynic acid (Edecrin) perfusion, decreasing renin secretion. This decreases preload and
bumetanide (Bumex) afterload, reducing cardiac work. Digitalis also has electrophysiologic
Chapter 31 • Nursing Care of Patients with Cardiac Disorders 931
Low serum potassium levels increase the risk of digitalis toxicity, as early manifestation of heart failure. Activity may be restricted to bed
do low magnesium and high calcium levels. Older adults are at par- rest during acute episodes of heart failure to reduce cardiac workload
ticular risk for digitalis toxicity. The AHA’s heart failure guidelines and allow the heart to compensate. Prolonged bed rest and contin-
(Yancy et al., 2013) note that the risk of toxicity outweighs the ben- ued activity limitations, however, are not recommended. A moder-
efits of this class of drug. Digitalis levels may be affected by a number ate, progressive activity program is prescribed to improve myocardial
of other drugs; check for potential interactions. function. Exercise should be performed 3 to 5 days per week, and
Dysrhythmias are common in patients with heart failure. each session should include a 10- to 15-minute warm-up period, 20
Although PVCs may be frequent, they are often not associated to 30 minutes of exercise at the recommended intensity, and a cool-
with an increased risk of ventricular tachycardia and fibrillation. down period. Walking is encouraged on nontraining days. As of
Because many antidysrhythmic medications depress left ventricu- November 21, 2013, the Centers for Medicare and Medicaid Services
lar function, PVCs are frequently left untreated in heart failure. announced a proposed decision memo that would extend cardiac re-
Amiodarone is the drug of choice to treat nonsustained ventricu- habilitation service coverage for patients with chronic heart failure
lar tachycardia, which is associated with a poor prognosis. (Refer (defined as patients with left ventricular ejection fraction of 35% or
to Chapter 30.) less and NYHA class II to IV symptoms despite being on optimal
heart failure therapy for at least 6 weeks).
Nutrition and Activity
A sodium-restricted diet is recommended to minimize sodium and Other Treatments
water retention. Intake is generally limited to 1.5 to 2 g of sodium per In end-stage heart failure, devices to provide circulatory assistance or
day, a moderate restriction. Box 10–2 in Chapter 10 includes patient surgery may be required. Surgery may be used to treat the underlying
teaching regarding a sodium-restricted diet. cause of failure (e.g., replacement of diseased valves) or to improve
Exercise intolerance, decreased ability to participate in activities quality of life. Valve replacement is discussed later in this chap-
using large skeletal muscles due to fatigue or dyspnea, is a common ter. Heart transplant is currently the only clearly effective surgical
932 Unit 8 • Responses to Altered Cardiovascular Function
BiDil for Treating Heart Failure in African Americans • Closely monitor for hypotension when administered concur-
rently with any potent parenteral antihypertensive agent.
BiDil, a fixed-dose combination of two vasodilators (hydralazine and
isosorbide), is indicated as an adjunctive treatment in African Ameri- Patient and Family Teaching
cans with heart failure. It has been shown to reduce symptoms, de- • Take this drug as prescribed.
crease the number of hospitalizations, and prolong life in Blacks. The • Headache is a common adverse effect of this drug, particularly
recommended dose is one to two tablets three times per day, although when first starting therapy. Headaches tend to subside with
the dose may be as low as 1/2 tablet three times a day if side effects continued treatment.
are intolerable. The approval of this combination drug has raised the • Notify your doctor if headaches continue after the first few
ethical issue of race-specific FDA approval. weeks of therapy, or if you develop chest pain or palpitations
while taking this drug.
Nursing Implications • This drug can cause a drop in blood pressure, particularly when
• Assess vital signs and fluid volume status before administering changing positions from lying to sitting or sitting to standing.
this drug, because hypotension (orthostatic hypotension in Change positions slowly and use caution to prevent falls.
particular) is a common effect. • Do not use drugs such as sildenafil (Viagra, Revatio), vardenafil
• Notify the physician if manifestations of systemic lupus erythe-
(Levitra), or tadalafil (Cialis) while taking this medication because
matosus, glomerulonephritis, or peripheral neuropathy develop. the combination may cause an extreme drop in blood pressure
• Use caution when administering concurrently with MAO
leading to fainting, chest pain, or a heart attack.
inhibitors.
treatment for end-stage heart failure; its use is limited by the avail- integrity of the suture line to prevent postoperative bleeding. Donor
ability of donor hearts. organs are obtained from people with no evidence of cardiac trauma.
Nursing care of the heart transplant patient is similar to care of
Circulatory Assistance Devices such as the intra-aortic any cardiac surgery patient (refer to Chapter 30). Bleeding is a ma-
balloon pump or a left-ventricular assist device may be used when jor concern in the early postoperative period. Chest tube drainage is
the patient is expected to recover or as a bridge to transplant (refer frequently monitored (initially every 15 minutes), as are the cardiac
to Chapter 30). Newer devices that will allow longer term support output, pulmonary artery pressures, and CVP. Cardiac tamponade
outside the hospital are in the developmental stages. These devices (compression of the heart) can develop, presenting as either a sud-
will serve either as a bridge to transplant or allow the myocardium to den event or a gradual process. Chest tubes are gently milked (not
heal over an extended period of time. stripped) as needed to maintain patency. Atrial dysrhythmias are rela-
tively common following cardiac transplant. Temporary pacing wires
Cardiac Transplantation Heart transplant is the are placed during surgery because surgical manipulation or postop-
treatment of choice for end-stage heart disease. Survival rates are erative swelling may disrupt the conduction system. Hypothermia
good: 83% at 1 year and 76% at 3 years. More than 90% of patients is induced during surgery; postoperatively, the patient is gradually
return to normal, unrestricted functional abilities following rewarmed over a 1- to 2-hour period. Prevention of rapid rewarm-
transplant. The most frequently used transplant procedure leaves the ing and shivering is important to maintain hemodynamic stability
posterior walls of the atria, the superior and inferior vena cavae, and and reduce oxygen consumption. Cardiac function is impaired in up
the pulmonary veins of the recipient intact (Figure 31–6A •). The to 50% of transplanted hearts during the early postoperative period.
atrial walls of the donor heart are then anastomosed to the recipient’s Inotropic agents such as low-dose dopamine, dobutamine, or milri-
atria (Figure 31–6B). The donor pulmonary artery and aorta are none may be required to support cardiac function and circulation.
anastomosed to the recipient’s vessels (Figure 31–6C). Care is taken Infection and rejection are major postoperative concerns; these
to avoid damaging the sinus node of the donor heart and to ensure are the chief causes of mortality in transplant patients. Rejection may
A B C
Figure 31–6 • Cardiac transplantation. A, The heart is removed, leaving the posterior walls of the atria intact. The donor heart is
anastomosed to the atria, B, and the great vessels, C.
Chapter 31 • Nursing Care of Patients with Cardiac Disorders 933
develop immediately after transplant (a rare occurrence), within ●◯● Nursing Care
weeks to months, or years after the transplant. Acute rejection usu-
ally presents within weeks of the transplant, developing when the Health Promotion
transplanted organ is recognized by the immune system as foreign. Health promotion activities to reduce the risk for and incidence of heart
Lymphocytes infiltrate the organ, and myocardial cell necrosis can be failure are directed at the risk factors. Teach patients about coronary
detected on biopsy. Acute rejection often can be treated using immu- heart disease, the primary underlying cause of heart failure. Discuss
nosuppressive drugs. These drugs are also given to prevent rejection CHD risk factors, and ways to reduce those risk factors (see Chapter 30).
of the transplanted organ, even when the tissue match is good (refer Hypertension also is a major cause of heart failure. Routinely
to Chapter 12). Although immunosuppressive medications help pre- screen patients for elevated blood pressure, and refer patients to a pri-
vent organ rejection, they impair the patient’s defenses against infec- mary care provider as indicated. Discuss the importance of effectively
tion. Early postoperative infections commonly are bacterial or fungal managing hypertension to reduce the future risk for heart failure.
(candida). Multiple invasive lines, prolonged ventilator support, and Likewise, stress the relationship between effective diabetes manage-
immunosuppressive therapy contribute to the transplant recipient’s ment and reduced risk of heart failure.
risk for infection. Aggressive nursing care directed at prevention of
infection is vital: limiting visitors with communicable diseases and Assessment
practicing pulmonary hygiene measures, early ambulation, and strict See the Manifestations and Interprofessional Care sections for the as-
aseptic technique. sessment of the patient with heart failure.
The donor heart is denervated during the transplant procedure. Obtain both subjective and objective data when assessing the
Lack of innervation by the autonomic nervous system affects the patient with heart failure.
heart rate (usually between 90 and 110 bpm in transplanted hearts),
its response to position changes, stress, exercise, and certain drugs. • Health history: complaints of increasing shortness of breath, dys-
pnea with exertion, decreasing activity tolerance, or paroxysmal
Other Procedures Other surgical procedures such as nocturnal dyspnea; number of pillows used for sleeping; recent
cardiomyoplasty and ventricular reduction surgery do not improve weight gain; presence of a cough; chest or abdominal pain; an-
the prognosis or quality of life in patients with end-stage heart failure. orexia or nausea; history of cardiac disease, previous episodes of
Cardiomyoplasty involves wrapping the latissimus dorsi muscle heart failure; other risk factors such as hypertension or diabetes;
around the heart to support the failing myocardium. The muscle is current medications; usual diet and activity and recent changes.
stimulated in synchrony with the heart, providing a more forceful Determine patient’s NYHA class.
contraction and increasing cardiac output. In ventricular reduction • Physical assessment: general appearance; ease of breathing, con-
surgery (or partial ventriculectomy), a portion of the anteriolateral left versing, changing positions; apparent anxiety; vital signs including
ventricular wall is resected to improve cardiac function. apical pulse; color of skin and mucous membranes; neck vein dis-
tention, peripheral pulses, capillary refill, presence and degree of
Complementary Therapies edema; heart and breath sounds; abdominal contour, bowel sounds,
Evidence supports the use of several complementary therapies for tenderness; right upper abdominal tenderness, liver enlargement.
heart failure. Hawthorn, a shrubby tree, contains natural cardiotonic
ingredients in its blossoms, leaves, and fruit. It increases the force of Priorities of Care
myocardial contraction, dilates blood vessels, and has a natural ACE Collaborating with the interprofessional team to ensure adequate
inhibitor. Hawthorn should never be used without consulting an ex- treatment of the underlying process while providing care that sup-
perienced herb practitioner and advising the physician. Nutritional ports the physical and psychologic responses to the disorder is a pri-
supplements of coenzyme Q10, magnesium, and thiamine may be ority of nursing care.
used in conjunction with other treatments. Coenzyme Q10 improves
mitochondria function and energy production. It can be lost with use Diagnoses, Outcomes, and Interventions
of antilipemics. Heart failure impacts quality of life, interfering with such daily activi-
ties as self-care and role performance. Reducing the oxygen demand
End-of-Life Care of the heart is a major nursing care goal for the patient in acute heart
Unless a cardiac transplant is performed, chronic heart failure is ul- failure. This includes providing rest and carrying out prescribed
timately a terminal disease. The patient and family need honest dis- treatment measures to reduce cardiac work, improve contractility,
cussions about the anticipated course of the disease and treatment
options. It is important to discuss advance directives such as a living
will and medical power of attorney, differentiating potential acute Evidence for Nursing Care
events from which recovery would be anticipated (e.g., reversible ex-
acerbation of heart failure, sudden cardiac arrest) from prolonged life The Patient with Heart Failure
support without reasonable expectation of functional recovery. Hos- A selected resource that nurses may find helpful when planning
pice services are available for patients with heart failure, and should evidence-based nursing care follows.
be offered when appropriate. Severe dyspnea is common in the final • Pere, K. (2012). Developing nursing expertise in caring for older
stages of the disease. It may be managed with narcotic analgesics or advanced stage heart failure patients and their families—palliative
and end-of-life care. Canadian Journal of Cardiovascular Nursing,
with frequent intravenous diuretics and continuous infusion of a 22(3), 12–17.
positive inotropic agent.
934 Unit 8 • Responses to Altered Cardiovascular Function
and manage symptoms. See also the accompanying Case Study & • Monitor intake and output. Notify the physician if urine output is
Nursing Care Plan for additional nursing diagnoses and interven- less than 30 mL/h. Weigh daily. Careful monitoring of fluid volume
tions for the patient with heart failure. is important during treatment of heart failure. Diuretics may reduce
circulating volume, producing hypovolemia despite persistent periph-
Decreased Cardiac Output eral edema. A fall in urine output may indicate significantly reduced
As the heart fails as a pump, stroke volume and tissue perfusion cardiac output and renal ischemia. Weight is an objective measure of
decrease. fluid status: 1 L of fluid is equal to 2.2 lb of weight.
Expected Outcome: Patient will demonstrate adequate cardiac output • Record abdominal girth every shift. Note complaints of a loss of
as evidenced by blood pressure and pulse rate and rhythm within appetite, abdominal discomfort, or nausea. Venous congestion can
normal limits. lead to ascites and may affect gastrointestinal function and nutri-
tional status.
