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

The pathomechanism of arrhythmias consecutive to a prolonged electrical systole --the long QT syndrome--was studied by local hypothermia in the heart. Local increase in the QT-interval (long QT with unhomogeneous repolarisation) was induced at a circumscribed area of the right ventricle by perfusion of the mid- and end-sections of the right coronary with cooled blood. The effect of local prolongation of QT on the arrhythmic susceptibility of the heart was studied by means of programmed electrical stimulation. Induced local hypothermia of the heart was found to increase the QT-interval of the ECG-tracings, also if QT had been corrected for heart rate. The local ECG tracings showed a considerable increase of the QT-interval at the selected right ventricular area under the effect of induced hypothermia but in relation to QT (ERP/QT) it diminished. The long QT in association with an unhomogeneous repolarization went hand in hand with an increased irritability of the heart. Early ventricular impulses were found to elicit extrasystolic runs, ventricular tachycardia or ventricular fibrillation. The results indicate that the cause of tachyarrhythmias consecutive to the long QT-syndrome may be ascribed to the inhomogeneity of repolarization on the one hand, and to the shortness of ERP in relation to the QT-duration on the other.
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PMID:Increased susceptibility of the heart to arrhythmia in response to QT-prolongation associated with unhomogeneous repolarization: further data concerning the pathomechanism of arrhythmias associated with long QT-syndrome. 718 48

A patient with severe hypothermia (core temperature of 22.2 C) and ventricular fibrillation had manual cardiopulmonary resuscitation for 3 1/2 hours while various rewarming technics raised her temperature to a level permitting successful electrical cardioversion. Laboratory testing revealed disseminated intravascular coagulation and several endocrinologic abnormalities. The need for prolonged, aggressive resuscitative measures and the possible role of corticosteroids in the management of profound hypothermia are discussed.
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PMID:Profound hypothermia: value of prolonged cardiopulmonary resuscitation. 722 65

The halothane-diethyl ether azeotrope was evaluated in dogs as the anesthetic agent for deep surface hypothermia with total circulatory arrest for open-heart operation. All 10 animals given azeotrope in 100% oxygen (O2) experienced atrial arrhythmias during cooling, and 1 had ventricular fibrillation prior to the completion of cooling at 18 degrees to 20 degrees C. After only 30 minutes' arrest, 8 of the 10 dogs had postoperative motor disturbances. Administering the azeotrope in 95% O2 and 5% carbon dioxide (CO2) yielded markedly improved results characterized by a rapid, smooth cooling course, easy resuscitation following circulatory arrest, and rapid rewarming, and 3 out of 10 dogs experienced mild motor disturbance after 60 minutes of circulatory arrest. This method, when compared with our standard method of ether in 100% O2, resulted in reduced blood lactates and a striking improvement in clinical status on the first postoperative morning. In limited clinical trials, infants undergoing repair of congenital cardiac defects have done well and responded as expected based on the laboratory experience. Since the results with the azeotrope in 95% O2 and 5% CO2 were at least as good as, and in several instances better than, those with the standard method employing either, the nonexplosive characteristic of the azeotrope warrants continued evaluation of this agent.
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PMID:Improved anesthesia for deep surface-induced hypothermia: the halothane-diethyl ether azeotrope. 735 62

A 15-year prospective study was carried out of 44 patients with accidental hypothermia (mean age 60 years) admitted to an intensive therapy unit. The lowest core temperature recorded in each patient ranged from 20.0 to 34.3 degrees C. The precipitating factors were poisoning (by drugs, alcohol, or coal gas) in 25 cases and various illnesses in 19. Rewarming was achieved in 42 patients by applying a radiant heat cradle over the torso, and in two patients by mediastinal irrigation with warmed fluids. Twelve patients died, but only two during the period of rewarming. Thus rewarming may be consistently and safely achieved irrespective of the cause of hypothermia, and normal body temperature may be regained as rapidly as is compatible with adequate tissue perfusion and oxygenation. Surface rewarming of the torso is perhaps the simplest technique available, but internal rewarming procedures may be desirable or essential in the presence of, for example, profound hypothermia, severe hypotension, or ventricular fibrillation. Mortality was attributable to underlying factors or disease and not to hypothermia.
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PMID:Treatment of accidental hypothermia: a prospective clinical study. 738 24

