Date of Award

8-1-2005

Document Type

Independent Study

Degree Name

Master of Science (MS)

Department

Nursing

Abstract

Neurosurgical procedures continue to be a challenging and intricate part of an anesthesia provider’s career. The anesthesia provider can control the physiological effects of improper auto-regulation of the brain that can occur with abnormal neurological pathology. The control of hyperventilation is one way that the anesthesia provider can manipulate cerebral physiology. This paper addresses the physiology of impaired brain autoregulation and the role in which carbon dioxide affects that physiology. Simply stated, carbon dioxide (C02) is the number one physiological factor that controls cerebral blood flow; increasing C02 dilates cerebral vessels thus increasing flow while decreasing C02 constricts cerebral vessels hence decreasing cerebral flow and intracranial pressure. Yet, decreasing blood flow also decreases oxygen transport, which is placing the brain at increased risk for continuing ischemia. Numerous research studies were critiqued regarding the usage of hyperventilation in neurosurgery. These findings were than compared and contrasted with pertinent findings discussed within the body of this paper. Overwhelming support dictates judicious usage of hyperventilation under anesthesia and suggests maintaining end tidal carbon dioxide levels no lower that 28-30mmHg to prevent decreasing oxygen flow at a time where it is greatly needed. A summary of pertinent findings is printed within the appendix of this paper. This paper concludes with implications for nursing research, practice, education, and policy development.

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