Heart failure—a syndrome characterized by poor tissue perfusion and signs of fluid overload—often occurs when the heart can no longer pump adequately to supply the tissues with the needed oxygen and nutrients after its compensatory mechanism is exhausted. As a result, decreased cardiac output (COP) and myocardial dysfunction may lead to vascular congestion, a condition also known as congestive heart failure (CHF).

Heart failure can be related to problems with heart contraction (systolic dysfunction) or heart filling (diastolic dysfunction), among others, and may occur with or without congestion. The underlying mechanism can be complex. In heart failure caused by systolic dysfunction, the ventricular contraction may be weakened with decreased cardiac output and ejection fraction; in heart failure caused by diastolic dysfunction, the ventricular filling is inadequate, possibly due to heart muscle being stiff and noncompliant. Heart failure can be associated with a variety of conditions, including myocardial infarction, long-standing hypertension, and coronary artery or other cardiovascular diseases.

The following major factors all affect cardiac output:

• Preload: the volume of blood in the ventricles at the end of diastole (when the heart dilates and fills with blood), which is related to the degree of heart muscle stretch
• Afterload: the resistance the left ventricle has to pump against
• Myocardial contractility: the force with which left ventricular ejection occurs (with systole)
• Heart rate
• Metabolic state

The symptoms of heart failure are often related to the side of the heart that fails. In many cases, however, heart failure (due to systolic or diastolic dysfunction) affects both sides of the heart, as each side depends on the adequate function of the other. Left-sided heart failure, involving congestion in the lungs, often presents with the following respiratory problems:

• Crackles of cardiac origin, which do not clear with coughing
• A dry, nonproductive cough
• Shortness of breath, decreased oxygen saturation rate, and signs of inadequate tissue perfusion
• Nocturia (possibly due to improved renal perfusion as a result of reduced cardiac workload during resting period)

Right-sided heart failure may occur secondary to left-sided heart failure, with manifestations of systemic fluid retention (as well as the respiratory symptoms):

• Weight gain
• Oliguria (decreased urine output)
• Hypertension
• Dependent edema, evident in the sacral area in bedridden patients
• Jugular vein distension (JVD), an indication of elevated venous pressure and failure of the heart as a pump

The earliest signs of heart failure may include:

• Increased heart rate (when the sympathetic nervous system is activated by a decrease in cardiac output)
• Fatigue due to decreased blood flow to the vital organs

1. Follow cardiac care protocols, which are usually updated on a regular basis depending on new theories, discoveries, or technologies. Perform comprehensive assessments, including taking vital signs, recording weight and fluid intake/output, observing activity tolerance, and assessing the severity of dyspnea by determining how many pillows the patient uses to sleep at night.
2. Alleviating pain and anxiety is important to reduce oxygen consumption. Supplemental oxygen should be given as indicated.
3. An upright position facilitates breathing. Placing a patient with heart failure who is experiencing difficulty breathing in a sitting position first, if possible, can reduce the heart's workload by decreasing the venous return and maximizing lung expansion, thereby decreasing pulmonary congestion. Elevating the patient's legs is not encouraged at this time, because increased venous return can worsen pulmonary congestion.
4. Assess for early signs of pulmonary edema, a common and serious complication of heart failure, such as increased heart rate and crackles. Monitor hemodynamic status; record daily weight, the extent of pitting edema, and abdominal girth.
5. Short-term nursing goals may include improved activity tolerance, such as being able to perform daily self-care routines or walking a short distance without dyspnea or air hunger.
6. Table salt and fluid intake may be restricted to manage fluid retention. If so ordered, the goal is to minimize water retention.
7. If a patient with heart failure suddenly develops severe edema in the lower extremities, reviewing the prior intake/output and weight record may help identify a sudden weight gain. This development may be a tell-tale sign of worsening cardiac functioning, indicating a need to adjust the treatment regimen or medication.

1. Angiotensin-converting enzyme (ACE) inhibitors, such as enalapril (Vasotec) and lisinopril (Prinivil/Zestril), can lower blood pressure by suppressing the renin‒angiotensin‒aldosterone system, decreasing secretion of aldosterone, and inhibiting conversion of angiotensin I to angiotensin II (a potent vasoconstrictor). When one of these agents is prescribed for management of heart failure (or for other uses), teach patients the measures to minimize its hypotensive effect. Sitting on the side of the bed and rising slowly before standing may help restore equilibrium and prevent dizziness. If an excessive decrease in blood pressure occurs, to offset the hypotensive effect, have the patient lie supine with the legs elevated, if appropriate.
2. When patients receive beta-adrenergic blockers, such as carvedilol (Coreg), watch for bradycardia as well as hypotension and dizziness, among other adverse effects. Check blood pressure and apical pulse before administering the medication.
3. Digoxin (Lanoxin) can increase the force of heart contraction and slow the heartbeat. It has a narrow therapeutic range. Before administering digoxin, it is essential to determine the patient's apical pulse rate, which is more accurately assessed with a stethoscope over the heart's apex (the pointed part) at the left fifth intercostal space (space between the ribs) in the midclavicular line. Digoxin should be withheld if pulse is less than 60 per minute, or as per protocol/order.
4. Digoxin toxicity may be manifested by GI upset (e.g., nausea, vomiting, or anorexia), neurologic problems (e.g., headache, weakness, and confusion), or visual disturbances (e.g., seeing greenish-yellow halos). Digoxin immune FAB (DigiFab) is an antidote in potentially life-threatening cases of digoxin toxicity.

1. Potassium-depleting diuretics, such as furosemide (Lasix), may cause potassium (and other electrolytes such as sodium or chloride) to be excreted in urine, causing hypokalemia. A patient's complaints of leg cramping and muscle twitching—signs of hypokalemia—should prompt the nurse to check the patient's serum potassium level and report low levels to the practitioner. Potassium, a major intracellular electrolyte, has a significant effect on both skeletal and cardiac muscle activities. Severe hypokalemia can lead to dysrhythmia and cardiac or respiratory arrest. (Hypokalemia may also predispose patients to digoxin toxicity.) Carefully observe the furosemide administration rate (without exceeding it) to prevent acute hypotensive episode and ototoxicity. Supplemental potassium is frequently prescribed along with furosemide. Some foods are naturally rich in potassium, such as bananas, orange juice, and potatoes.
2. Patients on potassium-sparing diuretics, such as spironolactone (Aldactone), should be monitored for signs of hyperkalemia (high potassium level), including GI discomfort, muscle twitching, flaccidity, dysrhythmia, or cardiac arrest, especially when patients already have renal insufficiency. Advise these patients to avoid using a potassium-containing salt substitute.