Respiratory muscle contribution to lactic acidosis in low cardiac output.

The role of the respiratory muscles in the evolution of experimental low cardiac output and lactic acidosis was studied in 2 groups of dogs. One group (6 dogs) was paralyzed and artificially ventilated, and the other (6 dogs) was breathing spontaneously. Shock was induced by cardiac tamponade; cardiac output during shock amounted to 25 to 35% of control values in both groups. All the spontaneously breathing dogs died from ventilatory failure (mean time, 2 h), whereas the artificially ventilated dogs were still alive 3 h after the onset of cardiogenic shock. At any given time after the onset of shock, arterial pH was significantly lower in the spontaneously breathing dogs than in the artificially ventilated ones. This was due to a greater increase in arterial blood lactate in the spontaneously breathing dogs than in the artificially ventilated ones (9.47 +/- 2.7 versus 4.74 +/- 56 mmoles/L at 2 h, respectively). Greater glycogen depletion associated with higher muscle lactate concentrations were found in the respiratory muscles of the spontaneously breathing dogs when compared with that in the artificially ventilated ones. It is concluded that artificial ventilation in cardiogenic shock decreases substantially the severity of lactic acidosis and prolongs survival.