Continuous compensatory mechanisms, the heart may be unable to maintain an adequate cardiac output. Decreased blood flow to the kidneys continues to stimulate sodium and water reabsorption, leading to hypervolemia, increased workload on the heart, and congestion in the pulmonary and systemic circulations. Since these hemodynamic changes occur at different times, the signs and symptoms can vary.
Impaired myocardial function
One of the earliest signs of compensation and decompensation is tachycardia (sleeping heart rate above 160 beats / minute in infants), as a direct result of sympathetic stimulation. It is elevated even during rest but becomes markedly rapid during the slightest exertion.
Increased blood volume causes the ventricles to dilate, stretching the myocardial fibers until they are no longer as contractile. Ventricular dilation results in extra heart sounds, S3 or S4. The addition of these extra sounds to S1 S2 produces a gallop rhythm. S3 is believed to be caused by vibrations against the ventricles can no longer accommodate the volume. It is heard immediately after the second heart sound (ventricular diastole gallop). S4 is believed to be caused by atrial contraction in response to ventricular resistance during filling of the ventricles. It occurs just before the first hear sound (atrial presystolic gallop). The presence of S3 and S4 is called a summation gallop. Each is best heard at the apex.
Variations in the strength of ventricular contractions result in pulsus alternans, regular alternation of one strong beat and one weak one. It is best detected by palpating the pulse while taking the blood pressure. The increased pressure from the inflated cuff occludes the weak beats, so that only the stronger beats are counted. As a result, the pulse is half the actual rate.
Cardiomegaly results from dilation of the ventricle to accommodate increasing volumes of blood and fom hypertrophy, as a result of persistent lengthening and thickening of the myocardial fibers. Although hypertrophy decreases the contractility of the fibers, it is partially compensated by an increase in muscle mass. Decreased cardiac output results in poor peripheral perfusion, which is characterized by cold extremities, weak pulses, low blood pressure, mottled skin, and ever growth retardation.
As the left ventricle fails, blood volume and pressure increase in the left atrium, pulmonary veins, and lungs. Occasionally, the pulmonary capillary pressure measures the plasma osmotic pressure, forcing fluid into tissues, causing pulmonary edema. The increased pressure also decrees the compliance (expansion) of the lungs.
Dyspnea is the earliest signs of failure and is thought to be caused by a decrease in the distensibility of the lungs. As a result, additional muscles must be used for respiration, cuasing costal retractions. Initially, dyspnea may only be evident on exertion but may progress to the point that even slight activity results in labored breathing. In infections, dyspnea at reat is a prominent sign and may be accompanied by flaring nares.
Tachypnea (respiratory rate above 60 breaths / .minute in infants) occurs in response to reduced lung compliance. Inability to feed with resultant weight loss is primarily a result of tachypnea and dyspnea on exertion.
Orthopnea (dyspnea in the recumbent position) is caused by increased blood flow to the heart and lungs from the extremities, It is relieved by sitting up, because blood pools in the lower extremities, decreasing venous return. In addition, this position decrees pressure from the abdominal organs on the diaphragm. In infects, orthopnea may be evident in their innability to lie supine and their desire to be held upright.]
Paroxysmal nocturnal dyspnea (PND) is a severe shortness of breath that occurs shortly after falling asleep. It is a result of reabsorption of fluid (from dependent edema), which increases blood volume, producing more severe pulmonary congestion. Edema of the bronchial mucosa may produce cardiac wheezing from obstruction to airflow. Mucosal swelling and irritation result in a persistent, dry, hacking cough. As pulmonary edema increases, the cough may be productive from increased secreations. Pressure on the laryngeal nerve results in hoarseness, A late sign of heart failure is gasping and grunting respirations. An uncommon sign in infants is rales.
Cyanosis may occur without a right-to-left shunt and is the result of impaired respiratory gas experience mottling of the skin or generalized transient duskiness. Extreme pallor or persistent duskiness is an ominous sign of Congestive Heart failure.
Systemic congestion is a primary consequence of right-ided failure due to the instability of the right ventricle to eject blood into the pulmonary circulation, resulting in increased pressure, and pooling of blood in the venous circulation. As was explained earlier, it can result as a late consequence of left-sided failure.
Hepatomegaly is usually the earliest sign of failure and occurs from pooling of blood in the portal circulation and transudation of fuid into the hepatic tissues. The liver may be tender on palpation and its size is an indication of the course of heart failure.
Edema forms as the sodium and water retention cause systemic vascular pressure to rise. The earliest sign is weight gain. However, as additional fluid accumulates, it leads to swelling of soft tissue that is dependent and flavors the flow of gravity, such as the sacrum and scrotum when recumbent and loose periorbital tissues. In infants, edema is usually generalized and difficult to detect. Gross fluid accumulation may produce ascites and pleural effusions.
Distended Neck and peripheral veins which are uncommon in infants, result from a consistently elevated central venous pressure. Normally neck and hand veins collapse when the head or hands are raised above the level of the heart, since the blood drains by gravity back to the heart. However, when the venous pressure is high, it prevails the back flow of blood. Causing the veins to remain distracted.
Diagnosis is made on clinical symptoms such as dyspnea (especially when at rest), flaring nares, moist grunting respirations, subcostal retractions, tachycardia, activity intolerance (particularly during feeding), excessive sweating, and unexplained weight gain from edema. Since the signs of pulmonary congestion from heart failure response respiratory infections, it is imperative to differentiate between the two. Signs selectively indicative of Cngestive heart failure are cardiac enlargement, edema, sweating, hepatomegaly, and auscultatory finsings such as tachycardia, gallop rhythm and pulsus alternans.
Care for children
The objectives of nursing care are to
• Assist in measures to improve cardiac function
• Decrease cardiac statements
• Reduce respiratory distress
• Maintain nutritional status
• Assist in measures to promote fluid loss, and
• Provide emotional support.
Although the objectives are the same, the interventions differ depending on the child's age, especially with infants as compared to older children. The doctor's responsibility in administrating digitalis included observing for signs of toxicity, calculating the correct dosage and instituting parental teaching regarding drug administration at home.