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Using the mouth occlusion pressure technique, we have studied the control of breathing in 10 hypercapnic patients with chronic obstructive pulmonary diseases and polycythemia before and after venesection. The mean hematocrit value was 59.9 +/- 5.5% which, following venesection (approximately 1,200-1,600 cm3 of blood was removed from each patient over three consecutive days), fell to 44.4 +/- 2.2%. Respiratory drive, expressed as P0.1 (mouth occlusion pressure 0.1 s after the onset of occluded inspiration at functional residual capacity) and as mean inspired flow (VT/TI), was diminished after venesection (p less than 0.001 and p less than 0.05); in contrast to that, we found no changes in respiratory timing (TI and TI/Ttot). The arterial PCO2 was decreased (p less than 0.001) and arterial PO2 was increased after venesection, these improvements are mainly attributed to decreased dead space ventilation (p less than 0.05). It seems that the improvements of blood gases after venesection is probably responsible for the decrease in respiratory drive.

Cerebral blood flow was measured before and after venesection in 6 patients with chronic obstructive pulmonary disease and secondary polycythemia. The hematocrit was decreased from a mean of 59.6 to 43.9%, and whole blood viscosity was decreased by 35%. The supratentorial blood flow increased 78.2% (p < 0.005) after venesection; subtentorial flow also increased, but not significantly. The improvement in cerebral blood flow appeared to be related to a decrease in blood viscosity, because pulmonary function and arterial blood gases did not change significantly. There was subjective improvement in all patients, and this improvement might have been due to the increased supratentorial blood flow.

A lack of respiratory centrogenic drive of undetermined origin is a rare cause of cyanosis. In this condition, voluntary hyperventilation restores arterial oxygen saturation to normal. Secondary changes consist of polycythemia, somnolence, headache and right heart failure. The present report of a 43-year-old thin man with idiopathic alveolar hypoventilation is combined with a review of 12 similar patients reported by others. His resting oxygen saturation increased from 60% to 98% with hyperventilation. The pulmonary artery pressure was 68/26 mm. Hg and cardiac output 12.3 l./min. Death resulted from pulmonary infarction, and no specific abnormalities were found in the brain.