After normothermic cardiac arrest in dogs, we found that mild hypothermia (34 degrees C) of 1-2 h reduced brain damage, providing that hypothermia was achieved within 15 min of reperfusion. A clinically feasible rapid brain-cooling method is needed. As head-neck surface cooling alone in dogs was found to be too slow (0.1 degrees C/min), we reviewed peritoneal cooling in the Introduction and Discussion sections. PRELIMINARY EXPERIMENTS WITHOUT CARDIAC ARREST: In 5 dogs with spontaneous circulation and IPPV, 2 L of Ringer's solution at 10 degrees C were instilled into the peritoneal cavity, left for 5 min, and drained. Brain (tympanic membrane) temperature (Tty) decreased by a mean of 0.3 degrees C/min (12 min to 34 degrees C). Core (pulmonary artery) temperature (Tpa) decreased by a mean of 0.8 degrees C/min (5 min to 34 degrees C). COOLING AFTER CARDIAC ARREST: In our reproducible dog model of normothermic ventricular fibrillation cardiac arrest of 11 min (no flow), brief low-flow normothermic cardiopulmonary bypass (CPB) was used for reperfusion and restoration of spontaneous circulation (ROSC) within 2 min. In 24 dogs, mild hypothermia was induced by head-neck surface cooling with ice bags, starting with reperfusion, plus peritoneal lavage as above, starting with ROSC. All 24 dogs were resuscitated. Initial head-neck surface cooling alone over 2 min decreased Tty by only 0.15 degrees C/min. Subsequent additional peritoneal lavage decreased Tty by a mean of 0.3 degrees C/min (11 min to 34 degrees C); and Tpa 0.6 degrees C/min (7 min to 34 degrees C). There were no significant physiologic effects. We conclude that peritoneal instillation of cold Ringer's solution is more rapidly effective than other non-intravascular cooling methods reported previously. Peritoneal cooling should be tried in patients during CPR.
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PMID:Peritoneal cooling for mild cerebral hypothermia after cardiac arrest in dogs. 748 Nov 3

Among 172 cases of coronary artery bypass grafting, 9 cases (5%) revealed severely atherosclerotic ascending aorta. In 3 of the 9 cases, total aortic cross-clamping in the distal anastomoses of saphenous vein graft (SVG) and partial aortic clamp in the proximal anastomoses of SVG were performed. In 1 case with this technique, cerebral infarction was occurred. In 4 cases, total aortic cross-clamping in the distal and proximal anastomoses of SVG was performed. In 2 of these cases with this technique, cerebral infarctions were occurred. Hypothermic circulatory arrest was performed in 2 of the rest. In one case that was predicted to have atherosclerosis of ascending aorta prior to operation, the left internal thoracic artery was anastomosed to the left anterior descending, and SVG to the right coronary artery with hypothermia and ventricular fibrillation. And during the proximal anastomoses of SVG, hypothermic circulatory arrest without aortic clamping was initiated. In another case, atherosclerosis of ascending aorta was noted after aortic cross-clamping. Then the aorta was declamped, hypothermic circulatory arrest was established, the aorta was opened, the diseased segment was resected, and proximal anastomoses of SVG was performed to Dacron patch which was implanted for aortic wall. There were no cerebral infarction in last two patients.
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PMID:[Coronary artery bypass grafting in cases with the atherosclerotic ascending aorta]. 756 18

This study was designed to investigate whether the calcium channel blocker diltiazem affects the threshold for ventricular fibrillation during hypothermia in dogs. Ten dogs were cooled from 37 to 25 degrees C and rewarmed to 37 degrees C. The threshold for ventricular fibrillation was determined at body temperatures 37, 34, 31, 28 and 25 degrees C by programmed electrical stimulation using a stimulation protocol which involved application of maximal five extrastimuli. At 25 degrees C, six dogs were given an i.v. bolus dose of 100 micrograms.kg-1 followed by a continuous infusion of 100 micrograms.kg-1.h-1 of diltiazem hydrochloride. The other four dogs, were given no drugs at 25 degrees C and served as a control group. The dogs were rewarmed, and the stimulus protocol was performed at the same temperatures as during cooling. Cooling from 37 to 25 degrees C reduced the threshold for ventricular fibrillation in both groups. Heart rate were reduced, monophasic action potential duration at the apex and base of the heart increased from 167 +/- 5 ms to 469 +/- 17 ms and from 164 +/- 5 ms to 466 +/- 17 ms, respectively, when the temperature was reduced. The ventricular effective refractory period increased from 176 +/- 9 ms at 37 degrees C to 472 +/- 15 ms at 25 degrees C. Cooling increased QRS time on the ECG from 55 +/- 4 ms to 138 +/- 13 ms. Addition of diltiazem at 25 degrees C did not affect the threshold for ventricular fibrillation during rewarming. Further, diltiazem at 25 degrees C did not affect the heart rate or refractoriness.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diltiazem does not increase ventricular fibrillation threshold during hypothermia. 757 17

We experienced reoperative coronary revascularization through a left thoracotomy in 12 patients between June 1992 and June 1994. All patients underwent grafting to the left coronary system except one, who underwent bypass procedure to the atrioventricular branch of the right coronary artery in addition to grafting to the left anterior descending artery, using the pedicled left internal thoracic artery, the gastroepiploic artery as a free graft, or a reversed saphenous vein graft. In one patient, revascularization was accomplished during temporary occlusion of the coronary artery without cardiopulmonary bypass. On the other hand, in 11 patients, cardiopulmonary bypass was used. Coronary bypass procedure was employed under the ventricular fibrillation with hypothermia in those but one, who underwent revascularization under the beating heart with cardiopulmonary support. All patients were hemodynamically stable in postoperative stage, and artificial ventilation time was not prolonged, with a mean time of 15.7 hours. Postoperative morbidity included reexploration for hemorrhage in one patient, convulsion in one, worsening of hemianopsia in one, ventricular arrhythmia in one, and wound complication in one, however, there were no hospital deaths. All patients underwent repeat coronary angiography, which revealed that all grafts were widely patient except one, which had inadequate flow due to diffuse narrowing. Based on these clinical results, we conclude that a left thoracotomy is a useful approach for reoperative coronary bypass procedures to reduce the surgical risk associated with a sternal reentry in properly selected patients.
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PMID:[Left thoracotomy approach for coronary reoperation]. 759 45

