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

Cardiac arrests (CA) occurring during anaesthesia and recovery can be classified into three groups: CA not related to anaesthesia (NACA), CA related to anaesthesia (ACA), whether partially (PACA) or totally (TACA). In the French survey, NACAs were three times more frequent than ACAs. Nearly 25% of ACAs occurred at induction and consisted mainly in TACAs. Another quarter of ACAs occurred during maintenance and consisted mainly in PACAs. About 50% of ACAs occurred after the end of anaesthesia and had the highest mortality rate. Cardiac arrest corresponds to the status of a heart unable to generate the minimum aortic blood flow required for functioning of vital organs. For the brain, a zero-blood flow of more than 4 seconds results in coma. Consequently CA exists when the time interval between two subsequent efficient systoles is greater than 4 seconds. Anaesthetic agents can result in CA by 1) overdose (absolute, relative), 2) anaphylactoid/anaphylactic reactions, 3) specific effects (acetylcholine-like effect, hyperkalaemia and malignant hyperthermia for succinylcholine; vagal effect of vecuronium and atracurium; cardiotoxicity of bupivacaine) and 4) drug interaction. In hypoxic CA, severe neurologic impairment often still exists at the time of onset of CA. The anaesthesia machine and controlled ventilation can induce CA by hypoxic ventilation, overdose of anaesthetic vapour, excessive CO2 reinhalation, hypoventilation, disconnection, excessive pressure in airways. Cardiac hypothermia can be a cause of CA as well as a cause of unsuccessful CPR. Massive infusion of unwarmed fluids and IPPV with unheated gases generate a temperature gradient within the heart which may result in severe arrhythmias and CA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cardiac arrest during anesthesia and recovery period]. 214 88

Between July 1985 and December 1986, 29 near-drowned children ranging in age between 6 months and 13 yr were admitted to the Pediatric ICU of Huntington Memorial Hospital. Eight patients suffered cardiopulmonary arrest and had an admission Glasgow Coma Score of 3 or 4. Hemodynamic monitoring was performed on five of these patients. Three received cerebral resuscitation with controlled hyperventilation, hypothermia, pentobarbital, and mannitol because of intracranial hypertension. After CPR, a low cardiac index (CI) and high systemic vascular resistance index (SVRI) were found. When cerebral resuscitative therapy was initiated later, it caused a reduction of SVRI, CI, mean arterial pressure, and cerebral perfusion pressure. Fluid volume therapy and inotropic cardiac support was necessary to maintain adequate cerebral perfusion pressure. These observations indicate that cerebral resuscitative therapy can affect cardiovascular function. The hemodynamic depressive effects might even worsen the outcome. For this reason, it is advisable to obtain CI and pulmonary capillary wedge pressure to optimize cerebral perfusion and potentially neurologic outcome.
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PMID:Cardiac performance in pediatric near-drowning. 276 77

Near-drowning and immersion hypothermia are important, preventable causes of mortality and morbidity. The most important consequences of an immersion accident are hypoxia and its effects on the cardiovascular system and the CNS. The mammalian diving reflex and hypothermia may offer some protection to the CNS despite prolonged hypoxia. The initial management of a nearly drowned victim must be focused on reversal of hypoxemia and acidosis. Prompt and effective on-site CPR is of paramount importance in ensuring optimal survival. The presence of immersion hypothermia must be recognized. Hypothermic patients should be managed according to the severity and the duration of hypothermia. Active external rewarming is adequate for acute and mild hypothermia, whereas active core rewarming may be necessary for chronic and severe hypothermia.
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PMID:Near-drowning: fresh, salt, and cold water immersion. 351 3

Accidental hypothermia is a health problem with a scope which has been underestimated by the medical community. Limited awareness and limited diagnostic equipment, along with hospital coding inaccuracies, make calculation of the true number of instances of accidental hypothermia nearly impossible. Severe hypothermia occurs when body temperature falls below 28 degrees C. The patient may be unconscious, with such severely depressed vital signs that he appears to be dead. All such patients, regardless of extremis upon presentation, should undergo vigorous cardiopulmonary resuscitation in addition to rewarming, because a reliable determination of death is nearly impossible without the restoration of body temperature. Rewarming must follow the implementation of adequate cardiovascular support, maintaining serum acid base balance, arterial oxygenation and intravascular volume levels within the appropriate physiologic ranges; otherwise, the reawakening of metabolic needs will outpace the recovery of cardiac function, and the patient will die of multiple organ infarction. In addition, standard mechanical or manual CPR can furnish adequate cardiovascular support for the severely failing myocardium. When cardiovascular resuscitation is performed first, followed by rewarming with a continual maintenance of optimum cardiovascular function, then all standard methods of rewarming (external rewarming with a fluid-circulated blanket, peritoneal lavage or partial cardiac bypass) should give equally good results. The preceding guidelines are extrapolated from a retrospective review of available clinical material as well as controlled prospective animal studies. Prospective clinical studies should be performed to confirm the acceptability of these guidelines; an inter-institutional study may be the best way to glean such data and should be considered by researchers interested in this problem.
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PMID:Accidental severe hypothermia. 351 93

