I. Pathophysiology
a. Remodeling of the myocardium (as a structural response to
injury) changes the heart from an efficient football shape
to an inefficient basketball shape, making coordinated
contractility difficult.
i. Ventricular dilation (systolic dysfunction) results in poor
contractility and inadequate emptying of chamber.
ii. Ventricular stiffening (diastolic dysfunction) impairs
ability of chamber to relax and receive and eject blood.
b. Failure of the left and/or right chambers of the heart results
in insufficient output to meet metabolic needs of organ and
tissues.
c. Cardiac-related elevation of pulmonary or systemic venous
pressures leads to organ congestion.
d. Backward heart failure (HF): passive engorgement of the
veins caused by elevated systemic venous pressure or a
“backward” rise in pressure proximal to the failing cardiac
chambers (right ventricular failure)
e. Forward HF: decreased cardiac output with reduced forward
flow into the aorta, systemic circulation (inadequate renal
blood flow leads to sodium and water retention), and increasing
pulmonary venous pressure results in fluid accumulation
in alveoli (left ventricular failure)
f. Myocardial muscle dysfunction associated with left ventricular
hypertrophy (LVH) causes decreased cardiac output, activating
neurohormones.
g. Elevated circulating or tissue levels of neurohormones,
norepinephrine, angiotensin II, aldosterone, endothelin,
vasopressin, and cytokines, causes sodium retention and
peripheral vasoconstriction, increasing hemodynamic
stresses on the ventricle.
II. Classification
a. New York Heart Association Functional Classification
System for HF (9th ed, 1994)
i. Class I—normal physical activity is not limited by
symptoms.
ii. Class II—ordinary physical activity results in fatigue,
dyspnea, or other symptoms.
iii. Class III—marked limitation in normal physical
activity
iv. Class IV—symptoms at rest or with any physical
activity
b. American College of Cardiology/American Heart
Association (ACC/AHA) 2005 Guidelines include specific
recommendations for each stage (Hunt et al, 2005).
i. Stage A—high risk for HF associated with such conditions
as hypertension, diabetes, and obesity. Treatment is
focused on comorbidity.
ii. Stage B—presence of structural heart disease, such as
left ventricular remodeling, LVH, or previous myocardial
infarction (MI), but is asymptomatic. Treatment is
focused on retarding the progression of ventricular
remodeling and delaying the onset of HF symptoms.
iii. Stage C—clients with past or current HF symptoms
associated with structural heart disease, such as
advanced ventricular remodeling. Treatment is focused
on modifying fluid and dietary intake and drug therapies
as well as nonpharmacological measures, such as
biventricular pacing and valvular or revascularization
surgery.
iv. Stage D—refractory advanced HF symptoms at rest or
with minimal exertion and frequently requiring intervention
in the acute setting. Treatment is focused on promoting
clinical stability including supportive therapy to sustain
life, such as left ventricular assist device, continuous
intravenous (IV) inotropic therapy, experimental surgery
or drugs, a heart transplant, or end-of-life or hospice care.
III. Etiology
a. Multifactoral
i. Complex clinical syndrome resulting from any structural
or functional cardiac disorder that impairs the ability of
the ventricle to fill with or eject blood (ACC/AHA 2005
Guidelines; see Hunt et al, 2005).
ii. Risk factors and comorbidities—hypertension; obesity;
diabetes; coronary artery disease (CAD); peripheral and
cerebrovascular disease; valvular heart disease with onset
of atrial fibrillation (AF); sleep disorders such as sleep
apnea; history of exposure to cardiotoxins, for example,
chemotherapy, alcohol, and cocaine; family history of
cardiomyopathy
IV. Statistics
a. High morbidity and mortality, particularly in clients with
New York Heart Association Class IV symptoms (Hunt et
al, 2005)
b. Morbidity: 5.2 million Americans have HF. (National
Heart, Lung and Blood Institute [NHLBI], 2007)
i. Approximately 550,000 new cases reported annually
(Centers for Disease Control and Prevention [CDC],
2006b).
ii. 1.1 million hospitalizations reported annually (CDC,
2006b).
c. Mortality: 287,000 deaths reported annually (CDC, 2006b).
d. Cost: $29.6 billion spent in 2006, making HF the most
common reason for hospitalization of Medicare clients
(CDC, 2006b).
