Congestive Heart Failure (CHF) Nursing Care Plan & Management

Description
  • Congestive Heart Failure or CHF is a severe circulatory congestion due to decreased myocardial contractility, which results in the heart’s inability to pump sufficient blood to meet the body’s needs.
  • About 80% of CHF cases occur before 1 year of age
Etiology
  1. The primary cause of CHF in the first 3 years of life is CHD.
  2. Other causes in children include:
    • Other myocardial disorders, such as cardiomyopathies, arrhythmias, and hypertension
    • Pulmonary embolism or chronic lung disease
    • Severe hemorrhage or anemia
    • Adverse effects of anesthesia or surgery
    • Adverse effects of transfusions or infusions
    • Increased body demands resulting from conditions such as fever, infection and arteriovenous fistula
    • Adverse effects of drugs, such as doxorubicin
    • Severe physical or emotional stress
    • Excessive sodium intake
  3. In general, causes can be classified according to the following:
    • Volume overload may cause the right ventricle to hypertrophy to compensate for added volume.
    • Pressure overload usually results from an obstructive lesion, such as COA
    • Decrease contractility can result from problems such as sever anemia, asphyxia, heart block and acidemia.
    • High cardiac output demands occur when the body’s need for oxygen exceeds the heart’s output s seen in sepsis and hyperthyroidism.
Pathophysiology
  • Right ventricular failure occurs when the right ventricle is unable to pump blood into the pulmonary circulation. Less blood is oxygenated and pressure increases in the right atrium and systemic venous circulation, which results in edema of the extremities.
  • Left ventricular failure occurs when the left ventricle in unable to pump blood into systemic circulation. Pressure increases in the left atrium and pulmonary veins; then the lungs become congested with blood, causing elevated pulmonary pressure and pulmonary edema.
  • To compensate, the cardiac muscle hypertrophies eventually resulting in decreased ventricular compliance. Decreased compliance requires higher filling pressure to produce the same stroke volume. Increased muscle mass impedes oxygenation of the heart muscle, which leads to decreased contraction force and heart failure.
  • As cardiac output fails, stretch receptors and baroreceptors stimulate the sympathetic nervous system, releasing catecholamines that increase the force and rate of myocardial contraction.
  • This causes increased systemic resistance, increased venous return, and reduced blood flow to the limbs, viscera and kidneys.
  • Sweating results from sympathetic cholinergic fibers, there is extra work for the heart muscle, and there is less systemic blood flow.
  • The renal system responds by releasing renin-angiotensin, which sets off a chain of events – vasoconstriction, leading to increased aldosterone release, causing sodium and water retention and, in turn, increasing preload. Finally, sodium and water retention becomes excessive, resulting in signs of systemic venous congestion and fluid overload.
Assessment
  1. Right ventricular failure
    • Signs of right ventricular failure are evident in the systemic circulation
    • Pitting, dependent edema in the feet, legs, sacrum, back, and buttocks
    • Ascites from portal hypertension
    • Tenderness of right upper quadrant, organomegaly
    • Distended neck veins
    • Pulsus alternans (regular alteration of weak and strong beats noted in the pulse)
    • Abdominal pain, bloating
    • Anorexia, nausea
    • Fatigue
    • Weight gain
    • Nocturnal diuresis
  2. Left ventricular failure
    • Signs of left ventricular failure are evident in the pulmonary system
    • Cough, which may become productive with frothy sputum
    • Dyspnea on exertion
    • Orthopnea
    • Paroxysmal nocturnal dyspnea
    • Presence of crackles on auscultation
    • Tachycardia
    • Pulsus alternans
    • Fatigue
    • Pallor
    • Cyanosis
    • Confusion and disorientation
    • Signs of cerebral anoxia
  3. Acute pulmonary edema
    • Severe dyspnea and orthopnea
    • Pallor
    • Tachycardia
    • Expectoration of large amounts of blood-tinged, frothy sputum
    • Wheezing and crackles on auscultation
    • Bubbling respirations
    • Acute anxiety, apprehension, restlessness
    • Profuse sweating
    • Cold, clammy skin
    • Cyanosis
    • Nasal flaring
    • Use of accessory breathing muscles
    • Tachypnea
    • Hypocapnia, evidenced by muscle cramps, weakness, dizziness, and paresthesias
Diagnostic Evaluation
  1. Chest radiography reveals cardiomegaly and pulmonary congestion
  2. CBC reveals dilution hyponatremia, hypochloremia, and hyperkalemia
  3. ECG reveals ventricular hypertrophy
Primary Nursing Diagnosis
  • Decreased CO related to an ineffective ventricular pump
Medical Management
  • Initial management of the patient with HF depends on severity of HF, seriousness of symptoms, etiology, presence of other illnesses, and precipitating factors. Medication management is paramount in patients with HF. The general principles for management are treatment of any precipitating causes, control of fluid and sodium retention, increasing myocardial contractility, decreasing cardiac workload, and reducing pulmonary and systemic venous congestion. The physician may also prescribe fluid and sodium restriction in an attempt to reduce volume and thereby reduce preload.