• Monitor vital signs and oxygen saturation as indicated. Decreased
• Monitor and record hemodynamic measurements. Report signif-
cardiac output stimulates the SNS to increase the heart rate in an
icant changes and negative trends. Hemodynamic measurements
attempt to restore CO. Tachycardia at rest is common. Diastolic blood
provide a means of monitoring the patient’s condition and response to
pressure may initially be elevated because of vasoconstriction; in late
treatment.
stages, compensatory mechanisms fail, and BP falls. Oxygen satura- • Restrict fluids as ordered. Allow choices of fluid type and timing
tion levels provide a measure of gas exchange and tissue perfusion.
of intake, scheduling most fluid intake during morning and af-
• Auscultate heart and breath sounds regularly. S1 and S2 may be
ternoon hours. Offer ice chips and frequent mouth care; provide
diminished if cardiac function is poor. A ventricular gallop (S3) is
hard candies if allowed. Providing choices increases the patient’s
an early sign of heart failure; atrial gallop (S4) may also be present.
sense of control. Ice chips, hard candies, and mouth care relieve dry
Crackles are often heard in the lung bases; increasing crackles, dys-
mouth and thirst and promote comfort.
pnea, and shortness of breath indicate worsening failure.
Activity Intolerance
SAFETY ALERT
Patients with heart failure have little or no cardiac reserve to meet
Report manifestations of decreased cardiac output and tissue perfu- increased oxygen demands. As the disease progresses and cardiac
sion: changes in mentation; decreased urine output; cool, clammy function is further compromised, activity intolerance increases. The
skin; diminished pulses; pallor or cyanosis; or dysrhythmias. These low cardiac output and inability to participate in activities may hinder
are manifestations of decreased tissue perfusion to organ systems. self-care.
Expected Outcome: Patient will participate in physical activity as
• Administer supplemental oxygen as needed. This improves oxy- tolerated.
genation of the blood, decreasing the effects of hypoxia and ischemia.
• Administer prescribed medications as ordered. Drugs are used PRACTICE ALERT!
to decrease the cardiac workload and increase the effectiveness of
contractions. Monitor vital signs and cardiac rhythm during and after activities.
• Encourage rest, explaining the rationale. Elevate the head of the Tachycardia, dysrhythmias, increasing dyspnea, changes in blood
pressure, diaphoresis, pallor, complaints of chest pain, excessive
bed to reduce the work of breathing. Provide a bedside commode, fatigue, or palpitations indicate activity intolerance. Instruct to rest if
and assist with ADLs. Instruct to avoid the Valsalva maneuver. manifestations are noted. The failing heart is unable to increase car-
These measures reduce cardiac workload. diac output to meet the increased oxygen demands associated with
activity. Assessing response to activities helps evaluate cardiac func-
Excess Fluid Volume tion. Decreasing activity tolerance may signal deterioration of cardiac
function, not overexertion.
As cardiac output falls, compensatory mechanisms cause salt and wa-
ter retention, increasing blood volume. This increased fluid volume
places additional stress on the already failing ventricles, making them • Organize nursing care to allow rest periods. Grouping activities to-
work harder to move the fluid load. gether allows adequate time to rest and recharge.
Expected Outcome: Patient will maintain normal fluid volume as evi- • Assist with ADLs as needed. Encourage independence within pre-
denced by weight loss and decreases in edema, jugular venous disten- scribed limits. Assisting with ADLs helps ensure that care needs are
tion, and abdominal distention. met while reducing cardiac workload. Involving the patient promotes
a sense of control and reduces helplessness.
• Assess respiratory status and auscultate lung sounds at least every
• Plan and implement progressive activities. Use passive and active
4 hours. Notify the physician of significant changes in condition.
ROM exercises as appropriate. Consult with physical therapist on
Declining respiratory status indicates worsening left heart failure.
activity plan. Progressive activity slowly increases exercise capacity by
SAFETY ALERT strengthening and improving cardiac function without strain. Activ-
ity also helps prevent skeletal muscle atrophy. ROM exercises prevent
Immediately notify the physician if the patient develops air hunger, an complications of immobility in severely compromised patients.
overwhelming sense of impending doom or panic, tachypnea, severe • Provide written and verbal information about activity after dis-
orthopnea, or a cough productive of large amounts of pink, frothy charge. Written information provides a reference for important
sputum. Acute pulmonary edema, a medical emergency, can develop
rapidly, necessitating immediate intervention to preserve life. information. Verbal information allows for clarification and valida-
tion of the material.
Chapter 31 • Nursing Care of Patients with Cardiac Disorders 935
Deficient Knowledge: Low-Sodium Diet • Desired and adverse effects of prescribed drugs; monitoring for
Diet is an important part of long-term management of heart failure to effects; importance of compliance with drug regimen to prevent
manage fluid retention. acute and long-term complications of heart failure
Expected Outcome: Patient will comply with sodium restrictions pre- • Prescribed diet and sodium restriction; practical suggestions for
scribed as evidenced by reduction in fluid retention and edema. reducing salt intake; recommend American Heart Association
materials and recipes
• Discuss the rationale for sodium restrictions. Understanding fos-
• Exercise recommendations to strengthen the heart muscle and
ters compliance with the prescribed diet.
improve aerobic capacity (Box 31–3)
• Consult with dietitian to plan and teach a low-sodium and, if
• The importance of keeping scheduled follow-up appointments to
necessary for weight control, low-kilocalorie diet. Provide a list
monitor disease progression and effects of therapy.
of high-sodium, high-fat, high-cholesterol foods to avoid. Pro-
vide American Heart Association materials. Dietary planning and Provide referrals for home healthcare and household assistance
teaching increase the patient’s sense of control and participation in (shopping, transportation, personal needs, and housekeeping) as
disease management. Food lists are useful memory aids. indicated. Referrals to community agencies, such as local cardiac
• Teach how to read food labels for nutritional information. Many rehabilitation programs, heart support groups, or the AHA, can pro-
processed foods contain hidden sodium, which can be identi- vide additional materials and psychosocial support.
fied by careful label reading. Knowledge about hidden sodium can
improve dietary selections.
• Assist the patient to construct a 2-day meal plan choosing foods
The Patient
low in sodium. This allows for learning assessment, clarification of with Pulmonary Edema
misunderstandings, and reinforcement of teaching. Pulmonary edema is an abnormal accumulation of fluid in the
• Encourage small, frequent meals rather than three heavy meals interstitial tissue and alveoli of the lung. Both cardiac and noncar-
per day. Small, frequent meals provide continuing energy resources diac disorders can cause pulmonary edema. Cardiac causes include
and decrease the work required to digest a large meal. acute myocardial infarction, acute heart failure, and valvular disease.
Cardiogenic pulmonary edema, the focus of this section, is a sign of se-
Delegating Nursing Care Activities vere cardiac decompensation. Noncardiac causes of pulmonary edema
As appropriate and allowed by the designated duties and responsibili- include primary pulmonary disorders, such as acute respiratory dis-
ties of unlicensed assistive personnel, the nurse may delegate nursing tress syndrome (ARDS), trauma, sepsis, drug overdose, or neurologic
care activities such as measuring fluid intake and output, collecting sequelae. Pulmonary edema due to ARDS is discussed in Chapter 37.
vital signs (including orthostatic vital signs), encouraging oral or
enteral fluid intake, and ensuring nonpharmacologic skin care. FAST FACTS
BOX 31–3 Home Activity Guidelines for the Patient with Heart Failure
• Perform as many activities as independently as you can. increase the distance and pace. A suggested schedule is pro-
• Space your meals and activities. vided next—but progress at your own speed. Take your time.
a. Eat six small meals a day. Aim for walking at least three times per week (every other day)
b. Allow time during the day for periods of rest and relaxation. (American College of Sports Medicine, 2013).
• Perform all activities at a comfortable pace.
a. If you get tired during any activity, stop what you are doing
Week 1 200–400 ft Twice a day, slow
and rest for 15 minutes.
(1/4 mile) leisurely pace
b. Resume activity only if you feel up to it.
• Stop any activity that causes chest pain, shortness of breath, Week 2 1/4 mile 15 min, minimum
dizziness, faintness, excessive weakness, or sweating. Rest. of 3 times per week
Notify your physician if your activity tolerance changes and if Weeks 2–3 1/2 mile 30 min, minimum
symptoms continue after rest. of 3 times per week
• Avoid straining. Do not lift heavy objects. Eat a high-fiber diet Weeks 3–4 1 mile 30 min, minimum
and drink plenty of water to prevent constipation. Use laxatives of 3 times per week
or stool softeners, as approved by your physician, to avoid con- Weeks 4–5 1 1/2 miles 30 min, minimum
stipation and straining during bowel movements. of 3 times per week
• Begin a graded exercise program. Walking is good exercise that
Weeks 5–6 2 miles 40 min, minimum
does not require any special equipment (except a good pair of
of 3 times per week
walking shoes). Plan to walk twice a day at a comfortable, slow
pace for the first couple of weeks at home, and then gradually
936 Unit 8 • Responses to Altered Cardiovascular Function
CASE STUDY & NURSING CARE PLAN A Patient with Heart Failure
One year ago, Arthur Jackson, 67 years old, had a large anterior • Auscultate heart and breath sounds every 4 hours and as
wall MI and underwent subsequent coronary artery bypass surgery. indicated.
On discharge, he was started on a regimen of enalapril (Vasotec), • Administer oxygen per nasal cannula at 2 L/min. Monitor
digoxin, furosemide (Lasix), warfarin (Coumadin), and a potassium oxygen saturation continuously. Notify physician if less
chloride supplement. He is now in the cardiac unit complaining than 94%.
of severe shortness of breath, hemoptysis, and poor appetite for • Place in high-Fowler’s or other position of comfort.
1 week. He is diagnosed with acute heart failure. • Notify physician of significant changes in laboratory values.
• Teach about all medications and how to take and record pulse.
Assessment Provide information about anticoagulant therapy and signs of
Mr. Jackson refuses to settle in bed, preferring to sit in the bedside bleeding.
recliner in high-Fowler’s position. He states, “Lately, this is the only • Design an activity plan with Mr. Jackson that incorporates pre-
way I can breathe.” Mr. Jackson states that he has not been able to ferred activities and scheduled rest periods.
work in his garden without getting short of breath. He complains of • Instruct about sodium-restricted diet. Allow meal choices within
his shoes and belt being too tight. allowed limits.
When Mr. Jackson’s nurse, Ms. Takashi, RN, obtains his nursing • Consult dietitian for planning and teaching Mr. and Mrs. Jackson
history, Mr. Jackson insists that he takes his medications regularly. about low-sodium diet.
He states that he normally works in his garden for light exercise. In
his diet history, Mr. Jackson admits a fondness for bacon and Chi- Evaluation
nese food and sheepishly admits to snacking between meals “even Mr. Jackson is discharged after 3 days in the cardiac unit. He
though I need to lose weight.” has lost 8 pounds during his stay and states it is much easier to
Mr. Jackson’s vital signs are BP 95/72 mmHg, HR 124 bpm and breathe and his shoes fit better. He is able to sleep in semi-Fowler’s
irregular, R 28/min and labored, and T 97.5°F (36.5°C). The cardiac position with only one pillow. His peripheral edema has resolved.
monitor shows atrial fibrillation. An S3 is noted on auscultation; the Mr. and Mrs. Jackson met with the dietitian, who helped them de-
cardiac impulse is left of the midclavicular line. He has crackles and velop a realistic eating plan to limit sodium, sugar, and fats. The dieti-
diminished breath sounds in the bases of both lungs. Significant tian also provided a list of high-sodium foods to avoid. Mr. Jackson
jugular venous distention, 3+ pitting edema of feet and ankles, and is relieved to know that he can still enjoy Chinese food prepared
abdominal distention are noted. Liver size is within normal limits by without monosodium glutamate (MSG) or added salt. Ms. Takashi
percussion. Skin cool and diaphoretic. Chest x-ray shows cardio- and the physical therapist designed a progressive activity plan with
megaly and pulmonary infiltrates. Mr. Jackson that he will continue at home. He remains in atrial fibril-
lation, a chronic condition. His knowledge of digoxin and Coumadin
Diagnoses has been assessed and reinforced. Ms. Takashi confirms that he
• Excess Fluid Volume related to impaired cardiac pump and salt is able to accurately check his pulse and can list signs of digoxin
and water retention toxicity and excessive bleeding.
• Activity Intolerance related to impaired cardiac output
• Impaired Health Maintenance related to lack of knowledge Clinical Reasoning in Patient Care
about diet restrictions 1. Mr. Jackson’s medication regimen remains the same after
discharge. What specific teaching does he need related
Expected Outcomes to potential interactions of these drugs?
• Patient will demonstrate loss of excess fluid by weight loss and
2. Mr. Jackson tells you, “Talk to my wife about my medications—
decreases in edema, jugular venous distention, and abdominal she’s Tarzan and I’m Jane now.” How would you respond?
distention. 3. Design an exercise plan for Mr. Jackson to prevent decon-
• Patient will demonstrate improved activity tolerance.
ditioning and conserve energy.
• Patient will verbalize understanding of diet restrictions.
4. Mr. Jackson tells you, “Sometimes I forget whether I have
Planning and Implementation taken my aspirin, so I’ll take another just to be sure. After all,
• Take hourly vital signs and hemodynamic pressure they are only baby aspirin. One or two extra a day shouldn’t
measurements. hurt, right?” What is your response?
• Administer and monitor effects of prescribed diuretics 5. Mr. Jackson is admitted to the neuro unit 6 months later with
and vasodilators. a cerebrovascular accident (CVA). What is the probable cause
• Weigh daily; strict intake and output. of his stroke?
• Enforce fluid restriction of 1500 mL/24 hours: 600 mL day shift, See Evaluating Your Response in Appendix B.
