Hyperventilation in the newborn piglet does not increase whole body oxygen consumption as seen in mature animals.
Hyperventilation has been shown to cause increased whole body oxygen consumption (VO2) and lactic acid production in human and animal mature subjects, but limited data are available in neonates. We investigated the effect of hypocarbic and normocarbic hyperventilation during normoxia and hypoxia (fractional inspired oxygen concentration = 0.14) upon the VO2 in anesthetized and paralyzed piglets. Systemic arterial, pulmonary arterial, and left and right atrial pressures as well as cardiac output and body temperature were continuously recorded. Hypocarbic hyperventilation (PaCO2 = 19 +/- 1 mm Hg; pH = 7.58 +/- 0.02) was associated with a significant decrease in systemic and pulmonary arterial pressures and cardiac output. These measurements returned to values similar to the initial normoventilation ones when PaCO2 was increased by adding CO2 to the inspired gas, whereas hyperventilation was continued. Neither hyperventilation alone nor in combination with hypoxia induced any significant change in VO2. We conclude that in the newborn pig, unlike what has been reported in mature subjects, cellular metabolic function is unaffected by hyperventilation as evidenced by the unchanged VO2.
D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism*; D002245:Carbon Dioxide / Q000008:administration & dosage; D006439:Hemodynamics; D006985:Hyperventilation / Q000209:etiology / Q000378:metabolism*; D000860:Hypoxia / Q000150:complications / Q000378:metabolism*; D010100:Oxygen / Q000008:administration & dosage / Q000378:metabolism*; D010276:Parasympatholytics / Q000633:toxicity; D012121:Respiration, Artificial / Q000009:adverse effects; D012133:Respiratory Paralysis / Q000139:chemically induced / Q000150:complications / Q000378:metabolism*; D013552:Swine / Q000378:metabolism
D010276:Parasympatholytics; D002245:Carbon Dioxide; D010100:Oxygen