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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the presented article, the course and results of anatomical correction of transposition of great arteries (TGA) in 7 neonates (2 females and 5 males) with mean body mass of 3250 g and 2 to 5 days old (mean 3 days) are reviewed. Surgery was performed in moderate hypothermia. St. Thomas cold cardioplegia was used. Mean aortic clamping time was 70 min (55-115), and the time of extracorporeal circulation was 165 min (117-210). Low cardiac output in all patients in the postoperative period required prolonged mechanical ventilation and positive inotropic drugs. Out of 7 patients operated, two died (29%). The cause of death in both cases was myocardial ischemia of right ventricle. The other 5 patients were discharged after healing of operational wound. In the control echocardiographic examination performed 3 to 12 months postoperatively, apart from one case of moderate pulmonary artery stenosis, no other haemodynamically significant complications were noted.
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PMID:[Anatomical correction of transposition of the great arteries in 7 newborn infants]. 143 31

Coronary artery bypass without cardioplegia remains the preferred technique at many centers around the world. This report describes in detail a technique that emphasizes intermittent cross-clamping of the aorta at mild hypothermia (30 degrees C). Since coronary bypass procedures require brief interruptions of coronary blood flow only for the distal anastomoses, the duration of myocardial ischemia with this technique is not prolonged by unexpected changes in the operative plan. Many bypass grafts can also be carried out without cross-clamping of the aorta by using local control of the coronary arteries. The increasing number of elderly patients with atherosclerotic aortas that cannot be safely clamped makes it helpful for all cardiac surgeons to be familiar with noncardioplegic techniques.
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PMID:Technical considerations for coronary artery bypass without cardioplegia. 148 26

Acute postoperative hypertension (APH) has been documented in the PACU. Over half of the patients who exhibit APH have pre-existing primary hypertension. Sustained blood pressure (BP) elevation increases the risk of myocardial ischemia, infarction, surgical site bleeding, or cerebral hemorrhage in these patients. Following surgery and anesthesia, increased sympathetic stimulation caused by a high level of circulating catecholamines can lead to APH. Some direct perioperative stimulants include pain, anxiety, hypoxia, hypercapnia, hypothermia, shivering, volume overload, and bladder distension. Nursing interventions are directed toward identifying and relieving the cause of APH. Antihypertensive drug therapy with vasodilators or adrenergic inhibitors is used if initial nursing interventions are not effective. Vasodilators frequently used are hydralazine, sodium nitroprusside, and nitroglycerin. Nicardipine has recently been introduced as an intravenous calcium channel blocker. Vasodilators are effective in BP reduction but may cause reflex tachycardia when used alone. Adrenergic inhibitors, such as esmolol and labetalol, block alpha and/or beta receptors to decrease heart rate and BP. Labetalol's effectiveness, relative freedom from side effects, and ease of administration have made it a useful drug in the treatment of APH.
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PMID:Acute postoperative hypertension in the hypertensive patient. 173 70

Low cardiac output after surgically induced myocardial ischemia is a major contributor to mortality and morbidity after operations for congenital heart defects, despite myocardial "protection" with the techniques of hypothermia and cardioplegia that have been effective in protecting mature myocardium. The purpose of this study was to investigate the effectiveness of topical cooling to 15 degrees C, crystalloid cardioplegia, and blood cardioplegia in protecting 28 isolated neonatal lamb hearts subjected to 2 hours of ischemia. Seven hearts were isolated and perfused in a similar manner with cooling to 15 degrees C but were then rewarmed without any ischemia to serve as a control group. All three groups (topical cooling, crystalloid cardioplegia, and blood cardioplegia) had recovery of systolic function (as measured by maximum developed pressure, maximum rate of pressure rise, peak developed pressure at a fixed volume, and peak rate of pressure rise at a fixed volume) equal to the control group; the exception was peak rate of pressure rise at a fixed volume in the blood cardioplegia group, in which recovery was worse than in the control group. No differences among three ischemia groups or in comparison with the control group were found for measures of diastolic function (ventricular diastolic pressure at a fixed volume or stiffness constant kA). Systolic function declined in all groups (including control) from baseline to the end of the experiment. These findings suggest that hypothermia exerted the dominant protective effect in these normal neonatal lamb hearts and there was no added protection from either crystalloid or blood cardioplegia.
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PMID:Myocardial preservation in neonatal lambs. Comparison of hypothermia with crystalloid and blood cardioplegia. 200 9