Care Setting
Although generally managed at the community level, an
in-client stay may be required for periodic exacerbation of
failure or development of complications.
Nursing Priorities
1. Improve myocardial contractility and systemic perfusion.
2. Reduce fluid volume overload.
3. Prevent complications.
4. Provide information about disease and prognosis, therapy
needs, and prevention of recurrences.
Discharge Goals
1. Cardiac output adequate for individual needs.
2. Complications prevented or resolved.
3. Optimum level of activity and functioning attained.
4. Disease process, prognosis, and therapeutic regimen
understood.
5. Plan in place to meet needs after discharge.
NURSING DIAGNOSIS: decreased Cardiac Output
May be related to
Altered myocardial contractility, inotropic changes
Alterations in rate, rhythm, electrical conduction
Structural changes, such as valvular defects and ventricular aneurysm
Possibly evidenced by
Increased heart rate (tachycardia), dysrhythmias, ECG changes
Changes in BP (hypotension, hypertension)
Extra heart sounds (S3, S4)
Decreased urine output
Diminished peripheral pulses
Cool, ashen skin and diaphoresis
Orthopnea, crackles, JVD, liver engorgement, edema
Chest pain
Desired Outcomes/Evaluation Criteria—Client Will
Cardiac Pump Effectiveness
Display vital signs within acceptable limits, dysrhythmias absent or controlled, and no symptoms of failure, for example,
hemodynamic parameters within acceptable limits and urinary output adequate.
Report decreased episodes of dyspnea and angina.
Cardiac Disease Self-Management
Participate in activities that reduce cardiac workload.
ACTIONS/INTERVENTIONS
Hemodynamic Regulation
Independent
Auscultate apical pulse; assess heart rate, rhythm, and document
dysrhythmia if telemetry available.
Note heart sounds.
Palpate peripheral pulses.
Monitor BP.
Inspect skin for pallor and cyanosis.
Monitor urine output, noting decreasing output and dark or
concentrated urine.
Note changes in sensorium, for example, lethargy, confusion,
disorientation, anxiety, and depression.
Encourage rest, semirecumbent in bed or chair. Assist with
physical care, as indicated.
Provide quiet environment, explain medical and nursing management,
help client avoid stressful situations, listen and
respond to expressions of feelings or fears.
Provide bedside commode. Have client avoid activities eliciting
a vasovagal response, for instance, straining during defecation
and holding breath during position changes.
Elevate legs, avoiding pressure under knee. Encourage active
and passive exercises. Increase ambulation and activity as
tolerated.
Check for calf tenderness; diminished pedal pulse; and
swelling, local redness, or pallor of extremity.
Withhold digoxin, as indicated, and notify physician if marked
changes occur in cardiac rate or rhythm or signs of digoxin
toxicity occur.
Collaborative
Administer supplemental oxygen, as indicated.
Administer medications, as indicated, for example:
Loop diuretics, such as furosemide (Lasix), ethacrynic acid
(Edecrin), and bumetanide (Bumex); thiazide and thiazidelike
diuretics, such as hydrocholorothiazide (HydroDiuril)
and metolazone (Zaroxolyn)
ACE inhibitors, such as benazepril (Lotensin), captopril
(Capoten), lisinopril (Prinivil), enalapril (Vasotec),
quinapril (Accupril), ramipril (Altace), and moexipril
(Univasc)
ARBs (also known as angiotensin II receptor antagonists),
such as candesartan (Atacand), losartan (Cozaar),
eprosartan (Teveten), ibesartan (Avapro), and valsartan
(Diovan)
Vasodilators, such as nitrates (Nitro-Dur, Isordil); arteriodilators
such as hydralazine (Apresoline); combination
drugs, such as prazosin (Minipress) and nesiritide
(Natrecor)
-adrenergic receptor antagonists (also called beta blockers),
such as carvedilol (Coreg), bisoprolol (Zebeta), and metoprolol
(Lopressor)
Digoxin (Lanoxin)
Inotropic agents, such as amrinone (Inocor), milrinone
(Primacor), and vesnarinone (Arkin-Z)
Aldosterone antagonist, such as eplerenone (Inspra)
Morphine sulfate
Anti-anxiety agents and sedatives
Anticoagulants, such as low-dose heparin and warfarin
(Coumadin)
Administer IV solutions, restricting total amount, as indicated.