Current basic life support (BLS) protocols do not address the physiologic effects of accidental hypothermia in prehospital care. The extreme levels of bradycardia, bradypnea, and peripheral vasoconstriction that often accompany profound hypothermia may complicate the accurate diagnosis of cardiopulmonary arrest in the unmonitored patient. Although CPR is indicated in the truly pulseless, apneic victim of hypothermia, chest compressions may convert nonpalpable but adequately perfusing sinus bradycardia to ventricular fibrillation. This dilemma had led to disagreement among clinicians and researchers in hypothermia about prehospital care protocols for the severely hypothermic patient. This article reviews the controversy and recommends the application of a normal BLS protocol to hypothermic patients presenting in apparent cardiopulmonary arrest.
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PMID:Cardiopulmonary resuscitation and hypothermia. 353 62

A multicenter survey evaluated the clinical presentation, treatment, and outcome of accidental hypothermia. Data were collected from 13 emergency departments, with 401 of the 428 cases presenting during a two-year study period. Core temperatures ranged from 35 C to 15.6 C (mean, 30.57 C +/- 3.53) with 272 cases (63.6%) less than or equal to 32.2 C. There were no significant differences by age in presenting temperature, rewarming strategies, or mortality. The first hour rewarming rate was significantly (P less than .05) faster in the population less than or equal to 59 years (1.08 +/- 1.39 C/hr) than in those greater than or equal to 60 years (0.75 +/- 1.16 C/hr). Male core temperatures averaged 30.27 +/- 3.44 C versus female temperatures of 31.1 +/- 3.61 C. There were no clinically significant differences in male (N = 296) versus female (N = 132) profiles. High ethanol levels (315 to 800 mg%) did not affect outcome. Nine of 27 (33%) patients who received CPR initiated in the field survived, versus six of 14 (43%) with CPR begun in the ED. The profile of the CPR versus non-CPR population differed significantly (P less than .05) in location (outdoors), initial temperature (24.8 +/- 3.77 C vs 30.94 +/- 3.12 C), third-hour rewarming rate (2.28 +/- 1.53 C vs 1.17 +/- 1.18 C/hr), and numerous laboratory parameters. Tracheal intubation was performed without incident in 117 cases, of which 97 were less than or equal to 32.2 C. There were 73 fatalities (17.1%). Of these, 84.9% (N = 62) were less than or equal to 32.2 C. Predisposing conditions in this group included "serious" illness (30), systemic infection (28), trauma (15), immersion (ten), frostbite (seven), and overdose (two). The initial pulse, hemoglobin, and first-hour rewarming rate was lower in the deceased population, while the potassium, urea nitrogen, creatinine, and phosphorus were elevated. Excluding treatment combinations, outcome with exclusive use of a single rewarming strategy was passive external rewarming, 14 deaths below 32.2 C, 13 above; active external rewarming, six deaths below 32.2 C, two above; active core rewarming, 38 deaths below 32.2 C, none above. Refinements of the American Heart Association's CPR standards in hypothermia and a Hypothermia Survival Index are proposed.
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PMID:Multicenter hypothermia survey. 363 69

Little is known about the efficacy of CPR in the setting of hypothermia-induced cardiac arrest. We measured organ blood flow produced by conventional closed-chest CPR in eight swine following normothermic KCl-induced cardiac arrest and in seven swine surface-cooled until cardiac arrest occurred. Radiomicrospheres were injected in the unanesthetized basal state, after five minutes of CPR, and after 20 minutes of CPR. After five minutes of CPR, the cardiac output and cerebral and myocardial blood flows (mean +/- SD) of hypothermic animals were 15.3 +/- 7.5 mL/min/kg, 0.16 +/- 0.11 mL/min/g, and 0.20 +/- 0.15 mL/min/g, respectively. Mean percentage flows were 7%, 15%, and 8%, respectively, of those measured in the unanesthetized prearrest state, and 50%, 55%, and 31%, respectively, of the flow produced during CPR in normothermic animals. Blood flow during hypothermic CPR did not change significantly over time; however, during normothermic CPR, cardiac output and cerebral and myocardial flows decreased so that at 20 minutes there were no significant differences from those values measured in hypothermic animals. The reduction in organ flow produced by external chest compression in hypothermic animals may be a result of the changes in the viscoelastic properties of the thorax that occur during profound hypothermia.
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PMID:Regional blood flow during hypothermic arrest. 395 70

