The best picture of anaerobic metabolism is scene in athletes after an 800 race. A 50 to 100 meter race is not long enough to develop the full effect of exceeding the limits of aerobic metabolism. In 800 meters (just about 2 minutes), runners are breathing deeply and forcefully to compensate for the metabolic acidosis they develop. In a marathon, runners have to limit themselves to activity similar to the limits of their aerobic capacity as a metabolic acidosis cannot continue beyond the severe level that develops at about 800 meters.
Relationship to Acute Cardiovascular Insufficiency
The metabolic physiology at the end of 800 meters is essentially the same as in Acute Cardiovascular Insufficiency. There is a severe metabolic acidosis with respiratory compensation. Such individuals are breathing with great depth and rate due to the metabolic acidosis and appear and feel dyspnic. A significant oxygen debt is present.
The dyspnea of the colloquially know Acute Pulmonary Edema is often attributed solely to the edema of the lungs. However much of it is also the same metabolic acidosis that occurs in 800 meter runners. In both cases the supply of oxygen is insufficient to the demand for it leading to metabolic acidosis and the resulting respiratory physiology. If one uses the moniker, Acute Pulmonary Edema it should be realized that the dyspnea stems from acute cardiovascular insufficiency and the lack of tissue oxygenation. Breathing is deep and rapid to compensate for metabolic acidosis. Compromised blood flow should be considered the primary abnormality. There is of course some effect from the edema itself. It is incorrect and often the case that the abnormalities are attributed enteriely to the edema of the lungs. The increased pulmonary venous pressure is a compensation for the insufficiency of blood flow. If the moniker of Acute Pulmonary Edema is used this still should be considered a cardiovascular disease and not a pulmonary disease. The term Acute Cardiovascular Insufficiency is preferred.