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

Changes in systemic haemodynamic variables (mean arterial pressure, MAP; heart rate, HR; cardiac output, Qc), in oxygen consumption, VO2, and in ventilation (minute ventilation, V; respiratory frequency, f; tidal volume, VT; and arterial blood gases) with particular attention to respiratory times (duration of inspiration, TI; duration of expiration, TE; duration of the breathing cycle, TTOT), to respiratory timing (TI/TTOT) and respiratory drive (VT/TI) were studied during moderate progressive hypothermia (36 degrees C to 28 degrees C) during stable halothane anaesthesia (MAC = 1.5) in six dogs. MAP, HR and Qc decreased; V and f decreased, the decrease in f being correlated with that in temperature (r = 0.66; P < 0.01). Tidal volume did not change. The PaO2 and pHa decreased while PaCO2 increased slightly. The decrease in ventilation was related to changes in respiratory times (TI and TE) which increased (TE more than TI) and in respiratory drive (VT/TI which decreased due to the increase in TI). The relation between VT/TI and TI/TTOT changes was not constant during cooling. Changes in respiratory times and drive could be due to the effect of cold on medullar respiratory control.
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PMID:[Respiratory effects of moderate hypothermia (36 degrees C-28 degrees C) in dogs under halothane anesthesia]. 146 37

The effects of dobutamine (DOB) on hemodynamics, critical cooling, and myocardial excitability were studied in dogs under simple deep hypothermia. Hypothermia was induced by surface cooling after the animals had been anesthetized with ether and triflupromazine (conventional method, group I). Continuous intravenous administration of DOB was combined with conventional method in group II, and surface cooling was performed with thiamylal in group III. The following results were obtained. The mean lowest temperature reached was 15.6 degrees C in group II. MAP, CO and V max of group II were maintained significantly higher than those of group I during cooling. Decrease in BE in group II was mild compared with group I. Catecholamine release during cooling was suppressed completely in group I and II, but increased markedly in group III. Myocardial threshold to artificial pacing in group II was elevated as the temperature fell, and restored during rewarming, while that of group III was unchanged during cooling. Ventricular fibrillation occurred by stimulation of pacemakers in some cases. Our results suggest that even in case of hypothermia, DOB retains a selective inotropic effect with no threat of arrhythmogenicity, and produces stable hemodynamics. These characteristics of DOB allow cooling down to 15 degrees C.
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PMID:[The effect of dobutamine on hemodynamics, critical cooling, and myocardia excitability during simple deep hypothermia]. 177 May 75

The endogenous opioids have been implicated as contributing factors to the cardiovascular dysfunction of shock. Opiate receptor antagonists improve cardiovascular function and long-term survival in laboratory animal models of shock. In this communication, evidence of the therapeutic efficacy of opiate antagonists in canine and primate hemorrhagic shock is presented. The animals were hemorrhaged into a reservoir to lower MAP to 45 mmHg and that pressure was maintained for 1 h at which time the reservoir was clamped and treatment initiated. The "shed blood" was returned at t = 120 min and treatment continued until t = 180 min. Opiate antagonists employed included naloxone, naltrexone and the mixed agonist/antagonist agent, nalbuphine. Both naloxone and naltrexone improved cardiac function at doses of 1 and 2 mg/kg. Animal survival was significantly enhanced in the high dose format. Nalbuphine also improved cardiovascular performance at doses from 1 to 4 mg/kg but at higher doses it depressed cardiac performance. The efficacy of the antagonists is attenuated by acidosis and hypothermia. Opiate antagonists may induce cardiac arrhythmias in combination with beta-adrenergic blocking drugs and the efficacy is reduced in animals that received high dose steroid therapy. Thus the use of opiate antagonists would be contraindicated in patients that received drugs such as propranolol or methylprednisolone. There have been no controlled clinical trials of opiate antagonists in human hemorrhagic shock; these are needed for final clarification.
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PMID:The therapeutic efficacy of opiate antagonists in hemorrhagic shock. 255 77

