Congestive heart failure
Definition and Origin
Congestive Heart Failure (CHF) is the most universally acquired heart disease in children. It most frequently occurs as a result of a congenital heart disorder or a disease such as Kawasaki disease, rheumatic fever, or infectious endocarditis. When the myocardium of the heart cannot pump and circulate adequate blood to bring in oxygen and nutrients to body cells, CHF occurs. A deluge of blood collects in the heart (excessive preload) or in the pulmonary venous systems. Etiology
CHF may happen as a result of a congenital defect
efficacy of the heart’s pumping action, or it may result from cardiac surgery or rheumatic fever, when the myocardium is weakened. Severe anemia, hypocalcemia, and myocarditis may play a role in the heart’s failure to operate efficiently. CHF most commonly occurs in children under 1 year of age. The heart can counteract the effects of CHF with the use of various regulatory mechanisms to move blood forward and attempt to increase cardiac output. The muscle fibers can lengthen, which triggers the ventricles to expand and handle more blood with each heart stroke (ventricular hypertrophy). The number of beats per minute can also increase. As long as these methods allow for sufficient cardiac output, the signs of heart failure are not apparent. Nonetheless, the heart’s aptitude for compensation is limited, predominantly in infants, an age group in which hypertrophy is restricted. Eventually, in children of all ages, the heart can no longer compensate and the heart becomes plagued by the amount of blood present, which cannot be pushed forward effectively. As blood flow to the kidneys decreases, the glomerular filtration rate slows, resulting in stimulation of the renin-angiotensin system, which causes fluid and sodium retention. Aldosterone secretion by the adrenal glands further promotes sodium retention in an attempt to increase blood flow to the kidneys. Antidiuretic hormone secretion by the pituitary is also increased to help retain fluid. Sympathetic nervous system stimulation causes the frequently seen symptoms of excessive sweating and pallor.
Signs and Symptoms
Tachycardia is one of the earliest signs of CHF as the heart attempts to beat faster to move blood forward more effectively; tachypnea soon follows. When a child has primary right heart failure, increased venous back pressure and hepatomegaly (enlarged liver) occur from back-pressure in the portal circulation. The child may feel irritable and restless from the abdominal pain caused by liver distention. Lower extremity edema, usually a primary sign in adults, is often a late sign of heart failure in children.
With left-sided heart failure, blood accumulates in the pulmonary system. Dyspnea is usually the dominant symptom, especially when the child lies in a supine position. Increased pulmonary congestion results in orthopnea. The child may have crackles (rales) and may produce bloody sputum on coughing caused by lung capillaries subjected to increased pulmonary blood pressure, thereby being broken. The child may appear cyanotic from interference with gas exchange in the alveoli, which begin to fill with fluid (pulmonary edema). Left-sided heart failure can ultimately lead to right-sided heart failure as extensive pressure in the pulmonary system prevents blood from leaving the right ventricle. In an infant, heart failure is often difficult to detect because it presents with very subtle signs. The infant becomes breathless from rapid respirations, easy fatigability, and has difficulty feeding because of the exhaustion and dyspnea present. Often the infant becomes diaphoretic from the effort of feeding. If edema is present, it is generalized rather than dependent and often is first noticed as periorbital edema. An
abrupt gain in weight may be the most obvious indication. On physical examination, the infant will have an enlarged liver, described as a liver palpable more than 2cm below the right costal margin, and may have ascites. The apical heartbeat is displaced laterally and downward. As a rule of thumb, if the width of the heart is more than half the width of the chest in a child more than 1 year of age, the heart is enlarged. Conversely, a galloping heart rhythm or an accentuated third heart sound may be heard because of the sudden distention of the ventricle during the rapid filling phase. Tachycardia and tachypnea are present. Heart failure may be confirmed by echocardiography, which reveals the enlarged heart. Ventricular hypertrophy can be confirmed by ECG.
Medical Management Evacuate the accumulated fluids using diuretics (furosemide; spironolactone) Slowing the heart rate and strengthening cardiac function by administering an inotropic drug (digoxin) Reducing afterload with vasodilators (hydrazaline; nifedepine; nitroprusside; captopril
Nursing Diagnosis Ineffective cardiopulmonary and peripheral tissue perfusion related to inadequate heart function. Risk for imbalanced nutrition, less than body requirements, related to fatigue. Fear related to child’s ill appearance and possible disease outcome. Excess fluid volume related to impaired cardiac contractility and venous congestion. Ineffective cardiopulmonary tissue perfusion related to impaired cardiac function and increased cardiac workload. Activity intolerance related to effects of heart failure and dyspnea.
Provide for rest periods. Position the client in a comfortable position (semi-Fowler’s).
Monitor oxygen saturation levels with pulse oximetry. Provide oxygen as necessary. Assess the nostrils of the child receiving oxygen with nasal prongs every 4 ors to prevent possible pressure and subsequent irritation and breakdown on the nostrils.