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

Intramyocardial pH and temperature data recorded in 100 patients undergoing cardiac operations were analyzed to elucidate the effects of ventricular fibrillation and reflow. All patients underwent a single period of aortic clamping. Systemic hypothermia (25 degrees C) and intermittent cold crystalloid K+ cardioplegia were employed for myocardial protection. Baseline myocardial pH was 6.88 +/- 0.03 at a temperature of 36.5 degrees +/- 0.2 degree C. During the period of hypothermic ventricular fibrillation prior to aortic clamping, ventricular fibrillation did not affect myocardial pH in 45 patients (Group 1). In 21 patients (Group 2), it caused a significant drop in intramyocardial pH despite cooling. Group 2 patients had a higher incidence of valvular heart disease and left ventricular hypertrophy. They also exhibited low intramyocardial pH values during the subsequent periods of aortic clamping and reflow, indicating inadequate myocardial protection. During the period of reflow, reperfusion acidosis (pH less than 6.8 at 32 degrees C) was encountered in 39 patients (Group B) as opposed to 37 patients (Group A) whose pH remained well above 6.8 during that period. Group B patients had a higher incidence of valvular heart disease and left ventricular hypertrophy, tended to have more ischemic anterior walls prior to cardiopulmonary bypass, sustained longer periods of aortic clamping, had intramyocardial pH evidence of suboptimal protection during aortic clamping, were affected more adversely by ventricular fibrillation during reflow, and tended to have a higher operative mortality. Thus: Depending on the underlying myocardial disease, the adequacy of protection during aortic clamping, and the conditions of reflow, intramyocardial pH in man can fall significantly during ventricular fibrillation and reflow. The metabolic correlate of injury with reflow is a reperfusion acidosis that can reach as low as pH 5.98. When encountered, reperfusion acidosis can be minimized by prompt defibrillation.
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PMID:Observations on 100 patients with continuous intraoperative monitoring of intramyocardial pH. The adverse effects of ventricular fibrillation and reperfusion. 396 2

The densely calcified ascending aorta presents a formidable challenge to the cardiac surgeon. Clamping such an aorta in the patient requiring myocardial revascularization may result in catastrophic cerebral embolism and mar an otherwise successful surgical outcome. Myocardial revascularization using ventricular fibrillation and hypothermia without aortic cross-clamping in 3 patients with severely calcified aortas is described.
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PMID:Revascularization without embolization: coronary bypass in the presence of a calcified aorta. 403 20

Hibernators are resistant to ventricular fibrillation (VF) induced by hypothermia. This is in contrast to non-hibernating mammals which develop circulatory arrest, usually VF, in the temperature region 15-20 degrees C. The hedgehog which is a hibernator showed resistance to VF also when VF-evoking procedures other than hypothermia were used, such as local application of aconitine on the epicardium, administration of 0.55 M CaCl2 to isolated hearts perfused with a potassium-free modified Tyrode solution, injection of procaine HCl into isolated hearts perfused with a modified Tyrode solution after previous adrenaline administration, and ligation of the left descending coronary artery. Electrical stimulation in the vulnerable period produced VF in some but not in all the hedgehogs but a greater current was necessary than in guinea-pigs, all of which developed VF. Factors of possible importance to explain this difference in VF resistance are the QT duration which is short in hibernators, adrenergic innervation (ventricular muscle fibres in hibernators lack sympathetic innervation), metabolic factors (different temperature activity curves in hibernators compared to nonhibernating mammals) and ultrastructure (less skeletin filament in the conduction system of the hedgehog heart).
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PMID:Ventricular repolarization and fibrillation threshold in hibernating species. 408 17

Effects of the use of 5% CO(2) and surface-rewarming or perfusion- rewarming on safe total circulatory occlusion time, blood gases and carbohydrate metabolism were studied in 25 dogs subjected to surface hypothermia (18 C) and 30 minutes of circulatory occlusion under halothane or ether anesthesia. Under halothane anesthesia, all animals with 100% 0(2) developed motor disorders while one of five surface-rewarmed dogs and none of the perfusion-rewarmed dogs developed motor disorders with 5% CO(2). Under ether anesthesia, all were normal with either 100% 0(2) or when 5% CO(2) was added. Ventricular fibrillation occurred in one dog at 21C under halothane anesthesia with 5% CO(2). Blood lactate levels remained low through hypothermic procedures when 5% CO(2) was used. Perfusion rewarming had little effect on lactate levels. The use of 100% 0(2) resulted in slightly higher lactate levels, especially in the ether anesthetized group, but these levels still remained within the upper limit of the normal range. Significant differences in lactate levels between halothane and ether anesthesia suggest different mechanisms of tissue circulation and metabolism during hypothermia. Halothane anesthesia can be useful with the use of CO(2) for surface hypothermia with 30 minutes circulatory occlusion but is still inferior to ether.
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PMID:A comparative study of the effects of carbon dioxide and perfusion rewarming on limited circulatory occlusion during surface hypothermia, under halothane and ether anesthesia. 485 91