600 mL evening shift, 300 mL at night.
Pulmonary edema is a medical emergency: The patient is liter- fluid leaking from the pulmonary capillaries congests interstitial tis-
ally drowning in the fluid in the alveolar and interstitial pulmonary sues, decreasing lung compliance and interfering with gas exchange.
spaces. Its onset may be acute or gradual, progressing to severe respi- As capillary and interstitial pressures increase further, the tight junc-
ratory distress. Immediate treatment is necessary. tions of the alveolar walls are disrupted, and the fluid enters the
alveoli, along with large red blood cells and protein molecules. Venti-
Pathophysiology lation and gas exchange are severely disrupted, and hypoxia worsens.
In cardiogenic pulmonary edema, the contractility of the left ven-
tricle is severely impaired. The ejection fraction falls as the ventricle Manifestations
is unable to eject the blood that enters it, causing a sharp rise in end- The patient with acute pulmonary edema presents with classic
diastolic volume and pressure. Pulmonary hydrostatic pressures rise, manifestations (see the accompanying box). Dyspnea, shortness of
ultimately exceeding the osmotic pressure of the blood. As a result, breath, and labored respirations are acute and severe, accompanied
Chapter 31 • Nursing Care of Patients with Cardiac Disorders 937
Expected Outcome: Patient will experience improved ventilation and positive inotropic medications (e.g., digoxin) as ordered. These
adequate oxygenation as evidenced by blood gas levels within normal drugs reduce cardiac work and improve contractility.
limits for the individual patient • Insert an indwelling catheter as ordered; record output hourly.
Urine output of less than 30 mL/h indicates impaired renal perfusion
• Ensure airway patency. A patent airway is absolutely vital for pul-
due to severely impaired cardiac output and a risk for renal failure or
monary function, including ventilation and gas exchange.
other complications.
• Assess the effectiveness of respiratory efforts and airway clearance.
• Keep accurate intake and output records. Restrict fluids as or-
Pulmonary edema increases the work of breathing. This increased
dered. Fluids may be restricted to reduce vascular volume and
effort can lead to fatigue and decreased respiratory effort.
cardiac work.
• Assess respiratory status frequently, including rate, effort, use of
accessory muscles, sputum characteristics, lung sounds, and skin
Fear
color. The status of a patient in acute pulmonary edema can change
Acute pulmonary edema is a very frightening experience for every-
rapidly for the better or worse.
one (including the nurse).
• Place in high-Fowler’s position with the legs dangling. The upright
position facilitates breathing and decreases venous return. Expected Outcome: Patient will demonstrate reduced fear as evi-
• Administer oxygen as ordered by mask, CPAP mask, or ventila- denced by verbal and nonverbal indicators that reflect understanding
tor. Supplemental oxygen promotes gas exchange; positive pressure by the patient and family of the current clinical condition.
increases the pressure within the alveoli, airways, and thoracic cav- • Provide emotional support for the patient and family members.
ity, decreasing venous return, pulmonary capillary pressure, and fluid Fear and anxiety stimulate the sympathetic nervous system, which
leak into the alveoli. can lead to ineffective respiratory patterns and interfere with coop-
• Encourage patient to cough up secretions; provide nasotracheal eration with care measures.
suctioning if necessary. Coughing moves secretions from smaller air- • Explain all procedures and the reasons for the procedures to the
ways into larger airways where they can be suctioned out if necessary. patient and family members. Keep information brief and to the
point. Use short sentences and a reassuring tone. Anxiety and
SAFETY ALERT fear interfere with the ability to assimilate information; brief, factual
information and reassurance reduce anxiety and fear.
Have emergency equipment readily available in case of respiratory ar-
rest. Be prepared to assist with intubation and initiation of mechanical • Maintain close contact with the patient and family, providing re-
ventilation. Fatigue, impaired gas exchange, and respiratory acidosis assurance that recovery from acute pulmonary edema is often as
can lead to respiratory and cardiac arrest. dramatic as its onset.
• Answer questions, and provide accurate information in a caring
manner. Knowledge reduces the anxiety and psychologic stress associ-
Decreased Cardiac Output ated with this critical condition.
Cardiogenic pulmonary edema usually is caused by either an acute
decrease in myocardial contractility or increased workload that
exceeds the ability of the left ventricle. The significant decrease in Delegating Nursing Care Activities
cardiac output increases pressure within the pulmonary vascular sys- As appropriate and allowed by the designated duties and responsibili-
tem and triggers compensatory mechanisms that increase the heart ties of unlicensed assistive personnel, the nurse may delegate nursing
rate and blood volume. These compensatory mechanisms further care activities such as measuring fluid intake and output, collecting
increase the workload of the failing heart. vital signs (including orthostatic vital signs), encouraging oral or
Expected Outcome: Patient will demonstrate adequate cardiac output enteral fluid intake, and ensuring nonpharmacologic skin care.
as evidenced by blood pressure and pulse rate and rhythm within
normal limits. Continuity of Care
• Monitor vital signs, hemodynamic status, and rhythm continu- During the acute period, teaching is limited to immediate care mea-
ously. Acute pulmonary edema is a critical condition, and cardiovas- sures. Once the acute episode of pulmonary edema has resolved,
cular status can change rapidly. teach the patient and family about its underlying cause and preven-
• Assess heart sounds for possible S3, S4, or murmurs. These ab- tion of future episodes. If pulmonary edema follows an acute myo-
normal heart sounds may be due to excess work or may indicate the cardial infarction (AMI), include information related to CHD and
cause of the acute pulmonary edema. the AMI, as well as information related to heart failure. Review the
• Initiate an intravenous line for medication administration. Ad- teaching and home care for patients with these disorders for further
minister morphine, diuretics, vasodilators, bronchodilators, and information.
The Patient with Rheumatic Endocardial inflammation, however, causes swelling and erythema
Fever and Rheumatic of valve structures and small vegetative lesions on valve leaflets. As
the inflammatory process resolves, fibrous scarring occurs, causing
Heart Disease deformity.
Rheumatic fever is a systemic inflammatory disease caused by an
Rheumatic heart disease (RHD) is a slowly progressive
abnormal immune response to pharyngeal infection by group A beta-
valvular deformity that may follow acute or repeated attacks of
hemolytic streptococci. Rheumatic fever usually is a self-limiting
rheumatic fever. Valve leaflets become rigid and deformed; com-
disorder, although it may become recurrent or chronic. Although the
missures (openings) fuse, and the chordae tendineae fibrose and
heart commonly is involved in the acute inflammatory process, only
shorten. This results in stenosis or regurgitation of the valve. In
about 10% of people with rheumatic fever develop rheumatic heart
stenosis, a narrowed, fused valve obstructs forward blood flow.
disease. Rheumatic heart disease frequently damages the heart valves
Regurgitation occurs when the valve fails to close properly (an
and is a major cause of the mitral and aortic valve disorders discussed
incompetent valve), allowing blood to flow back through it. Valves
in the next section of this chapter.
on the left side of the heart are usually affected; the mitral valve is
most frequently involved.
Incidence, Prevalence, and Risk Factors
In the United States and other industrialized nations, rheumatic fe-
Manifestations
ver and its sequelae are rare. The peak incidence of rheumatic fever
Manifestations of rheumatic fever typically follow the initial strepto-
is between ages 5 and 15; although it is rare after age 40, it may af-
coccal infection by about 2 to 3 weeks. Fever and migratory joint pain
fect people of any age. About 3% of people with untreated group A
are often initial manifestations. The knees, ankles, hips, and elbows
streptococcal pharyngitis develop rheumatic fever. Rheumatic fever
are common sites of swelling and inflammation. Erythema margin-
and rheumatic heart disease remain significant public health prob-
atum is a temporary nonpruritic skin rash characterized by red le-
lems in many developing countries. Highly virulent strains of group
sions with clear borders and blanched centers usually found on the
A streptococci have caused scattered outbreaks in the United States
trunk and proximal extremities. Neurologic symptoms of rheumatic
in recent years.
fever, although rare in adults, may range from irritability and an in-
Risk factors for streptococcal infections of the pharynx in-
ability to concentrate to clumsiness and involuntary muscle spasms.
clude environmental and economic factors such as crowded living
Manifestations of carditis include chest pain, tachycardia, a peri-
conditions, malnutrition, immunodeficiency, and poor access to
cardial friction rub, or evidence of heart failure. On auscultation, an
healthcare. Evidence also suggests an unknown genetic factor in sus-
S3, S4, or a heart murmur may be heard. Cardiomegaly or pericardial
ceptibility to rheumatic fever.
effusion may develop. Other manifestations of rheumatic fever are
listed in the accompanying box.
FAST FACTS
• The peak incidence of rheumatic fever is in children ages 5 to 15.
• Young adults (in late adolescence and the early 20s) are the pri-
●◯● Interprofessional Care
mary adult population affected by rheumatic fever. Management of the patient with rheumatic heart disease focuses on
• People past age 40 rarely develop the disease, unless it is a case
of recurrent rheumatic fever.
eradicating the streptococcal infection and managing the manifesta-
• Although crowded living conditions and lower socioeconomic tions of the disease. Carditis and resulting heart failure are treated
status are risk factors, a relatively recent outbreak in the United with measures to reduce the inflammatory process and manage
States occurred in people with ready access to healthcare. the heart failure. Activities are limited, but bed rest is not generally
ordered.
Pathophysiology
The pathophysiology of rheumatic fever is not yet totally under- MANIFESTATIONS OF RHEUMATIC FEVER
stood. It is thought to result from an abnormal immune response to
Cardiac
M proteins on group A beta-hemolytic streptococcal bacteria. These • Chest pain
antigens can bind to cells in the heart, muscles, and brain. They also • Friction rub
bind with receptors in synovial joints, provoking an autoimmune • Heart murmur
response. The resulting immune response to the bacteria also leads Musculoskeletal
to inflammation in tissues containing these M proteins. Inflamma- • Migratory polyarthritis: redness, heat, swelling, pain,
tory lesions develop in connective tissues on the heart, joints, and and tenderness of more than one joint
• Usually affects large joints of extremities
skin. The antibodies may remain in the serum for up to 6 months
following the initiating event. Refer to Chapters 11 and 12 for more Skin
information about the immune system and inflammatory response. • Erythema marginatum: transitory pink, nonpruritic, macular
Carditis, inflammation of the heart, develops in about 50% of lesions on trunk or inner aspect of upper arms or thighs
• Subcutaneous nodules over extensors of wrist, elbow, ankle,
people with rheumatic fever. The inflammatory process usually in-
and knee joints
volves all three layers of the heart—the pericardium, myocardium,
and endocardium. Aschoff bodies, localized areas of tissue necrosis Neurologic
• Sydenham’s chorea: irritability; behavior changes; sudden,
surrounded by immune cells, develop in cardiac tissues. Pericardial
jerky, involuntary movements
and myocardial inflammation tends to be mild and self-limiting.
940 Unit 8 • Responses to Altered Cardiovascular Function
Diagnosis pathogen and the risk for rheumatic fever. Characteristics of strep-
In addition to the history and physical examination, a number of tococcal sore throat include a red, fiery-looking throat, pain with
laboratory and diagnostic tests may be ordered for the patient with swallowing, enlarged and tender cervical lymph nodes, fever range
suspected rheumatic fever. Table 31–5 identifies tests and values of 38.3° to 40.0°C (101° to 104°F), and headache. Emphasize the im-
indicative of carditis associated with rheumatic fever. portance of finishing the complete course of medication to eradicate
the pathogen.
• Complete blood count (CBC) and erythrocyte sedimentation rate
(ESR) are indicators of the inflammatory process. The WBC
count is elevated, and the number of red blood cells may be low Assessment
due to the inflammatory inhibition of erythropoiesis. The ESR, See the Manifestations and Interprofessional Care sections for the as-
a general indicator of inflammation, is elevated. sessment of the patient with rheumatic fever/rheumatic heart disease.
• C-reactive protein (CRP) is positive in an active inflammatory Assess patients at risk for rheumatic fever (prolonged, untreated, or
process. recurrent pharyngitis) for possible manifestations.
• Antistreptolysin (ASO) titer is a test for streptococcal antibodies. It • Health history: complaints of recent sore throat with fever, diffi-
rises within 2 months of onset and is positive in most patients with culty swallowing, and general malaise; treatment measures; pre-
rheumatic fever. vious history of strep throat or rheumatic fever; history of heart
• Throat culture is positive for group A beta-hemolytic streptococ- murmur or other cardiac problems; current medications
cus in only 25% to 40% of patients with acute rheumatic fever. • Physical assessment: vital signs including temperature; skin color,
presence of rash on trunk or proximal extremities; mental status;
Medications
evidence of inflamed joints; heart and lung sounds.
As soon as rheumatic fever is diagnosed, antibiotics are started to
eliminate the streptococcal infection. Penicillin is the antibiotic of
choice to treat group A streptococci. Antibiotics are prescribed for Priorities of Care
at least 10 days. Erythromycin or clindamycin is used if the patient is Collaborating with the interprofessional team to ensure adequate
allergic to penicillin. Prophylactic antibiotic therapy is continued for treatment of the underlying process while providing care that sup-
5 to 10 years to prevent recurrences. Recurrences after 5 years or age ports the physical and psychologic responses to the disorder is a pri-
25 are rare. Penicillin G, 1.2 million units injected intramuscularly ority of nursing care.
every 3 to 4 weeks, is the prophylaxis of choice. Oral penicillin, amox-
icillin, sulfadiazine, or erythromycin may also be used. Diagnoses, Outcomes, and Interventions
Joint pain and fever are treated with salicylates (e.g., aspirin), ibu- The nursing care focus for the patient with RHD is on providing
profen, or another nonsteroidal anti-inflammatory drug (NSAID); supportive care and preventing complications. Teaching to prevent
corticosteroids may be used for severe pain due to inflammation or recurrence of rheumatic fever is extremely important. Pain and
carditis. Refer to Chapter 9 for information about the use of these Activity Intolerance are priority nursing diagnoses for the patient with
anti-inflammatory medications. rheumatic fever and RHD.
