Delayed-onset pulmonary insufficiency in primates resuscitated from hemorrhagic shock.
Forty-one unanesthetized cynomolgus monkeys were subjected to 2 hours of hemorrhagic hypotension at various mean arterial pressures (MAP) between 40 and 60 mm Hg. Resuscitation and maintenance of MAP were provided by lactated Ringer's solution and homologous blood. Thirty-eight per cent (57% of those surviving greater than 24 hours) developed a delayed-onset (18 to 24 hours) pulmonary insufficiency in spite of good urinary output, and which did not respond to furosemide. The group in which this caused death (24%) showed significantly decreased PaO2, PaCO2, dynamic compliance, and FECO2, and increased minute volume, Qs/Qt, pulmonary artery pressure, and VD/VT before death. Their lungs were heavier, with abnormal pressure/volume curves and increased minimum surface tension. During the entire post-resuscitation phase, this group remained in a high-output, low-resistance hemodynamic state in contract to survivors and those dying of shock. The implications regarding current practices of monitoring and resuscitating patients with traumatic shock are discussed.