The role of the anesthesiologist in myocardial protection is to optimize myocardial oxygen balance during the perioperative period. Nonpharmacological steps that can be taken to achieve this revolve around maintaining a satisfactory hemoglobin concentration and oxyhemoglobin saturation through maximizing ventilation. In addition, alkalosis and hypothermia should be prevented since they cause a left shift of the oxyhemoglobin dissociation curve, thus interfering with tissue oxygen delivery. Hypocarbia increases coronary vascular resistance. Blood volume must be adequate with an optimal hemoglobin concentration. Pharmacological measures should also be used, and it is important to continue through the perioperative period any previously administered cardioactive drugs. Furthermore, in the prebypass period, tachycardia may not be controlled by anesthetics; unless the tachycardia is paroxysmal, beta blockers are the drugs of choice. Depending on the cause, diastolic hypotension also needs to be treated either with volume, vasoconstrictors, or inotropes. Likewise, major hypertension can produce increased demand and, again depending on the cause, either anesthetics, vasodilators, beta blockers, or calcium blockers may be useful. Finally, myocardial ischemia without obvious cause probably should be treated with nitroglycerin or calcium blockers. During surgery, the effect of the anesthetic drugs on myocardial oxygen balance is important.
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PMID:Myocardial protection: what the anesthesiologist does. 213 51

With changing patient demographics resulting in greater risk of myocardial ischemia, avoidance of low-output states must begin with patient selection. From that point, a variety of well-established surgical techniques can be used to provide myocardial protection. Hypothermia and cardioplegia are fundamental among these; however, it should be recognized that alternate approaches must be considered. The well-documented deleterious effects of overdistension and hypoperfusion must be borne in mind. To this is added the complex formulation of contemporary cardioplegic solutions based on thorough understanding of the pathophysiology of ischemic injury. Specific deleterious consequences of ischemia and/or hypothermia are abnormalities of tissue volume regulation, lack of high-energy substrate availability, reduced capacity for postischemic oxidative metabolism, depressed availability of high-energy phosphate precursors, and the potential damage done by oxygen-induced free-radical-mediated oxidant injury.
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PMID:Myocardial protection: what the surgeon does. 213 52

The production and prevention of calcium paradox injury in myocardium was studied in a canine model of cardiopulmonary bypass with multidose, moderately hypothermic, crystalloid cardioplegic solution. During 4 1/2 hours of global ischemia, three groups of six dogs each received one of three histidine-buffered cardioplegic solutions (500 ml initially and 250 ml every 30 minutes) at 27 degrees C. Group 1 cardioplegic solution was calcium free, group 2 solution contained a trace amount of calcium chloride (70 mumols /L), and group 3 cardioplegic solution was calcium free but contained diltiazem (150 micrograms/kg body weight). Left ventricular function measured as percent control of developed pressure revealed significantly greater (p less than 0.05) recovery in groups 2 and 3. Triphenyltetrazolium chloride staining showed 35% +/- 9% (mean +/- standard error) of heart mass necrosis in group 1 versus 0% and 0.5% +/- 0.4% in groups 2 and 3, respectively (p less than 0.001). Electron microscopy revealed ultrastructural changes characteristic of calcium paradox injury in group 1 myocardium. Calcium paradox injury was produced in an in vivo model of global myocardial ischemia and multidose cardioplegia despite moderate hypothermia and non-coronary collateral flow. The addition of either trace levels of calcium or diltiazem to the cardioplegic solution was effective in preventing this injury.
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PMID:Calcium paradox in an in vivo model of multidose cardioplegia and moderate hypothermia. Prevention with diltiazem or trace calcium levels. 230 65

