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

Studies of the systemic circulation in dogs (n = 5) during hypothermia showed that cardiac output, mean arterial pressure, total peripheral resistance, pulse rate, work L. V. is reduced and the stroke volume is increased. The authors think that these effects are probably due to metabolic alterations during hypothermia.
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PMID:[Effect of induced hypothermia on the systemic circulation]. 297 71

The effects of postoperative external heat supply on shivering, oxygen uptake, carbon dioxide production, ventilatory requirements and haemodynamic variables were studied postoperatively after aortocoronary bypass surgery in 24 men with stable angina pectoris. After hypothermic cardiopulmonary bypass (CPB) at 25 degrees C, the patients were rewarmed to a nasopharyngeal temperature of at least 38 degrees C, resulting in a rectal temperature of about 34 degrees C before termination of CPB. Twelve patients, forming the control group, were given no other external heat supply. In another group (n = 12), the "radiant heat supply group", additional external heat was provided postoperatively, the main source of which was a thermal ceiling supplemented with heated, humidified respiratory gases. In this latter group the postoperative rewarming was accomplished earlier and was converted into a mainly passive process. Shivering, oxygen uptake, CO2 production and ventilation volumes were significantly reduced compared with the control group. Cardiac index and stroke index were higher and systemic oxygen extraction was lower in the radiant heat supply group. Postoperative hypertension and vasoconstriction were greatly decreased, suggesting that residual hypothermia is an important cause of the postoperative vasoconstriction.
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PMID:Postoperative ventilatory and circulatory effects of heating after aortocoronary bypass surgery. Postoperative external heat supply. 311 49

Recreational diving is a popular sport, although human ability to stay in and under water is severely limited physiologically. An understanding of these limitations enhances safety and enjoyment of sports diving. Breath-hold diving involves head-out water immersion, apnoea and submersion, exercise, cold stress, and pressure exposure. Each of these components, by itself, elicits prominent and specific physiological effects. Combination of these factors produces a unique and interesting physiological response generally known as diving reflex. Humans display weak diving responses, but exhibit no oxygen conservation function. Nevertheless, application of diving-induced physiological changes is now finding its way into clinical practice. Apnoea, face immersion, and head-out water immersion all show promise of clinical application. There are several spin-offs from diving research worth noting. Diuresis, enhancement of cardiac performance, and redistribution of blood flow, all produced by head-out water immersion, have been shown to be clinically useful, besides providing physiological data useful to space travel. Results from investigations on apnoea have been shown to be relevant to the following: treating some forms of cardiac arrhythmias; understanding drowning, sudden infant death syndrome and sleep apnoea; and confirming hyperventilation as the major cause of drowning. In comparison to marine mammals, humans are poor divers because of severe physiological constraints which limit their breath-hold time, diving depth, and ability to conserve body heat. Although under special circumstances humans can achieve unusually long breath-hold time and reach exceptional depth with a single breath, the sustainable working time and depth are only about 1 minute and 5 metres, respectively. Hypothermia inevitably results in divers working in the ocean. Without thermal protection, the intolerable limit of 35 degrees C is reached within 30 minutes in winter (10 degrees C) water and within 60 to 90 minutes in summer. Nevertheless, effective harvest work can be performed by humans in the ocean, and recreational benefits enhanced when these physiological limitations are respected. An unusual circulatory state exists during head-out water immersion in that there is a sustained increase of stroke volume. This results in 30% increase in cardiac output when the subject is resting in thermal neutral water, indicating a substantial overperfusion for the oxygen requirement. Furthermore, animal experiments showed that the elevated blood flow is preferentially channeled to the liver, fat, and the organs in the splanchnic region.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Applied physiology of diving. 327 55

