CEREBRAL VENOUS AND ARTERIAL BLOOD GASES DURING CHEYNE-STOKES RESPIRATION

Continuous graphs of arterial and cerebral venous blood gases and pH were obtained in eleven patients with Cheyne-Stokes respiration. In the phase of hyperventilation, arterial oxygen tension (PaO2), oxygen saturation and pH decreased while carbon dioxide tension (PCO2) increased. In the apneic phase, PaO2, arterial saturation and pH increased whereas PCO2 decreased. This is the opposite of changes that occur during voluntary hyperventilation and breathholding. The pattern of changes in cerebral venous blood oxygen levels showed some individual variations but these could be classified readily into two groups. In the younger age group, cerebral venous oxygen levels varied directly with changes in arterial carbon dioxide pressure (PaCO2) and inversely with arterial oxygen levels. In the older age group, cerebral venous oxygen levels passively followed the swings in arterial oxygenation. The administration of acetazolamide in a young patient increased cerebral blood flow but paralyzed cerebrovascular reactivity to changes in PaCO2. As a result, cerebral venous oxygen levels no longer varied according to changes in PaCO2 but passively followed the swings in arterial oxygen levels, mimicking the response of the older group. Thus, in the young patients with well preserved vasomotor capacitance, cerebral blood flow fluctuated rapidly in response to changes in PaCO2, increasing during hyperventilation and decreasing during apnea. In the older patients with diminished vasomotor capacitance, cerebral blood flow remained relatively constant and the cerebral venous oxygen delivery varied passively with up and down swings in the arterial blood. It is concluded that Cheyne-Stokes respiration is neurogenically mediated and results from depression of the respiratory center. This results in periods of apnea with a delayed rise in PaCO2 which tends to drive the respiratory center to hyperpnea. Hyperpnea is then followed by posthyperventilation apnea and the cycle renews itself. Periodic cerebral anoxia does not account for intermittent worsening of the electroencephalogram and neurologic status. It is postulated that they are also mediated by depression of the brain-stem with periodic improvement as the respiratory center is stimulated by the rise in PaCO2 of the arterial blood following apnea. © 1969.