[Function of the respiratory muscles in acute cardiac decompensation]

In anesthetized dogs the performance of the respiratory muscles during cardiogenic shock and their influence on its outcome was studied. Shock was induced by cardiac tamponade. Cardiac output during shock amounted to 25-35% of control and was kept constant. Minute ventilation (VE) initially increased and then progressively decreased until respiratory arrest. The latter was due to impairment of respiratory muscle contractility, the pressure generated by the diaphragm (Pdi) decreasing despite a marked increase in the diaphragmatic electromyogram and of the phrenogram. Mechanical ventilation during shock prolonged survival for the same decrease in cardiac output, and also decreased substantially the severity of lactic acidosis. Furthermore, blood flow to the respiratory muscles during shock was different in the animals breathing spontaneously (SB) from that in mechanically ventilated animals (MV). The fraction of cardiac output distributed to the respiratory muscles during control amounted to 1.85% in MV and 2.79% in SB. With shock this decreased to 1.55% in MV while in SB it decreased by 21%, which suggests that mechanical ventilation during shock preserves a large portion of cardiac output used by the respiratory muscles during spontaneous breathing, thus making it available to other organs.