The beneficial vs deleterious effects of hypothermia superimposed on hypoxia and hypotension have been argued and are clinically important. In this study, cerebral cytochrome a,a3 redox state and the quantity of intracerebral oxygenated hemoglobin (HbO2) were measured continuously and noninvasively in rats subjected to hemorrhagic hypotension (MAP = 30 mm Hg) and hypoxia (F1O2 = 7.5%) utilizing near infrared spectrophotometry. Prior to the experiment the rats were briefly respired on 100% oxygen to establish 100% oxidation of cytochrome a,a3 and hemoglobin, and at the conclusion of the experiment they were respired on 100% nitrogen to establish 100% reduction. Data are reported as percent oxidation within this range at baseline and after 15 and 30 min of hypoxic hypotension. Arterial blood gases were measured. Body temperature as monitored by a rectal probe was altered by placing anesthetized-paralyzed rats inside a circulating water jacket. Three groups of rats were studied: 38, 33, and 22 degrees C. Group III rats had a significantly (P less than 0.01) greater quantity of intracranial HbO2 than group I or II. Since MAP was held constant at 30 mm Hg, we assume this is largely due to the higher (P less than 0.01) arterial PO2 in group III (101.5) compared to group I and II (48.5, 51.3). Both groups II and III had a significantly (P less than 0.01) greater oxidation of cytochrome a,a3 indicating greater oxygen availability for a given metabolic rate. This was associated with improved survival inasmuch as all rats in groups II and III lived, and only one group I rat survived. It can be concluded that, as used in this study, hypothermia is beneficial and deserves further investigation.
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PMID:Effect of hypothermia during hypoxic hypotension on cerebral metabolism. 630 May 53

Etomidate is a nonbarbiturate hypnotic agent which, like the barbiturates, decreases the cerebral metabolic rate of oxygen consumption (CMRO2) 35-50%. The present studies assessed whether etomidate decreased CMRO2 through temperature-dependent mechanisms and whether the combination of etomidate and moderate hypothermia (28 degrees C) decreased CMRO2 more than hypothermia alone. Nineteen anesthetized dogs were treated with saline, etomidate (burst-suppressive doses), etomidate with hypothermia, or hypothermia alone. Etomidate did not affect (p > 0.05) the mean arterial pressure (MAP, mm Hg) but modestly lowered the heart rate [HR; 124 +/- 6 to 105 +/- 14, (mean +/- SEM); p < 0.05] whereas hypothermia (without or with etomidate) lowered (p < 0.05) both MAP (141 +/- 4 to 116 +/- 5 and 135 +/- 6 to 81 +/- 7) and HR (135 +/- 14 to 84 +/- 3 and 135 +/- 10 to 69 +/- 5, respectively). Etomidate administration did not result in a change (p > 0.05) in the esophageal, brain parenchymal, or subdural temperature. CMRO2 (ml/100 g/min) decreased (p < 0.05) during etomidate administration (3.2 +/- 0.4 to 1.7 +/- 0.2) and hypothermia (3.5 +/- 0.2 to 1.1 +/- 0.2), but the addition of etomidate to hypothermia did not further reduce CMRO2 in the animals (3.1 +/- 0.5 to 1.3 +/- 0.2) despite decreasing their brain hemispheric electrical activity from 9 +/- 1 Hz to a burst-suppressive state.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of etomidate and hypothermia on cerebral metabolism and blood flow in a canine model of hypoperfusion. 849 Mar 7

Renal failure after cardiac surgery using cardiopulmonary bypass (CPB) is well understood for infants, children and adults. The perioperative risk factors after CPB for immature kidneys in newborns are not well known. This retrospective study investigates perioperative risk factors for renal insufficiency in neonates. I) Preoperative: Age; weight, performed angiography, amount of dye used in angiography, renal disease and creatinine. II) Intraoperative: Duration of operation, duration of MAP < 40 mmHg, use of deep hypothermia, in-out fluid balance, duration of CPB, duration of circulatory arrest and cross-clamp time. III) Postoperative: Creatinine, use of catecholamines, use of nitroglycerine (NG) or phosphodiesterase inhibitors (PDI) and additional antibiotics. From Jan. 1990 to Dec. 1994 50 neonates underwent cardiac surgery using CPB (n = 23 transposition of the great arteries; n = 4 pulmonary atresia; n = 6 critical pulmonary stenosis; n = 5 hypoplastic left heart syndrome; n = 3 Ebstein's anomaly; n = 2 interrupted arch with hypoplastic left ventricle; n = 2 single ventricle; n = 1 each: double outlet right ventricle, tricuspid atresia, critical aortic stenosis, rhabdo-myosarkoma, corrected transposition of the great arteries.) Thirty-one patients entered the study. Depending on the postoperative creatinine level two groups (group I: creatinine <1 mg/dl and group II: >1 mg/dl) were created. The diureses between the two groups did not differ. Comparing the patients of group I vs. group II, patients of group I were younger (mean age: 7.7 d. vs. 11.4 d), lighter (mean weight: 3260 g vs. 3430 g), less had angiography (44% vs. 77%), received more dye (mean amount: 14 ml vs. 7 ml), the duration of MAP < 40 mmHg while on CPB was longer (mean duration 3 min vs. 21 min), more patients were operated on using deep hypothermia (55% vs. 27%), the postoperative in-out-fluid balance was more positive (mean balance +413 ml vs. +221 ml), received postop. more frequently high doses of catocholamines and less common NG or PDI, but more often additional antibiotics. The duration of circulatory arrest (mean time: 60 min vs. 55 min) and cross clamp time (mean time: 68 min vs. 65 min) seems not to be a risk factor and vasodilators given simultaneously with catecholamines may have preventive effects on postoperative renal insufficiency. Immature kidneys may play an outstanding role in the susceptibility of damaging factors. Further investigation with a larger number of patients allowing to obtain statistical significant risk factors are required.
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PMID:Renal insufficiency in neonates after cardiac surgery. 883 54

