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

We undertook a study to determine the ability of intravenous bretylium to cause "chemical defibrillation" or facilitate electrical defibrillation of hypothermia-induced ventricular fibrillation in the dog. Two groups of ten dogs were cooled to 22 C and placed into ventricular fibrillation. Following initiation of cardiopulmonary resuscitation, bretylium 15 mg/kg or normal saline was administered and the dogs were defibrillated according to a standard protocol. Both groups were equivalent in mean arterial pressure and arterial blood gases throughout the investigation. Seven dogs in each group were converted from ventricular fibrillation to an organized cardiac rhythm (P greater than .05). Despite the possible value of prophylactic bretylium in the setting of hypothermia, its use as active treatment for hypothermia-induced ventricular fibrillation in dogs does not seem to be beneficial.
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PMID:Bretylium in hypothermia-induced ventricular fibrillation in dogs. 648 52

Hypothermic potassium cardioplegia has become the most popular technique for myocardial preservation during coronary revascularization. However, an older technique continues to yield comparable results with some potential advantages. Myocardial preservation was achieved with systemic hypothermia to 28 degrees C, pericardial cooling, elective ventricular fibrillation, maintenance of systemic perfusion pressure between 80 and 100 mm Hg, routine left ventricular venting, and local vessel isolation during distal anastomoses without aortic occlusion. Proximal anastomoses were performed prior to atrial cannulation and cardiopulmonary bypass. Nonemergency isolated bypass grafting was performed in 500 consecutive patients, of whom 51% had had a prior myocardial infarction, 24% had unstable angina, and 21% had left main coronary stenosis. Primary grafting was performed in 483 patients and reoperations in 17. The mean number of grafts per patient was 3.8. Perioperative myocardial infarction occurred in 1.8%. Hospital mortality was 0.4%. Late follow-up was obtained for all survivors at a mean postoperative interval of 17.8 months. All survivors were asymptomatic or improved over their preoperative status. The 3 year actuarial survival rate was 95.8%, equivalent to that for the matched general population. Of 287 male patients under age 65, 68.4% were working preoperatively and 69.5% postoperatively. This technique provides results comparable to bypass grafting with cardioplegia and may be useful when aortic occlusion or administration of cardioplegic solutions is not desirable.
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PMID:Noncardioplegic myocardial preservation for coronary revascularization. 661 56

Anoxic cardiac arrest was studied for one hour in five groups of dogs. Groups I-III were given methylprednisolone (30 mg/kg b.w.) before aortic cross-clamping. Normothermia was used with electrically induced ventricular fibrillation in group I, and without such fibrillation in group II, while group III was studied in local hypothermia. Propranolol (10 micrograms/kg) was given to group IV and verapamil (0.2 mg/kg) to group V before the anoxic arrest in local hypothermia. Judged from the ability of the heart to take over the circulation after anoxic arrest, local cooling preceded by propranolol or verapamil gave working performance comparable with the pre-arrest values. In the cooled, steroid-pretreated hearts the work capacity was depressed to the same degree as in locally cooled hearts without steroid premedication. Methylprednisolone prevented ischemic contracture during normothermic arrest with induced fibrillation, but not in the absence of such fibrillation. As adjuvant to local cooling, pretreatment with metabolism-reducing drugs is favorable for cardiac performance after arrest. Steroid premedication should be considered when normothermic arrest with electrically induced ventricular fibrillation is planned.
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PMID:Myocardial preservation during anoxic arrest. Premedication with propranolol, verapamil or methylprednisolone. 664 2

During cardiac operations using hypothermia, the pH measured at 37 degrees C (and corrected to the patient's body temperature) is generally kept at 7.40. However, ectotherms (cold-blooded animals) regulate pH alkaline of 7.40 as temperature falls, e.g., pH 7.58 at 25 degrees C. Hypothermia and acidosis increase the propensity for ventricular fibrillation (VF). This study was undertaken to determine which scheme of pH regulation during hypothermia provided the highest level of cardiac electrical stability. Eleven dogs underwent median sternotomy and implantation of right ventricular and limb electrodes, aortic and central venous pressure catheters, and a probe to measure pulmonary artery blood temperature. To determine the VF threshold, a programmable stimulator was used to find the minimum current needed to produce VF by sweeping the vulnerable period of the cardiac cycle. The animals were divided into two groups for pH management: eight in the clinical scheme (pH 7.4) and seven in the ectothermic scheme, where pH varied with temperature. Control values were recorded prior to cooling and then repeated when core cooling had lowered the temperature to 25 degrees C. In the clinical group, the VF threshold decreased from 23.1 +/- 4.1 mA at 37 degrees C to 17.0 +/- 3.4 mA at 25 degrees C (p = 0.002); in the ectothermic group, the VF threshold was unchanged by hypothermia (23.7 +/- 3.2 to 22.8 +/- 2.8 mA). Heart rate and arterial and central venous pressures were not different between the groups at either temperature. Corrected arterial pH and PCO2 were unchanged from control in the clinical group at 25 degrees C (pH 7.40 +/- 0.01, arterial PCO2 34 +/- 2 torr), whereas arterial PCO2 was maintained at 20 +/- 1 torr to achieve pH 7.59 +/- 0.01 in the ectothermic group. Five of the eight dogs in the clinical group had spontaneous VF while cooling, as compared to one of the seven dogs in the ectothermic group. These studies demonstrate that allowing the corrected pH to rise with hypothermia and remain alkalotic relative to pH 7.4 improves the electrical stability of the heart during hypothermia, as evidenced by the VF threshold at 25 degrees C. Since the ectothermic scheme increases the electrical stability of the heart, it could decrease the incidence of VF during hypothermia and decrease the temperature at which VF occurs during hypothermic cardiopulmonary bypass.
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PMID:The effect of pH on the hypothermic ventricular fibrillation threshold. 670 Feb 51

