title: The effect of extracorporeal life support on the brain: cardiopulmonary bypass.
abstract: This article reviews the mechanisms of brain injury associated with cardiopulmonary bypass. These include embolic injury of both a gaseous and particulate nature as well as global hypoxic ischemic injury. Ischemic injury can result from problems associated with venous drainage or with arterial inflow including a steal secondary to systemic to pulmonary collateral vessels. Modifications in the technique of cardiopulmonary bypass have reduced the risk of global hypoxic/ischemic injury. Laboratory and clinical studies have demonstrated that perfusion hematocrit should be maintained above 25% and preferably above 30%. Perfusion pH is also critically important, particularly when hypothermia is employed. An alkaline pH can limit cerebral oxygen delivery by inducing cerebral vasoconstriction as well as shifting oxyhemoglobin dissociation leftwards. If deep hypothermia is employed, it is critically important to add carbon dioxide using the so-called "pH stat" strategy. Oxygen management during cardiopulmonary bypass is also important. Although there is currently enthusiasm for using air rather than pure oxygen, ie, adding nitrogen, this does introduce a greater risk of gaseous nitrogen emboli since nitrogen is much less soluble than oxygen. The use of pure oxygen in conjunction with CO2 to apply the pH stat strategy is recommended. Many of the lessons learned from studies focusing on brain protection during cardiopulmonary bypass can be applied to the patient being supported with extracorporeal membrane oxygenation.
authors.affiliation: Department of Cardiovascular Surgery, Children's National Medical Center, 111 Michigan Avenue NW, Washington, DC 20010, USA. rjonas@cnmc.org
authors.forename: Richard A
authors.initials: RA
authors.lastname: Jonas
mesh_terms: D001921:Brain; D002545:Brain Ischemia / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control / Q000628:therapy; D002315:Cardiopulmonary Bypass / Q000009:adverse effects*; D002561:Cerebrovascular Disorders / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control / Q000628:therapy; D002648:Child; D006400:Hematocrit; D006801:Humans; D006863:Hydrogen-Ion Concentration; D010100:Oxygen / Q000627:therapeutic use
chemical_list: D010100:Oxygen