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

Since the gradient between aortic pressure and left ventricular diastolic pressure is a major determinant of coronary blood flow, a change in left ventricular relaxation by its effect on early diastole could diminish early diastolic coronary flow. Two interventions that resulted in impaired left ventricular relaxation, hypothermia, and reperfusion following a left anterior descending coronary artery occlusion were studied to evaluate whether there were associated changes in coronary blood flow. With both interventions, there was a significant prolongation of left ventricular relaxation (p less than 0.01) accompanied by a significant decrease in early diastolic coronary blood flow (p less than 0.01). Verapamil did not have a significant effect on these hemodynamic changes during hypothermia. However, verapamil significantly blunted the effects of reperfusion following ischemia on ventricular relaxation (p less than 0.002) and early diastolic coronary blood flow (p less than 0.01). Thus, impaired left ventricular relaxation has an adverse impact on early diastolic coronary blood flow, which, under the condition of reperfusion following regional myocardial ischemia, can be alleviated with calcium channel blockade.
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PMID:Effect of changes in ventricular relaxation on early diastolic coronary blood flow in canine hearts. 366 79

The hypothesis of this study was that inadequate right ventricular hypothermia contributes to the right ventricular dysfunction occasionally observed after cardiac operations. Dogs were placed on cardiopulmonary bypass, and 60 minute periods of hypothermic myocardial ischemia were imposed. Left ventricular temperature was always maintained at 15 degrees C and right ventricular temperatures were maintained at 15 degrees C (Group I, n = 8), 25 degrees C (Group II, n = 8), and 35 degrees C (Group III, n = 8). These temperatures were produced by infusion of hypothermic crystalloid cardioplegic solution and appropriate topical cooling and heating of the left and right ventricles, respectively. Multiple indices of ventricular function were obtained 15, 30, 45, and 60 minutes after bypass and compared to prebypass control values. In all Group I animals (left ventricular temperature = 15 degrees C, right ventricular temperature = 15 degrees C), postischemic indices of right ventricular function were not different from control values (p = NS). In Group II (left ventricular temperature = 15 degrees C, right ventricular temperature = 25 degrees C), two animals died 30 and 45 minutes after bypass, respectively, of right ventricular failure. In the other six animals in Group II, all indices of right ventricular function were significantly reduced (p less than 0.05) except for right ventricular systolic pressure. In Group III (left ventricular temperature = 15 degrees C, right ventricular temperature = 35 degrees C), two animals could not be weaned from cardiopulmonary bypass because of right ventricular akinesia. Six animals were weaned from bypass, but two died 15 minutes, one died 30 minutes, and one 45 minutes after bypass. Two animals lived 60 minutes, but all indices of right ventricular function were decreased. Failure to maintain right ventricular temperatures below 25 degrees C during 1 hour of cardiac ischemia in the dog can result in fatal right ventricular failure.
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PMID:Acute right ventricular failure is caused by inadequate right ventricular hypothermia. 397 74

Since the hemodynamic response elicited by the administration of citrate is sensitive to alterations in the baseline cardiovascular status, we have investigated the consequences of peroperative myocardial ischemia upon this hemodynamic response. 19 dogs equipped with an electromagnetic flow probe positioned around the ascending aorta served as control (group I). 16 dogs were equipped similarly and in addition submitted to 1 h of myocardial ischemia combined with topical cardiac hypothermia (group II). Hemodynamic studies were carried out 3 h postoperatively and then daily for 1 month, before and during rapid intravenous administration of citrate. From baseline hemodynamic data, cardiac failure was only evident 3 h postoperatively in group II. Transient hypotension and myocardial depression resulted from administration of citrate in both groups with no evidence of peripheral vasodilation. Hypotension and the negative inotropic response were more pronounced in the presence of cardiac failure following peroperative myocardial ischemia. Long-term studies indicate that global myocardial ischemia did not interfere with the cardiovascular adaptability to this pharmacologic interference.
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PMID:Peroperative myocardial ischemia and citrate administration: cardiovascular adaptability in conscious dogs. 404 54