Homoiothermic organisms react to hypothermia by shivering and thermogenesis to retain their euthermic state. This reactive homeostatic mechanism recruits a strong sympathetic response, which must be suppressed by anesthesia and adjuvants during induced hypothermia. Below 30 degrees C there is significant neural and organ depression associated with cold narcosis. Cardiac arrhythmias and ventricular fibrillation are grave developments when the core temperature is below 28 degrees C. Proper cardiopulmonary support must be instituted in a patient who has induced or accidental hypothermia at these severely hypothermic levels.Although clinical hypothermia is used to protect the brain and the heart from ischemic insults during an operation, it induces a complex array of physiologic changes in the body that must be appreciated so that optimal care may be provided to a patient.
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PMID:Physiology and pharmacology of hypothermia. 683 26

The effects of hypothermia on survival time and ECGs were investigated in hemorrhagic-shocked rats. Acute blood loss corresponding to LD84 was achieved within 1 min through cannulation of the carotid artery. Immediately following the hemorrhagic episode, extracorporeal cooling was performed by placing the animals, with ice packs attached to their lateral sides, in a cold water bath. Rewarming was achieved by removing the ice packs and resetting the temperature of the water bath to 37 degrees C. With this system, the survival time of the hemorrhagic rats was lengthened from 40 to 60 min without rewarming and to 123 min with rewarming. ECGs showed sinus bradycardia, prolonged PR and QRS intervals, AV block, and finally ventricular fibrillation in both the control and hemorrhagic groups during extracorporeal cooling. During rewarming, the above ECG changes returned to normal in the control group as did body temperature. In contrast, animals in the hemorrhagic group did not survive. Body temperature in this group began to rise toward normal, and above ECG changes showed slight but not complete improvement. It is concluded that extracorporeal cooling can lengthen the survival time of hemorrhagic-shocked rats and that recovery of the disturbed conduction system is a prerequisite for survival from severe hypothermia.
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PMID:Effect of hypothermia on survival time and ECG in rats with acute blood loss. 688 Sep 71

Asystole can be the presenting ECG finding of accidental hypothermia when the core temperature is less than 28 degrees C. Even two hours of persistent asystole does not represent irreversible cardiac compromise. With cardiopulmonary support and active rewarming, resuscitation and survival without serious sequelae can be achieved. Case reports and electrophysiology studies suggest that asystole is a primary manifestation of hypothermia potentiated by carbon dioxide retention. However, ventricular fibrillation in this setting is probably a secondary complication of resuscitation efforts, being precipitated by hypocapnic alkalosis, physical manipulation of the heart, and rewarming.
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PMID:Recovery after prolonged asystolic cardiac arrest in profound hypothermia. A case report and literature review. 698 23

The homotransplanted heart is in severe failure in the immediate post-operative period, secondary to ischemia inherent to the technic of orthotopic transplantation. The present work was carried out to investigate if ventricular fibrillation followed by cold coronary perfusion could protect the homograft during implantation by evaluating the post-operative cardiac performance. In the control group, 7 hearts were excised, immediately immersed in physiological saline at 5 degrees C, and homotransplanted. In a second group of 4 grafts, ventricular fibrillation was induced and the coronary bed was perfused immediately with cold (5 degrees C) extracellular solution for a period of 10 minutes before orthotopic implantation. All animals were prepared at the end of surgery for hemodynamic studies to be carried out 3, 24 and 48 hours post-operatively in the resting state. In group I, the myocardial temperature dropped to 13.5 degrees C in 14.5 minutes. In group II, the hypothermia by perfusion was more rapid and deeper (11 degrees C within 10 minutes). Three hours post-operatively, cardiac function of group II was superior to that of group I as demonstrated by the increase of cardiac index (39%), stroke volume index (41%) mean systolic ejection rate index (44%), maximum systolic flow index (58%), maximum acceleration index (36%), stroke power index (88%), stroke work index (67%). Twenty-four and forty-eight hours post-operatively the cardio-vascular function improved in both groups but remained superior in group II. These results demonstrate that ventricular fibrillation followed by cold coronary perfusion increases protection of the homograft during the initial period of implantation.
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PMID:[Myocardial protection of the homograft. III - Evaluation of ventricular fibrillations with hypothermic coronary perfusion (author's transl)]. 703 51

Peri-operative myocardial damage during aortic valve replacement is evaluated by analysis of S-GOT and LDH in the early postoperative phase. Combining the mortality figures and enzyme changes postoperatively, it is demonstrated that the peri-operative myocardial damage is significantly lower in the group operated on under cold cardioplegia a.m. Bretschneider, than in the group operated on under normothermia or moderate hypothermia and induced ventricular fibrillation.
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PMID:Myocardial protection during aortic valve replacement. 707 44

With a view to increasing the severity of the arrhythmias that arise following coronary artery ligation in anesthetized rats, the influences of exposure to lowered environmental temperature (LET) (21 to 13 degrees C) and isolation stress were examined. Housing rats singly for 48 hr, prior to the induction of arrhythmias, caused the most marked changes in the severity of the model; the incidence of ventricular fibrillation and mortality were increase from 43 to 90% and 9 to 60%, respectively. Exposure of multiply housed rats to LET for 48 hr also significantly increased mortality from fibrillation. A combination of LET plus isolation stress, however, did not further increase the severity of the arrhythmias following ligation. Acute hypothermia (body temperature reduced to 30 or 25 degrees C) did not significantly enhance the severity of the model.
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PMID:Influences of hypothermia, cold, and isolation stress on the severity of coronary artery ligation-induced arrhythmias in rats. 709 99


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