Although hypothermia has been described as an emergency in suspended animation, severe degrees of hypothermia mandate appropriate aggressive intervention. Because of cardiac instability with core temperature below 28 C, aggressive invasive rewarming by F-F partial bypass is often ideal in this setting. In contrast, a gentle approach in other therapeutic maneuvers is equally important to prevent iatrogenic induction of VF in nonarrested victims. If the only definite criterion for diagnosis of death in hypothermia is failure to respond to resuscitation and rewarming, successful resuscitation must carefully balance aggressive and gentle interventions. Because CPR protocols involve legal as well as medical questions, additional prospective data are especially critical for resolving controversies in the initial management of profound exposure hypothermia.
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PMID:Severe exposure hypothermia: a resuscitation protocol. 398 47

We provide information that we believe should allow the establishment of rational guidelines for discontinuing, with physician supervision, unsuccessful prehospital CPR. Goldberg has advocated that CPR be terminated only after evidence of brain or cardiac death has persisted for more than one hour of adequately applied advanced CPR. This recommendation was made for inhospital resuscitation and does not reflect the limited capabilities of basic and advanced CPR techniques to sustain life outside the hospital. In addition, White and associates have demonstrated that after resuscitation from prolonged cardiac arrest, cerebral cortical blood flow is reduced severely. This state of hypoperfusion may last up to 18 hours. Because this condition can result in extensive neurologic damage, it may explain the poor survival rates after prolonged resuscitation. We propose that CPR be terminated in the ED when, despite adequate rescue attempts (intubation, defibrillation, IV medications, CCCM en route) by those responding at the scene of cardiac arrest, intrinsic cardiac activity has not been achieved in patients brought to the hospital with asystole or bradyarrhythmia. Additionally patients who have had advanced prehospital CPR for more than 45 minutes without generation of any intrinsic cardiac activity are not resuscitatable by current standard techniques, and CPR may be discontinued. These criteria must not be used for victims of hypothermia before a core temperature of 35 C to 36.1 C is achieved by active core rewarming during CPR. The available data suggest that if these criteria are implemented, many unproductive hospital-based resuscitative efforts can be eliminated without jeopardizing potential survivors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Guidelines for discontinuing prehospital CPR in the emergency department--a review. 405 Dec 75

In our previous report, the effect of CCPR (an intracarotid hypothermic infusion combined with the existing CPR) has been described by the authors on dogs in which cardiac arrest had been induced by the inhalation of nitrous oxide. This report contains a new continuous brain cooling method, using a Resusci Pump TM-1 which has been newly devised by us and which has a carotid-carotid bypass in order to reduce oxygen consumption and cerebral metabolism while maintaining a continuous cerebral blood flow. Cardiac arrest was induced experimentally by electrical stimulation. The duration of cardiac arrest was 5 to 10 min duration. The continuous brain cooling was carried out during the period of 10-30 min. Through the experiment, we have investigated vital signs, acid base balance, cardiac output, carotid arterial blood flow, oxygen availability of the brain tissue, and regional cerebral blood flow in both groups of CPR and CCPR . As for the clinical signs and cardiac output, there were no significant differences between two groups. Oxygen availability of the brain tissue and regional blood flow were much more improved in CCPR group than in CPR group. The brain was selectively cooled by means of the continuous brain cooling. This resulted in the minimum effect on circulatory and respiratory system as compared to the effects caused by general hypothermia. Furthermore, the continuous brain cooling decreased cerebral metabolism and CMRO2, and prevented a progressive development of cerebral hypoxia Cerebral perfusion at a given constant pressure may protect the brain tissue from the disturbance of cerebral microcirculation. Therefore, we might expect the continuous brain cooling to have a beneficial effect on cerebral respiration, circulation and metabolism.
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PMID:Second report of an experimental study of cerebrocardiopulmonary resuscitation (CCPR) in dogs with reference to a new continuous brain cooling method, using a Resusci Pump TM-1. 633 Aug 28


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