THE commonly recognized causes of respiratory distress during infancy are pulmonary or tracheobronchial pathology, cardiac failure, and cerebral disease. The various mechanisms by which cardiac disease may produce increased respiratory effort are not, however, generally appreciated, with resultant confusion in the management of the underlying problem.
The major pathological physiologic disturbances producing respiratory distress (in association with heart disease) are pulmonary edema and severe metabolic acidosis. Pulmonary edema occurs either in left ventricular failure or in association with lesions resulting in an obstruction of the pulmonary venous return. Metabolic acidosis is related to severe hypoxia which is the major manifestation of several types of cardiac anomaly.
The respiratory pattern associated with pulmonary edema is that of tachypnea to rates of 60-100/min, with initially only mild increased effort. Rales are not usually heard until a considerable amount of fluid has entered the alveoli; thus absence of this clinical sign does not exclude the diagnosis. In advanced pulmonary edema, marked air hunger appears and in young infants head retraction with gasping respiration may occur, presenting an appearance of an obstructed airway. Cyanosis is usually only of mild degree unless associated with cyanotic congenital heart disease.
Left ventricular failure and pulmonary venous congestion are far more frequently observed in heart disease in infancy than right-sided failure. It is surprising that most descriptions of heart failure in infancy stress hepatomegaly as one of the earliest signs of failure. However, respiratory distress as manifested by tachypnea and dyspnea is usually the first evidence of cardiac failure in infancy, and hepatomegaly and other evidences of right-sided failure occur much later.
ACUTE LEFT VENTRICULAR FAILURE PRESENTING AS UNILATERAL PULMONARY EDEMA: THE RESULT OF RARE UNILATERAL CONGENITAL PULMONARY VASCULAR ANOMALY
