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Relation of oxygen transport patterns to the pathophysiology and therapy of shock states
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LITERATURE REVIEW
heart size and reduced need for other therapy for congestive failure. At 12 months mortality remained lower in the enalapril group (36% v 52% in controls). The only side effect was hypotension, requiring discontinuation of enalapril in seven patients, but controllable in other patients by reduction of dosage to 2.5 mg daily. Enalapril modifies the progression of heart failure, which significantly decreases mortality.
Rotmensch HH, Rotmensch S, Elkayam U: Management of cardiac arrhythmias during pregnancy. Current concepts. Drugs 33~623-633, 1987 In contrast to the numerous case reports of the management of pregnant patients with various cardiac arrhythmias, this article reviews the diagnostic evaluation of patients with arrhythmias, the significance of arrhythmias on fetal well being, and the pharmacology of antiarrhythmic drugs during pregnancy. Cardiac arrhythmias resulting from underlying cardiac disease can present for the first time during pregnancy as the hemodynamic burden increases. Treatment of the primary cardiac condition, rather than the arrhythmia, is essential. Antiarrhythmic drugs should be given in minimal effective doses when absolutely necessary for maternal and fetal well being. Certain antiarrhythmic drugs are “safer” than others during pregnancy. Examples include digoxin, quinidine, lidocaine, procainamide, and some beta-blocking drugs such as labetalol, metoprolol, and atenolol. Based on available reports, the authors suggest that disopyramide, mexiletine, amiodarone, verapamil, or phenytoin need additional studies to determine their safety in the pregnant patient. Cardioversion, however, can be safely performed during pregnancy although data is limited.
Shoemaker WC: Relation of oxygen transport patterns to the pathophysiology and therapy of shock states. Intensive Care Med 13:230-243, 1987 Oxygen transport and delivery are critically evaluated in this and a related article: Schumacker PT, Cain SM: The concept of a critical oxygen delivery. Intensive Care Med 13:223-229, 1987. Reduced or inadequate oxygen consumption is the common component of all types of shock. Oxygen transport is significantly related to survival in shock. The first recognized clinical features of shock are often the compensatory responses to inadequate oxygen consumption such as tachycardia, increased cardiac output and contractility, and tachypnea. Therapy including fluids, vasoactive drugs, blood, and other measures can be guided by determination of oxygen consumption and oxygen delivery (product of cardiac index and arterial oxygen content). In healthy humans, decreases in oxygen delivery do not decrease oxygen consumption because tissue oxygen extraction increases. As oxygen delivery decreases to a critical point, however, oxygen consumption decreases and blood lactate increases because tissue oxygen extraction cannot increase proportionately to the reduced delivery. An increase in the extraction ratio (ratio of arteriovenous oxygen content difference/ arterial oxygen content) occurs. The critical limit remains undefined with values for oxygen delivery between 8 mL/min/kg and 21 mL/min/kg being the critical point in different populations of patients. Nevertheless, the clinical
admonition of both of these articles is to maximize systemic oxygen delivery by alteration of cardiac output, hemoglobin, and arterial Pot.
Langer GA, Weiss JN, Schelhert HR: Cardiac ischemia. Part I-Metabolic and physiologic responses. Langer GA, Buckberg GD, Tillisch JH: Cardiac ischemia. Part II-Reperfusion and treatment. West J Med 146713-723 and 14754-61, 1987 (Also the accompanying editorial: Jennings RB: Treatment of acute myocardial ischemia. West J Med 147~62-64, 1987) Widely diverse therapies have been reported to decrease the size of myocardial infarctions. However, recently recognized difficulties in the measurement of infarct size and the variability of infarctions produced under controlled conditions (because of collateral circulation, hemodynamic factors, etc) invalidate much earlier experimental work. Myocardial cell death resulting from reduction in arterial flow can be prevented by restoration of arterial flow after brief ischemic intervals. These articles summarize discussions from an interdepartmental conference at UCLA. Normal cardiac metabolism and its alteration with ischemia is reviewed. However, the precise molecular change or changes causing cellular death from ischemia is unknown. The desirability of restoring stable cardiac electrophysiology by modification of ionic concentrations or accumulation of metabolic by-products is recognized. Positron emission tomography can evaluate the metabolic consequences of ischemia, providing an objective measure of myocardial salvage if the ischemic myocytes have a distinctive metabolic state with an isotopic marker. Finally, the effects of reperfusion are reviewed. Careful control of the composition of the reperfusate and the conditions under which it is infused enhances myocardial salvage and functional recovery. Because clinical studies suggest excellent recovery after surgical reperfusion (coronary bypass grafting and use of substrate-enriched cardioplegia), a preliminary report of a method to permit controlled coronary reperfusion without thoracotomy is described.
ACKNOWLEDGMENT The papers reviewed for this issue include those published in the following journals: Acta Anaesthesiologica Scandinavica. American Heart Journal, American Journal of Cardiology, American Review of Respiratory Disease, Anaesthesia. Anesthesia and Analgesia, Anesthesiology, Angiology, Annals of Thoracic Surgery, British Heart Journal, Canadian Journal of Anaesthesia, Cardiovascular Research, Chest, Circulation, Circulation Research, Critical Care Medicine, International Journal of Cardiology, Journal of the American College of Cardiology, Journal of Applied Physiology, Journal of Cardiovascular Pharmacology, Journal of Molecular and Cellular Cardiology, Journal of Pharmacology and Experimental Therapeutics, Journal of Thoracic and Cardiovascular Surgery, Journal of Trauma, Journal of Vascular Surgery, New England Journal of Medicine, Pace, Progress in Cardiovascular Diseases, Stroke, Thorax, Thrombosis and Haemostasis. Transfusion, Vascular Surgery, and Western Journal of Medicine.