The intensity of lipid peroxidation (LPO) and antioxidant system activity (ASA) have been studied using chemiluminescent technique in 15 patients with ischemic heart disease subjected to surgery under moderate hypothermia. Two types of responses to surgical intervention and cardiopulmonary bypass have been demonstrated depending on baseline LPO intensity. Low baseline intensity of free-radical reactions at the beginning of perfusion is first enhanced and then attenuated by the end of perfusion, which is accompanied by ASA activation. This indicates adequate protective and adaptation body reactions. The same group of patients was characterized by a significant correlation between the parameters studied in venous blood and blood outflowing from the myocardium prior to and following the aorta clamping. With high LPO intensity that remained unchanged in the course of the intervention no correlation between LPO and ASA parameters has been observed in venous and coronary sinus blood. These patients develop various cardiovascular complications in the postperfusion period. It has been concluded that high baseline LPO level is prognostically unfavourable, with no correlations between the parameters under study observed in venous blood and blood outflowing from the myocardium.
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PMID:[Lipid peroxidation in open-heart operations]. 235 38

The possible myocardial protective effect of oral propranolol in combination with potassium cardioplegia and hypothermia was investigated in 30 greyhounds, divided into 2 sub-groups, by determining the changes in myocardial ATP and CP levels, ultrastructural changes and the changes in hemodynamics after a 2-hour period of myocardial ischemia. In group 1, in animals with multiple doses of cardioplegia during the 2-hour ischemic period, preoperative treatment with propranolol did not have a significant myocardial protective effect. In group 2, in animals with a single dose of cardioplegia, during the 2-hour ischemic period, propranolol resulted in a trend of improved survival, although the myocardial ATP and CP levels were the same in both sub-groups. In addition, the multiple doses of cardioplegia in group 1 caused increased subcellular edema in the myocardium. This study suggests that oral propranolol treatment may provide additional myocardial protection during ischemic periods when used with potassium cardioplegia and hypothermia. The mechanism of this effect is not established, but could relate to reduced transmembrane calcium influx.
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PMID:Oral beta-blockade with hypothermic potassium cardioplegia in cardiac surgery: is there an additive protective effect? 242 43

A hyperemic response on dog hearts following myocardial ischemia for 10 minutes has been studied in reference to myocardial protection with cardioplegia and hypothermia. Experimental animals were divided into four groups according to the difference in temperature and with or without cardioplegia during ischemia of the hearts. Group I (n = 7) succumbed to a normothermic ischemia. Group II (n = 6) had normothermic ischemia following infusion of 8 ml/kg of a normothermic cardioplegic solution. Group III (n = 7) had ischemia under moderate hypothermia (28 degrees C). Group IV [n = 7) had hypothermic ischemia following infusion of 8 ml/kg of hypothermic cardioplegic solution. A percent repayment of the flow debts in groups I, II, III, and IV were 234.6 +/- 38.3%, 101.5 +/- 40.8%, 134.5 +/- 50.0% and 112.8 +/- 36.5%, respectively. There was significant difference between group I and group II and IV (p less than 0.001) and group III (p less than 0.02). Peak flow in reactive hyperemia compared with control flow were 605.4 +/- 131.1%, 328.3 +/- 60.2%, 288.8 +/- 79.7% and 282.2 +/- 65.4% in each group I, II, III, and IV, respectively. The value in group I was significantly high in comparison with others (p less than 0.005). Depression of oxygen consumption was observed in groups with hypothermia as well as with cardioplegia. A hyperemic response was low in cardioplegia and/or hypothermia group. These data are suggestive of a beneficial use of cardioplegia and hypothermia on cardiac surgery through the observation of coronary reactive hyperemia after myocardial ischemia.
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PMID:[Experimental study of coronary reactive hyperemia--effects of hypothermia and potassium cardioplegia]. 260 Apr 63


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