Acute Pain
●◯● Nursing Care Joint and chest pain due to acute inflammation is common in rheu-
Health Promotion matic fever. Pain and inflammation may interfere with rest and healing.
Rheumatic fever is preventable. Prompt identification and treat- Expected Outcome: Patient will achieve adequate pain control as
ment of streptococcal throat infections help decrease spread of the evidenced by physical well-being.
Chapter 31 • Nursing Care of Patients with Cardiac Disorders 941
• Administer anti-inflammatory drugs as ordered. Promptly report • Preventive dental care and good oral hygiene to maintain oral
manifestations of aspirin toxicity, including tinnitus, vomiting, health and prevent gingival infections, which can lead to recur-
and gastrointestinal bleeding. Give aspirin and other NSAIDs rence of the disease.
with food, milk, or antacids to minimize gastric irritation. Joint • Early recognition of streptococcal sore throat and appropriate
pain and fever may be treated with anti-inflammatory agents such as treatment for both the patient and family members.
aspirin and NSAIDs. Steroids may be prescribed for severe carditis. • Early manifestations of heart failure to report to the physician.
• Provide warm, moist compresses for local pain relief of acutely in- • Prescribed medications, including their dosage, route, intended
flamed joints. Moist heat helps relieve pain associated with inflamed and potential adverse effects, and manifestations to report to the
joints by reducing inflammation. physician.
• Auscultate heart sounds as indicated (every shift or each home • Dietary sodium restriction if ordered or recommended. A high-
visit). Notify the physician if a pericardial friction rub or a new carbohydrate, high-protein diet may be recommended to facili-
murmur develops. A friction rub is produced as inflamed pericar- tate healing and combat fatigue.
dial surfaces rub against each other. This also stimulates pain recep-
Refer for home health services or household assistance as indicated.
tors, and may increase discomfort.
Manifestations
The manifestations of infective endocarditis often are nonspecific
(see the accompanying box). A temperature above 39.4°C (101.5°F)
and flu-like symptoms develop, accompanied by cough, shortness
Figure 31–7 • A vegetative lesion of bacterial endocarditis. of breath, and joint pain. The presentation of acute staphylococcal
Source: M. English/Custom Medical Stock Photo, Inc. endocarditis is more severe, with a sudden onset, chills, and a high
fever. Heart murmurs are heard in 90% of persons with infective en-
drug use; or as a result of infectious processes such as urinary tract or docarditis. An existing murmur may worsen, or a new murmur may
upper respiratory infection. develop.
The initial lesion is a sterile platelet-fibrin vegetation formed Splenomegaly is common in chronic disease. Peripheral mani-
on damaged endothelium (Figure 31–7 •). In acute infective en- festations of infective endocarditis result from microemboli or
docarditis, these lesions develop on healthy valve structures, al- circulating immune complexes. These manifestations include the
though the mechanism is unknown. In subacute endocarditis, following:
they usually develop on already damaged valves or in endocardial
• Petechiae: small, purplish-red hemorrhagic spots on the trunk,
tissue that has been damaged by abnormal pressures or blood flow
conjunctiva, and mucous membranes
within the heart.
• Splinter hemorrhage: hemorrhagic streaks under the fingernails or
Organisms that have invaded the blood colonize these veg-
toenails
etations. The vegetation enlarges as more platelets and fibrin are at-
• Osler’s nodes: small, reddened, painful raised growths on finger
tracted to the site and cover the infecting organism. This covering
and toe pads
“protects” the bacteria from quick removal by immune defenses such
• Janeway lesions: small, nontender, purplish-red macular lesions on
as phagocytosis by neutrophils, antibodies, and complement. Veg-
the palms of the hands and soles of the feet
etations may be singular or multiple. They expand while loosely at-
• Roth’s spots: small, whitish spots (cotton-wool spots) seen on the
tached to edges of the valve. Friable vegetations can break or shear
retina.
off, embolizing and traveling through the bloodstream to other organ
systems. When they lodge in small vessels, they may cause hemor-
rhages, infarcts, or abscesses. Ultimately, the vegetations scar and de- Complications
form the valves and cause turbulence of blood flowing through the Embolization of vegetative fragments may affect any organ system,
heart. Heart valve function is affected, either obstructing forward particularly the lungs, brain, kidneys, and the skin and mucous
blood flow, or closing incompletely. membranes, with resulting organ infarction. Other common compli-
Endocarditis is classified by its acuity and disease course cations of infective endocarditis include heart failure, abscess, and an-
(Table 31–6). Acute infective endocarditis has an abrupt onset and is eurysms due to infiltration of the arterial wall by organisms. Without
a rapidly progressive, severe disease. Although almost any organ- treatment, endocarditis is almost universally fatal; fortunately, antibi-
ism can cause infective endocarditis, virulent organisms such as otic therapy is usually effective to treat this disease.
TABLE 31–7 Updated Recommendations for Antibiotic Prophylaxis for Infective Endocarditis
to the physician. Provide practical information about measures to • The importance of maintaining contact with the physician for
reduce the risk of superinfection (e.g., consuming 8 oz of yogurt follow-up care and monitoring for long-term effects such as pro-
or buttermilk containing live bacterial cultures daily). Careful com- gressive valve damage and dysfunction.
pliance with prescribed drug therapy is vital to eradicate the infecting • If appropriate, explain the risks associated with intravenous
organism. Antibiotic therapy can, however, cause superinfections such drug use.
as candidiasis due to elimination of normal body flora.
Provide educational materials on infective endocarditis from
• Teach about the function of heart valves and the effects of endo-
the American Heart Association. Refer as appropriate to home health
carditis on heart function. Include a simple definition of endocar-
or home intravenous therapy services. Refer the patient and family
ditis, and explain the risk for its recurrence. Information helps the
members or significant others as appropriate to a drug or substance
patient and family understand endocarditis, its treatment, and its ef-
abuse treatment program or facility. Provide follow-up care to ensure
fects. Understanding increases compliance.
compliance with the referral and treatment plan.
• Describe the manifestations of heart failure to be reported to the
physician. Evidence of heart failure may necessitate modification of
the treatment regimen or replacement of infected valves. The Patient with Myocarditis
• Stress the importance of notifying all care providers of valve dis- Myocarditis is inflammation of the heart muscle. It usually results
ease, heart murmur, or valve replacement before undergoing in- from an infectious process, but also may occur as an immunologic
vasive procedures. Invasive procedures provide a portal of entry for response, or due to the effects of radiation, toxins, or drugs. In the
bacteria. A history of valve disease increases the risk for the develop- United States, myocarditis is usually viral, caused by coxsackievirus
ment or recurrence of endocarditis. B. Approximately 10% of people with HIV disease develop myocardi-
• Encourage good dental hygiene and mouth care and regular den- tis due to infiltration of the myocardium by the virus. Bacterial myo-
tal checkups. Teach how to prevent bleeding from the gums and carditis, much less common, may be associated with endocarditis
avoid developing mouth ulcers (e.g., gentle tooth brushing, en- caused by Staphylococcus aureus, or with diphtheria. Parasitic infec-
suring that dentures fit properly, and avoiding toothpicks, dental tions caused by Trypanosoma cruzi (Chagas disease) are common in
floss, and high-flow water devices). The oropharynx harbors strep- Central and South America.
tococci, which are common causes of endocarditis. Bleeding gums of-
fer an opportunity for bacteria to enter the bloodstream. Incidence and Risk Factors
• Encourage the patient to avoid people with upper respiratory Myocarditis may occur at any age, and it is more common in men
infections. Streptococci are normal pathogens in the upper respira- than women. Factors that alter immune response (e.g., malnutrition,
tory tract; exposure to people with upper respiratory infections may alcohol use, immunosuppressive drugs, exposure to radiation, stress,
increase the risk of infection. and advanced age) increase the risk for myocarditis. It also is a com-
• If anticoagulant therapy is ordered, explain its actions, adminis- mon complication of rheumatic fever and pericarditis.
tration, and major side effects. Identify manifestations of bleed-
ing to be promptly reported to the physician. Patients with valve Pathophysiology
disease or a prosthetic valve following infective endocarditis may re- In myocarditis, myocardial cells are damaged by an inflammatory
quire continued anticoagulant therapy to prevent thrombi and em- process that causes local or diffuse swelling and damage. Infectious
boli. Knowledge is vital for appropriate management of anticoagulant agents infiltrate interstitial tissues, forming abscesses. Autoimmune
therapy and prevention of complications. injury may occur when the immune system destroys not only the
invading pathogen but also myocardial cells. The extent of damage
Delegating Nursing Care Activities to cardiac muscle ultimately determines the long-term outcome of
As appropriate and allowed by designated duties and responsibilities the disease. Viral myocarditis usually is self-limited; it may progress,
of assistive personnel, the nurse may delegate nursing care activities however, to become chronic, leading to dilated cardiomyopathy.
such as measuring fluid intake and output, collecting vital signs (in- Severe myocarditis may lead to heart failure.
cluding orthostatic vital signs), encouraging oral or enteral fluid in-
take, and ensuring nonpharmacologic skin care. Manifestations
The manifestations of myocarditis depend on the degree of myocar-
Continuity of Care dial damage. The patient may be asymptomatic. Nonspecific mani-
When preparing the patient with infective endocarditis for home festations of inflammation such as fever, fatigue, general malaise,
care, provide teaching as outlined for the nursing diagnosis Ineffective dyspnea, palpitations, arthralgias, and sore throat may be present. A
Health Maintenance. In addition, discuss the following topics: nonspecific febrile illness or upper respiratory infection often pre-
cedes the onset of myocarditis symptoms. Abnormal heart sounds
• Although serious and frightening, infective endocarditis can usu- such as muffled S1, an S3, murmur, and pericardial friction rub may
ally be treated effectively with intravenous antibiotics. be heard. In some cases, manifestations of myocardial infarction,
• The importance of promptly reporting any unusual manifesta- including chest pain, may occur.
tion, such as a change in vision, sudden pain, or weakness, so
that interventions to control complications can be promptly
implemented.
●◯● Interprofessional Care
• The rationale for all treatments and procedures. Myocarditis treatment focuses on resolving the inflammatory pro-
• Preventing recurrences of infective endocarditis. cess to prevent further damage to the myocardium.
946 Unit 8 • Responses to Altered Cardiovascular Function
Complications
Pericardial effusion, cardiac tamponade, and constrictive pericarditis Figure 31–8 • Cardiac tamponade. Note increased volume in
are possible complications of acute pericarditis. the right ventricle during inspiration in both the normal heart and
the heart affected by a pericardial effusion. In tamponade, fluid
Pericardial Effusion in the pericardial sac and the distended right ventricle restrict
A pericardial effusion is an abnormal collection of fluid between the filling of the left ventricle and, consequently, cardiac output.
pericardial layers that threatens normal cardiac function. The fluid
may consist of pus, blood, serum, lymph, or a combination. The
manifestations of a pericardial effusion depend on the rate at which inspiration. A drop in systolic blood pressure of more than 10 mmHg
the fluid collects. Although the pericardium normally contains about during inspiration also indicates pulsus paradoxus.
30 to 50 mL of fluid, the sac can stretch to accommodate a gradual ac- Other manifestations of cardiac tamponade include muffled
cumulation of fluid. Over time, the pericardial sac can accommodate heart sounds, dyspnea and tachypnea, tachycardia, a narrowed pulse
up to 2 L of fluid without immediate adverse effects. Conversely, a pressure, and distended neck veins (see the accompanying box).
rapid buildup of pericardial fluid (as little as 100 mL) does not allow
the sac to stretch and can compress the heart, interfering with myo- Chronic Constrictive Pericarditis
cardial function. This compression of the heart is known as cardiac Chronic pericardial inflammation can lead to scar tissue formation
tamponade. Slowly developing pericardial effusion is often painless between the pericardial layers. This scar tissue eventually contracts,
and has few manifestations. Heart sounds may be distant or muffled. restricting diastolic filling and elevating venous pressure. Constric-
The patient may have a cough or mild dyspnea. tive pericarditis may follow viral infection, radiation therapy, or heart
surgery. Its manifestations include progressive dyspnea, fatigue, and
Cardiac Tamponade weakness. Ascites is common; peripheral edema may develop. Neck
Cardiac tamponade is a medical emergency that must be aggressively veins are distended, and may be particularly noticeable during in-
treated to preserve life. Cardiac tamponade may result from pericar- spiration (Kussmaul’s sign). This occurs because the right atrium is
dial effusion, trauma, cardiac rupture, or hemorrhage. Rapid collec- unable to dilate to accommodate increased venous return during in-
tion of fluid in the pericardial sac interferes with ventricular filling spiration. See Figure 31–9 •.
and pumping, critically reducing cardiac output.
