ObjectivesTo determine the hemodynamic responses to a wide range of specific, controlled, graded levels of hypoxic hypoxia over 120 mins in a neonatal porcine model and to identify the PaO2threshold for altered hemodynamic homeostasis.DesignProspective, experimental, animal study.SettingUniversity cardiovascular research laboratory.SubjectsThree-day-old domestic swine.InterventionsAnesthetized, intubated, and ventilated 3-day-old pigs (n = 88) were assigned to one of five predetermined graded PaO2groups: Group I (normoxia, PaO2= 80 torr [10.7 kPa]); group II (PaO2= 60 torr [8.0 kPa]); group III (PaO2= 40 torr [5.3 kPa]); group IV (PaO2= 30 torr [4.0 kPa]); or group V (PaO2= 20 torr [2.7 kPa]).Measurements and Main ResultsHemodynamic parameters including heart rate, systolic blood pressure, diastolic blood pressure, mean arterial pressure (MAP), and pulse pressure were evaluated. Acid-base status (arterial pH and lactate) was monitored in each experimental group over the 120-min study period. Hemodynamic and acid-base parameters were unaltered in animals in groups I and II. In group III animals, blood pressure was maintained (partly by increased heart rate), and acid-base balance was unaltered. In contrast, group IV animals had a gradual and progressive decrease in systolic blood pressure, diastolic blood pressure, and MAP, and slightly decreased pulse pressure, despite sustained tachycardia. Group IV animals also developed mild lactic acidosis. Group V animals exhibited a biphasic hemodynamic response, while the heart rate response was characterized by tachycardia at the induction of hypoxia, which was reduced in magnitude by 120 mins. The biphasic hemodynamic response in this group of animals included an initial increase in systolic and pulse pressures, followed by a gradual and progressive decrease in systolic and diastolic blood pressures, MAP, and pulse pressure. In addition, group V animals also developed profound progressive lactic acidosis.ConclusionsIn anesthetized neonatal pigs, tachycardia occurred in response to a PaO2of 40 torr (5.3 kPa), and thus marked the threshold for altered hemodynamic homeostasis. Beyond this threshold, both the 30 torr (4.0 kPa) and 20 torr (2.7 kPa) groups had a PaO2-dependent "late" hypotension, while only the 20 torr (2.7 kPa) group had a significant biphasic hemodynamic response characterized by "early" hypertension. The "late" hypotension which occurred in these two profound hypoxia groups indicates an inability to adequately adjust hemodynamics during prolonged hypoxic hypoxia.(Crit Care Med 1996; 24:1886-1892)