The Pathophysiology of Cerebral Arterial Gas Embolism

¹ The Wesley Centre for Hyperbaric Medicine, Brisbane, Australia
² Faculty of Medicine and Health Sciences, University of Auckland, Auckland, New Zealand

^* Address correspondence to: Dr. Simon Mitchell, The Wesley Centre for Hyperbaric Medicine, P.O. Box 2056, Milton Q 4064, Brisbane, Australia. E-mail: smitchell@wesley.com.au

Received: 3 September 2001
Accepted: 20 January 2002

Abstract

Bubbles are introduced to the arterial circulation in many patients undergoing cardiac surgical procedures, and some of these distribute to the cerebral vessels. Larger bubbles may arrest in cerebral arterioles, causing ischemia and neuronal injury in the downstream territory. Smaller bubbles may redistribute through the cerebral circulation, but this is not a benign event. Their passage may cause transient ischemia and cause damage to endothelium. Margination and activation of leukoctyes follows, and may cause a secondary ischemia. Although the potential of large bubbles to cause cerebral injury is not disputed, there is controversy over the significance of exposure to small bubbles in cardiac surgery. It is known that postsurgical neuropsychological deficits do correlate positively with numbers of emboli to which patients are exposed, but to date, the technology to distinguish between gaseous and particulate emboli or to size emboli accurately is not readily available. Until this technology becomes available and is applied in large studies designed to determine the importance of small bubbles, it seems prudent to take all practical steps to prevent introduction of arterial bubbles in cardiac surgery.