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Intracellular calcium homeostasis and cardiac myocytes
LITERATURE REVIEW
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loss, and use of homologous blood. Ann Thorac Surg 55:1460-1466,1993 The effects of aprotinin (25,000 U/kg after induction of anesthesia, 25,000 U/kg added to the pump prime, and 25,000 U/kg every hour of cardiopulmonary bypass) on blood loss and platelet function were studied in 60 randomized children during cardiovascular operations. Maximum platelet aggregation in children less than 10 kg was lower at preoperative baseline than in children greater than 10 kg. Platelet aggregation was reduced significantly following cardiopulmonary bypass in both patient weight groups. Treatment with aprotinin did not improve platelet function, reduce blood loss or homologous blood use in either group compared to nontreated controls.
Sawchuk CWT, Ong B, Unruh HW, et ah ‘Ihoracic versus lumbar epidural fentanyl for post-thoracotomy pain. Ann Thorac Surg 55:1472-1476,1993 Thirty patients were prospectively randomized to receive thoracic or lumbar epidural fentanyl infusion for postthoracotomy pain. Postoperatively, patients received epidural fentanyl in titrated doses until visual analog scale score (O-10) was less than 4 or until maximum fentanyl dose of 150 p,g by bolus and an infusion rate of 150 &g/h was reached. Visual analog scale score was decreased more rapidly by thoracic fentanyl administration than by lumbar administration. Infusion rate required to maintain a visual analog score less than 4 was lower in the thoracic group (1.55 kg/kg/h) than in the lumbar group (2.06 kg/kg/h). Four patients in the lumbar group required naloxone intravenously for respiratory depression and somnolence. REVIEW ARTICLES
Brutsaert DL, Sys SU, Gillebert TC: Diastolic failure: Pathophysiology and therapeutic implications. J Am Co11Cardiol22:318-325,1993 Primary diastolic ventricular dysfunction results from increased resistance to ventricular filling, which leads to upward shift of the diastolic pressure-volume relationship, particularly during exercise. Causes of diastolic failure are inappropriate tachycardia, decreased diastolic compliance, and impaired systolic relaxation. The authors suggest that optimal therapy requires the cause of diastolic dysfunction be determined by echocardiography, Doppler analysis of ventricular filling, and cardiac catheterization when necessary, both at rest and during exercise. Tachycardia may be treated with l3-adrenergic antagonists, calcium channel blocking agents, or digitalis. Regression of myocardial changes (remodeling) reducingventricular compliance may be permitted by angiotension converting enzyme inhibitors and antialdosterone agents. Impaired systolic relaxation is treated by drugs with lusitropic actions. These may include calcium channel blockers, vasodilators, l3agonists, and phosphodiesterase inhibitors. The authors emphasize that drugs are not easily classified as negative or positive lusitropic agents and
a given drug’s lusitropic action depends on the type of myocardial disease underlying the diastolic dysfunction.
Barry WH, Bridge JI-IB: Intracellular calcium homeostasls and cardiac myocytes. Circulation 87:18061815,1993 In this Research Advances’ series article, the authors review the structure and function of the ion channels and transport proteins involved in calcium ion homeostasis. The control of resting myocyte calcium concentration, calcium ion fluxes during excitationcontraction coupling, and myocyte relaxation are described. The mechanisms by which digitalis, catacholamines, and phosphodiesterase inhibitors alter calcium ion homeostasis and improve inotropit function are briefly described.
Rubin LJ: Primary pulmonary hypertension. Chest 104:236-250,1993 This review article for the clinician describes the etiology, pathophysiology, diagnosis, and treatment of idiopathic primary pulmonary hypertension. The pathogenesis of primary pulmonary hypertension remains speculative. The pathophysiology including elevated pulmonary vascular resistance, right ventricular hypertrophy and dilation, right ventricular volume overload, tricuspid regurgitation, is well understood by cardiac anesthesiologists. Progressive right ventricular failure and sudden death due to arrhythmia, pulmonary hemorrhage, and right ventricular ischemia are common mechanisms of death. The author details diagnostic findings in the history and physical examination, and hemodynamic tests ranging from the electrocardiogram and echocardiography to cardiac catheterization, lung biopsy, and magnetic resonance imaging. There is no uniformly accepted or successful therapeutic approach. Oxygen therapy is not effective in primary pulmonary hypertension when hypoxic pulmonary vasoconstriction does not contribute to the pathogenesis of pulmonary vascular disease. There is little evidence digitalis is effective. Diuretics are useful in reducing right heart volume overload but must be titrated to avoid a fall in cardiac output. Anticoagulant therapy is provided for thromboembolism prophylaxis. The primary goal of drug therapy is pulmonary vasodilation and reduction in right ventricular afterload. This is most frequently attempted with oral calcium channel blocking agents. However in some patients vasodilators reduce systemic blood pressure without altering pulmonary artery pressure or cardiac output. Prostacyclin and prostaglandin El are the only intravenous vasodilators discussed by the author. ACKNOWLEDGMENT Papers reviewed in this issue were selected from those published in the following journals: American Heart Journal, Annals of Thoracic Swgery, Chest, Circulation, Clinical Pharmacology and Therapeutics, Journal of the American College of Cardiology, Journal of the American Medical Association, and Journal of Thoracic and Cardiovascular Surgery.