1. Physostigmine (0.1 mg/kg i.v.) given at 37 degrees C and 25 degrees C rectal temperatures, completely protected the hypothermic dog heart against ventricular fibrillation.2. Pentolinium, atropine, vagotomy and reserpine did not significantly alter the incidence of ventricular fibrillation.3. The incidence of ventricular fibrillation under hypothermia could be significantly increased by ligating the anterior descending branch of the left coronary artery. The incidence of ventricular fibrillation in coronary ligated hypothermic dogs was reduced to half by physostigmine pretreatment.4. Hypothermia produced ventricular glycogen depletion and physostigmine prevented ventricular glycogenolysis under hypothermia. However, in the normothermic state physostigmine itself produced a significant decrease in cardiac glycogen.5. The relation between the antifibrillatory and antiglycogenolytic effects of physostigmine under hypothermia are discussed.
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PMID:Effect of physostigmine on ventricular fibrillation and myocardial glycogen in hypothermic dogs. 504 Jun 57

Myocardial oxygen consumption (MVO2) and coronary blood flow (CBF) distribution were studied in 21 isolated, metabolically supported dog hearts. Measurements of MVO2 and CBF distribution were carried out in three different experimental conditions : empty beating heart (EBH), ventricular fibrillation (VF) and high potassium-induced cardiac arrest (CA). MVO2 was approximately the same in EBH and VF (4.09 +/- 0.77 and 4.28 +/- 0.68 ml O2 min-1 100 g-1 respectively), and significantly lower in the group with CA (2.40 +/- 0.18 ml O2 min-1 100 g-1, P less than 0.05). Total CBF showed no significant differences among the three groups (84 +/- 7 ml/min in EBH; 78 +/- 7 ml/min in VF and 83 +/- 7 ml/min in CA). Subendocardial CBF per unit of tissue mass was significantly lower in hearts with VF (0.43 +/- 0.01 ml/min-1 g-1, P less than 0.05) when tested against the other two groups of experiments (0.69 +/- 0.03 ml min-1 g-1 in EBH and 0.65 +/- +/- 0.04 ml min-1 g-1 in CA). This was also reflected in the endo/epi ratio, that was significantly lower in VF (1.41 +/- 0.07, P less than 0.05) with respect to the other two groups (2 +/- 0.09 in EBH and 2.21 +/- 0.07 in CA). From data presented here we can conclude that cardioplegia, even in absence of hypothermia, is a method that will assure myocardial protection providing : (1) a lower subendocardial MVO2; (2) a higher subendocardial CBF, which helps for a prompt recovery during reperfusion.
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PMID:Myocardial flow distribution. II : Empty beating heart, ventricular fibrillation and cardiac arrest. 617 93

Two hundred and sixty six consecutive patients who underwent aortocoronary bypass surgery at our institution were studied to assess the incidence of developing new fascicular conduction disturbance. The first 66 patients (Group I) were operated on using systemic hypothermia and ventricular fibrillation while the next 200 patients (Group II) were operated on using systemic hypothermia plus 4 degrees C potassium cardioplegia. Twelve patients in Group I (18%) developed new fascicular conduction defects, an incidence similar to previous studies of patients operated on using similar conditions. A significantly higher incidence of new fascicular conduction defects occurred in Group II patients where 87 patients (43.5%) developed new defects (p less than .001). The most likely explanations for the marked increase in fascicular conduction defects in Group II patients were either local effects of high concentrations of potassium on the conduction system or excessive cooling of the posterior wall of the heart.
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PMID:Fascicular conduction disturbances following aortocoronary bypass surgery: the role of hypothermia versus potassium-arrest cardioplegia. 633 88

