ABSTRACT. Redistribution of regional blood flow is an important compensatory response to acute hypoxemia which preserves oxygen delivery to the most vital organs. It is not known if this change in blood flow persists when hypoxemia is prolonged, as occurs in cyanotic congenital heart disease. Chronic hypoxemia was produced in newborn lambs by creating pulmonary stenosis and an atrial septal defect. Oxygen saturation was maintained at 60-70% of control for 2 wk. Distribution of cardiac output was then measured with radionuclide-labeled microspheres. As compared with control, chronic hypoxemia did not alter total cardiac output. Regional blood flow was redistributed, however, the pattern of this redistribution 'was different from that seen during acute hypoxemia. Myocardial and cerebral blood flows, which increase during acute hypoxemia, return to control levels during chronic hypoxemia. Renal, splenic, gastrointestinal, carcass, and skin blood flows remain decreased. Hemoglobin gradually increases so that after 2 wk of hypoxemia total systemic oxygen delivery returns toward control. However, oxygen delivery to all organs except the heart and brain is reduced. Thus, although cardiac output and total systemic oxygen delivery return toward normal during chronic hypoxemia, these measurements may not reflect important regional variations in blood flow and oxygen delivery. Decreased oxygen and substrate delivery to the gastrointestinal tract, liver, and carcass may account for the alterations of metabolism and growth seen in the newborn with cyanotic congenital heart disease. (Pediatr Res 22: 389-393, 1987) When arterial oxygen content is acutely decreased, several compensations occur to maintain adequate tissue oxygen delivery. Two of these compensations are an increase in cardiac output and an increase in oxygen extraction in several vascular beds. However, because the increase in cardiac output may be insufficient to maintain normal systemic oxygen delivery, blood flow is redistributed to the most vital and most metabolically active organs (I, 2). During acute hypoxemia, blood flow increases to the myocardium and brain and decreases to the kidneys, gastrointestinal tract, and skin (3, 4). During chronic hypoxemia, such Received December 11, 1986; accepted May 5, 1987
3Eas occurs in newborns with cyanotic congenital heart disease, additional compensatory mechanisms are invoked. These hemodynamic, hematologic, respiratory, hormonal, and neural adjustments either increase systemic oxygen delivery or reduce oxygen demands.In a previous study of newborn lambs with experimentally produced cyanotic heart disease, we demonstrated that the major compensations to chronic hypoxemia are a decrease in growth and an increase in hemoglobin concentration (5). The decrease in growth may reduce systemic oxygen utilization (3, 5). The increase in hemoglobin increases the blood oxygen-carrying capacity and returns systemic oxygen content to normal. Systemic oxygen delivery can thus be maintained without a chronic increase in cardia...