Carbicarb, sodium bicarbonate, and sodium chloride in hypoxic lactic acidosis. Effect on arterial blood gases, lactate concentrations, hemodynamic variables, and myocardial intracellular pH.

The effects of Carbicarb, sodium bicarbonate, and sodium chloride on arterial blood gases, lactate concentrations, hemodynamics, and myocardial intracellular pH were compared in hypoxic lactic acidosis with controlled carbon dioxide elimination. Twenty-one young mongrel dogs were anesthetized, mechanically ventilated, and randomly allocated into one of three treatment groups. After hypoxic lactic acidosis was induced and maintained, 2.5 mEq/kg of one of the agents was infused over 30 min. Arterial blood gases, pH, lactate concentrations, and hemodynamic variables were measured immediately prior to the infusion of the agent and 30 min after the infusion was completed. With sodium bicarbonate administration, there was a significant increase in arterial PCO2 as compared to both Carbicarb or sodium chloride administration. With Carbicarb administration, there was a significant increase in arterial pH, base excess, and cardiac index, without a significant increase in arterial lactate concentration as compared to sodium bicarbonate or sodium chloride administration. Stroke volume index was also increased significantly with decreased heart rate. The data suggest that Carbicarb administration in hypoxic lactic acidosis improved hemodynamics compared with sodium bicarbonate or sodium chloride administration. The increased stroke volume and cardiac contractility appear to be due to improved myocardial intracellular pH.

Drowning and near-drowning.

The incidence, epidemiology, and pathophysiology of drowning and near-drowning are presented. Particular attention is paid to the neurologic and pulmonary pathophysiology indicators for monitoring and laboratory tests. Special attention to transportation of patients is given, and treatment in the field, emergency department, and pediatric intensive care unit is delineated.