Studies of cerebral circulation in brain injury IV.—Ischemia and hypoxemia of the brain stem and respiratory center

Abstract

Concurrent studies of local blood flow, oxygen availability, steady potential (SP) and pH of the respiratory center and carotid body have been made together with continuous recording of blood pressure and respirations. The EPG electrode placed in the wall of the carotid artery records changes in the partial pressure of oxygen of the blood rather than changes in oxygen saturation. The first effect of anoxic anoxia is stimulation of respiration by the carotid body reflex, continued anoxic anoxia or ischemic anoxia damages the respiratory center, resulting in various patterns of dysrhythmia such as slowed respiration, Cheyne-Stokes breathing, apneusis, gasping and finally respiratory arrest. Incomplete anoxia of the respiratory center causes respiratory arrest due to a state of reversible anoxic neuronal paralysis. In this state of reversible paralysis the respiratory neurones continue to metabolize oxigen but at a reduced rate. Anoxic damage to the respiratory center is associated with local acidity and hyperemia. Whenever respirations fail there is an accompanying injury potential (SP shift) of the respiratory center with respect to the spinal cord white matter. Seven per cent CO 2 and oxygen causes hyperpnea which appears to be mediated in the first few seconds by its action on the carotid body and later by its additional action on the respiratory center. Occlusion of the carotid arteries cause hyperpnea which is mainly due to resultant hypoxemia of the carotid body. There is an increased blood flow in the collateral circulation from the vertebral, basilar and dorsal spinal arteries. Occlusion of the vertebral arteries causes incomplete ischemic anoxia of the brain stem. Respiration continues because the posterior communicating arteries provide a collateral circulation. Additional occlusion of the carotid arteries causes medullary anoxia and respiratory arrest. Repeated anoxia lowers the threshold of the respiratory neurones to its paralytic effects. Patterns of periodic breathing, resulting from ischemia or anoxemia of the brain under the conditions of these experiments, do not appear to be mediated by periodic fluctuations of oxygen availability of carotid body and respiratory center or rhythmic fluctuations in pH of the respiratory center. They appear to result from anoxic damage to various levels of the brain stem and are reversible. Brief carbon monoxide breathing lowers the oxygen saturation of the blood without reducing the partial pressure of blood oxygen, the oxygen dissolved in the plasma may provide a critical supply sufficient for the metabolic needs of the respiratory center as the normal oxygen carrying capacity of the blood is slowly restored.