The relationship of respiratory failure to the oxygen consumption of, lactate production by, and distribution of blood flow among respiratory muscles during increasing inspiratory resistance.

An animal model was developed to determine if blood flow to the respiratory muscles limits oxygen delivery and thus work output during inspiratory resistance. With incremental increases in the rate of work of breathing to 15 times the resting level, blood flow to the diaphragm rose exponentially 26-fold. Blood flow to other inspiratory and a few expiratory muscles increased to a much smaller extent, often only at the greater work loads. Cardiac output and blood pressure did not change. Arterial-venous oxygen content difference across the diaphragm became maximal at low work rates and thereafter all increases in oxygen delivery during higher work rates were accomplished by increments in blood flow. Oxygen consumption of the respiratory musculature calculated by blood flow times oxygen extraction increased exponentially with increasing work of breathing and was less than the increase in total body oxygen consumption at each work load. Hypoxemia and respiratory acidosis occurred when the animals inspired through the highest resistance; blood flow and oxygen consumption were even higher than that observed during previous resistances and there was no evidence of a shift to anaerobic metabolsim in blood lactate and pyruvate levels. Respiratory failure did not appear to be a consequence of insufficient blood flow in this model.