Avoid saline solutions.
Monitor and replace electrolytes, as indicated.
Monitor serial ECG and chest x-ray changes.
Measure cardiac output and other functional parameters, as
indicated.
Prepare for insertion and maintain pacemaker or
pacemaker/defibrillator, if indicated.
Prepare for surgery, such as valve replacement, angioplasty,
coronary artery bypass grafting (CABG), as indicated:
Cardiomyoplasty
Transmyocardial revascularization
Assist with and maintain mechanical circulatory support
system, such as intra-aortic balloon pump (IABP) or leftventricular
assist device (LVAD), when indicated.
RATIONALE
Tachycardia is usually present, even at rest, to compensate for
decreased ventricular contractility. Premature atrial contractions
(PACs), paroxysmal atrial tachycardia (PAT), PVCs,
multifocal atrial tachycardia (MAT), and AF are common
dysrhythmias associated with HF, although others may also
occur. Note: Intractable ventricular dysrhythmias unresponsive
to medication suggest ventricular aneurysm.
S1 and S2 may be weak because of diminished pumping
action. Gallop rhythms are common (S3 and S4), produced
as blood flows into noncompliant, distended chambers.
Murmurs may reflect valvular incompetence and stenosis.
Decreased cardiac output may be reflected in diminished radial,
popliteal, dorsalis pedis, and post-tibial pulses. Pulses may
be fleeting or irregular to palpation, and pulsus alternans
may be present.
In early, moderate, or chronic HF, BP may be elevated because
of increased SVR. In advanced HF, the body may no longer
be able to compensate, and profound or irreversible
hypotension may occur. Note: Many clients with HF have
consistently low systolic BP (80 to 100 mm Hg) due to their
disease process and the medications they take, and most
tolerate these BPs without incident (Wingate, 2007).
Pallor is indicative of diminished peripheral perfusion secondary
to inadequate cardiac output, vasoconstriction, and
anemia. Cyanosis may develop in refractory HF. Dependent
areas are often blue or mottled as venous congestion
increases.
Kidneys respond to reduced cardiac output by retaining water
and sodium. Urine output is usually decreased during the
day because of fluid shifts into tissues, but may be
increased at night because fluid returns to circulation when
client is recumbent.
May indicate inadequate cerebral perfusion secondary to
decreased cardiac output.
Physical rest should be maintained during acute or refractory
HF to improve efficiency of cardiac contraction and to
decrease myocardial oxygen consumption and workload.
Physical and psychological rest helps reduce stress, which can
produce vasoconstriction, elevating BP and increasing heart
rate and work.
Commode use decreases work of getting to bathroom or
struggling to use bedpan. Vasovagal maneuver causes
vagal stimulation followed by rebound tachycardia, which
further compromises cardiac function and output.
Decreases venous stasis and may reduce incidence of thrombus
and embolus formation.
Reduced cardiac output, venous pooling and stasis, and
enforced bedrest increases risk of thrombophlebitis.
Incidence of toxicity is high (20%) because of narrow margin
between therapeutic and toxic ranges. Digoxin may have to
be discontinued in the presence of toxic drug levels, a slow
heart rate, or low potassium level. (Refer to CP:
Dysrhythmias; ND: risk for Poisoning: digoxin toxicity.)
Increases available oxygen for myocardial uptake to combat
effects of hypoxia and ischemia.
A variety of medications (usually a combination of a
diuretic, an ACEI, or ARB and beta blocker) may be used
to increase stroke volume, improve contractility, and
reduce congestion.
Diuretics, in conjunction with restriction of dietary sodium and
fluids, often lead to clinical improvement in clients with
stages I and II HF. In general, type and dosage of diuretic
depend on cause and degree of HF and state of renal function.
Preload reduction is most useful in treating clients with
a relatively normal cardiac output accompanied by congestive
symptoms. Loop diuretics block chloride reabsorption,
thus interfering with the reabsorption of sodium and water.