Eight healthy horses premedicated with xylazine and induced with ketamine were used to evaluate sevoflurane in oxygen for maintenance of anaesthesia during elective exploratory laparotomy. After orotracheal intubation, horses were hoisted, placed in dorsal recumbency on a padded surgery table, and received sevoflurane in oxygen for maintenance of anaesthesia. The horses were allowed to breathe spontaneously until instrumented; then, they were mechanically ventilated to maintain the PaCO2 between 35 and 45 mmHg. Systolic (SAP), diastolic (DAP), and mean (MAP) arterial blood pressures, heart rate (HR), ECG, respiratory rate, an estimation of the saturation of haemoglobin with oxygen in peripheral arterial blood (S(p)O2), nasal temperature, end-tidal CO2(ET(CO2)), end-tidal sevoflurane (ET(SEVO)), and vaporiser concentration were recorded every 5 min post induction; arterial blood samples were obtained soon after induction, at 30 min after induction, and every hour thereafter until surgery was completed. Recovery data including times from the sevoflurane vaporiser being turned off to first movement, to sternal recumbency, and to standing, number of attempts to stand, and recovery score (between 1 = safe, smooth and 6 = stormy, major injury to horse) were collected. Analysis of variance was performed using physiological data collected over 195 min of anaesthesia, the longest time period during which all 8 horses were instrumented. Time effects (P<0.05) for HR, SAP, DAP, MAP, and nasal temperature were identified. Heart rate peaked at 45 min and declined over the course of the procedure. Arterial blood pressure generally decreased over time. Body temperature decreased over time. From 15 to 195 min mean ET(SEVO)concentration ranged from 2.0 to 3.3%, while mean vaporiser settings ranged from 3.7 to 5.5%. Three horses received intra-operative ketamine; all horses received dobutamine infusions; and 2 horses received intra-operative calcium-dextrose. Total anaesthesia time was 222-316 min (mean+/-s.d.269+/-31 min). Time from turning the sevoflurane vaporiser off to first movement was mean +/-s.d.18+/-15 min; to sternal recumbency was 54+/-22 min; to standing was 65+/-27 min; and to returning the horse to the stall in the ward was 78+/-24 min. Six horses stood on the first attempt; 2 horses stood on the second attempt. The median recovery score was one (1-3). In conclusion, sevoflurane provided a stable, easily controllable anaesthetic plane during prolonged exploratory laparotomies; horses experienced smooth, safe recoveries after maintenance of anaesthesia with sevoflurane following routine anaesthetic induction and post operative xyalzine administration.
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PMID:Maintenance of anaesthesia with sevoflurane and oxygen in mechanically-ventilated horses subjected to exploratory laparotomy treated with intra- and post operative anaesthetic adjuncts. 975 97

