CONGENITAL HEART DISEASE
Congenital heart disease refers to cardiac lesions present at birth. Even though these abnormalities exist before birth, they often become clinically evident at the time of delivery, when profound physiological changes occur in the circulatory system, or months or years after birth. Congenital heart disease (excluding bicuspid aortic valve) occurs in approximately 0.8 per cent of live births and results from both genetic and environmental factors. Congenital heart disease may be familial in some instances, although a distinct pattern of inheritance is usually not recognized. It is more common in children of older mothers. Ventricular septal defect and patent ductus arteriosus are relatively common in premature infants. Environmental factors such as teratogens and maternal rubella are commonly recognized risk factors.
Congenital cardiac defects that are compatible with the fetal circulation (see Chapter 1) may produce symptoms once the child is born. The persistence of normal fetal structures in an infant, such as a patent ductus arteriosus allowing a left-to-right shunt, may be detrimental. However, an abnormal connection may be necessary for an infant to survive in the presence of another congenital anomaly, such as transposition of the great arteries, which must have a connection between the two circuits (e.g., atrial septal defect, patent ductus arteriosus) to allow oxygenation of systemic blood and survival for any period of time after birth. Those at risk for developing endocarditis (see Chapter 10) should receive prophylactic antibiotics at appropriate times.
Congenital defects can be classified generally into acyanotic and cyanotic groups. The acyanotic congenital defects are those either without a shunt or with left-to-right shunts. Cyanosis occurs in the presence of a right-to-left shunt. In addition, it is important to identify whether malformations arise in the left or the right heart, the site of shunts if present, the status of the pulmonary blood flow (increased, normal, or decreased), and the presence of pulmonary hypertension (Tables 4-1, 4-2, and 4-3).
- SYMPATHOMIMETIC AMINES
- HIGH-OUTPUT STATES
- PHYSIOLOGY OF THE SYSTEMIC CIRCULATION
- NONPHARMACOLOQICAL MANAGEMENT OF HEART FAILURE
- PATENT DUCTUS ARTERIOSUS
- ATRIAL SEPTAL DEFECT
- GROSS ANATOMY
- PHYSIOLOGY OF THE CORONARY CIRCULATION
- CARDIAC DEVELOPMENT
- MYOCARDIAL METABOLISM
- CARDIOVASCULAR RESPONSE TO EXERCISE
- ACYATJOTIC LESIONS
- VENTRICULAR SEPTAL DEFECT
- PHYSIOLOGY OF THE PULMONARY CIRCULATION
- SHOCK
- MANAGEMENT OF ACUTE PULMONARY EDEMA
- ELECTROPHYSIOLOGY
- CONGENITAL HEART DISEASE
- EVALUATION OF THE PATIENT WITH CARDIOVASCULAR DISEASE
- MICROSCOPIC ANATOMY
- CIRCULATORY PHYSIOLOGY