The effects of left ventricular venting and distention on myocardial protection during heterogenous distribution of cardioplegic solution remain undefined. This study was undertaken to determine if left ventricular venting enhances and distention impairs myocardial cooling and recovery of global and regional left ventricular function. Twenty-one pigs were placed on cardiopulmonary bypass and subjected to 80 minutes of ischemic arrest with the mid-left anterior descending artery occluded. Hearts were protected with multidose potassium (25 mEq/L) crystalloid cardioplegic solution supplemented with topical (4 degrees C) and systemic (28 degrees C) hypothermia. During arrest, the left ventricle was vented in seven pigs, seven pigs were not vented, and seven others had systemic pump blood infused into the left ventricle to maintain an end-diastolic pressure of 15 mm Hg. Parameters measured included left ventricular temperature, stroke work index, compliance (end-diastolic pressure-end-diastolic volume curves) and wall motion scores (two-dimensional echocardiography). Distended hearts had the lowest mean left ventricular temperature beyond the left anterior descending arterial occlusion (10.1 degrees +/- 1.8 degrees C distended [p less than 0.025 from vented and nonvented groups] versus 14.2 degrees +/- 0.7 degrees C vented versus 15.5 degrees +/- 1.2 degrees C nonvented), the highest postischemic stroke work index (0.78 +/- 0.09 gm-m/kg distended versus 0.62 +/- 0.07 gm-m/kg vented versus 0.66 +/- 0.07 gm-m/kg nonvented at end-diastolic pressure = 10 mm Hg), and the best wall motion scores (0.7 +/- 0.04 distended [p less than 0.025 from vented and nonvented groups] versus 5.5 +/- 1.80 vented versus 4.8 +/- 1.20 nonvented). Postischemic end-diastolic pressure-end-diastolic volume curves were unchanged from preischemic values in each group. We conclude that during heterogenous cardioplegic arrest, left ventricular venting offers no additional myocardial protection and may negate the beneficial effects of moderate (end-diastolic pressure = 15 mm Hg) left ventricular distention.
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PMID:Effects of left ventricular venting and distention during heterogenous distribution of cardioplegic solution. 334 57

Controversy has surrounded the role of local hypothermia as a preoperative treatment in amputations of the lower extremity. A study was undertaken to determine the effectiveness of amputation under cryoanesthesia in decreasing postoperative morbidity and mortality in below-knee (BK) amputations. Of 154 BK amputations, only 91 with unreconstructable vascular disease, gangrene, or both, were included in this study. Group I consisted of 48 patients (mean age 63.9 years) who had undergone a routine BK amputation; group II consisted of 43 patients (mean age 65.7 years) who were acutely ill and too unstable to undergo a major surgical procedure. Group II patients were treated by amputation while under cryoanesthesia before any definitive operative intervention. The patients in group II were significantly (p less than 0.05) more ill preoperatively than those in group I. Group II patients had a higher prevalence of previous myocardial infarction, previous stroke, diabetes mellitus, osteomyelitis, and wet gangrene. Seventy percent of the patients in group II had three or more risk factors vs. 46% in group I. Early postoperative mortality rates did not differ significantly between groups (group I, 8%; group II, 9%); the average length of hospital stay for group I patients was 24.2 days compared with 17.7 days in group II. Group II patients sustained slightly more postoperative complications. Amputation under cryoanesthesia appears to be of value in reducing postoperative morbidity and mortality and length of hospital stay in the acutely ill patient with unreconstructable vascular disease, gangrene, or both.
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PMID:Below-knee physiologic cryoanesthesia in the critically ill patient. 334 56

Recent experimental studies have shown that pressure-controlled intermittent coronary sinus occlusion effectively reduces both infarct size and myocardium at risk after coronary artery occlusion. This study was undertaken to determine whether this modality was equally effective in altering reperfusion damage after a period of ischemic arrest. Fourteen pigs were placed on cardiopulmonary bypass and subjected to 2 hours of ischemic arrest with multidose potassium crystalloid cardioplegia supplemented with topical and systemic hypothermia (28 degrees C). During arrest, the mid-left anterior descending artery was occluded with a snare, which was released immediately after aortic unclamping. In seven pigs, a 7F balloon-tipped catheter was positioned in the coronary sinus and pressure-controlled intermittent coronary sinus occlusion was performed for 60 minutes after aortic unclamping. Seven other pigs served as controls. Parameters measured included stroke work index, ejection fraction, and myocardial pH in the distribution of the distal left anterior descending artery. Pigs treated with pressure-controlled intermittent coronary sinus occlusion had a significantly higher myocardial pH (6.99 +/- 0.06 versus 6.67 +/- 0.05, p less than 0.01), ejection fraction (50% +/- 2% versus 33% +/- 6%, p less than 0.01), and stroke work index (0.87 +/- 0.07 versus 0.61 +/- 0.05 gm-m/kg, p less than 0.01) after 60 minutes of reperfusion compared with those of the group not treated in this way. We conclude that pressure-controlled intermittent coronary sinus occlusion effectively reverses reperfusion damage after periods of ischemic arrest.
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PMID:Reversal of reperfusion injury after ischemic arrest with pressure-controlled intermittent coronary sinus occlusion. 335 98

