T J Morgan1. 1. Intensive Care Facility, Division of Anaesthesiology and Intensive Care, Royal Brisbane Hospital, Brisbane, Queensland. morgant@health.qld.gov.au
Abstract
OBJECTIVE: To review the status of haemoglobin-oxygen affinity in critical illness and investigate the potential to improve gas exchange, tissue oxygenation and outcome by manipulations of the oxyhaemoglobin dissociation curve. DATA SOURCES: Articles and published peer-review abstracts. SUMMARY OF REVIEW: The P50 of a species is determined by natural selection according to animal size, tissue metabolic requirements and ambient oxygen tension. In right to left shunting mathematical modeling indicates that an increased P50 defends capillary oxygenation, the one exception being sustained hypercapnia. Increasing the P50 should also be protective in tissue ischaemia, and this is supported by modeling and experimental evidence. Most studies of critically ill patients have indicated reduced 2,3-DPG concentrations. This is probably due to acidaemia, and the in vivo P50 is likely to be normal despite low 2,3-DPG levels. It may soon be possible to achieve significant P50 elevations without potentially harmful manipulations of acid-base balance or hazardous drug therapy. CONCLUSIONS: Despite encouraging theoretical and experimental data, it is not known whether manipulations of the P50 in critical illness can improve gas exchange and tissue oxygenation or improve outcome. The status of the P50 may warrant more routine quantification and consideration along with the traditional determinants of tissue oxygen availability.
OBJECTIVE: To review the status of haemoglobin-oxygen affinity in critical illness and investigate the potential to improve gas exchange, tissue oxygenation and outcome by manipulations of the oxyhaemoglobin dissociation curve. DATA SOURCES: Articles and published peer-review abstracts. SUMMARY OF REVIEW: The P50 of a species is determined by natural selection according to animal size, tissue metabolic requirements and ambient oxygen tension. In right to left shunting mathematical modeling indicates that an increased P50 defends capillary oxygenation, the one exception being sustained hypercapnia. Increasing the P50 should also be protective in tissue ischaemia, and this is supported by modeling and experimental evidence. Most studies of critically illpatients have indicated reduced 2,3-DPG concentrations. This is probably due to acidaemia, and the in vivo P50 is likely to be normal despite low 2,3-DPG levels. It may soon be possible to achieve significant P50 elevations without potentially harmful manipulations of acid-base balance or hazardous drug therapy. CONCLUSIONS: Despite encouraging theoretical and experimental data, it is not known whether manipulations of the P50 in critical illness can improve gas exchange and tissue oxygenation or improve outcome. The status of the P50 may warrant more routine quantification and consideration along with the traditional determinants of tissue oxygen availability.
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