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What is Heart Failure and Its Pathophysiology:Nursing Case Study

Sunday, 9 March 2014

Heart failure is the heart's inability to pump and circulate the oxygen and nutrients needed to maintain the metabolic requirements that sustain life. In a neonate, this condition usually results from a congenital defect that causes fluid overload or left‑to‑right shunt through the ductus or from surgical correction of the defect. The onset may occur soon after birth or in the first month or year, depending on the cause. A weak myocardium that can't meet normal demands as a result of asphyxia is the usual cause of heart failure in the first few days after birth. Such defects as a narrowed passage or an obstruction, a fistula, and a shunt lesion hinder blood flow and increase the heart's workload, causing heart failure in the first few weeks after birth.

Pathophysiology
Cardiac dysfunction activates sympathetic nervous system compensatory mechanisms, producing peripheral vasoconstriction, which diverts blood from the skin and renal circulation to the heart and brain. The decrease in renal perfusion activates the angiotensin‑aldosterone mechanism, causing hyperaldosteronism. The results are sodium and water retention and increased blood volume.

Ventricular dysfunction increases end‑diastolic pressure and produces systemic venous or pulmonary venous engorgement, depending on which ventricle is affected. The ventricles dilate and hypertrophy. Because a neonate's myocardium is less compliant (able to adapt to changes in volume and pressure) and contains less contractile mass, a small increase in ventricular volume increases the pressure, but the ventricles may be unable to enlarge in response to the increased pressure. This produces signs and symptoms of heart failure (usually left-sided and right-sided) with resulting systemic and venous engorgement. Deterioration occurs more rapidly in a preterm neonate than in a full‑term neonate because a preterm neonate has even less compliance and less contractile mass than a full‑term neonate.

Complications
■ End-stage cardiomyopathy
■ Metabolic acidosis
■ Acute renal failure
■ Death

Assessment
Health perception and management

■ Poor health due to congenital heart defect, asphyxia, and diseases affecting cardiac function

Physical examination

General appearance and nutrition
■ Prematurity
■ Low Apgar score (1 to 4) with hypoxia and bluish skin

Mental status and behavior
■ Irritability
■ Agitation
■ Lethargy
■ Difficulty bonding and interacting with parent

Integumentary
■ Pale or mottled skin and nail beds
■ Cyanosis
■ Periorbital edema
■ Peripheral edema on the backs of the hands and feet and dependent edema on the flank and scalp

Respiratory
■ Tachypnea and dyspnea, with rates as high as 100 breaths/minute
■ Intercostal muscle retractions
■ Rhonchi and crackles on auscultation

Cardiovascular
■ Tachycardia, with rates as high as 200 beats/minute
■ Peripheral vasoconstriction with cool arms and legs
■ Increased central venous pressure (CVP)
■ Distended neck veins and, occasionally, superficial veins

Gastrointestinal
■ Poor feeding with prolonged feeding time and poor sucking
■ Propensity to fall asleep during feedings because of exhaustion
■ Vomiting after feedings
■ Gastric distention
■ Hepatomegaly or splenomegaly

Neurologic
■ Restlessness and irritability
■ Lethargy

Renal and urinary
■ Oliguria despite adequate fluid intake

Diagnostic studies
■ Echocardiography identifies heart abnormalities.
■ Electrocardiogram (ECG) identifies arrhythmias.
■ Cardiac catheterization shows cardiac abnormalities, cardiac output, and ejection fraction.
■ Chest X‑ray shows heart enlargement in response to increased workload.
■ Decreases in the hemoglobin (Hb) level and hematocrit (HCT) suggest anemia.
■ Decreased serum glucose level and reagent strip testing for blood glucose levels suggest hypoglycemia.
■ Cardiac glycoside serum level determines therapeutic levels of digoxin (Lanoxin).
■ White blood cell count and neutrophil studies may indicate infection.
■ Decreased platelet count and coagulation studies show impaired clotting functions.
■ Arterial blood gas (ABG) analysis may show acidosis.
■ Serum electrolytes are abnormal.
■ Blood urea nitrogen and serum creatinine monitor renal function.

Teaching: Procedure/treatment
Teaching checklist

■ Disease process and signs and symptoms
■ Procedures, tests, and equipment in use
■ Normal development of the neonate, based on gestational age
■ Developmental tasks of the neonate in relation to health status
■ Medications utilized and their administration, if appropriate
■ Personal care of the neonate (bathing, diapering, feeding, sleeping position)
■ Ways to nurture the ill neonate
■ Infection control and safety needs of the neonate
■ Resources for support, information, and assistance through interdisciplinary team and the community
■ Issues relevant to discharge planning
■ Ways to contact the practitioner during and after usual hours
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