ACE inhibitors represent first-line therapy to control HF by
decreasing ventricular filling pressures and SVR, while
increasing cardiac output with little or no change in BP and
heart rate.
Antihypertensive and cardioprotective effects are attributable
to selective blockade of AT1 (angiotensin II) receptors and
angiotensin II synthesis. Note: ARBs used in combination
with ACE inhibitors and beta blockers are thought to have
decreased hospitalizations for HF clients.
Vasodilators are used to increase cardiac and renal output,
reducing circulating volume (preload and afterload), and
decreasing SVR, thereby reducing ventricular workload.
Note: Nesiritide is used in acutely decompensated congestive
HF and has been used with digoxin, diuretics, and ACE
inhibitors. Parenteral vasodilators are reserved for clients
with severe HF or those unable to take oral medications.
Useful in the treatment of HF by blocking the cardiac effects of
chronic adrenergic stimulation. Many clients experience
improved activity tolerance and EF.
Increases force of myocardial contraction when diminished
contractility is the cause of HF and slows heart rate by
decreasing conduction velocity and prolonging refractory
period of the atrioventricular (AV) junction to increase cardiac
efficiency and output.
These medications are useful for short-term treatment of HF
unresponsive to cardiac glycosides, vasodilators, and diuretics
in order to increase myocardial contractility and produce
vasodilation. Positive inotropic properties have reduced
mortality rates (by 50%) and improved quality of life.
Approved by the Food and Drug Administration (FDA) in 2003,
eplerenone has been shown to improve survival in HF,
especially following MI.
Decreases vascular resistance and venous return, reducing
myocardial workload, especially when pulmonary congestion
is present.
Allays anxiety and breaks the feedback cycle of anxiety to
catecholamine release to anxiety. Promotes rest and relaxation,
reducing oxygen demand and myocardial workload.
May be used prophylactically to prevent thrombus and embolus
formation in the presence of risk factors, such as venous
stasis, enforced bedrest, cardiac dysrhythmias, and history
of previous thrombolic episodes.
Because of existing elevated left ventricular pressure, client
may not tolerate increased fluid volume (preload). Clients
with HF also excrete less sodium, which causes fluid retention
and increases myocardial workload.
Fluid shifts and use of diuretics can alter electrolytes (especially
potassium and chloride), which affect cardiac rhythm and
contractility.
ST-segment depression and T-wave flattening can develop
because of increased myocardial oxygen demand, even if
no CAD is present. Chest x-ray may show enlarged heart
and changes of pulmonary congestion.
Cardiac index, preload and afterload, contractility, and cardiac
work can be measured noninvasively by using thoracic
electrical bioimpedance (TEB) technique. TEB is useful in
determining effectiveness of therapeutic interventions and
response to activity.
May be necessary to correct bradydysrhythmias unresponsive
to drug intervention, which can aggravate congestive
failure and produce pulmonary edema. Note: Biventricular
pacemaker and cardiac defibrillators are designed to provide
resynchronization for the heart by simultaneous electrical
activation of both the right and left sides of the heart,
thereby creating a more effective and efficient pump.
HF due to ventricular aneurysm or valvular dysfunction may
require aneurysmectomy or valve replacement to improve
myocardial contractility and function. Revascularization of
cardiac muscle by CABG may be done to improve cardiac
function.
Cardiomyoplasty, an experimental procedure in which the
latissimus dorsi muscle is wrapped around the heart and
electrically stimulated to contract with each heartbeat, may
be done to augment ventricular function while the client is
awaiting cardiac transplantation or when transplantation is
not an option.
Other new surgical techniques include transmyocardial revascularization,
such as percutaneous transmyocardial revascularization
(PTMR), using CO2 laser technology, in which a
laser is used to create multiple 1-mm-diameter channels in
viable but underperfused cardiac muscle.
An IABP may be inserted as a temporary support to the failing
heart in the critically ill client with potentially reversible HF.
A battery-powered LVAD may also be used positioned
between the cardiac apex and the descending thoracic or
abdominal aorta. This device receives blood from the left
ventricle and ejects it into the systemic circulation, often
allowing client to resume a nearly normal lifestyle while
awaiting heart transplantation, or in some instances,
allowing the heart to recover and regain its function. With
end-stage HF, cardiac transplantation may be indicated.
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