LITERATURE REVIEW
heart size and reduced need for other therapy for congestive failure. At 12 months mortality remained lower in the enalapril group (36% v 52% in controls). The only side effect was hypotension, requiring discontinuation of enalapril in seven patients, but controllable in other patients by reduction of dosage to 2.5 mg daily. Enalapril modifies the progression of heart failure, which significantly decreases mortality.
Rotmensch HH, Rotmensch S, Elkayam U: Management of cardiac arrhythmias during pregnancy. Current concepts. Drugs 33~623-633, 1987 In contrast to the numerous case reports of the management of pregnant patients with various cardiac arrhythmias, this article reviews the diagnostic evaluation of patients with arrhythmias, the significance of arrhythmias on fetal well being, and the pharmacology of antiarrhythmic drugs during pregnancy. Cardiac arrhythmias resulting from underlying cardiac disease can present for the first time during pregnancy as the hemodynamic burden increases. Treatment of the primary cardiac condition, rather than the arrhythmia, is essential. Antiarrhythmic drugs should be given in minimal effective doses when absolutely necessary for maternal and fetal well being. Certain antiarrhythmic drugs are “safer” than others during pregnancy. Examples include digoxin, quinidine, lidocaine, procainamide, and some beta-blocking drugs such as labetalol, metoprolol, and atenolol. Based on available reports, the authors suggest that disopyramide, mexiletine, amiodarone, verapamil, or phenytoin need additional studies to determine their safety in the pregnant patient. Cardioversion, however, can be safely performed during pregnancy although data is limited.
Shoemaker WC: Relation of oxygen transport patterns to the pathophysiology and therapy of shock states. Intensive Care Med 13:230-243, 1987 Oxygen transport and delivery are critically evaluated in this and a related article: Schumacker PT, Cain SM: The concept of a critical oxygen delivery. Intensive Care Med 13:223-229, 1987. Reduced or inadequate oxygen consumption is the common component of all types of shock. Oxygen transport is significantly related to survival in shock. The first recognized clinical features of shock are often the compensatory responses to inadequate oxygen consumption such as tachycardia, increased cardiac output and contractility, and tachypnea. Therapy including fluids, vasoactive drugs, blood, and other measures can be guided by determination of oxygen consumption and oxygen delivery (product of cardiac index and arterial oxygen content). In healthy humans, decreases in oxygen delivery do not decrease oxygen consumption because tissue oxygen extraction increases. As oxygen delivery decreases to a critical point, however, oxygen consumption decreases and blood lactate increases because tissue oxygen extraction cannot increase proportionately to the reduced delivery. An increase in the extraction ratio (ratio of arteriovenous oxygen content difference/ arterial oxygen content) occurs. The critical limit remains undefined with values for oxygen delivery between 8 mL/min/kg and 21 mL/min/kg being the critical point in different populations of patients. Nevertheless, the clinical
admonition of both of these articles is to maximize systemic oxygen delivery by alteration of cardiac output, hemoglobin, and arterial Pot.
Langer GA, Weiss JN, Schelhert HR: Cardiac ischemia. Part I-Metabolic and physiologic responses. Langer GA, Buckberg GD, Tillisch JH: Cardiac ischemia. Part II-Reperfusion and treatment. West J Med 146713-723 and 14754-61, 1987 (Also the accompanying editorial: Jennings RB: Treatment of acute myocardial ischemia. West J Med 147~62-64, 1987) Widely diverse therapies have been reported to decrease the size of myocardial infarctions. However, recently recognized difficulties in the measurement of infarct size and the variability of infarctions produced under controlled conditions (because of collateral circulation, hemodynamic factors, etc) invalidate much earlier experimental work. Myocardial cell death resulting from reduction in arterial flow can be prevented by restoration of arterial flow after brief ischemic intervals. These articles summarize discussions from an interdepartmental conference at UCLA. Normal cardiac metabolism and its alteration with ischemia is reviewed. However, the precise molecular change or changes causing cellular death from ischemia is unknown. The desirability of restoring stable cardiac electrophysiology by modification of ionic concentrations or accumulation of metabolic by-products is recognized. Positron emission tomography can evaluate the metabolic consequences of ischemia, providing an objective measure of myocardial salvage if the ischemic myocytes have a distinctive metabolic state with an isotopic marker. Finally, the effects of reperfusion are reviewed. Careful control of the composition of the reperfusate and the conditions under which it is infused enhances myocardial salvage and functional recovery. Because clinical studies suggest excellent recovery after surgical reperfusion (coronary bypass grafting and use of substrate-enriched cardioplegia), a preliminary report of a method to permit controlled coronary reperfusion without thoracotomy is described.
ACKNOWLEDGMENT The papers reviewed for this issue include those published in the following journals: Acta Anaesthesiologica Scandinavica. American Heart Journal, American Journal of Cardiology, American Review of Respiratory Disease, Anaesthesia. Anesthesia and Analgesia, Anesthesiology, Angiology, Annals of Thoracic Surgery, British Heart Journal, Canadian Journal of Anaesthesia, Cardiovascular Research, Chest, Circulation, Circulation Research, Critical Care Medicine, International Journal of Cardiology, Journal of the American College of Cardiology, Journal of Applied Physiology, Journal of Cardiovascular Pharmacology, Journal of Molecular and Cellular Cardiology, Journal of Pharmacology and Experimental Therapeutics, Journal of Thoracic and Cardiovascular Surgery, Journal of Trauma, Journal of Vascular Surgery, New England Journal of Medicine, Pace, Progress in Cardiovascular Diseases, Stroke, Thorax, Thrombosis and Haemostasis. Transfusion, Vascular Surgery, and Western Journal of Medicine.