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loss, and use of homologous blood. Ann Thorac Surg 55:1460-1466,1993 The effects of aprotinin (25,000 U/kg after induction of anesthesia, 25,000 U/kg added to the pump prime, and 25,000 U/kg every hour of cardiopulmonary bypass) on blood loss and platelet function were studied in 60 randomized children during cardiovascular operations. Maximum platelet aggregation in children less than 10 kg was lower at preoperative baseline than in children greater than 10 kg. Platelet aggregation was reduced significantly following cardiopulmonary bypass in both patient weight groups. Treatment with aprotinin did not improve platelet function, reduce blood loss or homologous blood use in either group compared to nontreated controls.
Sawchuk CWT, Ong B, Unruh HW, et ah ‘Ihoracic versus lumbar epidural fentanyl for post-thoracotomy pain. Ann Thorac Surg 55:1472-1476,1993 Thirty patients were prospectively randomized to receive thoracic or lumbar epidural fentanyl infusion for postthoracotomy pain. Postoperatively, patients received epidural fentanyl in titrated doses until visual analog scale score (O-10) was less than 4 or until maximum fentanyl dose of 150 p,g by bolus and an infusion rate of 150 &g/h was reached. Visual analog scale score was decreased more rapidly by thoracic fentanyl administration than by lumbar administration. Infusion rate required to maintain a visual analog score less than 4 was lower in the thoracic group (1.55 kg/kg/h) than in the lumbar group (2.06 kg/kg/h). Four patients in the lumbar group required naloxone intravenously for respiratory depression and somnolence. REVIEW ARTICLES
Brutsaert DL, Sys SU, Gillebert TC: Diastolic failure: Pathophysiology and therapeutic implications. J Am Co11Cardiol22:318-325,1993 Primary diastolic ventricular dysfunction results from increased resistance to ventricular filling, which leads to upward shift of the diastolic pressure-volume relationship, particularly during exercise. Causes of diastolic failure are inappropriate tachycardia, decreased diastolic compliance, and impaired systolic relaxation. The authors suggest that optimal therapy requires the cause of diastolic dysfunction be determined by echocardiography, Doppler analysis of ventricular filling, and cardiac catheterization when necessary, both at rest and during exercise. Tachycardia may be treated with l3-adrenergic antagonists, calcium channel blocking agents, or digitalis. Regression of myocardial changes (remodeling) reducingventricular compliance may be permitted by angiotension converting enzyme inhibitors and antialdosterone agents. Impaired systolic relaxation is treated by drugs with lusitropic actions. These may include calcium channel blockers, vasodilators, l3agonists, and phosphodiesterase inhibitors. The authors emphasize that drugs are not easily classified as negative or positive lusitropic agents and
a given drug’s lusitropic action depends on the type of myocardial disease underlying the diastolic dysfunction.
Barry WH, Bridge JI-IB: Intracellular calcium homeostasls and cardiac myocytes. Circulation 87:18061815,1993 In this Research Advances’ series article, the authors review the structure and function of the ion channels and transport proteins involved in calcium ion homeostasis. The control of resting myocyte calcium concentration, calcium ion fluxes during excitationcontraction coupling, and myocyte relaxation are described. The mechanisms by which digitalis, catacholamines, and phosphodiesterase inhibitors alter calcium ion homeostasis and improve inotropit function are briefly described.
Rubin LJ: Primary pulmonary hypertension. Chest 104:236-250,1993 This review article for the clinician describes the etiology, pathophysiology, diagnosis, and treatment of idiopathic primary pulmonary hypertension. The pathogenesis of primary pulmonary hypertension remains speculative. The pathophysiology including elevated pulmonary vascular resistance, right ventricular hypertrophy and dilation, right ventricular volume overload, tricuspid regurgitation, is well understood by cardiac anesthesiologists. Progressive right ventricular failure and sudden death due to arrhythmia, pulmonary hemorrhage, and right ventricular ischemia are common mechanisms of death. The author details diagnostic findings in the history and physical examination, and hemodynamic tests ranging from the electrocardiogram and echocardiography to cardiac catheterization, lung biopsy, and magnetic resonance imaging. There is no uniformly accepted or successful therapeutic approach. Oxygen therapy is not effective in primary pulmonary hypertension when hypoxic pulmonary vasoconstriction does not contribute to the pathogenesis of pulmonary vascular disease. There is little evidence digitalis is effective. Diuretics are useful in reducing right heart volume overload but must be titrated to avoid a fall in cardiac output. Anticoagulant therapy is provided for thromboembolism prophylaxis. The primary goal of drug therapy is pulmonary vasodilation and reduction in right ventricular afterload. This is most frequently attempted with oral calcium channel blocking agents. However in some patients vasodilators reduce systemic blood pressure without altering pulmonary artery pressure or cardiac output. Prostacyclin and prostaglandin El are the only intravenous vasodilators discussed by the author. ACKNOWLEDGMENT Papers reviewed in this issue were selected from those published in the following journals: American Heart Journal, Annals of Thoracic Swgery, Chest, Circulation, Clinical Pharmacology and Therapeutics, Journal of the American College of Cardiology, Journal of the American Medical Association, and Journal of Thoracic and Cardiovascular Surgery.