The influence of normothermic and hypothermic cardiopulmonary bypass on defibrillation energy requirements and transcardiac impedance is not well characterized. However, this relationship is of clinical importance during automatic defibrillator implantation done with concomitant cardiac surgery, and there is anecdotal information that criteria for successful implantation are harder to achieve after such operations. We studied the effect of controlled hypothermia on defibrillation energy requirements and transcardiac impedance in a canine model of cardiopulmonary bypass in which 26 animals underwent right atrial and femoral arterial cannulation, as well as continuous hemodynamic and intramyocardial temperature monitoring. The defibrillation energy requirements were evaluated at 60-minute intervals with an epicardial patch system, and transcardiac impedance was measured before and after the multiple inductions and terminations of ventricular fibrillation. In group 1 (n = 10) defibrillation energy requirements were evaluated immediately after initiation of cardiopulmonary bypass at 37 degrees C (T0), after gradual cooling to 28 degrees C (T1), and after rewarming to 37 degrees C (T2). Group 2 (n = 16) comprised time controls that were identically instrumented and studied, but maintained at 37 degrees C throughout. Percent successful defibrillation was plotted against delivered energy, and the raw data fit by logistic regression. The energy at which 50% of shocks were successful (E50) was 3.23 +/- 0.89 joules at T0, 5.12 +/- 1.85 joules at T1, and 4.42 +/- 1.22 joules at T2 in group 1; this was not significantly different from the corresponding group 2 E50 values, which were 3.11 +/- 1.39 joules, 4.95 +/- 2.47 joules, and 5.59 +/- 3.18 joules, respectively. Both groups demonstrated a significant increase in E50 during the first hour of cardiopulmonary bypass (mean increase from T0 to T1 was 1.89 joules in group 1 and 1.84 joules in group 2, p < 0.05). Transmyocardial impedance fell progressively during the group 2 experiments from 73.6 +/- 12.9 omega at the beginning of the T0 shock series to 61.4 +/- 8.9 omega at the end of the T2 shock series. A similar reduction in transmyocardial impedance was observed during the course of all the group 1 experiments; however, at the beginning of the T1 shock series impedance was significantly elevated to 77.4 +/- 12.3 omega (p < 0.05 compared with group 2 and with end T0 in group 1). There was no relationship between defibrillation energy requirements and transcardiac impedance; there was also no correlation between either of these parameters and intramyocardial extracellular pH or left ventricular end-diastolic pressure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The effects of normothermic and hypothermic cardiopulmonary bypass on defibrillation energy requirements and transmyocardial impedance. Implications for implantable cardioverter-defibrillator implantation. 773 60

How bretylium tosylate affected the ventricular fibrillation threshold, electrophysiological parameters, and plasma catecholamine levels during hypothermia in dogs was studied. Threshold for ventricular fibrillation was determined by programmed electrical stimulation using a stimulation protocol that involved applying a maximum of five extrastimuli at body temperatures 37, 34, 31, 28, and 25 degrees C, and at the same temperatures during rewarming. Electrocardiogram, epicardial monophasic action potentials (MAP), and electrograms were recorded, and ventricular effective refractory period (VERP) was determined at each of the above temperatures. In one group (n = 7), a bolus dosage of bretylium tosylate (BT), 6 mg/kg body wt, was administered at 25 degrees C before rewarming. Another group (n = 4) was exposed to cooling and rewarming without addition of BT. Cooling to 25 degrees C reduced ventricular fibrillation threshold linearly, reduced heart rate, increased VERP and MAP, and slowed myocardial conduction velocity in both groups. There was no overall increase in plasma catecholamine levels during cooling. Addition of BT at 25 degrees C increased ventricular fibrillation threshold during rewarming compared with cooling. Addition of BT at 25 degrees C increased VERP by +/- 32 milliseconds and the corrected JT time by 0.06 +/- 0.02 seconds. VERP and JTc increased during rewarming with BT compared with cooling with no drug. BT had no effect on conduction velocity, and plasma catecholamine levels were not reduced. The antiarrhythmic effect of BT during hypothermia was attributed to an increased wavelength of refractoriness by its increase in the refractory period. This increased wavelength of refractoriness may prevent excitable gaps or increase circuit pathway in the setting of reentry arrhythmias.
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PMID:Effect of bretylium tosylate on ventricular fibrillation threshold during hypothermia in dogs. 803 22


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