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Query: UMLS:C0020672 (hypothermia)
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After normothermic cardiac arrest in dogs, we found that mild hypothermia (34 degrees C) of 1-2 h reduced brain damage, providing that hypothermia was achieved within 15 min of reperfusion. A clinically feasible rapid brain-cooling method is needed. As head-neck surface cooling alone in dogs was found to be too slow (0.1 degrees C/min), we reviewed peritoneal cooling in the Introduction and Discussion sections. PRELIMINARY EXPERIMENTS WITHOUT CARDIAC ARREST: In 5 dogs with spontaneous circulation and IPPV, 2 L of Ringer's solution at 10 degrees C were instilled into the peritoneal cavity, left for 5 min, and drained. Brain (tympanic membrane) temperature (Tty) decreased by a mean of 0.3 degrees C/min (12 min to 34 degrees C). Core (pulmonary artery) temperature (Tpa) decreased by a mean of 0.8 degrees C/min (5 min to 34 degrees C). COOLING AFTER CARDIAC ARREST: In our reproducible dog model of normothermic ventricular fibrillation cardiac arrest of 11 min (no flow), brief low-flow normothermic cardiopulmonary bypass (CPB) was used for reperfusion and restoration of spontaneous circulation (ROSC) within 2 min. In 24 dogs, mild hypothermia was induced by head-neck surface cooling with ice bags, starting with reperfusion, plus peritoneal lavage as above, starting with ROSC. All 24 dogs were resuscitated. Initial head-neck surface cooling alone over 2 min decreased Tty by only 0.15 degrees C/min. Subsequent additional peritoneal lavage decreased Tty by a mean of 0.3 degrees C/min (11 min to 34 degrees C); and Tpa 0.6 degrees C/min (7 min to 34 degrees C). There were no significant physiologic effects. We conclude that peritoneal instillation of cold Ringer's solution is more rapidly effective than other non-intravascular cooling methods reported previously. Peritoneal cooling should be tried in patients during CPR.
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PMID:Peritoneal cooling for mild cerebral hypothermia after cardiac arrest in dogs. 748 Nov 3

The intravascular administration and the high blood resorption of local anesthetic agents are known to induce neurotoxic accidents. However, the use of potent local anesthetic drugs such as bupivacaine is responsible for serious cardiotoxic accidents with a mortality of about 50%. Indeed, bupivacaine induces both electrophysiologic and haemodynamic disturbances with the occurrence of conduction blocks, arrhythmias and cardiovascular collapse. Moreover, cardiotoxicity is worsened by: bupivacaine-induced sympathetic activation which facilitates tachycardia and arrhythmias, metabolic abnormalities such as hypoxia, acidosis, hyperkaliemia and hypothermia, pregnancy, diazepam pretreatment, and the antiarrhythmic drugs. In case of cardiac arrest, CPR must be made. In the other cases, the first treatment is to oxygenate, to intubate the trachea and to ventilate the lungs, and then to stop convulsions. Specific cardiac resuscitation remains controversial because it is based principally on experimental results. We demonstrated that the combination of clonidine and dobutamine is efficient to reverse both haemodynamic and electrophysiologic impairments induced by a large dose of bupivacaine in anesthetized dogs. Whatever the efficiency of specific resuscitation, it must be emphasized that prevention of toxic accident must always include: the best choice of local anesthetic drug (e.g.: lidocaine+alpha-2 agonist vs bupivacaine), test dose, aspiration and slow administration. Finally, the monitoring of regional anaesthesia must be similar to that in use for general anaesthesia and drugs and devices for resuscitation must be ready.
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PMID:[Cardiotoxicity of local anesthetics]. 828 99

Significant hypothermia is an increasing clinical problem that requires a rapid response with properly trained personnel and techniques. Although the clinical presentation may be such that the victim appears dead, aggressive management may allow successful resuscitation in many instances. Initial management should include CPR if the victim is not breathing or is pulseless. Further core heat loss should be prevented by removing wet garments, insulating the victim, and ventilating with warm humidified air/oxygen to help stabilize core temperature. Core temperature and cardiac rhythm should be monitored in the prehospital setting, if possible, and CPR should be continued during transport. In-hospital management should consist of rapid core rewarming in the severely hypothermic victim with heated humidified oxygen, centrally administered warm IV fluids (43 C), and peritoneal dialysis until extracorporeal rewarming can be accomplished. Postresuscitation complications should be monitored; they include pneumonia, pulmonary edema, cardiac arrhythmias, myoglobinuria, disseminated intravascular thrombosis, and seizures. The decision to terminate resuscitative efforts must be individualized by the physician in charge.
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PMID:Hypothermia. 843 36

