vasopressor therapy in cardiac resuscitation

LITERATURE REVIEW 633 within 3 hours of air embolism during cardiopulmonary bypass. Four adults in whom hyperbaric oxygenation was delayed for 17-20 hours showed no or partial neurologic improvement. REVIEW ARTICLES Butler J, Rocker GM, Westaby S: Inflammatory response to cardiopulmonary bypass. Ann Thorac Surg 55:552-559,1993 Surgical trauma, blood contact with the extracorporeal circuit, and lung reperfusion are causes of the systemic inflammatory response seen after cardiopulmonary bypass. This succinct review outlines the components of this response and their pathophysiologic actions. Bypass-related alterations and complement, coagula- tion and fibrinolysis, leukocytes, elastase and antiproteases, oxygen free radicals, endotoxin and cytokines and their pathophysiologic effects are described. Effective clinical anti-inflammatory therapy does not exist. Experimental methods including oxygen radical scavengers, neutrophil inhibition, neutrophil granule stabilizers, aprotinin, and specific monoclonal antibodies are briefly reviewed. Kloner RA: Does reperfusion injury exists in hu- mans? J Am Co11Cardiol21:537-545,1993 Timely coronary reperfusion is advocated to reduce myocardial infarct size. Oxygen radical generation at the time of reperfusion has been implicated as a cause of further myocardial damage. Four types of reperfusion injury (lethal reperfusion injury, microvascular injury, stunned myocardium, reperfusion arrhythmias) and the experimental and clinical evidence both for and against these concepts are reviewed. McLean AS: Vasopressor therapy in cardiac resuscitation. Anaesth Intens Care 20:431-438,1992 This review examines the use of adrenalin (epinephrine) for cardiac resuscitation. Studies suggest that currently recommended doses of 0.5 to 1.0 mg may be inadequate, a dose of 3 to 15 mg being more appropriate although associated with increased myocardial oxygen consumption. Noradrenalin (norepinephrine), with similar o-agonist activity and ability to raise aortic diastolic pressure, improves the ratio of myocardial oxygen delivery and consumption possibly due to its selectivity for @t-receptors mediating coronary vasodilatation. Noradrenalin may be more efficacious than adrenalin in cardiac arrest. Pure cxt- and PI-agonists are generally contraindicated. Angiotensin II needs to be studied. ACKNOWLEDGMENT Papers reviewed in this issue were selected from those published in the following journals: American Heart Journal, American Review of Respiratory Disease, Anaesthesia and Intensive Care, Annals of Thoracic Surgery, British Heart Journal, Circulation, European Heart Journal, Journal of the American College of Cardiology, Journal of Thoracic and Cardiovascular Surgery, and Lancet. Contributions to the Literature Review in this issue were made by Dr J.G. Bovill, Leiden, The Netherlands and Dr Michael Davies, Melbourne, Australia.

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Page 1: Vasopressor therapy in cardiac resuscitation

LITERATURE REVIEW 633

within 3 hours of air embolism during cardiopulmonary bypass. Four adults in whom hyperbaric oxygenation was delayed for 17-20 hours showed no or partial neurologic improvement.

REVIEW ARTICLES

Butler J, Rocker GM, Westaby S: Inflammatory response to cardiopulmonary bypass. Ann Thorac Surg 55:552-559,1993

Surgical trauma, blood contact with the extracorporeal circuit, and lung reperfusion are causes of the systemic inflammatory response seen after cardiopulmonary bypass. This succinct review outlines the components of this response and their pathophysiologic actions. Bypass-related alterations and complement, coagula- tion and fibrinolysis, leukocytes, elastase and antiproteases, oxygen free radicals, endotoxin and cytokines and their pathophysiologic effects are described. Effective clinical anti-inflammatory therapy does not exist. Experimental methods including oxygen radical scavengers, neutrophil inhibition, neutrophil granule stabilizers, aprotinin, and specific monoclonal antibodies are briefly reviewed.

Kloner RA: Does reperfusion injury exists in hu- mans? J Am Co11 Cardiol21:537-545,1993

Timely coronary reperfusion is advocated to reduce myocardial infarct size. Oxygen radical generation at the time of reperfusion has been implicated as a cause of further myocardial damage. Four types of reperfusion injury (lethal reperfusion injury, microvascular

injury, stunned myocardium, reperfusion arrhythmias) and the experimental and clinical evidence both for and against these concepts are reviewed.

McLean AS: Vasopressor therapy in cardiac resuscitation. Anaesth Intens Care 20:431-438,1992

This review examines the use of adrenalin (epinephrine) for cardiac resuscitation. Studies suggest that currently recommended doses of 0.5 to 1.0 mg may be inadequate, a dose of 3 to 15 mg being more appropriate although associated with increased myocardial oxygen consumption. Noradrenalin (norepinephrine), with similar o-agonist activity and ability to raise aortic diastolic pressure, improves the ratio of myocardial oxygen delivery and consumption possibly due to its selectivity for @t-receptors mediating coronary vasodilatation. Noradrenalin may be more efficacious than adrenalin in cardiac arrest. Pure cxt- and PI-agonists are generally contraindicated. Angiotensin II needs to be studied.

ACKNOWLEDGMENT

Papers reviewed in this issue were selected from those published in the following journals: American Heart Journal, American Review of Respiratory Disease, Anaesthesia and Intensive Care, Annals of Thoracic Surgery, British Heart Journal, Circulation, European Heart Journal, Journal of the American College of Cardiology, Journal of Thoracic and Cardiovascular Surgery, and Lancet.

Contributions to the Literature Review in this issue were made by Dr J.G. Bovill, Leiden, The Netherlands and Dr Michael Davies, Melbourne, Australia.

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