During fetal life, both the right and left ventricles generate the same pressure. They both empty into the aorta, the left directly and the right via the ductus arteriosus. Pulmonary vascular resistance is high and pulmonary blood flow is low. The presence of a large ventricular septal defect, therefore, is of little or no consequence in the fetus.
Large VSD - newborn infant
In the newborn infant, pulmonary vascular resistance normally decreases rapidly. This permits left-to-right flow to begin through a large ventricular septal defect, resulting in pulmonary vascular engorgement. Flow gradually increases, and over the first weeks of life, the infant can develop congestive heart failure, a group of symptoms and signs reflecting the hemodynamic effects of the large left-to-right shunt.
Large VSD - infant
In the infant, a large shunt through a ventricular septal defect causes left atrial and left ventricular dilation and may significantly elevate left ventricular filling pressure, thereby, raising left atrial pressure. These phenomena cause fluid extravasation into both the pulmonary interstitial space and the alveoli, resulting in small airway compression, gas trapping, carbon dioxide accumulation and hypoxemia.
Respiratory pattern - grunting video
The pulmonary effects of a large ventricular septal defect result in the respiratory pattern of tachypnea, intercostal retractions and nasal flaring, reflecting the infant's attempts to increase respiratory volume. The infant also demonstrates forced expiration in an attempt to raise airway pressure. These features are demonstrated in the video that follows. Note also the audible grunting.
Large VSD - CHF
Pulmonary vascular congestion, cardiac dilation and increased right ventricular diastolic pressure lead to increased systemic venous pressure. The liver becomes congested and, therefore, enlarged. Effects on the kidneys cause salt and water retention, causing increased vascular volume and tachycardia.