In 1961, in Pittsburgh, PA, "cerebral" was added to the cardiopulmonary resuscitation system (CPR --> CPCR). Cerebral recovery is dependent on arrest and cardiopulmonary resuscitation times, and numerous factors related to basic, advanced, and prolonged life support. Postischemic-anoxic encephalopathy (the cerebral postresuscitation disease or syndrome) is complex and multifactorial. The prevention or mitigation of this syndrome requires that there be development and trials of special, multifaceted, combination treatments. The selection of therapies to mitigate the postresuscitation syndrome should continue to be based on mechanistic rationale. Therapy based on a single mechanism, however, is unlikely to be maximally effective. For logistic reasons, the limit for neurologic recovery after 5 mins of arrest must be extended to achieve functionally and histologically normal human brains after 10 to 20 mins of circulatory arrest. This goal has been approached, but not quite reached. Treatment effects on process variables give clues, but long-term outcome evaluation is needed for documentation of efficacy and to improve clinical results. Goals have crystallized for clinically relevant cardiac arrest-intensive care outcome models in large animals. These studies are expensive, but essential, because positive treatment effects cannot always be confirmed in the rat forebrain ischemia model. Except for a still-elusive breakthrough effect, randomized clinical trials of CPCR are limited in their ability to statistically document the effectiveness of treatments found to be beneficial in controlled outcome models in large animals. Clinical studies of feasibility, side effects, and acceptability are essential. Hypertensive reperfusion overcomes multifocal no-reflow and improves outcome. Physical combination treatments, such as mild resuscitative (early postarrest) hypothermia (34 degrees C) plus cerebral blood flow promotion (e.g., with hypertension, hemodilution, and normocapnia), each having multiple beneficial effects, achieved complete functional and near-complete histologic recovery of the dog brain after 11 mins of normothermic, ventricular fibrillation cardiac arrest. Calcium entry blockers appear promising as a treatment for postischemic-anoxic encephalopathy. However, the majority of single or multiple drug treatments explored so far have failed to improve neurologic outcome. Assembling and evaluating combination treatments in further animal studies and determining clinical feasibility inside and outside hospitals are challenges for the near future. Treatments without permanent beneficial effects may at least extend the therapeutic window. All of these investigations will require coordinated efforts by multiple research groups, pursuing systematic, multilevel research--from cell cultures to rats, to large animals, and to clinical trials. There are still many gaps in our knowledge about optimizing extracerebral life support for cerebral outcome.
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PMID:Cerebral resuscitation from cardiac arrest: treatment potentials. 860 8

Early milestones of resuscitation research culminated in the 1950s in the documentation of modern external cardiovascular resuscitation (CPR) steps "ABC," followed by advanced and prolonged life support. Implementation of guidelines has been suboptimal. Self-training of the public in life-supporting first aid, including CPR-ABC-available since the 1970s-is only now being re-evaluated and hopefully implemented. Standard external CPR potency is inadequate for reliably restoring spontaneous circulation and saving the brain after prolonged arrests or in patients with sick hearts. Ultra-advanced life-support methods such as open-chest CPR and emergency cardiopulmonary bypass should be tried for bridging standard external CPR-resistant hearts to recovery or repair. Outcome studies in large animals can be fully controlled, in contrast to randomized clinical outcome trials, which have limitations. The HIV paranoia must not lead to abandoning the teaching of steps A and B, which are essential for any kind of coma, asphyxial arrest, and prolonged ventricular fibrillation arrest. Sternal compressions alone can produce some ventilation in animals, but not reliably in comatose humans. For cerebral resuscitation after cardiac arrest, the outcome benefit of the hypertensive bout, other cerebral blood flow-promoting measures, and mild resuscitative hypothermia have been documented in outcome models of large animals and are ready for clinical feasibility trials. The Wolf Creek CPR researchers' conferences I, II, and III were meant to advise the guidelines-setting committees of the American Heart Association and other agencies. The ten topics of Wolf Creek IV, published in this issue of New Horizons, were different in design and objective. There was an appropriate emphasis on fully automatic external defibrillation by lay rescuers, which has the potential for a breakthrough effect. Wolf Creek V, which we recommend to be conducted around the turn of the millennium, should focus on the pathophysiology and therapeutics of respiratory, cardiac, and cerebral resuscitation in general, and on organ, cellular, and molecular level research into how cells, organs, and organisms die, and how acute dying processes might be reversed. What to teach whom and how should be left to guideline conferences of agencies.
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PMID:Introduction to Wolf Creek IV Conference. 915 38

A 31-yr-old woman demonstrated intact neuropsychological functioning after being submerged for at least 30 minutes in icy cold water. Following submersion, the patient received CPR for approximately 1 hr. Eight hours after submersion, the patient's temperature was 31 degrees C (87 degrees F). She remained nonresponsive for 2 days after the accident. Extensive neuropsychological testing was completed 3 mo after the accident with no objective or subjective deficits evidenced. This case of hypothermically mediated neuroprotection from anoxia in an adult supports the need for further research on the putative neurophysiological mechanisms invoked and the potential for application of clinically induced hypothermia in the acute management of other types of cerebral insults.
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PMID:Near drowning in frigid water: a case study of a 31-year-old woman. 937 92

