Korean J Pediatr 2011;54(5):192-200 • DOI: 10.3345/kjp.2011.54.5.192 193 Introduction Respiratory syncytial virus (RSV) is the most common cause of lower respiratory tract infection in infants and toddlers worldwide, including Korea. According to the biweekly reports of Korea Centers for Disease Control and Prevention, the seasonal outbreaks of RSV infection occur during the winter months, September through March, even in Korea. Almost all children have RSV infection until the age of 2 years, and nearly half of those will be infected two episodes on the average1-3). About half the children may develop bronchiolitis and pneumonia which might require hospitalization. Often for some cases, an intensive care with mechanical ventilation is necessary. RSV infection in particular pediatric groups produces significant morbidity and mortality: especially in premature infants with <35 weeks gestational age and in patients with chronic lung disease, such as bronchopulmonary dysplasia (BPD) or hemodynamically significant congenital heart disease (HS-CHD)4,5). CHD patients with RSV infection were more likely to be hospitalized, and had greater morbidity and mortality associated with bronchiolitis than non-CHD infants, particularly associated with undertaking corrective surgery in CHD patients with a history of recent RSV bronchiolitis. In Korea, there were a few of initial reports for intervening in serious and fatal cases with CHD superimposed by RSV infection, and those still remains as painful memories for some pediatric cardiologists4-6). For the past 10 years, with advances in operative skills as well as transcatheter intervention and intensive care, RSV prophylaxis with palivizumab were introduced for these high- risk infants7,8). This review is to describe about the impact of RSV infection on infants with CHD and the recent trends according to global and Korean standardization. Impact of Respiratory Syncytial virus on infants with hemodynamically significant congenital heart diseases Lung compliance and airway resistance contributes to how much effort a patient needs for breathing. The airways of infants have greater resistance compared with the older children due to their smaller diameter. Increased peripheral resistance affects the distribution of air ventilation, and makes infants more vulnerable to hypoxemia. Spontaneous ventilation is characterized by a functional residual capacity, that is relatively small in infants and then the infant is prone to potential ventilation-perfusion mismatch and is at higher risk for respiratory compromise5,9-12). Depending upon the types of cardiac defect which is present, the lung of the infant may be over-circulated, as in the setting of ventricular septal defect, or under-circulated as with tetralogy of Fallot with pulmonary stenosis9,10). Pulmonary over-circulation associated with left-to-right shunting may result in mucosal edema, and luminal narrowing, as well as vascular or cardiac compression of the large bronchuses. During the typically delayed transition of the circulation in infant with CHD, usually occurring within the first few months, decreased pulmonary arteriolar resistance leads to increasing left-to-right shunt (LR shunt). There is a decrease in lung compliance and an increase in respiratory rate. Infants also may have significantly increased pulmonary blood flow, capillary wedge pressure and left atrial pressure. The result may be pulmonary edema, which leads to further decreases in functional residual capacity, potentiating ventilation-perfusion mismatch and become susceptible to hypoxia. In addition increased alveolar edema will lead to decreased lung volume and decreased compliance of the lung bed9,12). In the under-circulated lung, as seen with right-to-left shunting, those patients with cyanotic congenital heart disease typically include tetralogy of Fallot. The basic physiology is obstruction to pulmonary outf low due to stenosis. These patients are prone to increased hypoxemia because the degree of pulmonary stenosis increases over time, and there may be reduced lung volume and airway hypoplasia. Where there is increased ventilation compared with perfusion, dead space ventilation may lead to further hypoxemia. With decreased alveolar saturation, compliance of the lungs may be increased. However, small airway obstruction may also be present, leading to increase airway resistance. At baseline, these cyanotic patients are at risk for increasing hypoxemia, and RSV infection can precipitate significant cyanosis5,9). Many infants with complex CHD have both manifestations of cyanosis and relatively increased pulmonary blood flow. Examples of such patients include those with most forms of single ventricle including hypoplastic left heart syndrome and hypoplastic right heart of tricuspid atresia, or pulmonary atresia. The majority of infants with complex univentricular heart will have undergone palliative surgery early period with risk of increasing ventilation-perfusion mismatch, which is potentiated by RSV infection. Compromised ventricular function may contribute to higher pulmonary venous pressures, which may lead to capillary leak and pulmonary edema. In addition, those patients with oxygen saturations 85% have a relatively large amount of pulmonary blood flow, which can contribute to risk for respiratory complications in this setting. The result of this mixed physiology may be the reason for the poor tolerance in a superimposed respiratory infection, such as with RSV5,9,10,12).