Although it is well established that coronary revascularization can reverse exercise-induced ischemic dysfunction, the effects on resting ventricular performance are controversial. From a group of 183 patients receiving surgical therapy for ischemic heart disease, 166 underwent bypass graft arteriography at an average of 7 to 14 days postoperatively. In 149 patients, satisfactory preoperative and postoperative biplane left ventriculograms were obtained. Regional wall motion was assessed by the 100 segment method of Sheehan and Dodge, and a perioperative change in shortening greater than 2 standard deviations of normal variability over 20 or more adjacent segments was considered significant. Ninety-five patients had stable or progressive angina, 88 had medically refractory unstable angina, 155 were in New York Heart Association Class IV, and 37 had a preoperative left ventricular ejection fraction of less than 0.4. Myocardial integrity was preserved with crystalloid cardioplegia and topical hypothermia. Seven hundred ninety-eight bypass grafts were performed (522 vein grafts and 276 mammary artery grafts), and 13 patients had concomitant left ventricular aneurysmectomy. Hospital mortality was 2.2%. The overall early graft patency rate was 95.9% (93.7% for vein grafts and 100% for mammary arteries). Only one patient had a decrement in regional wall motion, and 51 (37%) had significant postoperative improvement (27 in the unstable angina group and 24 in the stable angina group); in the patients with improved regional wall motion, ejection fraction increased by an average of 0.18 (p less than 0.01). Ejection fraction also improved after aneurysmectomy, and the increment seemed to result from both a reduction in end-diastolic volume and improved regional wall motion. Thus, reversible ischemic myocardial dysfunction appears to be common in the general population of patients undergoing coronary artery bypass grafting; 40% of patients with unstable angina and 34% of those with stable angina can be expected to have improved regional wall motion after successful revascularization. Finally, ventricular aneurysm resection significantly enhances left ventricular performance as assessed by ventriculographic ejection fraction.
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PMID:The effects of coronary revascularization on left ventricular function in ischemic heart disease. 406 32

During the past decade, efforts to limit the extent of myocardium exhibiting infarction once ischemia has been initiated have focused on manipulation of myocardial oxygen supply and demand as well as the process of injury itself. Interventions of promise range from the conventional, moderate increase in inspired oxygen content, to administration of hyaluronidase or intracoronary thrombolysis to augment oxygen supply; use of beta-adrenergic blocking drugs and nitroglycerin to diminish demand; and administration of calcium antagonists and prostaglandin synthesis inhibitors to limit the injury process. The ultimate effects on infarct size and long-term mortality have yet to be established unequivocally for any of these approaches in the clinical setting of acute myocardial infarction, but significant preservation of ischemic myocardium with hypothermia and with administration of nifedipine during coronary-artery bypass surgery have been documented. Several prospective, large-scale, blinded, and random sample selection clinical trials are currently in progress. Their results should definitively elucidate the clinical utility of specific interventions under defined conditions and should help to further improve the management of patients with ischemic heart disease.
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PMID:Pharmacological salvage of myocardium. 612 93

In order to perform intracardiac repair safely during aortic cross clamping, we designed this study to evaluate the protective effect of coenzyme Q10 (CoQ10) on hypertrophied ischemic myocardium from the aspect of energy metabolism. Six to nine months preceding the study, aortic bandings were carried out on 14 puppies to produce left ventricular hypertrophy (LVH). These dogs with LVH were then subjected to total cardiopulmonary bypass and were evenly divided into control and CoQ10-treated groups (10 mg/kg of intravenous administration plus 1 mg/kg per hr of intracoronary injection). Myocardial ischemia was induced by aortic cross clamping for 2 hr under moderate systemic hypothermia. The results indicated that the administration of CoQ10 had a protective effect on hypertrophied ischemic myocardium, since depletion of high-energy phosphate (HEP) was uniformly prevented, and accumulation of lactate was simultaneously decreased during the 2 hr of aortic cross clamping. On the other hand, there were marked exhaustion of HEP and rapid increase in lactate following the 2 hr of ischemia in the control group, these being much more predominant in the subendocardial layer.
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PMID:Effect of coenzyme Q10 on hypertrophied ischemic myocardium during aortic cross clamping for 2 hr, from the aspect of energy metabolism. 622 44

