Heart Failure Nursing Care Management: A Study Guide

You will manage heart failure on almost every medical floor. It is the pump failing to move enough blood to meet the tissues' demand for oxygen and nutrients, and it shows up as fluid overload, poor perfusion, or both. Your priorities are recognizing decompensation early, managing volume, and protecting the patient from the side effects of the drugs that keep them out of the hospital.

What Is Heart Failure?

Heart failure (congestive heart failure) is a clinical syndrome of fluid overload or inadequate tissue perfusion. It signals myocardial disease with a problem in contraction (systolic dysfunction) or filling (diastolic dysfunction) that may or may not cause pulmonary or systemic congestion. It is usually a progressive, lifelong condition managed with lifestyle changes and medications to prevent episodes of acute decompensation.

Classification

Heart failure is left-sided or right-sided. In left-sided (left ventricular) failure, the left ventricle cannot pump blood effectively into the aorta and systemic circulation. Pulmonary venous volume and pressure rise, forcing fluid from the pulmonary capillaries into the tissues and alveoli, causing pulmonary interstitial edema and impaired gas exchange. In right-sided failure, congestion predominates in the peripheral tissues and viscera: the right ventricle cannot eject blood or accommodate all the venous return, so venous pressure rises, producing JVD and increased capillary hydrostatic pressure throughout the venous system.

The American College of Cardiology and American Heart Association stage heart failure:

• Stage A: high risk for left ventricular dysfunction but no structural heart disease or symptoms.
• Stage B: left ventricular dysfunction or structural heart disease without symptoms.
• Stage C: left ventricular dysfunction or structural heart disease with current or prior symptoms.
• Stage D: refractory end-stage heart failure requiring specialized interventions.

Pathophysiology

Heart failure follows cardiovascular conditions such as chronic hypertension, coronary artery disease, and valvular disease. As it develops, the body activates neurohormonal compensation. Systolic HF reduces the blood volume ejected from the ventricle. The sympathetic nervous system releases epinephrine and norepinephrine. Decreased renal perfusion triggers renin release, which promotes angiotensin I; ACE converts angiotensin I to angiotensin II, which constricts vessels and stimulates aldosterone release, causing sodium and fluid retention. Muscle fiber contractility falls as the workload rises, and the heart compensates by thickening the heart muscle.

Statistics

Like coronary artery disease, the incidence of HF rises with age. More than 5 million people in the United States have HF, with 550,000 new cases diagnosed each year per the American Heart Association. It is most common in people older than 75 years and is now considered epidemic in the United States. HF is the most common reason for hospitalization in people older than 65 years and the second most common reason for office visits. The estimated economic burden is more than $33 billion annually in direct and indirect costs and is still expected to rise.

HF affects both women and men, though mortality is higher among women. Death rates are higher in African Americans than in non-Hispanic whites at all ages. It is primarily a disease of older adults, affecting 6% to 10% of those older than 65, and is the leading cause of hospitalization in older people.

Causes

Atherosclerosis of the coronary arteries is the primary cause; coronary artery disease is found in more than 60% of HF patients. Ischemia deprives heart cells of oxygen and leads to acidosis from lactic acid accumulation. HF from cardiomyopathy is usually chronic and progressive. Systemic or pulmonary hypertension raises afterload, increasing the workload and causing hypertrophy of myocardial fibers. Valvular disease makes forward blood flow harder, raising intracardiac pressure and cardiac workload.

Clinical Manifestations

The manifestations of different HF types are similar, so they do not distinguish the types, but they track with the ventricle affected.

In left-sided HF, dyspnea may be triggered by minimal to moderate activity. The cough is initially dry and nonproductive. Bibasilar crackles appear early and, as it worsens, can be heard across all lung fields. Oxygen saturation may fall from increased pulmonary pressures.

In right-sided HF, the liver enlarges from venous engorgement, fluid accumulates in the peritoneal cavity and presses on the stomach and intestines (GI distress), and appetite drops from venous engorgement and stasis in the abdominal organs.

Prevention

Prevention is mostly lifestyle. Avoiding fatty and salty foods improves cardiovascular health. Cardiovascular exercise three times a week keeps the system running. Smoking cessation matters because nicotine causes vasoconstriction that raises vessel pressure.

Complications

Most HF therapy problems relate to diuretics. Excessive, repeated diuresis can cause hypokalemia, while ACE inhibitors, ARBs, or spironolactone can cause hyperkalemia. Prolonged diuretic therapy can cause hyponatremia, leading to disorientation, fatigue, apprehension, weakness, and muscle cramps. Volume depletion from excessive fluid loss can cause dehydration and hypotension.

Assessment and Diagnostic Findings

HF may go undetected until pulmonary and peripheral edema appear. The ECG may show hypertrophy, axis deviation, ischemia, damage patterns, dysrhythmias, and ST-T abnormalities. Chest x-ray may show an enlarged cardiac shadow or an abnormal contour suggesting ventricular aneurysm. Echocardiography (including Doppler and transesophageal) reveals chamber dimensions, valvular function and structure, and ventricular dilation and dysfunction. A MUGA heart scan measures cardiac volume, ejection fraction, and wall motion. Exercise or pharmacologic stress myocardial perfusion detects ischemia and wall motion abnormalities, and PET is a sensitive test for ischemia and viability. Cardiac catheterization assesses pressures, differentiates right- from left-sided failure, and evaluates coronary artery patency. Supporting labs include liver enzymes (elevated in liver congestion), digoxin and other cardiac drug levels (therapeutic range), bleeding and clotting times, electrolytes, pulse oximetry, ABGs, BUN/creatinine, serum albumin and transferrin, CBC, ESR, and thyroid studies.

Medical Management

The goals are to relieve symptoms, improve functional status and quality of life, and extend survival.

Pharmacologic therapy: ACE inhibitors slow HF progression, improve exercise tolerance, reduce hospitalizations, and promote vasodilation and diuresis by lowering afterload and preload. ARBs block angiotensin I conversion at the angiotensin II receptor, lowering blood pressure and systemic vascular resistance and improving cardiac output. Beta blockers reduce the harm of constant sympathetic stimulation. Diuretics remove excess extracellular fluid by increasing urine output in patients with fluid overload. Calcium channel blockers cause vasodilation and reduce systemic vascular resistance but are contraindicated in systolic HF.

Nutritional therapy: a low-sodium diet of 2 to 3 g/day reduces fluid retention, eases peripheral and pulmonary congestion, and lowers circulating volume and myocardial work. Compliance matters, since dietary indiscretion can drive severe exacerbations requiring hospitalization.

Additional therapy: supplemental oxygen is based on the degree of pulmonary congestion and hypoxia. Cardiac resynchronization therapy uses a biventricular pacemaker for electrical conduction defects. Ultrafiltration is an option for severe fluid overload. Cardiac transplant is the only option for long-term survival in some patients with end-stage disease.

Nursing Management

Despite treatment advances, HF morbidity and mortality remain high, and nurses have a major impact on outcomes through assessment, volume monitoring, medication management, and patient teaching.