Classic manifestations of cardiac tamponade result from ris-
ing intracardiac pressures, decreased diastolic filling, and decreased MANIFESTATIONS OF CARDIAC TAMPONADE
cardiac output. A hallmark of cardiac tamponade is a paradoxical
pulse, or pulsus paradoxus. A paradoxical pulse markedly decreases • Paradoxical pulse
in amplitude during inspiration. Intrathoracic pressure normally • Narrowed pulse pressure, hypotension
• Tachycardia
drops during inspiration, enhancing venous return to the right heart. • Weak peripheral pulses
This draws more blood into the right side of the heart than the left, • Distant, muffled heart sounds
causing the interventricular septum to bulge slightly into the left • Jugular venous distention
ventricle. When ventricular filling is impaired by excess fluid in the • High central venous pressure
pericardial sac, this bulging of the interventricular septum decreases • Decreased level of consciousness
• Low urine output
cardiac output during inspiration (Figure 31–8 •). On palpation of • Cool, mottled skin
the carotid or femoral artery, the pulse is diminished or absent during
948 Unit 8 • Responses to Altered Cardiovascular Function
Medications
Drug treatment for pericarditis addresses its manifestations. Aspirin
and acetaminophen may be used to reduce fever. NSAIDs are used to
reduce inflammation and promote comfort. In severe cases or with
recurrent pericarditis, corticosteroids may be given to suppress the
inflammatory response.
Pericardiocentesis
Pericardiocentesis may be done to remove fluid from the pericardial
sac for diagnostic or therapeutic purposes (refer to Figure 29–18).
The physician inserts a large (16- to 18-gauge) needle into the peri-
cardial sac and withdraws excess fluid. The needle is attached to an
ECG monitoring lead to help determine if the needle is touching the
epicardial surface, which helps prevent piercing the myocardium.
Pericardiocentesis may be an emergency procedure for the patient
with cardiac tamponade. Nursing implications for pericardiocentesis
are outlined in the box on page 843 of Chapter 29.
Surgery
For recurrent pericarditis or recurrent pericardial effusion, a rectan-
gular piece of the pericardium, or “window,” may be excised to allow
collected fluid to drain into the pleural space. Constrictive pericardi-
tis may necessitate a partial or total pericardiectomy, removal of part
Figure 31–9 • Constrictive pericarditis. or all of the pericardium, to relieve the ventricular compression and
allow adequate filling.
●◯● Interprofessional Care
Care for the patient with pericarditis focuses on identifying its cause ●◯● Nursing Care
if possible, reducing inflammation, relieving symptoms, and prevent-
ing complications. The patient is closely monitored for early manifes- Health Promotion
tations of cardiac tamponade so that it can be treated promptly. Although it may not yet be possible to identify many patients at risk
for acute pericarditis or to prevent it, early identification and treat-
Diagnosis ment of the disorder can reduce the risk of complications. Promptly
There are no specific laboratory tests to diagnose pericarditis, but report a pericardial friction rub or other manifestations of pericardi-
tests are often performed to differentiate pericarditis from myocar- tis in patients with recent AMI, cardiac surgery, or systemic diseases
dial infarction. associated with a risk for pericarditis.
• CBC shows elevated WBCs and an ESR greater than 20 mm/h
Assessment
indicating acute inflammation.
• Cardiac enzymes may be slightly elevated because the inflamma- See the Manifestations and Interprofessional Care sections for the
tory process extends to involve the epicardial surface of the heart. assessment of the patient with pericarditis.
Cardiac enzymes are typically much lower in pericarditis than Assessment data to collect from the patient with suspected peri-
in myocardial infarction. carditis includes the following:
• Electrocardiography shows typical changes associated with peri- • Health history: complaints of acute substernal or precordial chest
carditis, such as diffuse ST-segment elevation in all leads. This pain, effect of movement and breathing on discomfort, pain ra-
resolves more quickly than changes of AMI and is not associ- diation, associated symptoms; recent AMI, heart surgery, or other
ated with the QRS-complex and T-wave changes typically seen in cardiac disorder; current medications; chronic conditions such as
MI. With a large pericardial effusion, the QRS amplitude may be renal failure or a connective tissue or autoimmune disorder
decreased. Atrial dysrhythmias may occur in acute pericarditis. • Physical assessment: vital signs including temperature, variation in
• Echocardiography is used to assess heart motion, for pericardial systolic BP with respirations; strength of peripheral pulses, varia-
effusion, and the extent of restriction. tions with respiratory movement; apical pulse, clarity, changes
• Hemodynamic monitoring may be used in acute pericarditis or peri- with respiratory movement, presence of a friction rub; neck vein
cardial effusion to assess pressures and cardiac output. Elevated distention; level of consciousness, skin color, and other indicators
pulmonary artery pressures and venous pressures occur with im- of cardiac output.
paired filling due to pericardial effusion or constrictive pericarditis.
• Chest x-ray may show cardiac enlargement if a pericardial effusion Priorities of Care
is present. Collaborating with the interprofessional team to ensure adequate
• Computed tomography (CT scan) or magnetic resonance imaging treatment of the underlying process while providing care that sup-
(MRI) may be used to identify pericardial effusion or constrictive ports the physical and psychologic responses to the disorder is a
pericarditis. priority of nursing care.
Chapter 31 • Nursing Care of Patients with Cardiac Disorders 949
Diagnoses, Outcomes, and Interventions complication can also occur with chronic pericardial effusion if the
Nursing care for the patient with pericarditis may occur in the acute amount of fluid exceeds the ability of the pericardial sac to expand.
or community setting. Closely observe for early manifestations of Constrictive pericarditis increases the risk for decreased cardiac out-
increasing effusion or cardiac tamponade. Priority nursing diagno- put because of restricted cardiac filling.
ses relate to comfort, the risk for tamponade, and effects of the acute Expected Outcome: Patient will demonstrate adequate cardiac output
inflammatory process. as evidenced by blood pressure and pulse rate and rhythm within
normal limits.
Acute Pain
• Document vital signs hourly during the acute inflammatory pro-
Inflamed pericardial layers rubbing against each other and the lung
pleura stimulate phrenic nerve pain fibers in the lower portion of the cesses. Frequent assessment allows early recognition of manifesta-
parietal pericardium. Pain is usually acute and may be severe until tions of decreased cardiac output, such as tachycardia, hypotension,
inflammation resolves. or changes in pulse pressure.
Expected Outcome: Patient will experience adequate pain control as SAFETY ALERT
evidenced by physical well-being.
Assess heart sounds and peripheral pulses, and observe for neck vein
• Assess chest pain using a standard pain scale and noting the quality distention and paradoxical pulse hourly. Promptly report distant, muf-
and radiation of the pain. Note nonverbal cues of pain (grimacing, fled heart sounds, new murmurs or extra heart sounds, decreasing
guarding behaviors), and validate with the patient. Careful assess- quality of peripheral pulses, and distended neck veins. Acute pericar-
ment helps identify the cause of pain. The pain of pericarditis may dial effusion interferes with normal cardiac filling and pumping, caus-
ing venous congestion and decreased cardiac output. As the amount
radiate to the neck or back and is aggravated by movement, coughing,
of fluid increases in the pericardial sac, heart sounds are obscured.
or deep breathing. A pain scale allows evaluation of the e ffectiveness A drop in systolic blood pressure of more than 10 mmHg on inspiration
of interventions. signifies an abnormal response to changes in intrathoracic pressure.
• Auscultate heart sounds every 4 hours. Presence of a pericardial
friction rub often correlates with the location and severity of the pain.
• Report significant changes or trends in hemodynamic parameters
• Administer NSAIDs on a regular basis as prescribed with food.
and dysrhythmias. Compression of the heart interferes with venous
Document effectiveness. NSAIDs reduce fever, inflammation, and
return, increasing CVP and right atrial pressures; dysrhythmias may
pericardial pain. They are most effective when administered around
also occur.
the clock on a consistent basis. Administering the medications with
• Promptly report other signs of decreased cardiac output: de-
food helps decrease gastric distress.
• Maintain a quiet, calm environment, and position of comfort.
creased level of consciousness; decreased urine output; cold,
clammy, mottled skin; delayed capillary refill; and weak periph-
Offer back rubs, heat/cold therapy, diversional activity, and
eral pulses. These signs of decreased organ and tissue perfusion indi-
emotional support. Supportive interventions enhance the effects of
cate a significant drop in cardiac output.
the medication, may decrease pain perception, and convey a sense
• Maintain at least one patent intravenous access site. The patient in
of caring.
cardiac tamponade may require rapid intravenous fluid infusion to
Ineffective Breathing Pattern restore blood volume and administration of emergency drugs to sup-
Respiratory movement intensifies pericardial pain. In an effort to de- port the circulation.
crease pain, the patient often breathes shallowly, increasing the risk • Prepare for emergency pericardiocentesis and/or surgery as neces-
for pulmonary complications. sary. Provide appropriate explanations and reassurance. Observe
for adverse responses during pericardiocentesis. Excess pericardial
• Document respiratory rate, effort, and breath sounds every 2 to fluid must be rapidly evacuated to prevent further compromise of car-
4 hours. Report adventitious or diminished breath sounds. Shal- diac output and death. Emotional support and explanations reduce
low, guarded respirations may lead to increased respiratory rate and the patient’s and family’s anxiety and promote a caring atmosphere.
effort. Poor ventilation of peripheral alveoli may lead to congestion or
atelectasis. Activity Intolerance
• Encourage deep breathing and use of the incentive spirometer. In chronic constrictive pericarditis, pericardial adhesions and scar-
Provide pain medication before respiratory therapy, as needed. ring restrict pericardial compliance, which in turn restricts heart
Deep breathing and an incentive spirometer promote alveolar ventila- filling and movement. Restricted filling and ineffective cardiac con-
tion and prevent atelectasis. Analgesia prior to respiratory treatments traction decrease the cardiac output. The heart cannot compensate
improves their effectiveness by decreasing guarding. for increased metabolic demands by increasing cardiac output, and
• Administer oxygen as needed. Supplementary oxygen promotes op- cardiac reserve falls significantly.
timal gas exchange and tissue oxygenation. Expected Outcome: Patient will participate in an activity program
• Place in Fowler’s or high-Fowler’s position. Assist to a position of without suffering any complications
comfort. Appropriate positioning reduces the work of breathing and
decreases chest pain due to pericarditis. • Document vital signs, cardiac rhythm, skin color, and temperature
before and after activity. Note any subjective complaints of fatigue,
Risk for Decreased Cardiac Output shortness of breath, chest pain, palpitations, or other symptoms
The acute inflammatory process of pericarditis can lead to significant with activity. These parameters help determine the response to in-
pericardial effusion and cardiac tamponade. This potentially fatal creased cardiac work. Increased heart rate and respiratory rate and
950 Unit 8 • Responses to Altered Cardiovascular Function
effort, decreased blood pressure, and dysrhythmias are indicators of Continuity of Care
activity intolerance. Pallor or cyanosis and cool, clammy, mottled Include the following topics when teaching the patient and family in
skin are signs of decreased tissue perfusion. Complaints of weakness, preparation for home care:
shortness of breath, fatigue, dizziness, or palpitations are further evi-
dence of activity intolerance. • The importance of continuing anti-inflammatory medications as
• Work with the patient and physical therapist to develop a realistic, ordered. Advise to take NSAIDs with food, milk, or antacids to
progressive activity plan. Monitor response. Encourage indepen- minimize gastric distress, and to notify the physician if unable to
dence, but provide assistance as needed. Patient involvement in tolerate the drug. Instruct to avoid aspirin or preparations con-
planning increases the likelihood of success, as well as the patient’s self- taining aspirin while taking NSAIDs because it may interfere with
esteem and sense of control. Promoting self-care provides additional activity.
control and independence and enhances self-image. Activity that sig- • Prescribed medications, including dose, desired and possible ad-
nificantly increases the heart rate (more than 20 bpm over resting) verse effects, and interactions with other drugs or food.
should be stopped and reassessed for intensity. • Monitoring weight twice weekly because NSAIDs may cause fluid
• Plan interventions and care activities to allow uninterrupted rest retention.
and sleep. This supports healing and restoration of physical and emo- • Maintaining fluid intake of at least 2500 mL/day to minimize the
tional health. risk of renal toxicity due to NSAID use.
• Measures to maintain activity restriction if ordered. Activity
Delegating Nursing Care Activities will be gradually increased once the inflammatory process has
resolved.
As appropriate and allowed by the designated duties and responsibili- • Manifestations of recurrent pericarditis, and the importance of
ties of unlicensed assistive personnel, the nurse may delegate nursing
reporting these manifestations promptly to the physician.
care activities such as measuring fluid intake and output, collecting
vital signs (including orthostatic vital signs), encouraging oral or en-
teral fluid intake, and ensuring nonpharmacologic skin care.
Physiology Review
The heart valves direct blood flow within and out of the heart. The
valves are fibroelastic tissue supported by a ring of fibrous tissue (the
annulus) that provides support.
The atrioventricular (AV) valves, the mitral (or bicuspid) valve
on the left and the tricuspid valve on the right, separate the atria
from the ventricles. These valves normally are fully open during di-
astole, allowing blood to flow freely from the atria into the ventricles.
Rising pressure within the ventricles at the onset of systole (contrac-
tion) closes the AV valves, creating the S1 heart sound (“lub”). The
leaflets of the AV valves are connected to ventricular papillary mus- A Thickened and B Retracted
cles by fibrous chordae tendineae. The chordae tendineae prevent the stenotic valve fibrosed valve
valve leaflets from bulging back into the atria during systole. leaflets openings
The semilunar valves, the aortic and pulmonic valves, sepa- Figure 31–10 • Valvular heart disorders. A, Stenosis of a heart
rate the ventricles from the great vessels. They open during systole, valve. B, An incompetent or regurgitant heart valve.