Multidose administration of cardioplegic solution during cardiac operation is intended to maintain both electromechanical arrest of the heart and myocardial hypothermia as well as to remove accumulated metabolites of anaerobic glycolysis. This study was conducted to assess the effect of multidose infusion of three different types of cardioplegic solution on tissue acidosis during global myocardial ischemia. Three groups of five dogs each were placed on cardiopulmonary bypass and the aorta was cross-clamped for 3 hours. The hearts were maintained at a constant temperature (20 degrees C) and cardioplegic solution was infused at an initial dose of 500 ml and five supplementary doses of 250 ml administered every 30 minutes. Group 1 received a crystalloid solution weakly buffered with sodium bicarbonate, Group 2 received a blood-based solution, and Group 3 received a crystalloid solution strongly buffered with histidine (Bretschneider's solution). The buffering capacities of the solutions used in Groups 2 and 3 were 40 and 60 times, respectively, that of the solution used in Group 1. The average myocardial tissue pH at the end of 3 hours of ischemia was 6.54 +/- 0.07 in Group 1, 7.23 +/- 0.05 in Group 2, and 7.19 +/- 0.06 in Group 3 (Group 1 significantly lower than Groups 2 and 3). Multidose infusion of a cardioplegic solution with low buffering capacity was unable to prevent the progressive development of tissue acidosis during 3 hours of ischemia. However, the multidose infusion of either blood-based or crystalloid solutions with high buffering capacity completely prevented any further reduction of tissue pH after the first 30 minutes of ischemia.
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PMID:Effect of multidose cardioplegia and cardioplegic solution buffering on myocardial tissue acidosis. 628 76

Because hypotension induced by the administration of hypertonic sodium bicarbonate is more severe when cardiac performance is impaired, the authors evaluated the hemodynamic consequences of peroperative myocardial ischemia upon the response of conscious dogs to an intravenous bolus of sodium bicarbonate. Twenty-two control dogs (group 1) were equipped with an electromagnetic flow probe positioned around the ascending aorta. Seventeen dogs (group 2), equipped in the same manner, were subjected to 1 hour of myocardial ischemia combined with topical cardiac hypothermia. Hemodynamic studies were performed daily for 1 month before and during the administration of sodium bicarbonate. Baseline hemodynamic values in group 1 were always within normal limits. In group 2, cardiac failure was evident in the immediate postoperative period but hemodynamic values reached normal limits 24 hours postoperatively. For both groups, the peak hypotensive response to sodium bicarbonate was combined with a substantial reduction in all hemodynamic values reflecting the left ventricular performance. However, this response is significantly (p less than 0.01) more pronounced in group 2 during the first 4 postoperative days, being maximal 3 and 24 hours after operation. Afterwards, the hemodynamic response to sodium bicarbonate was similar in both groups. These results indicated that an intravenous bolus of sodium bicarbonate decreases left ventricular performance and that this decrement is greater when cardiac performance is impaired following peroperative myocardial ischemia. Long-term hemodynamic studies show that this temporary myocardial ischemia is not deleterious to cardiovascular adaptability to hypertonic sodium bicarbonate administration.
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PMID:Effects of peroperative myocardial ischemia on early and late hemodynamic response to hypertonic sodium bicarbonate in dogs. 632 87

