{"title":"Perioperative Management of the Patient Undergoing Abdominal Aortic Surgery","authors":"M. Cobas, T. Smaka, D. Lubarsky","doi":"10.1097/ASA.0B013E3181EAE211","DOIUrl":null,"url":null,"abstract":"Cardiovascular Changes Gelman et al. established the basis of our understanding of the pathophysiology of hemodynamic changes that occur with aortic clamping and unclamping. Aortic cross clamping increases mean arterial pressure and systemic vascular resistance (SVR) up to 50%. These sudden increases are due to an increase in mechanical afterload, activation of renin, and release of catecholamines, prostaglandins, and other vasoconstrictors. This increase in SVR causes an initial reflexive decrease in cardiac output (see Supplemental Digital Content 1, http://links.lww.com/ASA/A1). Some of the initial changes in hemodynamics associated with cross clamping can be offset by the sympathectomy caused by a thoracic epidural or with boluses of a vasodilator administered immediately before placement of the clamp. Shortacting pharmacologic agents (e.g., 0.3-0.7 mcg/kg of nitroprusside, 80-200 mcg of nitroglycerin or 200-600 mcg nicardipine) offset the mechanical effect of cross clamping, allowing the body to adapt. Preload changes are more variable than changes in SVR. Higher central venous and pulmonary artery occlusion pressures occur with higher clamp placement due to central redistribution of blood. In the patient with coronary disease, nitrate therapy during cross clamp will not necessarily prevent wall motion abnormalities, and care should be exercised when using any vasodilator so that perfusion pressure below the aortic cross clamp remains sufficient to avoid visceral/spinal cord ischemia. We will allow a systolic blood pressure (SBP) as high as 180-200 mm Hg provided there is no contraindication and the surgeon has acceptable operating conditions. Relative hypotension (less than 20% below baseline mean arterial pressure) probably should be avoided unless other means, such as shunts, are used to provide perfusion below the clamp. The level of clamping and the chronicity of occlusive disease can dramatically affect the hemodynamic response. The hemodynamic response is greater when the clamp is more proximal along the aorta (proximal descending thoracic aorta 4 supraceliac 4 suprarenal 4 infrarenal). There is an even smaller hemodynamic response when","PeriodicalId":91163,"journal":{"name":"Refresher courses in anesthesiology","volume":"38 1","pages":"23-29"},"PeriodicalIF":0.0000,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/ASA.0B013E3181EAE211","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Refresher courses in anesthesiology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1097/ASA.0B013E3181EAE211","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Cardiovascular Changes Gelman et al. established the basis of our understanding of the pathophysiology of hemodynamic changes that occur with aortic clamping and unclamping. Aortic cross clamping increases mean arterial pressure and systemic vascular resistance (SVR) up to 50%. These sudden increases are due to an increase in mechanical afterload, activation of renin, and release of catecholamines, prostaglandins, and other vasoconstrictors. This increase in SVR causes an initial reflexive decrease in cardiac output (see Supplemental Digital Content 1, http://links.lww.com/ASA/A1). Some of the initial changes in hemodynamics associated with cross clamping can be offset by the sympathectomy caused by a thoracic epidural or with boluses of a vasodilator administered immediately before placement of the clamp. Shortacting pharmacologic agents (e.g., 0.3-0.7 mcg/kg of nitroprusside, 80-200 mcg of nitroglycerin or 200-600 mcg nicardipine) offset the mechanical effect of cross clamping, allowing the body to adapt. Preload changes are more variable than changes in SVR. Higher central venous and pulmonary artery occlusion pressures occur with higher clamp placement due to central redistribution of blood. In the patient with coronary disease, nitrate therapy during cross clamp will not necessarily prevent wall motion abnormalities, and care should be exercised when using any vasodilator so that perfusion pressure below the aortic cross clamp remains sufficient to avoid visceral/spinal cord ischemia. We will allow a systolic blood pressure (SBP) as high as 180-200 mm Hg provided there is no contraindication and the surgeon has acceptable operating conditions. Relative hypotension (less than 20% below baseline mean arterial pressure) probably should be avoided unless other means, such as shunts, are used to provide perfusion below the clamp. The level of clamping and the chronicity of occlusive disease can dramatically affect the hemodynamic response. The hemodynamic response is greater when the clamp is more proximal along the aorta (proximal descending thoracic aorta 4 supraceliac 4 suprarenal 4 infrarenal). There is an even smaller hemodynamic response when