Chapter 31 • Nursing Care of Patients with Cardiac Disorders 951
volume. Because stenotic valves also do not close completely, some workload of the heart exceed its blood supply, causing ischemia and
backflow of blood occurs when the valve should be fully closed. chest pain. Eventually, necrosis occurs and functional muscle is lost.
Regurgitant valves (called insufficient or incompetent valves) do Contractile force, stroke volume, and cardiac output decrease. High
not close completely (Figure 31–10B). This allows regurgitation, or pressures on the left side of the heart are reflected backward into the
backflow of blood, through the valve into the area it just left. Regur- pulmonary system, causing pulmonary edema, pulmonary hyper-
gitation can result from deformity or erosion of valve cusps caused tension, and, eventually, right ventricular failure.
by the vegetative lesions of bacterial endocarditis, by scarring or tear- Valvular disorders interfere with the smooth flow of blood
ing from myocardial infarction, or by cardiac dilation. As the heart through the heart. The flow becomes turbulent, causing a murmur, a
enlarges, the valve annulus (supporting ring of the valve) is stretched, characteristic manifestation of valvular disease. Table 31–8 describes
and the valve edges no longer meet to allow complete closure. the murmurs associated with various types of valvular disorders.
Valvular disease causes hemodynamic changes both in front Blood forced through the narrowed opening of a stenotic valve
of and behind the affected valve. Blood volume and pressures are or regurgitated from a higher pressure chamber through an incom-
reduced in front of the valve, because flow is obstructed through a petent valve creates a jet stream effect (much like water spurting out
stenotic valve and backflow occurs through a regurgitant valve. By of a partially occluded hose opening). The physical force of this jet
contrast, volumes and pressures characteristically increase behind stream damages the endocardium of the receiving chamber, increas-
the diseased valve. These hemodynamic changes may lead to pulmo- ing the risk for infective endocarditis.
nary complications or heart failure. Higher pressures and compen- The higher pressures on the left side of the heart subject its valves
satory changes to maintain cardiac output lead to remodeling and (the mitral and aortic valves) to more stress and damage than those
hypertrophy of the heart muscle. on the right side of the heart (the tricuspid and pulmonic). Pulmonic
Stenosis increases the work of the chamber behind the affected valve disease is the least common of the valvular disorders.
valve as the heart attempts to move blood through the narrowed
opening. Excess blood volume behind regurgitant valves causes dila- Mitral Stenosis
tion of the chamber. In mitral stenosis, for example, the left atrium Mitral stenosis narrows the mitral valve, obstructing blood flow from
hypertrophies to generate enough pressure to open and deliver its the left atrium into the left ventricle during diastole. It is usually caused
blood through the narrowed mitral valve. Not all of the blood is de- by rheumatic heart disease or bacterial endocarditis; it rarely results
livered before the valve closes, leaving blood to accumulate in the left from congenital defects. It affects females more frequently (66%) than
atrium. This chamber dilates to accommodate the excess volume. males. Mitral stenosis is chronic and progressive.
Eventually, cardiac output falls as compensatory mechanisms In mitral valve stenosis, fibrous tissue replaces normal valve tis-
become less effective. The normal balance of oxygen supply and de- sue, causing valve leaflets to stiffen and fuse. Resulting changes in
mand is upset, and the heart begins to fail. Increased muscle mass blood flow through the valve lead to calcification of the valve leaf-
and size increase myocardial oxygen consumption. The size and lets. As calcium is deposited in and on the valve, the leaflets become
S1 S2
Aortic regurgitation Diastole (early) 3rd ICS, left sternal border Decrescendo, continuous
(LSB)
S2 S1
S1 S2
952 Unit 8 • Responses to Altered Cardiovascular Function
more rigid and narrow the opening further. As the valve leaflets be- right heart failure, including jugular venous distention, hepatomegaly,
come less mobile, the chordae tendineae fuse, thicken, and shorten. ascites, and peripheral edema, develop. Crackles may be heard in
Thromboemboli may form on the calcified leaflets. the lung bases. In severe mitral stenosis, cyanosis of the face and
The narrowed mitral opening impairs blood flow into the left extremities may be noted. Chest pain is rare but may occur.
ventricle, reducing end-diastolic volume and pressure, and decreas- On auscultation, a loud S1, a split S2, and a mitral opening snap
ing stroke volume. The narrowed opening also forces the left atrium may be heard. The opening snap reflects high left atrial pressure. The
to generate higher pressure to deliver blood to the left ventricle. This murmur of mitral stenosis occurs during diastole, and is typically a
leads to left atrial hypertrophy. The left atrium also dilates as ob- low-pitched, rumbling, crescendo–decrescendo sound. It is heard
structed blood flow increases its volume. As the resistance to blood best with the bell of the stethoscope in the apical region. It may be
flow increases, high atrial pressures are reflected back into the pul- accompanied by a palpable thrill (vibration).
monary vessels, increasing pulmonary pressures (Figure 31–11 •).
Complications Atrial dysrhythmias, particularly atrial fibril
Pulmonary hypertension increases the workload of the right ventricle,
lation, are common due to chronic atrial distention. Thrombi may form
causing it to dilate and hypertrophy. Eventually, heart failure occurs.
and subsequently embolize to the brain, coronary arteries, kidneys,
Manifestations Mitral stenosis may be asymptomatic or spleen, and extremities—potentially devastating complications.
cause severe impairment. Its manifestations depend on cardiac Women with mitral stenosis may be asymptomatic until preg-
output and pulmonary vascular pressures. Dyspnea on exertion nancy. As the heart tries to compensate for increased circulating vol-
(DOE) is typically the earliest manifestation. Others include cough, ume (30% more in pregnancy) by increasing cardiac output, left atrial
hemoptysis, frequent pulmonary infections such as bronchitis and pressures rise, tachycardia reduces ventricular filling and stroke vol-
pneumonia, paroxysmal nocturnal dyspnea, orthopnea, weakness, ume, and pulmonary pressures increase. Sudden pulmonary edema
fatigue, and palpitations. As the stenosis worsens, manifestations of and heart failure may threaten the lives of the mother and fetus.
Mitral Regurgitation
Mitral regurgitation or insufficiency allows blood to flow back into
the left atrium during systole because the valve does not close fully.
Rheumatic heart disease is a common cause of mitral regurgitation.
1 Men develop mitral regurgitation more frequently than women.
Degenerative calcification of the mitral annulus may cause mitral
3 regurgitation in older women. Processes that dilate the mitral an-
nulus or affect the supporting structures, papillary muscles, or the
chordae tendineae may cause mitral regurgitation (e.g., left ventricu-
lar hypertrophy and MI). Congenital defects also may cause mitral
regurgitation.
In mitral regurgitation, blood flows into both the systemic circu-
lation and back into the left atrium through the deformed valve dur-
ing systole. This increases left atrial volume (Figure 31–12 •). The left
atrium dilates to accommodate its extra volume, pulling the posterior
4 valve leaflet further away from the valve opening and worsening the
defect. The left ventricle dilates to accommodate its increased preload
and low cardiac output, further aggravating the problem.
5 Manifestations Mitral regurgitation may be asymptomatic
or cause symptoms such as fatigue, weakness, exertional dyspnea,
and orthopnea. In severe or acute regurgitation, manifestations of
left-sided heart failure develop, including pulmonary congestion
2 and edema. High pulmonary pressures may lead to manifestations of
right-sided heart failure.
The murmur of mitral regurgitation is usually loud, high
pitched, rumbling, and holosystolic (occurring throughout systole).
It is often accompanied by a palpable thrill and is heard most clearly
Blood flow
at the cardiac apex. It may be characterized as a cooing or gull-like
Reduced blood flow
sound or as having a musical quality.
Backward pressure against flow
1 1
3
2
heart disease is the cause, mitral valve deformity is also often present. output causes manifestations of left ventricular failure. Dyspnea
Rheumatic heart disease destroys aortic valve leaflets, with fibrosis on exertion, angina pectoris, and exertional syncope are classic
and calcification causing rigidity and scarring. In the older adult, cal- manifestations of aortic stenosis. Pulse pressure, an indicator of stroke
cific aortic stenosis may result from degenerative changes associated volume, narrows to 30 mmHg or less. Hemodynamic monitors show
with aging. Constant wear and tear on this valve can lead to fibrosis increased left atrial pressure and pulmonary artery wedge pressure, as
and calcification. Idiopathic calcific stenosis generally is mild and well as decreased stroke volume and cardiac output.
does not impair cardiac output. Aortic stenosis produces a harsh systolic murmur best heard
As aortic stenosis progresses, the valve annulus decreases in size, in the second intercostal space to the right of the sternum. This
increasing the work of the left ventricle to eject its volume through crescendo–decrescendo murmur is produced by turbulence of blood
the narrowed opening into the aorta. To compensate, the ventricle entering the aorta through the stenotic valve. A palpable thrill is of-
hypertrophies to maintain an adequate stroke volume and cardiac ten felt. The murmur may radiate to the carotid arteries. Ventricular
output (Figure 31–14 •). Left ventricular compliance also decreases. hypertrophy displaces the cardiac impulse to the left of the midcla-
The additional workload increases myocardial oxygen consumption, vicular line. As aortic stenosis progresses, S3 and S4 heart sounds
which can precipitate myocardial ischemia. Coronary blood flow may may be heard, indicating heart failure and reduced left ventricular
also decrease in aortic stenosis. As left ventricular end-diastolic pres- compliance.
sure increases because of reduced stroke volume, left atrial pressures As cardiac output falls, tissue perfusion decreases. Late in the
increase. These pressures also affect the pulmonary vascular system; disease, pulmonary hypertension and right ventricular failure de-
pulmonary vascular congestion and pulmonary edema may result. velop. Untreated, symptomatic aortic stenosis has a poor prognosis;
10% to 20% of these patients experience sudden cardiac death.
Course and Manifestations Aortic stenosis may be
asymptomatic for many years. As the disease progresses and
Aortic Regurgitation
compensation fails, usually between ages 50 and 70, obstructed cardiac
Aortic regurgitation, also called aortic insufficiency, allows blood to
flow back into the left ventricle from the aorta during diastole. It is
more common in males (75%) in its “pure” form; in females, it is com-
1 monly associated with coexisting mitral valve disease. Most aortic re-
gurgitation (67%) results from rheumatic heart disease. Other causes
include congenital disorders, infective endocarditis, blunt chest
trauma, aortic aneurysm, syphilis, Marfan syndrome, and chronic
3
hypertension.
In aortic regurgitation, thickened and contracted valve cusps,
scarring, fibrosis, and calcification impede complete valve closure.
Chronic hypertension and aortic aneurysm may dilate and stretch
5 the aortic valve opening, increasing the degree of regurgitation.
In aortic regurgitation, volume overload affects the left ventricle
as blood from the aorta adds to blood received from the atrium during
diastole. This increases diastolic left ventricular pressure. Increased
6
preload causes more forceful contractions and a high stroke volume
(Figure 31–15 •). With time, muscle cells hypertrophy to compen-
2 sate for increased cardiac work and afterload; eventually this hyper-
trophy compromises cardiac output and increases regurgitation.
High left-ventricular pressures increase left atrial workload
4
and pressure. This pressure is transmitted to the pulmonary vessels,
causing pulmonary congestion. The workload of the right ventricle
increases as a result, and right-sided heart failure may develop. Acute
aortic regurgitation from traumatic injury or infective endocarditis
causes a rapid decline in hemodynamic status from acute heart failure
and pulmonary edema, because compensatory mechanisms do not
Blood flow have time to develop.
Reduced blood flow Manifestations Aortic regurgitation may be asymptomatic
Backward pressure against flow for many years, even when severe. The increased stroke volume
may cause complaints of persistent palpitations, especially when
Figure 31–14 • Aortic stenosis. The narrowed aortic valve
orifice (1) decreases the left ventricular ejection fraction during
recumbent. A throbbing pulse may be visible in arteries of the neck;
systole (2) and cardiac output (3). The left ventricle hypertrophies the force of contraction may cause a characteristic head bob (Musset’s
(4). Incomplete emptying of the left atrium (5) causes backward sign) and shake the whole body. Other symptoms include dizziness
pressure through pulmonary veins and pulmonary hypertension. and exercise intolerance.
Elevated pulmonary artery pressure (6) causes right ventricular Fatigue, exertional dyspnea, orthopnea, and paroxysmal noctur-
strain. nal dyspnea are common in aortic regurgitation. Anginal pain may
Chapter 31 • Nursing Care of Patients with Cardiac Disorders 955
Priorities of Care
Collaborating with the interprofessional team to ensure adequate • Elevate the head of the bed. Administer supplemental oxygen as or-
treatment of the underlying process while providing care that sup- dered. These measures improve alveolar ventilation and oxygenation.
ports the physical and psychologic responses to the disorder is a pri- • Provide for physical, emotional, and mental rest. Physical and psy-
ority of nursing care. chologic rest decreases the cardiac workload.