Previous studies have suggested benefit of mild hypothermia during hemorrhagic shock (HS). This finding needs additional confirmation and investigation into possible mechanisms. Proinflammatory cytokines are mediators of multiple organ failure following traumatic hemorrhagic shock and resuscitation. We hypothesized that mild hypothermia would improve survival from HS and may affect the pro- and anti-inflammatory cytokine response in a rat model of uncontrolled HS. Under light halothane anesthesia, uncontrolled HS was induced by blood withdrawal of 3 mL/100 g over 15 min followed by tail amputation. Hypotensive (limited) fluid resuscitation (to prevent mean arterial pressure [MAP] from decreasing below 40 mmHg) with blood was started at 30 min and continued to 90 min. After hemostasis and resuscitation with initially shed blood and Ringer's solution, the rats were observed for 72 h. The animals were randomized into two HS groups (n = 10 each): normothermia (38 degrees C +/- 0.5 degrees C) and mild hypothermia (34 degrees C +/- 0.5 degrees C) from HS 30 min until resuscitation time (RT) 60 min; and a sham group (n = 3). Venous blood samples were taken at baseline, RT 60 min, and days 1, 2, and 3. Serum interleukin (IL)-1beta, IL-6, IL-10, and tumor necrosis factor (TNF)-alpha concentrations were quantified by ELISA. Values are expressed as median and interquartile range. Survival time by life table analysis was greater in the hypothermia group (P = 0.04). Survival rates to 72 h were 1 of 10 vs. 6 of 10 in the normothermia vs. hypothermia groups, respectively (P = 0.057). All cytokine concentrations were significantly increased from baseline at RT 60 min in both HS groups, but not in the shams. At RT 60 min, in the normothermia vs. hypothermia groups, respectively, IL-1beta levels were 185 (119-252) vs. 96 (57-135) pg/mL (P = 0.15); IL-6 levels were 2242 (1903-3777) vs. 1746 (585-2480) pg/mL (P = 0.20); TNF-alpha levels were 97 (81-156) vs. 394 (280-406) pg/mL (P= 0.02); and IL-10 levels were 1.7 (0-13.3) vs. 15.8 (1.9-23.0) pg/mL (P = 0.09). IL-10 remained increased until day 3 in the hypothermia group. High IL-1beta levels (>100 pg/mL) at RT 60 min were associated with death before 72 h (odds ratio 66, C.I. 3.5-1255). We conclude that mild hypothermia improves survival time after uncontrolled HS. Uncontrolled HS induces a robust proinflammatory cytokine response. The unexpected increase in TNF-alpha with hypothermia deserves further investigation.
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PMID:Effects of mild hypothermia on survival and serum cytokines in uncontrolled hemorrhagic shock in rats. 1206 91

Neurologic complications after severe brain injuries are the result of primary injuries in the moment of impact and secondary injuries which evolve over the minutes and days later. According to statistics, secondary injuries were documented in about 90 percent of patients who died after traumatic brain injury. Low oxygen delivery in hypotension, hypoxia, oedema, intracranial hypertension or changes in cerebral blood flow all account for development of secondary injuries. Primary injuries are more or less complete, but secondary injuries could be prevented with adequate therapy. Understanding mechanisms of secondary injuries could help identify potentially beneficial therapies. Important elements of therapy are: head position, normoglycemia, osmotherapy, normal body temperature, optimal blood pressure, adequate oxygenation, barbiturate therapy. Neutral head and neck position is recommended to prevent intracranial hypertension. Hyperglycemia with less ATP leads to ishaemic acidosis, hypoglycemia enhances decomposition of phospholipids and release of fat acids, what makes the cellular damage worse. Normocapnia is recommended and adequate oxygenation (PaO2 higher than 90%). To prevent dehydration and electrolyte imbalance, serum electrolytes should be examined every 4-6 h as well as osmolarity. Moderate therapeutic hypothermia could be of benefit, and maintaining of optimal blood pressure (MAP above 90 mmHg), especially in the first period after injury. As these have a lot of adverse effects, barbiturates are recommended only when conventional therapies show no effect. Patients should be hydrated well before induction of barbiturates. In organized trauma centers and with adequate intensive care the mortality from traumatic brain injury decreased from 50% in 1970, to about 30% now days.
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PMID:[Prevention of secondary brain injuries]. 1501 66

Neurologic complications after severe brain injuries are the result of primary injuries in the moment of impact and secondary injuries which evolve over the minutes and days later. According to statistics, secondary injuries were documented in about 90 percent of patients who died after traumatic brain injury. Low oxygen delivery in hypotension, hypoxia, oedema, intracranial hypertension or changes in cerebral blood flow all account for development of secondary injuries. Primary injuries are more or less complete, but secondary injuries could be prevented with adequate therapy. Understanding mechanisms of secondary injuries could help identify potentially beneficial therapies. Important elements of therapy are: head position, normoglycemia, osmotherapy, normal body temperature, optimal blood pressure, adequate oxygenation. barbiturate therapy. Neutral head and neck position is recommended to prevent intracranial hypertension. Hyperglycemia with less ATP leads to ishaemic acidosis, hypoglycemia enhances decomposition of phospholipids and release of fat acids, what makes the celulare damage worse. Normocapnia is recommended and adequate oxygenation (PaO2 higher than 90%). To prevent dehydration and electrolyte imbalance, serum electrolytes should be examined every 4-6 h as well as osmolarity. Moderate therapeutic hypothermia could be of benefit, and maintaining of optimal blood pressure (MAP above 90 mmHg), especiallz in the first period after injury. As thez have a lot of adverse effects, barbiturates are recommended only when conventional therapies show no effect. Patients should be hydrated well before induction of barbiturates. In organized trauma centers and with adequate intensive care the mortality from traumatic brain injury decreased from 50% in 1970, to about 30% nowdays.
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PMID:[Prevention of secondary brain injury]. 1652 33


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