- Etiology
- Pathogenesis, Pathology & Pathophysiology
- Epidemiology
- Management & Treatment
- Prevention
- Complications
- Prognosis
- Research Frontier
- Clinical Case Studies
- Study Questions
VSD results from abnormal growth and fusion of the ventricular septal system. The majority of VSDs involve defects of the membranous septum, with fewer involving outlet and inlet defects.
The defects are dynamic, and 50 percent close within 2 years. Usually smaller defects close spontaneously.
VSDs allow shunting of blood from the high-pressure left ventricle to the low-pressure right ventricle (see Figure 29-1).
VSD results from abnormal growth and fusion of the ventricular septal system. The majority of VSDs involve defects of the membranous septum, with fewer involving outlet and inlet defects. The defects are dynamic, and 50 percent close within 2 years. Usually smaller defects close spontaneously. VSDs allow shunting of blood from the high-pressure left ventricle to the low-pressure right ventricle. This is not evident until after delivery, after which there is a rise in the left ventricular pressure compared with the right. The resultant shunting of blood from left to right can lead to increased blood flow to the lungs and pulmonary vascular changes, pulmonary hypertension, and heart failure.
Schematic representation of a normal heart and a heart with ventricular septal defect.
This is not evident until after delivery, after which there is a rise in the left ventricular pressure compared with the right. The resultant shunting of blood from left to right can lead to increased blood flow to the lungs and pulmonary vascular changes, pulmonary hypertension, and heart failure.
Ventricular septal defects are the most common congenital heart defects; they affect approximately 5 per 1000 live births and represent approximately 30 percent of all congenital heart defects. In approximately 25 percent of patients, there are coexisting extracardiac anomalies.
¶ The timing of the initial follow-up with the pediatric cardiologist corresponds to the timing of the normal decline in PVR during the newborn period.????????
Infants with moderate to large VSDs usually become symptomatic within the first months of life. The primary care provider should monitor the infant during the first weeks of life for manifestations of heart failure (eg, tachypnea, increased work of breathing, poor weight gain or failure to thrive, and diaphoresis, particularly with feeding). Infants who develop symptoms before the first follow-up with the pediatric cardiologist should be referred for urgent evaluation and management. For infants with trivial muscular VSDs (ie, initial imaging and Doppler demonstrate a very small, very restrictive defect), follow-up is not generally necessary until three to six months of age, by which time many will have closed.
Δ Symptoms of heart failure in infancy include poor feeding (eg, tiring during feeds), poor weight gain, tachypnea, increased work of breathing, and diaphoresis, particularly with feeding. "Asymptomatic" refers to infants who lack symptoms of heart failure, have normal growth, and do not have evidence (clinical or echocardiographic) of PH. Mild symptoms of heart failure may include mild tachypnea or diaphoresis while feeding; however, growth is typically adequate. Moderate heart failure in an infant is characterized by tachypnea or diaphoresis with feeding and signs of growth failure. Severe heart failure is characterized by respiratory distress (tachypnea, grunting, retractions, or diaphoresis) at rest and failure to thrive.
◊ Infants who develop symptoms of heart failure before their next scheduled follow-up with the pediatric cardiologist should be referred for more urgent evaluation.
§ Since heart failure is not expected in association with small VSDs, the development of new symptoms, particularly late, should prompt reassessment of the original diagnosis and evaluation for other causes of the symptoms.
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