The mechanism of CO2 retention in cardiac pulmonary edema

We studied a 58-year-old woman during an acute episode of cardiac pulmonary edema complicated by carbon dioxide (CO2) retention. As pulmonary wedge pressure became greater, metabolic production of CO2 increased by 38 ml/min and minute ventilation by 1.53 L; by contrast, alveolar ventilation remained unchanged due to a concomitant rise in physiologic dead space and, as a result, arterial CO2 tension increased up to 61 mm Hg. With treatment, all these variables returned to baseline values. Subsequent measurement of mouth occlusion pressure (p 0.1) during a CO2 rebreathing trial showed that neuromuscular inspiratory drive response to CO2 was preserved, but that ventilatory response was markedly reduced, presumably because of the severe restrictive and obstructive ventilatory defect and of the loss of inspiratory muscle force demonstrated in the patient. We conclude that CO2 retention in cardiac pulmonary edema involves a combination of: (1) increased CO2 production, (2) rise in physiologic dead space, and (3) severe respiratory mechanical impairment.