Pulmonary and systemic hemodynamics during hemorrhagic shock in baboons.
The pulmonary and systemic hemodynamic response to four hours of hemorrhagic shock and resuscitation has been studied in 17 baboons using both open and closed chest models. No pulmonary artery (PA) hypertension occurred during shock or resuscitation except for an increase in lft ventricular end diastolic pressure (LVEDP) secondary to intravascular volumee overload with Dextran. Pulmonary vascular resistance (PVR) increased during shock but returned to control levels with reinfusion of shed blood and correction of acidosis. PVR was moderately elevated following reinfusion of shed blood if acidosis was not corrected or if volum resuscitation was inadequate. No increase in gradients occurred between PA pressure and left atrial (LA) pressure or LVEDP and there was no gradients between small pulmonary vein and LA pressure. Arterial PO2 uniformly increased during shock and remained at or above control levels of reinfusion. Gross or histologic evidence of "congestive atelectasis" or "shock lung" was not observed. These observations suggest that in the subhuman primate, hemorrhage alone does not produce significant injury to the lung during shock or the immediate postresuscitation interval. Hemorrhage alone did not produce changes in the lung which would result in increased pulmonary microvascular hydrostatic pressure following appropriate resuscitation.
D000818:Animals; D001794:Blood Pressure; D001815:Bloodletting; D002245:Carbon Dioxide / Q000097:blood; D002302:Cardiac Output; D000882:Haplorhini; D006439:Hemodynamics; D006863:Hydrogen-Ion Concentration; D008168:Lung / Q000098:blood supply; D008833:Microcirculation; D009200:Myocardial Contraction; D010100:Oxygen / Q000097:blood; D010215:Papio; D011652:Pulmonary Circulation; D012128:Respiratory Distress Syndrome / Q000209:etiology; D012151:Resuscitation; D012771:Shock, Hemorrhagic / Q000503:physiopathology*; D013997:Time Factors; D014655:Vascular Resistance
D002245:Carbon Dioxide; D010100:Oxygen