Knowledge of the effects of hypothermia has increased greatly over the past 25 yr. Thousands of patients have been cooled intentionally in the operating room, and hundreds of thousands of living hearts have been temporarily stopped by cold cardioplegia and restarted without difficulty or apparent ill-effect. Yet in spite of the acquisition of this vast body of clinical experience an aura of mystery stills surrounds the patient who becomes hypothermic accidentally. The best treatment in any particular case is not always clear, and published accounts do not always give the impression that the hypothermic patient is treated with the same rational approach with which other sick and comatose patients are treated. In summarizing, therefore, conclusions that might be reached from reviewing past experience several important points emerge. The severely hypothermic patient should be treated in an intensive care unit where appropriate monitoring of temperature, cardiovascular function and respiratory function are available, and where full respiratory support including assisted ventilation can be given. The final outcome depends upon the etiology. The young healthy victim of exposure has a good chance of surviving. The patient poisoned by alcohol or barbiturates has a good chance of surviving provided the level of intoxication is not itself lethal. The elderly without severe underlying disease have a good chance of surviving. The patient with severe underlying disease of the endocrine, cardiovascular or neurologic system probably has, at best, a 50% chance of surviving and, at worst, a chance of only 10-20%, depending upon the associated disease. There is no statistical evidence that any one method of rewarming is significantly better than any other. But there is anecdotal evidence that in the absence of full monitoring and support systems slow rewarming is safer than over-energetic external rewarming. Internal rewarming, peritoneal dialysis, hemodialysis, inhalation of warmed oxygen and extracorporeal circulation are effective in severe cases and can be used with safety. The causes of, and triggering mechanism for, ventricular fibrillation are still largely unknown but the onset of ventricular fibrillation in a very cold patient may often be an irreversible complication. The place of modern anti-arrhythmic drugs in the prevention and management of this complication has yet to be elucidated. Cardiopulmonary resuscitation is difficult in profoundly hypothermic patients but should be maintained until a body temperature of 30 degrees C has been achieved.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Accidental hypothermia. 636 3

The preferred treatment for ventricular fibrillation (VF) refractory to maximal electrical defibrillation remains controversial, as evidenced by recent changes in the American Heart Association's treatment algorithm. To date there have been no published studies conclusively proving one mode of therapy to be superior to another. There is, however, an abundance of animal and clinical data suggesting that bretylium tosylate (BT) is the drug of choice in this setting. In animal studies BT has been shown to lower the canine defibrillation threshold, to facilitate conversion of hypothermia-induced ventricular fibrillation, and to effect spontaneous defibrillation. In 15 years of clinical use as a drug of last resort, and more recently as a first-line drug, BT has developed an impressive track record. Most of the clinical reports are uncontrolled and/or retrospective, but they share a central theme: BT is effective in the treatment of VF refractory to standard therapy. Several small studies have reported successful conversion of VF to a stable rhythm with BT after failure of standard electrical and pharmacologic therapy. Recent studies suggest that earlier use of BT may be associated with improved outcome. Finally, as in animal studies, spontaneous defibrillation has been reported. It is important to note that no drug currently used in the treatment of countershock-refractory VF has been proven effective. The use of some of these drugs is based on tradition rather than scientific evidence. The bulk of currently available scientific data indicates that BT is superior to other commonly used antiarrhythmics in the treatment of VF resistant to countershock.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antifibrillatory drugs: the case for bretylium tosylate. 647 47

Susceptibility of the ventricles to fibrillation has been related to the degree of spatial inhomogeneity in the repolarization process. We studied the pattern of beat-to-beat fluctuations in ventricular repolarization processes in order to determine whether a relationship also exists between the temporal variability of ventricular repolarization and susceptibility to ventricular fibrillation. We used the morphology of the T-wave recorded in surface and epicardial leads as a measure of the ventricular repolarization process. The Ventricular Fibrillation Threshold (VFT) was used as the standard measure of cardiac susceptibility to fibrillation. In dog experiments, T-wave morphologic indices were computed on 1,024 sequential beats. Histogram, autocorrelation and power spectrum analyses were performed on the sequence of T-wave morphologic indices. A series of 27 experiments were performed on 20 dogs in which VFT was reduced by several different interventions--hypothermia, tachycardia and coronary artery ligation. For all three interventions we observed the same characteristic change in the pattern of T-wave morphology fluctuations. In particular, we found that as the VFT was reduced, a pattern of T-wave alternans developed. This pattern was generally not detectable by visual inspection of the ECG. It was, on the other hand, easily quantified in terms of a T-wave alternans index (TWAI) which we computed from the power spectrum of the T-wave fluctuations. In 26 of the 27 experiments, measured VFT decreased (p less than .001); in 20 of these experiments the TWAI computed from the surface ECG increased (decreased) when VFT decreased (increased) (p less than .01). In 17 experiments epicardial electrograms were recorded. In 16 of these experiments VFT decreased (p less than .001). In 16 of these 17 experiments TWAI computed from the epicardial ECG increased (decreased) when the VFT decreased (increased) (p less than .001). We conclude that statistical analysis of fluctuations in ECG complex morphology may provide a sensitive probe of ventricular vulnerability to fibrillation.
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PMID:Fluctuations in T-wave morphology and susceptibility to ventricular fibrillation. 648 Dec 77


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