Pulmonary Complications in Patients with Brain Injury.
The severity of brain injury is the main determinant of morbidity and mortality in neurocritical patients. However, the role of other associated extracranial complications should not be disregarded1with pulmonary complications being among the most common ones. Major respiratory complications associated with injury to the Central Nervous System are caused by airways dysfunction, respiratory muscles dysfunction or intrinsic pulmonary disorders.
The occurrence of such complications could potentially cause hypoxemia, which would secondarily aggravate the brain damage. The objective of the present article was to offer an up to date review of theories and available evidence on relation between the cerebral alterations and the interactions to pulmonary level.
The interaction between the CNS and the respiratory system is evidenced at the physiological level since the respiratory center, located in the brain stem, controls involuntary respiratory activity and a second, less defined, center in the brain controls for the voluntary respiratory activity.
The ventilatory activity of airways and chest muscles is triggered by spinal cord and carotid sinuses, which are in turn
stimulated by CO2 and Hydrogen ion [H+] concentrations. Carotid sinuses also respond to changes in PaO2. Current theories proposed to explain the pathophysiological mechanisms of respiratory complications in case of brain injury are summarized as follows.
When brain injury occurs, an initial sympathetic discharge elevates plasmatic adrenaline
levels to about 1200 times the normal value within seconds. Although the level of
adrenaline subsequently falls, it keeps 3 times higher than normal for about ten days.
Pulm Res Respir Med Open J. 2(1): 69-74. doi: 10.17140/PRRMOJ-2-110
