Cardiovascular effects of d-tubocurarine and pancuronium in newborn lambs during normoxia and hypoxia.

Nondepolarizing muscle relaxants are administered to hypoxic neonates (including those with severe cyanotic congenital heart disease) to reduce oxygen consumption. However, it is unknown whether paralysis actually reduces oxygen consumption or whether the drugs used affect the cardiovascular system of neonates. Therefore, we studied the effects of d-tubocurarine and pancuronium induced muscle paralysis on oxygen consumption, cardiac output, and tissue oxygen delivery in healthy normoxic and hypoxic 1- to 3-day-old lambs. We measured intravascular pressures, cardiac output and its distribution (microspheres), and blood gases and pH during: 1) spontaneous respiration with room air (control); 2) spontaneous respiration with a Pao2 of 27-33 mm Hg (hypoxia); 3) mechanical ventilation with room air; 4) mechanical ventilation with room air and paralysis with d-tubocurarine (0.3 mg/kg) or pancuronium (0.1 mg/kg); and 5) mechanical ventilation with hypoxia and paralysis. Mechanical ventilation, with or without muscle paralysis, had no effect on the oxygen delivery or oxygen consumption of normoxic animals. Hypoxia and spontaneous ventilation had no effect on oxygen consumption, but hypoxia, paralysis, and mechanical ventilation reduced it 35% (p less than 0.002 d-tubocurarine) and 50% (p less than 0.001 pancuronium). Cardiac output was unaffected by oxygenation, mechanical ventilation, or muscle paralysis. However, blood flow to the brain and heart increased during hypoxia, which maintained normal oxygen delivery to these organs. During hypoxia and spontaneous ventilation, mean pulmonary arterial pressures increased 34% (d-tubocurarine) and 54% (pancuronium) above control; during hypoxia, muscle paralysis, and mechanical ventilation, it increased 81%.(ABSTRACT TRUNCATED AT 250 WORDS)