This study evaluated a possible protective and therapeutic effect of moderate hypothermia in the treatment of severe hemorrhagic shock. A modified Wiggers shock preparation was used. Normothermic dogs (Group I, N = 6) were maintained at normal body temperature throughout hemorrhagic shock and resuscitation. In Group II, hypothermia was initiated after 15 minutes of hemorrhagic shock (N = 12) and maintained for 60 minutes after fluid resuscitation. Animals were then rewarmed with Group IIA (N = 7) receiving sodium bicarbonate to correct acidosis, while Group IIB (N = 5) did not; all dogs were studied for an additional 120 minutes. During shock heart rate was lower in both hypothermic groups (IIA and IIB) compared to normothermic dogs (85.0 +/- 3.9, 77.7 +/- 4.6 vs. 136.7 +/- 4.2, respectively, p less than 0.05), while +dP/dt (mmHg/s) remained stable in all dogs. Furthermore, pH was lower in the hypothermic (Groups IIA and IIB) compared to normothermic animals at this time period (Group IIA: 7.19 +/- 0.02, Group IIB: 7.13 +/- 0.02 vs. Group I: 7.24 +/- 0.02). Arterial pCO2 was higher in the hypothermic hemorrhagic shock Groups IIA and IIB compared to normothermic group (34.5 +/- 2.2, 37.4 +/- 2.2 vs. 20.3 +/- 20,3 +/- 2.0, p less than 0.05) due to hypothermia-depressed respiration. A higher myocardial O2 consumption and a negative myocardial lactate balance occurred in the normothermic animals during hemorrhagic shock. After resuscitation and rewarming, stroke volume (mL/beat) and cardiac output (L/min) were lower in hypothermic animals with persistent acid-base derangements (12.6 +/- 2.5, 1.3 +/- 3.0, respectively) compared to hypothermic dogs with acid-base correction (20.1 +/- 3.3, 2.2 +/- 0.3) and normothermic dogs (24.6 +/- 3.0, 3.0 +/- 0.3, p less than 0.05), while myocardial O2 extraction and myocardial lactate production were higher. Results suggest hypothermia decreases the metabolic needs and maintains myocardial contractile function in hemorrhagic shock. Hypothermia may have a beneficial effect and, with normalization of acid-base balance, a therapeutic role in hemorrhagic shock.
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PMID:Effect of moderate hypothermia in the treatment of canine hemorrhagic shock. 335 70

Maximal aerobic power is the highest peak oxygen uptake that an individual can obtain during dynamic exercise using large muscle groups during a few minutes performed under normal conditions at sea level. In most subjects maximal aerobic power is limited by the central circulation. It is obvious that stroke volume is one very important factor. Another important one is the oxygen content of the arterial blood. If the oxygen content of the arterial blood is increased the maximal aerobic power and physical performance is increased. If it is decreased--except when there is an acute volume expansion--or if the heart rate is depressed the circulation can not compensate for it and the maximal aerobic power is decreased. Certain mainly external factors like drugs or induced hypothermia influences on circulation, thus reducing maximal aerobic power and physical performance. Despite all these possible ways of influencing circulation during maximal exercise, it is interesting to note that repeated measurements of maximal aerobic power show a fairly low variation from day to day.
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PMID:Factors determining maximal aerobic power. 347 Oct 53

