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

Coronary artery bypass grafting (CABG) was performed in a patient with cryoglobulinemia. In order to decrease the concentration of cryoglobulin, the patient underwent double filtration plasmapheresis (DFPP) pre- and postoperatively as well as during cardiopulmonary bypass. Bypass surgery was performed under total cardiopulmonary bypass, moderate systemic hypothermia, and ventricular fibrillation without aortic crossclamping. No adverse effects of cryoglobulin appeared during the peri- and postoperative course. Technical considerations for open heart surgery in patients with cryoglobulinemia are described.
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PMID:Coronary artery bypass grafting in a patient with cryoglobulinemia. 201 Apr 52

Cardiac transmembrane potentials and Na and Ca currents were recorded at different temperatures in rat and hedgehog ventricular muscle. At 35 degrees C in both species resting potential was about -80 mV and upstroke velocity (Vmax) of the action potential above 100 V/s. The shape of the action potential in hedgehog ventricular cells at 35 degrees C was similar to that in the rat showing a fast repolarization phase. When temperature was decreased, the membrane resting potential depolarized and action potential amplitude and Vmax declined. In rat ventricular cells at 10 degrees C, the resting potential was about -40 to -50 mV and Vmax was reduced to about 5 V/s. In hedgehog ventricular cells, however, the transmembrane potentials and Vmax were better maintained at low temperature. Phase 3 of the action potential was markedly prolonged below 20 degrees C in hedgehog but not in rat ventricular cells. When temperature was decreased to 10 degrees C the availability curve of the Na current shifted toward more negative potentials and ICa.peak declined in rat ventricular cells. In hedgehog cardiac preparations, the Na current was less influenced by the cooling and ICa.peak did not change very much at low temperatures. A transient inward current usually considered to induce cardiac arrhythmias could be recorded in rat ventricular cells below 20 degrees C but not in hedgehog preparations. These features of hedgehog cardiac membranes may contribute to the cold tolerance and the resistance to ventricular fibrillation during the hypothermia in mammalian hibernators.
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PMID:Temperature effects on the Na and Ca currents in rat and hedgehog ventricular muscle. 201 64

'Floating' microelectrodes were used to examine the transmembrane potentials of left and right ventricular cardiomyocytes in the guinea pig exposed to deep cooling. In the wide range of temperatures (37 to 20 degrees C), the transmembrane potentials did not substantially change, no fibrillation occurred. There may be a spontaneous reversible ventricular fibrillation in hypothermia where asynchronous excitation of myocardial cells occurs during cell membrane depolarization, which is essentially less than at normal body temperature.
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PMID:[Spontaneous ventricular defibrillation in hypothermia]. 204 39

We reported a 65-year-old male with the history of both cerebral and myocardial infarctions. Simultaneous carotid endarterectomy and myocardial revascularization (coronary artery bypass grafting = CABG) were performed. Ascending aorta was severely calcified. CABG was performed without aortic cross clamp under systemic moderate hypothermia and elective ventricular fibrillation. The wean off from extracorporeal circulation was successful. The postoperative course was uneventful. We recommend the simultaneous revascularization for the carotid and coronary artery obstructive diseases. CABG under ventricular fibrillation without aortic cross clamp was useful and unhazardous in patients presenting calcified ascending aorta.
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PMID:[An experience with simultaneous carotid endarterectomy and myocardial revascularization in a patient with calcified ascending aorta]. 223 Mar 97

Isolated rat hearts were used to examine whether reperfusion-induced arrhythmias may be caused by washout of substances accumulating during ischemia. This was achieved by subjecting hearts to 10 min of regional ischemia and rendering them transiently inexcitable during the first 1.5 min of reperfusion. Transient inexcitability was induced by switching to cold solution (4 degrees C) shortly before reperfusion (-1.5 min). In controls (no hypothermia), the incidences of ventricular tachycardia (VT) and ventricular fibrillation (VF) were 83% and 92%, respectively, during the first 1.5 min of reperfusion. Transient hypothermia caused inexcitability and asystole, impaired recovery of coronary flow and abolished VT and VF (all P less than 0.05). On subsequent rewarming to 37 degrees C, coronary flow and sinus rate recovered in all hearts. However, VT and VF occurred in only 58% and 25%, respectively (P less than 0.05). These values were similar to those of new episodes of VT and VF occurring in controls during the equivalent period. Therefore arrhythmias had been abolished during transient hypothermia, not merely delayed. The relative contributions of transient impairment of recovery of coronary flow and transient asystole to the antiarrhythmic effects were examined in a further 10 groups of hearts (n = 12/group) in which reperfusion conditions were transiently manipulated. We utilized combinations of hypothermia, ventricular pacing, acetylcholine (ACh) 55 microM (to cause asystole and impairment of recovery of coronary flow), and right atrial excision and left atrial pacing (to permit bradycardia to be transiently induced during reperfusion by temporarily switching off the pacemaker). The results indicated that transient hypothermia was antiarrhythmic as a result of a reduction of excitability, not because of bradycardia or impairment of recovery of flow. The data support the hypothesis that reperfusion unmasks (disinhibits) latent arrhythmogenic components of ischemia (particularly during the first 1.5 min of reperfusion) and that, by inducing inexcitability, transient hypothermia allows these substances to be washed out without their arrhythmogenic effects being manifested. The identities of the arrhythmogenic and antiarrhythmic substances remain to be determined; we suggest that cyclic AMP and potassium, respectively, are likely candidates.
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PMID:Are reperfusion-induced arrhythmias caused by disinhibition of an arrhythmogenic component of ischemia? 223 48

