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

Electrocardiographic and electron microscopic alterations in the myocardium were investigated in rats subjected to hypothermia with and without injection of dextran. Twenty-two animals were divided into four groups and studied. The first group of five rats served as the control group. The second group of six rats, which were subjected to total body hypothermia developed arrhythmia (from first degree atrioventricular block to complete heart block) at a mean rectal temperature of 18 degrees C., with prolongation of P,P-R, and QRS duration, as well as a marked separation of intercalated discs, articularly at the level of the fascia adherens. The third group of six rats was subjected to hypothermia and to an injection of dextran. The resulting threshold temperature tthe temperature at which the arrhythmia appeared) was lower (16 degrees C.) than in the preceding group (p less than 0.005), but neither advanced atrioventricular block nor remarkable subcellular structural changes developed. The fourth group of five rats was sacrificed 18 to 24 hours following recovery from hypothermia and, at that time, showed no significant electrocardiographic or electron microscopic alterations.
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PMID:Myocardium of hypothermic rats with and without administration of dextran. Electrocardiographic and electron microscopic studies. 116 Mar 53

The changes in ECG and arterial pressure were analysed during "simple" deep hypothermia and radical surgery in 52 children with various congenital heart diseases. A comparatively high senitivity of the myocardium to mechanical trauma under body temperatures below 28 degrees C (especially below 25 degrees C) indicates the rationale of conducting all the intrathoracic manipulations, performed prior to the exclusion of the heart from the circulation, under superficial hypothermia. The necessity of fixation of epicardial electrodes is supported by the usefulness of electric stimulation immediately prior to surgery in case the signs of atrioventricular block persist when the body temperature reaches 29 degrees C at rewarming.
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PMID:[Changes of ECG and arterial pressure at different periods of deep hypothermia during heart surgery in young children]. 122 64

Two hundred twenty-seven patients who underwent open heart surgery with retrograde continuous cold blood cardioplegia (RC-CBCP) were investigated to manifest the incidence of postoperative conduction disturbances (CD) and to determine factors related to the occurrence of CD. The incidence of CD in patients with RC-CBCP was 16.7%, which was lower than that (24.4%) in 41 patients with antegrade continuous cold blood cardioplegia. In addition, the CD resolved by the time of hospital discharge in 65% of the patients. There were no patients with new complete atrioventricular block requiring a pacemaker. The development of postoperative CD was related to topical cooling with slushed ice and lower myocardial temperature of the left ventricle, but not to kinds of diseases, duration of aortic cross-clamp, or the distribution of RC-CBCP evaluated from myocardial temperature at the end of initial infusion of cold cardioplegic solution. Furthermore, terminal warm blood cardioplegia reduced the occurrence of CD. We conclude that the occurrence of CD in patients with RC-CBCP is lower than that in patients with antegrade cardioplegia, and is most related to local hypothermia with slushed ice. This suggests that the most likely mechanism for the development of CD would be ischemic or reperfusion injury to the specialized conduction system with the disturbance of microcirculation because of rouleaux formation in CBCP at very low myocardial temperature.
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PMID:[Postoperative conduction disturbances in patients with retrograde continuous cold blood cardioplegia]. 149 Nov 93

An extensive literature suggests that there are minimal complications of systemic hypothermia in humans at and above 30 degrees C for periods of several days. Intracranial hemorrhage has been found to complicate profound hypothermia (10-15 degrees C), and ventricular arrhythmias occur at temperatures below 30 degrees C. Our initial clinical studies were with 21 patients undergoing elective craniotomy cooled to 30-32 degrees C for 1-8 h (mean 4 h). Hypothermia was induced by surface cooling with water blankets. No complications were found. Among 11 patients with severe brain injury, cooling to levels below 32 degrees C was associated with ventricular arrhythmias in 1 patient and atrioventricular block in 1 patient. Asymptomatic hypokalemia was found routinely and treated with potassium replacement. No intracranial hemorrhage or other complications were found. With surface cooling, intravascular temperature dropped at 1.6 degrees C/h. Based on the safety of surface cooling to a core temperature of 32 degrees C for 48 h, we are conducting a randomized study of this level of hypothermia in patients with severe brain injury, cooled within 6 h of injury.
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PMID:Systemic hypothermia in treatment of brain injury. 161 8