• Administer prescribed medications as ordered to reduce cardiac
Diagnoses, Outcomes, and Interventions workload. Diuretics, ACE inhibitors, and direct vasodilators may be
Nursing priorities include maintaining cardiac output, managing prescribed to reduce fluid volume and afterload, reducing cardiac work.
manifestations of the disorder, teaching about the disease process Activity Intolerance
and its management, and preventing complications. Nursing care of Altered blood flow through the heart impairs delivery of oxygen and
the patient undergoing valve surgery is similar to that of the patient nutrients to the tissues. As the heart muscle fails and is unable to com-
having other types of open-heart surgery (refer to Chapter 30), with pensate for altered blood flow, tissue perfusion is further compromised.
increased attention to anticoagulation and preventing endocarditis. Dyspnea on exertion is often an early symptom of valvular disease.
Decreased Cardiac Output Expected Outcome: Patient will participate in physical activity as tolerated.
Nearly all valve disorders affect ventricular filling and/or emptying,
• Monitor vital signs before and during activities. A change in heart rate
reducing cardiac output. Stenosis of the AV valves impairs ventricular
of more than 20 bpm, a change of 20 mmHg or more in systolic BP, and
filling and increases atrial pressures. Regurgitation of these valves re-
complaints of dyspnea, shortness of breath, excessive fatigue, chest pain,
duces cardiac output as a portion of the blood in the ventricle regur-
diaphoresis, dizziness, or syncope may indicate activity intolerance.
gitates into the atria during systole. Stenosis of the semilunar valves
• Encourage self-care and gradually increasing activities as allowed
obstructs ventricular outflow to the great vessels; regurgitation allows
and tolerated. Provide for rest periods, uninterrupted sleep, and
blood to flow back into the ventricles, creating higher filling pres-
adequate nutritional intake. Gradual progression of activities avoids
sures. When compensatory measures fail, heart failure develops.
excessive cardiac stress. Encouraging self-care increases the patient’s
Expected Outcome: Patient will demonstrate adequate cardiac output self-esteem and sense of power. Adequate rest and nutrition facilitate
as evidenced by blood pressure and pulse rate and rhythm within healing, decrease fatigue, and increase energy reserves.
normal limits. • Provide assistance as needed. Suggest use of a shower chair, sitting
• Monitor vital signs and hemodynamic parameters, reporting while brushing hair or teeth, and other energy-saving measures.
changes from the baseline. A fall in systolic blood pressure and Reducing energy expenditure helps maintain a balance of oxygen sup-
tachycardia may indicate decreased cardiac output. Increasing pul- ply and demand.
monary artery and pulmonary wedge pressures may also indicate • Consult with a cardiac rehabilitation specialist or physical thera-
decreased cardiac output, causing increased congestion and pressure pist for in-bed exercises and an activity plan. In-bed exercises may
in the pulmonary vascular system. help improve strength.
• Discuss ways to conserve energy at home. Information provides
PRACTICE ALERT! practical ways to deal with activity limitations and empowers the
patient to manage these limitations.
Promptly report changes in level of consciousness; distended neck
veins; dyspnea or respiratory crackles; urine output less than 30 mL/h; Risk for Infection
cool, clammy, or cyanotic skin; diminished peripheral pulses; or slow Damaged and deformed valve leaflets and turbulent blood flow
capillary refill. These findings indicate decreased cardiac output and
through the heart significantly increase the risk of infective endocar-
impaired tissue and organ perfusion.
ditis. Invasive diagnostic and monitoring lines (e.g., cardiac catheter-
ization, hemodynamic monitoring) and disrupted skin with surgery
• Monitor intake and output; weigh daily. Report weight gain of also increase the risk of infection.
1.4 to 2.3 kg (3 to 5 lb) within 24 hours. Fluid retention is a com
Expected Outcome: The patient will exhibit effective infection man-
pensatory mechanism that occurs when cardiac output decreases;
agement as evidenced by skin integrity and body temperature within
1 kg (2.2 lb) of weight equals 1 L of fluid.
normal range.
• Restrict fluids as ordered. Fluid intake may be restricted to reduce car-
diac workload and pressures within the heart and pulmonary circuit. • Use aseptic technique for all invasive procedures. Invasive proce-
• Monitor oxygen saturation continuously and ABGs as ordered. dures breach the body’s protective mechanisms, potentially allowing
Report oxygen saturation less than 95% (or as specified) and bacteria to enter. Aseptic technique reduces this risk.
abnormal ABG results. Oxygen saturation levels and ABGs allow • Record temperature every 4 hours; notify physician if temperature
assessment of oxygenation. exceeds 38.5°C (100.5°F). Fever may be an early indication of infection.
Chapter 31 • Nursing Care of Patients with Cardiac Disorders 959
• Assess wounds and catheter sites for redness, swelling, warmth, To prepare the patient and family for home care, discuss the follow-
pain, or evidence of drainage. These signs of inflammation may ing topics:
signal infection.
• Management of symptoms, including any necessary activity
• Administer antibiotics as ordered. Ensure completion of the full
restrictions or lifestyle changes
course. Antibiotics are used to prevent and treat infection. Comple-
• The importance of adequate rest to prevent fatigue
tion of the full course of therapy prevents drug-resistant organisms
• Diet restrictions to reduce fluid retention and symptoms of heart
from multiplying.
failure
• Monitor WBC and differential. Notify physician of leukocytosis
• Information about prescribed medications, including purpose,
or leukopenia. A high WBC and increased percentage of immature
desired and possible adverse effects, scheduling, and possible
WBCs (bands) may indicate bacterial infection; a low WBC count
interactions with other drugs
may indicate an impaired immune response and increased suscepti-
• The importance of keeping follow-up appointments to monitor
bility to infection.
the disease and its treatment
• Notifying all healthcare providers about valve disease or surgery
Ineffective Protection
Anticoagulant therapy commonly is prescribed for patients with to facilitate prescription of prophylactic antibiotics before inva-
chronic atrial fibrillation, a history of emboli, and following valve sive procedures or dental work
• Manifestations to immediately report to the healthcare provider:
replacement surgery. Although chronic anticoagulant therapy de-
creases the risk of clots and emboli, it increases the risk for bleeding increasing severity of symptoms, especially of worsening heart
and hemorrhage. failure or pulmonary edema; signs of transient ischemic attacks
or other embolic events; evidence of bleeding, such as joint pain,
Expected Outcome: Patient will remain free of any evidence of new easy bruising, black and tarry stools, bleeding gums, or blood in
bleeding and take precautions to prevent bleeding.
the urine or sputum.
Pathophysiology
Delegating Nursing Care Activities The cardiomyopathies are categorized by their pathophysiology and
As appropriate and allowed by the designated duties and responsibili- presentation into three groups: dilated, hypertrophic, and restrictive.
ties of unlicensed assistive personnel, the nurse may delegate nursing Table 31–10 compares the causes, pathophysiology, manifestations,
care activities such as measuring fluid intake and output, collecting and management of the cardiomyopathies.
vital signs (including orthostatic vital signs), encouraging oral or
Dilated Cardiomyopathy
enteral fluid intake, and ensuring nonpharmacologic skin care.
Dilated cardiomyopathy is the most common type of cardiomyopathy,
accounting for 87% of cases (AHA, 2013). Dilated cardiomyopathy
Continuity of Care also is a common cause of heart failure, accounting for about one
For most patients, valvular disease is a chronic condition. The patient in three cases. It is primarily a disease of middle age males; African
has primary responsibility for managing the effects of the disorder. American males have a higher risk than Whites.
960 Unit 8 • Responses to Altered Cardiovascular Function
CASE STUDY & NURSING CARE PLAN A Patient with Mitral Valve Prolapse
Julie Snow, a 22-year-old college student, sees a nurse practitioner • Allow to verbalize feelings and share concerns about MVP.
at the college health clinic for a physical examination after experi- Encourage to attend an MVP support group meeting.
encing palpitations, fatigue, and a headache during midterm ex- • Discuss the prognosis for MVP, emphasizing that most patients
aminations. Ms. Snow tells Lakisha Johnson, FNP, “I’m scared that live normal lives using diet and lifestyle management.
something is wrong with me.” • Instruct to keep a weekly record of symptoms and their
During the past few months, Ms. Snow has had occasional pal- frequency for 1 month.
pitations that she describes as “feeling like my heart is doing flip- • Discuss lifestyle changes to manage symptoms: aerobic
flops.” Rarely, these palpitations have been accompanied by a sharp, exercise with warm-up and cool-down periods; maintaining
stabbing pain in her chest that lasts only a few seconds. She initially adequate fluid intake, especially during hot weather or exer-
attributed her symptoms to stress, but she is increasingly concerned cise; relaxation techniques (e.g., meditation, deep-breathing
because the “attacks” are becoming more frequent. Ms. Snow states exercises, music therapy, yoga, guided imagery, heat therapy,
that she has “always been healthy,” does not smoke, uses alcohol or progressive muscle relaxation) to perform daily; avoiding
socially, and exercises, albeit intermittently. Ms. Snow admits that she caffeine and crash diets; forming healthy eating habits.
has been drinking a lot of coffee and cola and eating a lot of junk • Teach about infective endocarditis risk and prevention with
food lately. prophylactic antibiotics. Encourage notifying dentist and other
healthcare providers of MVP before dental or any other invasive
Assessment procedures.
Ms. Johnson’s assessment of Ms. Snow documents the following:
height 168 cm (66 in.), weight 63.6 kg (140 lb), T 37.4°C (99.3°F), Evaluation
BP 118/64 mmHg, P 82 bpm, and R 18/min. Slightly anxious but in After several educational sessions at the college health clinic,
no acute distress. Systolic click and soft crescendo murmur grade II/ Ms. Snow verbalizes an understanding of MVP by explaining heart
VI noted on auscultation. Apical impulse at 5th ICS left MCL. Lungs valve function, listing common manifestations of MVP, and describ-
clear to auscultation. Review of remaining systems reveals no ap- ing indications of deteriorating heart function. She states she will
parent abnormalities. An ECG shows sinus rhythm with occasional report these manifestations to her cardiologist if they occur. She is
PACs. Based on the admission history, manifestations, and physical given a booklet on MVP for additional reading. She verbalizes un-
assessment, Ms. Johnson suspects mitral valve prolapse (MVP). derstanding of the risk of endocarditis, and states that she will notify
her doctors of her MVP and the need for antibiotics before invasive
Diagnoses procedures. Ms. Snow is attending a monthly MVP support group
• Anxiety related to fear of heart disease and implications for lifestyle (led by a cardiology clinical nurse specialist) on campus and states,
• Powerlessness related to unpredictability of symptoms “I am so glad to know I’m not alone! It really helps to know that
• Risk of Infection (endocarditis) related to altered valve function others are living well with MVP.” Her weekly symptom log shows
Expected Outcomes her symptoms are associated with late-night studying and drinking
• Patient will verbalize an understanding of MVP and its large amounts of coffee and cola. Ms. Snow has moderated her
management. caffeine intake and increased her fluids, relieving her symptoms.
• Patient will discuss ways to decrease or relieve MVP In addition, Ms. Snow is taking a relaxation music therapy class.
symptoms. Ms. Snow states that she realizes that she has “the ability to control
• Patient will acknowledge the risk for endocarditis and identify my life through the choices I make.”
precautions to prevent it. Clinical Reasoning in Patient Care
Planning and Implementation 1. Develop an action plan for Ms. Snow that outlines specific
• Consult with and refer to the cardiologist for continued monitor- activities she can use to manage symptoms of MVP.
ing and follow-up. 2. Why are patients with symptomatic MVP encouraged to
• Teach about MVP, including heart valve anatomy, physiology, include regular exercise in their health habits?
and function, common manifestations of MVP, and treatment 3. How does the support of family, friends, and other people with
rationale. MVP assist MVP patients in managing their condition?
• Discuss symptoms of progressive mitral regurgitation, and the 4. What manifestations would indicate a progressive worsening
need to report these to the cardiologist. of Ms. Snow’s mitral regurgitation?
• Discuss recommended follow-up care and its rationale. See Evaluating Your Response in Appendix B.
The cause of dilated cardiomyopathy is unknown, although it Manifestations and Course Manifestations of dilated
appears to frequently result from toxins, metabolic conditions, or cardiomyopathy develop gradually. Heart failure often presents
infection. Reversible dilated cardiomyopathy may develop due to al- years after the onset of dilation and pump failure. Both right- and
cohol and cocaine abuse, chemotherapeutic drug use, pregnancy, and left-sided failure occur, with dyspnea on exertion, orthopnea,
systemic hypertension. Up to 20% of cases of dilated cardiomyopathy paroxysmal nocturnal dyspnea, weakness, fatigue, peripheral
may be genetic in origin, most commonly transmitted in an autoso- edema, and ascites. Both S3 and S4 heart sounds are commonly heard,
mal dominant pattern, although autosomal recessive, X-linked, and as well as an AV regurgitation murmur. Dysrhythmias are common,
mitochondrial patterns of inheritance also are seen. including supraventricular tachycardias, atrial fibrillation, and
In dilated cardiomyopathy, heart chambers dilate and ventric- complex ventricular tachycardias. Untreated dysrhythmias can
ular contraction is impaired. Both end-diastolic and end-systolic lead to sudden death. Mural thrombi (blood clots in the heart wall)
volumes increase, and the left ventricular ejection fraction is substan- may form in the left ventricular apex and embolize to other parts of
tially reduced, decreasing cardiac output. Left ventricular dilation is the body.
prominent; left ventricular hypertrophy is usually minimal. The right The prognosis of dilated cardiomyopathy is grim; most patients
ventricle also may be enlarged. Extensive interstitial fibrosis (scar- get progressively worse and 50% die within 5 years after the diagnosis;
ring) is evident; necrotic myocardial cells also may be seen. 75% die within 10 years (AHA, 2013).
