METABOLIC ACIDEMIA WITH HYPOXIA ATTENUATES THE HEMODYNAMIC-RESPONSES TO EPINEPHRINE DURING RESUSCITATION IN LAMBS

Objective: To examine the effects of metabolic acidemia and hypoxia on the hemodynamic responses to epinephrine in an intact neonatal animal model. Design: Multi-experiment, randomized, controlled trial. Settin g: Animal research laboratory of a university hospital. Subjects: Sixt een lambs, ranging in age hom 2 to 14 days. Interventions: The lambs w ere chronically catheterized; the ductus arteriosus was ligated; and a pulmonary arterial flow probe was inserted to measure cardiac output, blood pressure (BP), and heart rate. In the first protocol, hemodynam ic responses to epinephrine during pure metabolic acidemia or metaboli c alkalosis were studied in eight lambs. Each lamb was studied on four different days at a different arterial pH: 6.9, 7.1, 7.4, and 7.6. Ve ntilation was controlled to maintain Pco(2) at 35 to 45 torr(4.66 to 5 .99 kPa). Acidemia was induced by the infusion of lactic acid and alka losis by the infusion of sodium bicarbonate. When the appropriate arte rial pH was achieved, 10 mu g/kg of epinephrine was administered intra venously. In a second protocol, hemodynamic responses to epinephrine d uring metabolic acidemia or alkalosis plus hypoxia were studied in eig ht lambs. When the appropriate arterial pH was achieved, hypoxia was i nduced until cardiac output decreased to 40% of baseline. Epinephrine bolus was given, and after 90 secs, the lambs were resuscitated with o xygen. Measurements and Main Results: Epinephrine administered during uncompromised hemodynamics led to hypertension, bradycardia, and decre ased cardiac output that were unaffected by arterial pH values between 6.9 and 7.6. Acidemia with hypoxia compromised hemodynamics with decr eases in heart rate and cardiac output. Epinephrine administered durin g this compromised condition did not improve cardiac output, heart rat e, or BP before resuscitation with oxygen at any arterial pH studied. Resuscitation with epinephrine and oxygen during hemodynamically compr omised states led to increases in heart rate, BP, sued cardiac output with significant attenuation of these hemodynamic responses during met abolic acidemia at pH values of 6.9 and 7.1.