Moderate hypothermia (30 degrees C) induced before circulatory arrest is known to improve neurologic outcome. We explored, for the first time in a reproducible dog outcome model, moderate hypothermia induced during reperfusion after cardiac arrest (resuscitation). In three groups of six dogs each (N = 18), normothermic ventricular fibrillation cardiac arrest (no blood flow) of 17 minutes was reversed by cardiopulmonary bypass--normothermic in control group I (37.5 degrees C) and hypothermic to 3 hours in groups II (32 degrees C) and III (28 degrees C). Defibrillation was achieved in less than or equal to 5 minutes and partial bypass was continued to 4 hours, controlled ventilation to 20 hours, and intensive care to 96 hours. All 18 dogs survived. Electroencephalographic activity returned significantly earlier in groups II and III. Mean +/- SD best neurologic deficit between 48 and 96 hours was 44 +/- 8% in group I, 38 +/- 12% in group II, and 35 +/- 7% in group III (differences not significant). Best overall performance category 2 (good outcome) between 48 and 96 hours was achieved in none of the six dogs in group I and in four of the 12 dogs in the combined hypothermic groups II and III (difference not significant). Mean +/- SD brain total histologic damage score was 130 +/- 22 in group I, 93 +/- 28 in group II (p = 0.05), and 80 +/- 26 in group III (p = 0.03). Gross myocardial damage was greater in groups II and III than in group I--numerically higher overall and significantly higher in group III for the right ventricle alone (p = 0.02). Moderate hypothermia after prolonged cardiac arrest may or may not improve cerebral outcome slightly and can worsen myocardial damage.
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PMID:Moderate hypothermia after cardiac arrest of 17 minutes in dogs. Effect on cerebral and cardiac outcome. 223 54

We previously found mild hypothermia (34-36 degrees C), induced before cardiac arrest, to improve neurologic outcome. In this study we used a reproducible dog model to evaluate mild hypothermia by head cooling during arrest, continued with systemic cooling (34 degrees C) during recirculation and for 1 h after arrest. In four groups of dogs, ventricular fibrillation (no flow) of 12.5 min at 37.5 degrees C was reversed with cardiopulmonary bypass and defibrillation in less than or equal to 5 min, and followed by controlled ventilation to 20 h and intensive care to 96 h. In Study A we resuscitated with normotension and normal hematocrit; Control Group A-I (n = 12) was maintained normothermic, while Treatment Group A-II (n = 10) was treated with hypothermia. In Study B we resuscitated with hypertension and hemodilution. Control Group B-I (n = 12) was maintained normothermic (6 of 12 were not hemodiluted), while Treatment Group B-II (n = 10) was treated with hypothermia. Best overall performance categories (OPCs) achieved between 24 and 96 h postarrest were in Group A-I: OPC 1 (normal) in 0 of 12 dogs, OPC 2 (moderate disability) in 2, OPC 3 (severe disability) in 7, and OPC 4 (coma) in 3 dogs. In Group A-II, OPC 1 was achieved in 5 of 10 dogs (p less than 0.01), OPC 2 in 4 (p less than 0.001), OPC 3 in 1, and OPC 4 in 0 dogs. In Group B-I, OPC 1 was achieved in 0 of 12 dogs, OPC 2 in 6, OPC 3 in 5, and OPC 4 in 1 dog. In Group B-II, OPC 1 was achieved in 6 of 10 dogs (p less than 0.01), OPC 2 in 4 (p less than 0.05), and OPC 3 or 4 in 0 dogs. Mean neurologic deficit and brain histopathologic damage scores showed similar significant group differences. Morphologic myocardial damage scores were the same in all four groups. We conclude that mild brain cooling during and after insult improves neurologic outcome after cardiac arrest.
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PMID:Mild cerebral hypothermia during and after cardiac arrest improves neurologic outcome in dogs. 229 37