The protective effect of cardioplegia upon neonatal myocardium during ischemia has not been clearly established. This study evaluated the effects of cardioplegia on left ventricular function in isolated working neonatal rabbit hearts (aged 1 week) subjected to 120 minutes of global ischemia at 28 degrees C. Four groups were studied: Group 1, hypothermia alone; Group 2, intermittent washout with an oxygenated noncardioplegic solution; Group 3, multidose cardioplegia; Group 4, single-dose cardioplegia. After ischemia, cardiac output was reduced to 72% +/- 5% (mean +/- standard error of the mean) of control (p less than 0.02) in Group 1 and to 56% +/- 4% in Group 2 (p less than 0.001). In contrast, there was no significant reduction from baseline cardiac output in those animals receiving cardioplegic solution (Group 3, 93% +/- 6%, and Group 4, 97% +/- 4%). Group 2 hearts demonstrated significantly worse recovery of cardiac output and stroke volume than all other groups. After ischemia, the first derivative of left ventricular pressure fell to 73% +/- 13% of control in Group 1 (p less than 0.1) and to 89% +/- 5% in Group 2 (p less than 0.05). However, the first derivative of left ventricular pressure was restored to control values in Group 3 (118% +/- 11%) and Group 4 (114% +/- 9%). When compared to baseline, creatine kinase was higher 30 minutes after reperfusion in Group 1 (40 +/- 8 versus 143 +/- 32 IU/L/gm, p less than 0.05) and in Group 2 (39 +/- 7 versus 163 +/- 33 IU/L/gm, p less than 0.05). Creatine kinase remained unchanged from baseline in Groups 3 and 4. This study demonstrates excellent preservation of left ventricular function in the neonatal rabbit heart protected with cardioplegic solution. In contrast, neither hypothermia alone nor intermittent washout with an oxygenated noncardioplegic solution was effective in preventing myocardial dysfunction. As in adults, the administration of cardioplegic solution preserves ventricular function during ischemia in neonatal hearts.
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PMID:Protection of the neonatal myocardium during hypothermic ischemia. Effect of cardioplegia on left ventricular function in the rabbit. 359 97

Recent reports indicate that small-amplitude electrical activity may be present in the cold potassium-arrested heart. Twenty-four mongrel dogs were placed on cardiopulmonary bypass and cooled to a rectal temperature of 26 degrees C. Myocardial preservation was provided with a combination of systemic hypothermia 26 degrees C. potassium (20 mEq/L) crystalloid cardioplegic solution (10 ml/kg) infused initially and every 30 minutes during 90 minutes of ischemic arrest, and topical hypothermia. Myocardial temperature was maintained between 8 degrees and 10 degrees C. Electrical activity and transmural myocardial temperature were monitored with specially designed plunge electrodes. Left ventricular stroke work index, cardiac index, and maximum rate of rise of left ventricular pressure were measured before bypass and 45 minutes after ischemic arrest. Biopsy specimens were taken before bypass and at 15 and 45 minutes after ischemic arrest. The specimens were used to measure adenosine triphosphate and to analyze electron microscopic ultrastructure. Small-amplitude electrical activity was present in 16 of 24 animals during cardioplegic arrest. Cardiac index decreased 18 ml/min/kg (not significant), left ventricular stroke work index fell by 0.28 +/- 0.1 gm-m/beat/kg (p less than 0.007), and maximum rate of rise of left ventricular pressure decreased 409 mm Hg/sec (p less than 0.01) in the eight animals without small-amplitude electrical activity. Adenosine triphosphate concentration was unchanged and electron microscopic ultrastructure was well preserved. In contrast, small-amplitude electrical activity (16 animals) resulted in a decrease in cardiac index of 67 ml/min/kg (p less than 0.001), a decrease in left ventricular stroke work index of 0.79 +/- 0.8 gm-m/beat/kg (p less than 0.001), and a fall in maximum rate of rise of left ventricular pressure of 775 mm Hg/sec (p less than 0.001). Adenosine triphosphate concentration decreased from 25 to 21 mumol/gm (p less than 0.04) and electron microscopic ultrastructure was poorly preserved (p less than 0.001). This study demonstrates that small-amplitude electrical activity in the cardioplegia-arrested heart at 10 degrees C impairs myocardial preservation.
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PMID:Effect of small-amplitude electrical activity on myocardial preservation in the cold potassium-arrested heart. 370 77


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