The effect of verapamil administered before aortic cross-clamping was assessed in 40 patients undergoing elective coronary artery bypass grafting. Myocardial protection consisted of cold blood potassium cardioplegia, topical ice slush, and moderate (28 degrees C) systemic hypothermia. Patients were randomly divided into two groups: group 1 (18 patients) received verapamil (0.1 mg/kg up to 10 mg) intravenously three to five minutes before aortic cross-clamping; group 2 (22 patients) did not (control). Myocardial injury was assessed by cumulative release of the cardiac-specific isoenzyme of creatine kinase (CK-MB) after release of the aortic cross-clamp. Release of CK-MB was significantly lower in the verapamil group (44.9 +/- 6.2 versus 72.2 +/- 9.0 IU at 24.5 hours, p = 0.005). Calculated total infarct size was also lower in the verapamil group (6.0 +/- 0.9 versus 8.9 +/- 1.0 g-Eq, p = 0.035). Individual CK-MB release curves showed either one or two peaks. The two-peak pattern was more frequent in control patients (18 of 21 control patients versus 6 of 18 verapamil patients, p = 0.001) and was associated with a larger infarct size. Atrioventricular pacing was not required in any verapamil patient, but was needed in 1 control patient. We conclude that verapamil administered before aortic cross-clamping protects against myocardial injury during coronary artery bypass grafting with no increase in the incidence of atrioventricular block.
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PMID:Reduction of myocardial injury with verapamil before aortic cross-clamping. 231 Feb 48

In 1951 in our laboratory in Stockholm, we successfully used our experimental pump oxygenator: the first dogs survived 40 minutes of total cardiopulmonary bypass with right ventricular cardiotomy. In the same year extracorporeal circulation was combined with hypothermia (26 degrees to 28 degrees C) to allow lower perfusion flows, thus diminishing blood trauma and the risk of perfusion complications. To avoid air emboli during cardiotomies, the heart was "arrested" with electrically induced ventricular fibrillation (1952). Our standard perfusion technique used cooling and rewarming with left ventricular bypass, the oxygenator was used only during intracardiac manipulations and when the right ventricle was unable to maintain a sufficient pulmonary circulation. Left ventricular bypass was continued until normal body temperature was reached and the heart could be weaned off the pump. In July 1954 we successfully extirpated a left atrial myxoma in our first patient undergoing open heart surgery, a 40-year-old woman, who is still alive today. Other successful applications of open heart surgery involved resection of a huge left ventricular aneurysm after infarction in 1955, correction of supracardiac total anomalous venous return in 1956, and the first hemodynamic correction of transposition of the great arteries by atrial switch method in 1958. Also in 1958, the first totally implantable pacemaker was inserted in a patient with total atrioventricular block to eliminate the infections that occurred along the percutaneous pacemaker leads. In October 1958, we also operated on a patient with severe angina pectoris with stenosis of the left anterior descending and circumflexed arteries and occluded right coronary artery. Endarterectomy of the left coronary arteries was performed, and the arteriotomies were repaired with saphenous vein patches.
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PMID:Developments in cardiac surgery in Stockholm during the mid and late 1950s. 268 18

The finding of second-degree and high-grade atrioventricular block in a patient with severe accidental hypothermia is described. Additional findings included atrial fibrillation, severe sinus bradycardia, and prominent J (Osborn) waves. This case represents, to the authors' knowledge, the first report of advanced spontaneous AV block not induced by atrial pacing in severe accidental hypothermia. Reversal of the block, and other characteristic changes, suggest a relationship to low temperature.
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PMID:Atrioventricular block in accidental hypothermia--a case report. 291 Jan 45