The basic physiologic characteristics of acid-base equilibria during hypothermia were briefly reviewed. By graphic analysis, four possible clinical strategies for managing the acid-base status of the patient undergoing H-CPB were documented. The effect of hemodilution on buffer capacity was charted in a manner applicable to common current operative procedures. During hypothermia for cardiac operations as presently conducted, the perfusionist is in control of the temperature of the body and the perfusion preservation of the body and brain; the surgeon must assume responsibility for preservation of the heart. The literature pertinent to the relationship of the acid-base state to the functions and structural preservation of the heart and brain during the conditions of cooling to and rewarming from deep hypothermia associated with cardiopulmonary bypass, aortic cross clamping, cardioplegia and total circulatory arrest have been reviewed. The evidence is overwhelming that myocardial anoxia caused by aortic occlusion or total circulatory arrest at any temperature to 15 degrees C. result in progressive acidosis which, of itself, is myotoxic. In contrast, alkalinity is ionotropic. Myocardial ischemia, in both adults and infants, should be prevented and treated by alkaline perfusion cooling and by frequent coronary perfusion of a cardiopreservative solution which is extremely cold (4 to 8 degrees C.), oxygenated, has a pH of 7.8, slightly hyperosmolar and which has a hematocrit of 20 per cent (imidazole, erythrocytes and plasma protein colloid), a cardioplegic ionic pattern and energy substrates. Reperfusion of the heart should begin at a 37 pH of 7.8. Evidence is strong that the use of CO2 added to any gas mixture is harmful. It increases myocardial acidosis; it does not increase cerebral blood flow during hypothermia. Protection of the unperfused brain of an infant should emphasize prevention of circulatory arrest prolonged to more than 40 minutes. Temporary reperfusion at that time limit should be used. Probably the best general management of the body for H-CPB is alpha-stat, which preserves biologic neutrality. The uncorrected analyzer reads pH 7.4 and Pco2 at any temperature. However, the need for preservation of the hypoxic heart is overwhelming and, thus, the best acid-base management for cardiac hypothermic operations is significant respiratory alkalosis. The most appropriate sites for the collection of blood samples for gas analysis and measuring temperatures were discussed; "body temperature" is the most unreliable parameter measured. The major characteristics of an "ideal" cardiopreservative solution were described.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The importance of acid-base management for cardiac and cerebral preservation during open heart operations. 642 51

The gaseous microemboli (GME) production and gas transfer characteristics of two series of bubble oxygenators (Harvey H-1500 and Bentley BOS-10) were evaluated during clinical perfusion in 33 adult patients during open heart surgery for acquired valvular and ischaemic heart disease. For each oxygenator series, patients were divided into two groups, depending upon the method of measurement (intermittent or continuous) of the arterial PO2(PaO2). Using the data available, the perfusionist altered the gas:blood flow ratio in an attempt to maintain the PaO2 within the normal range. In the first group (I = intermittent), where PaO2 data were available only intermittently, the PaO2 values were well above normal, and large numbers of GME were detected in the arterial blood. In the second group (C = continuous), where the PaO2 data were available continuously, there was significantly better control of the PaO2 (P less than 0.001 and P less than 0.01 for the H-1500 and BOS-10, respectively) and significantly fewer GME (P less than 0.01 and P less than 0.05 for the H-1500 and BOS-10, respectively). The Bentley BOS-10 oxygenator used a lower gas:blood flow ratio to achieve physiological levels (range 9 to 13 kPa at 37 degrees C) of PaO2 than did the Harvey H-1500 oxygenator, but there was no difference in the number of GME detected. The lower gas:blood flow ratios for the BOS-10 oxygenators in group C resulted in significantly higher PaCO2 values well outside the physiological range (4 to 6 kPa at 37 degrees C) during the rewarming phase (mean PaCO2 = 7.6 +/- 0.8 kPa) of cardiopulmonary bypass than did the H-1500 oxygenator (mean PaCO2 = 6.3 +/- 0.7 kPa). Mean values for the PaCO2 for both oxygenators during other phases of bypass (cooling and hypothermia) were within the physiological range. If the CO2 retention was corrected by increasing the gas:blood flow ratio the PaO2 values and GME counts became elevated.
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PMID:A clinical evaluation of the gas transfer characteristics and gaseous microemboli production of two bubble oxygenators. 644 73


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