Hypothermia is a common intraoperative and immediate postoperative complication. Hypothermia causes morbidity from shivering, hypotension, cyanosis, and respiratory diseases. In severe cases, bradycardia, premature ventricular contractions, and even ventricular fibrillation may occur. The various causes of excessive heat loss, both intraoperatively and during the postanesthesia period, the methods of prevention, and the rewarming measures are important factors in administering patient care. Predisposing factors are large exposed body surface areas, open body cavities, prolonged exposure to low operating room temperature, rapid infusion of cold blood and intravenous (IV) fluids, cold irrigating solutions, ventilation with cold gases in long surgical procedures, age over 60 years, premedication that relaxes muscle tone, and the subcutaneous vasodilatation that occurs during anesthesia. Attempted prevention measures include active warming blankets, increased ambient temperatures, warmed IV and irrigating solutions, and metallized plastic sheeting. Restoration of normal body temperature is achieved by radiant heaters, heated mattresses, and heated humidifiers. Astute assessment, quick response, and correct interventions by the nurse can often minimize risk of postanesthesia hypothermia. These principles are illustrated in a case study of a PACU patient in a large teaching trauma hospital.
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PMID:Help! This postanesthesia care unit patient is hypothermic. 235 57

The effectiveness of various methods of myocardial protection were evaluated retrospectively in 59 infants less than 12 months of age who underwent open heart surgery for ventricular septal defect with severe pulmonary hypertension. Intermittent aortic clamping and electrically induced ventricular fibrillation (EF) were employed in 13 infants (Group I), and potassium induced cold cardioplegia and topical cardiac cooling (TC) were used in 14 infants (Group II). Six infants in Group II had additional EF after declamping of the aorta (Group II-A) but the rest of Group II infants did not have any EF (Group II-B). Profound hypothermia and circulatory arrest were utilized in 17 infants (Group III). Cold blood cardioplegia with TC were used in 15 infants (Group IV). Moderate hypothermia were used during cardiopulmonary bypass in Group I, II and IV. The operative mortality for Group I was 15% and was 0% for Group II, III and IV. The incidence of spontaneous resumption of cardiac beat following declamping of the aorta were 33.3, 0, 100, 94.1, 93.3% for Group I, II-A, II-B, III and IV respectively. The urinary output obtained in the postoperative 72 hours was significantly lower in Group I than in Group II, III and IV (Group I less than II less than IV less than III).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical evaluation of various methods of myocardial protections during open heart surgery in infants with ventricular septal defect and severe pulmonary hypertension]. 239 43

Sixteen patients (age 13-53 years) with accidental deep hypothermia have been rewarmed in our clinic during the last 10 years, 14 by femoro-femoral cardiopulmonary bypass (CPB) of whom 11 had a cardiopulmonary arrest (asystole in 5 and ventricular fibrillation in 6). On admission, the latter were clinically dead showing wide non-reactive pupils and being supported by ventilation and external heart massage. In the survivors, the mean length of cold exposure was 4.4 h (2-5.5 h) and mean arrest interval until initiation of CPB was 2.5 h (1.4-3.7 h). Rectal temperature on admission ranged from 17.5 degrees C to 26 degrees C (mean 22.5 degrees C). The causes for hypothermia were fall into a crevasse (5), avalanche (1), drowning (2) and cold exposure (3) including 2 suicide attempts. Results are summarized in the following table: [table: see text] Eight of the 11 patients with deep hypothermia and cardiac arrest were rewarmed and resuscitated successfully with CPB. Three patients, including 2 cases of asphyxia (avalanche and drowning), could not be weaned from CPB despite adequate rewarming. The other drowned patient (53 years) died on the 3rd postoperative day (POD) from ARDS. The main complication was pulmonary edema (57%) and transient neurological deficits. All survivors became conscious during the first POD and resumed, their professional activity. We conclude that patients with accidental deep hypothermia and even prolonged cardiopulmonary arrest should be rewarmed and resuscitated rapidly by cardiopulmonary bypass. These measures are very promising particularly if the cause of accident and the circumstances suggest that cardiopulmonary arrest was induced by hypothermia alone without other asphyxiating mechanisms.
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PMID:Accidental deep hypothermia with cardiopulmonary arrest: extracorporeal blood rewarming in 11 patients. 239 32


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