Observations on colloid osmotic pressure, hematocrit, and plasma osmolality during cardiac arrest.

A porcine model of cardiac arrest with irreversible electromechanical dissociation was associated with highly significant decreases in colloid osmotic pressure in the absence of increases in hematocrit during the initial half hour of CPR. Pulmonary edema was typically observed. These observations are best explained by increases in capillary permeability to plasma proteins. The progression of acidemia was remarkably slow; arterial blood pH remained normal for more than 16 min. Even though there was significant lactic acidosis, concurrent respiratory alkalosis during CPR accounted for the greatly delayed onset of acidemia. There was also an as-yet unexplained increase in plasma osmolality.