Chapter 31 • Nursing Care of Patients with Cardiac Disorders 961
Causes Usually idiopathic; may be secondary Hereditary; may be secondary to Usually secondary to amyloidosis,
to chronic alcoholism or myocarditis chronic hypertension radiation, or myocardial fibrosis
Pathophysiology Scarring and atrophy of myocardial Hypertrophy of ventricular muscle Excess rigidity of ventricular walls
cells mass restricts filling
Thickening of ventricular wall Small left ventricular volume Myocardial contractility remains
Dilation of heart chambers Septal hypertrophy may obstruct relatively normal
Impaired ventricular pumping left ventricular outflow
Increased end-diastolic and end- Left atrial dilation
systolic volumes
Mural thrombi common
Manifestations Heart failure Dyspnea, anginal pain, syncope Dyspnea, fatigue
Cardiomegaly Left ventricular hypertrophy Right-sided heart failure
Dysrhythmias Dysrhythmias Mild to moderate cardiomegaly
S3 and S4 gallop; murmur of mitral Loud S4 S3 and S4 heart sounds
regurgitation Sudden death Mitral regurgitation murmur
Management Management of heart failure Beta-blockers Management of heart failure
ICD as needed Calcium channel blockers Exercise restriction
Cardiac transplantation Antidysrhythmic agents
ICD, dual-chamber pacing
Surgical excision of part of the
ventricular septum
Hypertrophic Cardiomyopathy contractility. They may develop suddenly during or after physical
Hypertrophic cardiomyopathy is characterized by decreased compli- activity; in children and young adults, sudden cardiac death may
ance of the left ventricle and hypertrophy of the ventricular muscle be the first sign of the disorder. Hypertrophic cardiomyopathy is
mass. This impairs ventricular filling, leading to small end-diastolic the probable or definite cause of death in 36% of young athletes
volumes and low cardiac output. About half of all patients with hy- who die suddenly (AHA, 2013). It is hypothesized that sudden
pertrophic cardiomyopathy have a family history of the disease. It is cardiac death is due to ventricular dysrhythmias or hemodynamic
genetically transmitted in an autosomal dominant pattern. factors. Predictors of sudden cardiac death in this population
The pattern of left ventricular hypertrophy is unique in that the include age of less than 30 years, a family history of sudden death,
muscle may not hypertrophy equally. In a majority of patients, the in- syncopal episodes, severe ventricular hypertrophy, and ventricular
terventricular septal mass, especially the upper portion, increases to tachycardia seen on ambulatory ECG monitoring. For a brief
a greater extent than the free wall of the ventricle. The enlarged upper synopsis of a nursing research study regarding family presence
septum narrows the passageway of blood into the aorta, impairing during CPR and invasive procedures, see the Moving Evidence into
ventricular outflow. For this reason, this disorder is also known as id- Action box.
iopathic hypertrophic subaortic stenosis (IHSS) or hypertrophic obstruc- The usual manifestations of hypertrophic cardiomyopathy are
tive cardiomyopathy (HOCM). dyspnea, angina, and syncope. Angina may result from ischemia
due to overgrowth of the ventricular muscle, coronary artery abnor-
Manifestations and Course Hypertrophic cardiomyo malities, or decreased coronary artery perfusion. Syncope may occur
pathy may be asymptomatic for many years. Symptoms typically when the outflow tract obstruction severely decreases cardiac output
occur when increased oxygen demand causes increased ventricular and blood flow to the brain. Ventricular dysrhythmias are common;
962 Unit 8 • Responses to Altered Cardiovascular Function
atrial fibrillation also may develop. Other manifestations of hyper- and Chapter 30 for specific treatment strategies. Treatment of hy-
trophic cardiomyopathy include fatigue, dizziness, and palpitations. pertrophic cardiomyopathy focuses on reducing contractility and
A harsh, crescendo–decrescendo systolic murmur of variable inten- preventing sudden cardiac death. Strenuous physical exertion is
sity heard best at the lower left sternal border and apex is character- restricted, because it may precipitate dysrhythmias or sudden car-
istic in hypertrophic cardiomyopathy. An S4 may also be noted on diac death. Dietary and sodium restrictions may help diminish the
auscultation. manifestations.
vasodilators, and digitalis (see the previous section of this chapter). vasodilators, however, are avoided. If surgery is performed, nursing
Beta-blockers also may be used with caution in patients with di- care is similar to that for any patient undergoing open-heart s urgery
lated cardiomyopathy. Anticoagulants are given to reduce the risk or cardiac transplant. Discuss the genetic transmission of hyper-
of thrombus formation and embolization. Antidysrhythmic drugs trophic cardiomyopathy, and suggest screening of close relatives
are avoided if possible due to their tendency to precipitate further (parents and siblings).
dysrhythmias. Provide pre- and postoperative care and teaching as appro-
Beta-blockers are the drugs of choice to reduce anginal symp- priate for patients undergoing invasive procedures or surgery for
toms and syncopal episodes associated with hypertrophic cardiomy- cardiomyopathy.
opathy. The negative inotropic effects of beta-blockers and calcium Nursing diagnoses that may be appropriate for patients with car-
channel blockers decrease the myocardial contractility, decreasing diomyopathy include the following:
obstruction of the outflow tract. Beta-blockers also decrease heart
• Decreased Cardiac Output related to impaired left ventricular fill-
rate and increase ventricular compliance, increasing diastolic filling
ing, contractility, or outflow obstruction
time and cardiac output. Vasodilators, digitalis, nitrates, and diuret-
• Fatigue related to decreased cardiac output
ics are contraindicated. Amiodarone may be used to treat ventricular
• Ineffective Breathing Pattern related to heart failure
dysrhythmias.
• Fear related to risk for sudden cardiac death
Surgery • Ineffective Role Performance related to decreasing cardiac function
Without definitive treatment, patients with cardiomyopathy develop and activity restrictions
end-stage heart failure. Cardiac transplant is the definitive treatment • Anticipatory Grieving related to poor prognosis.
for dilated cardiomyopathy. Ventricular assist devices may be used
to support cardiac output until a donor heart is available. Transplan- Delegating Nursing Care Activities
tation is not a viable option for restrictive cardiomyopathy because
As appropriate and allowed by the designated duties and responsibili-
transplantation does not eliminate the underlying process causing in-
ties of unlicensed assistive personnel, the nurse may delegate nursing
filtration or fibrosis, and eventually the transplanted organ is affected
care activities such as measuring fluid intake and output, collecting
as well. See the section on heart failure for more information about
vital signs (including orthostatic vital signs), encouraging oral or
cardiac transplantation.
enteral fluid intake, and ensuring nonpharmacologic skin care.
In severely symptomatic patients with obstructive hypertrophic
cardiomyopathy, excess muscle may be surgically resected from the
aortic valve outflow tract. The septum is incised, and tissue is re- Continuity of Care
moved. This procedure provides lasting improvement in about 75% Cardiomyopathies are chronic, progressive disorders generally man-
of patients. aged in home and community care settings unless surgery or a trans-
An implantable cardioverter–defibrillator (ICD) often is inserted plant is planned or end-stage heart failure develops. When teaching
to treat potentially lethal dysrhythmias, reducing the need for antidys- the patient and family for home care, include the following topics:
rhythmic medications. A dual-chamber pacemaker also may be used
• Activity restrictions and dietary changes to reduce manifestations
to treat hypertrophic cardiomyopathy.
and prevent complications
• Prescribed drug regimen, its rationale, intended and possible
●◯● Nursing Care adverse effects
• The disease process, its expected ultimate outcome, and treatment
Nursing assessment and care for patients with dilated and restrictive
options
cardiomyopathy are similar to those provided to patients with heart
• Cardiac transplantation, including the procedure, the need for life-
failure. Teaching about the disease process and its management is vital.
time immunosuppression to prevent transplant rejection, and the
Some degree of activity restriction often is necessary; assist to conserve
risks of postoperative infection and long-term immunosuppression
energy while encouraging self-care. Support coping skills and adapta-
• Symptoms to report to the physician or for which immediate care
tion to required lifestyle changes. Provide information and support
is needed
for decision making about cardiac transplantation if that is an option.
• Cardiopulmonary resuscitation procedures and available training
Discuss the toxic and vasodilator effects of alcohol, and encourage
sites.
abstinence. See the Nursing Care section for heart failure earlier in this
chapter for nursing diagnoses and suggested interventions. Refer the patient and family for home and social services and coun-
The patient with hypertrophic cardiomyopathy requires care seling as indicated. Provide information about community resources
similar to that provided for myocardial ischemia; nitrates and other such as support groups or the AHA.
CHAPTER HIGHLIGHTS
• Heart failure is the most common cardiac disorder, a condi- and effective treatment to preserve life. The nurse’s role in manag-
tion in which the heart is unable to pump effectively to meet ing pulmonary edema focuses on supporting respiratory and car-
the body’s need to provide blood and oxygen to the tissues. diac function through careful assessment and early intervention,
• Heart failure is due to impaired myocardial contraction and administering prescribed medications, and providing reassurance
is most commonly caused by coronary heart disease and to the patient and family.
myocardial ischemia or infarct. • Inflammatory and infectious processes, such as rheumatic fever,
• Heart failure can also occur due to long-standing excessive workload endocarditis, myocarditis, and pericarditis, can affect any layer of
of the heart muscle such as in hypertension or valvular disorders. the heart. While some, such as myocarditis and pericarditis, typi-
• When the heart starts to fail, compensatory mechanisms are ac- cally are mild and self-limiting, others can have long-term effects
tivated to help maintain tissue perfusion. Although these mecha- on cardiac structure and function.
nisms, including increased contractile force, vasoconstriction, • Processes such as rheumatic heart disease, endocarditis, and
sodium and water retention, and remodeling of the heart, effec- congenital conditions can affect the structure and function of the
tively maintain cardiac output in the short term, in the long term heart valves, resulting in either stenosis (narrowing) of the valve
they hasten deterioration of heart function. and restricted flow through it, or regurgitation, backflow of blood
• Goals of heart failure management are to reduce the work- through a valve that does not fully close. The mitral and aortic
load and improve its function. Medical management includes valves are commonly affected due to the higher pressures and
medication use including ACE inhibitors, beta-blockers, di- increased workload of the left side of the heart.
uretics, and vasodilators to reduce the cardiac workload. • Valve disorders may be mild, producing a heart murmur but no
• As of 2009, the AHA guideline recommendation reflected that digi- functional impairment for the patient, or severe, causing symptoms
talis was no longer recommended as a first-line therapy due to the of heart failure even at rest. Repair or replacement of the valve may
risk for digitalis toxicity outweighing the benefit due to the narrow ultimately be required.
therapeutic window. • Cardiomyopathies affect the heart muscle and its ability to stretch
• Nursing care of the patient with heart failure is primarily sup- during filling and to contract effectively. Dilated cardiomyopathy,
portive and educative, providing the patient and family with the most common type, is progressive, ultimately necessitating
the necessary knowledge and resources to manage this heart transplant. Hypertrophic cardiomyopathy affects both ven-
chronic condition. tricular filling and outflow through the aortic valve. Surgical resec-
• Cardiogenic pulmonary edema, a manifestation of severe cardiac tion of excess tissue may relieve its manifestations.
decompensation, is a medical emergency, requiring immediate
964
Chapter 31 • Nursing Care of Patients with Cardiac Disorders 965
7. The nurse is planning care for a patient with acute infective 10. The parents of a young athlete who collapsed and died due
endocarditis. What would be an appropriate goal of nursing to hypertrophic cardiomyopathy ask how it is possible that
care for this patient? their son had no symptoms of this disorder before experiencing
1. Resume usual activities within 1 week of treatment. sudden cardiac death. How should the nurse respond to the
2. Relate the benign and self-limiting nature of the disease. parents?
3. Consider cardiac transplantation as a viable treatment option. 1. “It is likely that your son had symptoms of the disorder
4. State the importance of continuing intravenous antibiotic before he died, but he may not have thought them important
therapy as ordered. enough to tell someone about.”
8. The nurse is assessing heart sounds of a patient scheduled for 2. “In this type of cardiomyopathy, the ventricle does not fill
mitral valve replacement surgery. Which sound should the nurse normally. During exercise, the heart may not be able to meet
expect to auscultate in this patient? the body’s needs for blood and oxygen.”
1. cardiac heave 3. “Cardiomyopathy results in destruction and scarring of
2. muffled heart sounds cardiac muscle cells. As a result, the ventricle may rupture
3. S3 and S4 heart sounds during strenuous exercise, leading to sudden death.”
4. diastolic murmur heard at the apex 4. “Exercise causes the heart to contract more forcefully,
9. A patient considering heart valve replacement asks if a biologic and can lead to changes in the heart’s rhythm or the out-
or mechanical valve is better to use. How should the nurse re- flow of blood from the heart in people with hypertrophic
spond to the patient? cardiomyopathy.”
1. Biologic valves tend to be more durable than mechanical See Test Yourself answers in Appendix B.
valves.
2. The need to take drugs to prevent rejection of biologic tissue
is a major consideration.
3. Clotting is a risk with mechanical valves, necessitating
anticoagulant drug therapy after insertion.
4. Endocarditis is a risk following valve replacement that is
more easily treated with mechanical valves.
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