Effects of arterial carbon dioxide tension on the newborn lamb’s cardiovascular responses to rapid hemorrhage

Nineteen newborn lambs, spontaneously breathing room air, were hemorrhaged of 50% of their measured blood volume over a 30-min period. They were then observed for the following 90 min. No fluid or blood was reinfused during the study. Eight of the 19 lambs survived beyond the study period, the other 11 died at the end of the hemorrhage or during the recovery period. All lambs became hypotensive and bradycardic during the hemorrhage. All became tachycardic after the hemorrhage. Blood pressure of the survivors returned towards baseline levels whereas it continued to fall in the non-survivors. All animals became anemic, acidotic, and hypocarbic but remained normoxemic. Myocardial blood flow fell to approximately 50% of baseline levels in both survivors and non-survivors during, and at the end of the hemorrhage. It returned to near baseline levels in the survivors by 90 min posthemorrhage. Cerebral blood flow remained at baseline levels during the hemorrhage in the survivors but cerebral oxygen delivery decreased. Flow rose 10% above baseline levels 90 min after hemorrhage but oxygen delivery remained low. In the non-survivors, cerebral blood flow fell to 60% of baseline and cerebral oxygen delivery was 50% of baseline by the end of the hemorrhage. A group of five lambs was hemorrhaged and studied in the same fashion as the 19, except that they breathed 4.5% CO₂ beginning 15 min before the hemorrhage, during the hemorrhage and 90 min recovery period. Four of these five survived the study period. They remained normocarbic and became more acidotic than the animals that breathed room air. Blood pressure and heart rate fell during hemorrhage but these decreases were less than in either group of room air breathing animals. During recovery they became tachy-cardic and blood pressure returned to baseline levels. Myocardial blood flow increased 20% above baseline by the end of hemorrhage and 40% above baseline by 90 min posthemorrhage. Cerebral blood flow increased 40% above baseline during the hemorrhage and remained at that level at the end of hemorrhage and 90 min afterwards. The increase in brain blood flow was sufficient to maintain oxygen delivery to the brain at baseline levels throughout the experiment.