The present study was undertaken to demonstrate and characterize potentiation of ventricular overdrive suppression by adenosine. To substantiate that adenosine has an enhanced effect on overdrive suppression, it would be necessary to demonstrate that adenosine increases pause duration independent of slowing spontaneous pre-drive rate. In isolated perfused guinea pig hearts with surgically induced complete atrioventricular block, the effect of adenosine (2-20 microM) on pause duration was compared to two alternative means of slowing the pre-drive rate, i.e., hypothermia (28.0 degrees C to 34.0 degrees C) and cesium chloride (0.3-1.0 mM). The slope value of the linear regression line describing the relationship between pre-drive cycle length and pause duration for adenosine (15.8) was significantly greater than control (1.7), hypothermia (1.7), and cesium chloride (5.4). The competitive adenosine antagonist, aminophylline (60 microM), when infused at the initiation of overdrive during adenosine administration, significantly reduced the effect of adenosine on pause duration by 72.9 +/- 4.2% (mean +/- SEM). The reduction in pause duration by aminophylline was specific for adenosine and did not occur under control conditions or during cesium chloride administration. During hypoxia, aminophylline and adenosine deaminase, when infused at the initiation of overdrive, caused 72.3 +/- 5.6 and 63.3 +/- 6.1% reductions in pause duration, respectively. Endogenous adenosine levels rose significantly with hypoxia (1,687 +/- 202 vs. 36 +/- 4 pmol/min per g during normoxia) and increased significantly further during hypoxic overdrive (3,004 +/- 323 pmol/min per g). In isolated guinea pig Purkinje fibers (n = 4), adenosine (20 microM) increased pause duration by 73.6 +/- 9.9% while only minimally affecting the pre-drive cycle length (7.6 +/- 3.8%). These fibers, when stimulated at 1.5 Hz, also displayed an adenosine-induced reduction in action potential duration at 90% repolarization (16 +/- 2 msec). In addition, we demonstrated that adenosine had an enhanced effect on pause duration in the presence of ouabain (1 microM)-induced attenuation of overdrive suppression. Thus, in isolated Purkinje fibers, it is unlikely that the potentiating effect of adenosine on pause duration, which is independent of its chronotropic effect, is mediated via an enhancement of sodium potassium adenosine triphosphatase pump activity. The effect of adenosine is likely to be secondary to a direct action on outward potassium conductance.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of adenosine on ventricular overdrive suppression in isolated guinea pig hearts and Purkinje fibers. 404 82

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

We studied the effects of mild hypothermia on cardiac contractility in isolated rabbit hearts perfused with Krebs-Henseleit solution according to the technique of Langendorff. Isovolumetric left ventricular pressure (LVP) was measured with a fluid-filled balloon. Hearts were paced after induction of atrioventricular block. At low heart rates ( < 30 bpm) mild hypothermia (cooling to 30 degrees C) induced a 32% increase in LVp (146.5 +/- 10 mm Hg at 30 degrees C vs 110.7 +/- 13 mm Hg at 37 degrees C) but this positive inotropic response was progressively lost by increasing heart rate. At pacing rates > or = 90 bpm, lower systolic LVP, higher diastolic LVP, and lower positive and negative LV dP/dt were obtained in hypothermic (93 +/- 12 mm Hg, 55 +/- 18 mm Hg, 584 +/- 137 mm Hg/s, and 323 +/- 57 mm Hg/s at 210 bpm, respectively) compared to normothermic hearts (123 +/- 4 mm Hg, 10 +/- 4 mm Hg, 1705 +/- 145.5 mm Hg/s, and 1155 +/- 78 mm Hg/s at 210 bpm, respectively.) The duration of mechanical diastole was reduced or suppressed in these hearts. Exposure to the beta-adrenoreceptor agonist, isoproterenol, improved this diastolic dysfunction during hypothermia and pacing at high rates, suggesting that the sarcoplasmic reticulum Ca2+ uptake might be involved. Our data are also consistent with an increase in myofilament Ca2+ sensitivity that is opposed by isoproterenol during hypothermia.
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PMID:Interaction of heart rate and hypothermia on global myocardial contraction of the isolated rabbit heart. 861 Sep 9


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