We report two patients with out-of-hospital cardiac arrest who recovered after hypothermia therapy. A 25-year-old man and a 16-year-old boy were transferred to our hospital after cardiopulmonary arrest due to idiopathic ventricular fibrillation and hypertrophic cardiomyopathy, respectively. We carried out hypothermia therapy using cooling blankets, and the patients were maintained at 32-33 degrees C for 96 and 36 h, respectively. After slow rewarming, they regained consciousness and recovered. During hypothermia, hypokalemia and arrhythmia occurred. Their arrest times (no spontaneous circulation and no CPR) were 10 min and 8 min, and CPR times (no spontaneous circulation while CPR was being performed) were 24 min and 20 min, respectively. In cases where the duration of ischemia is prolonged, the prognosis is expected to be poor. Therefore, we believe that hypothermia therapy is beneficial for such patients.
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PMID:[Recovery from out-of-hospital cardiac arrest after mild hypothermia: report of two cases]. 969 97

Profound hypothermia (core temperature of less than 28 degrees C) is a life threatening state and a medical emergency associated with a high mortality rate. The prognosis depends on underlying diseases, advanced or very early age, the duration prior to treatment, the degree of hemodynamic deterioration, and especially, the methods of treatment, including active external or internal rewarming. This is a case study of an 80-year-old female patient with severe accidental hypothermia (core temperature 27 degrees C). She was found in her home lying immobile on the cold floor after a fall. The patient was in a profound coma with cardiocirculatory collapse, and the medical staff treating her was inclined to pronounce her deceased. On her arrival at the hospital, she was resuscitated, put on a respirator and actively warmed. Very severe metabolic disorders were found, including a marked metabolic acidosis composed of diabetic ketoacidosis (she had suffered from insulin treated type 2 diabetes mellitus) and lactic acidosis with a very high anion gap (42) and a hyperosmotic state (blood glucose 1202 mg/dl). There were pathognomonic electrocardiographic abnormalities, J-wave of Osborn and prolonged repolarization. Slow atrial fibrillation with a ventricular response of 30 bpm followed by a nodal rhythm of 12 bpm and reversible cardiac arrest were recorded. The pulse and blood pressure were unobtainable. Despite the successful resuscitation and hemodynamic and cognitive improvement, rhabdomyolysis (CKP 6580 u/L), renal failure and hepatic damage developed. She was extubated and treated with intravenous fluids containing dopamine, bicarbonate, insulin and antibiotics. Her medical condition gradually improved, and she was discharged clear minded, functioning very well and independent. Renal and liver tests returned eventually to normal limits. Progressive bradycardia, hypotension and death due to ventricular fibrillation or asystole commonly occur during severe hypothermia. Respiratory and metabolic, sometimes lactic, acidosis, lethargy and coma, hypercoagulopathy, hyperosmolar state, acute pancreatitis and renal and hepatic failure are frequent complications of hypothermia. Underlying predisposing causes of hypothermia are diabetic ketoacidosis, cerebrovascular disease, mental retardation, hypothyroidism, pituitary and adrenal insufficiency, malnutrition, acute alcoholism, liver damage, hypoglycemia, sepsis, hypothalamic dysfunction, sepsis and polypharmacy, and especially, the use of sedative and narcotic drugs. Our case demonstrates once again that CPR once begun should continue until the successful rewarming because "no one is dead until warm and dead".
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PMID:[Severe accidental hypothermia in an elderly woman]. 1175 73

The charts of all adult patients with accidental hypothermia who were admitted to a single academic hospital during a 10 year period were retrospectively retrieved. The aim was to identify factors associated with survival of those with hypothermic cardiac arrest. Of 75 admitted patients, 44 were found to be haemodynamically stable and not to require invasive rewarming measures. Of the remaining 31 patients, 23 were in refractory cardiac arrest due to primary hypothermia and rewarmed using cardiopulmonary bypass (CPB). The aetiology of hypothermia was immersion in cold water in 48%, exposure to cold environment in 39% and submersion in 13% of these patients. Their median age was 50 years, and 83% were males. The patients received a total of 70 min of conventional CPR before institution of CPB. Fourteen of these patients (61%) survived to discharge from hospital. Factors associated with survival were age (P=0.015), arterial pH (P=0.011), PaCO2 (P=0.003), and serum potassium (P=0.007). Logistic regression analysis showed that of the 23 patients, 22 could be correctly classified as survivor or nonsurvivor based on the level of serum potassium and arterial pCO2. It is concluded that patients with cardiac arrest due to primary hypothermia tolerate long periods of conventional CPR before institution of CPB. The possible predictive role of serum potassium and arterial pCO2 needs further evaluation.
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PMID:Outcome from severe accidental hypothermia in Southern Finland--a 10-year review. 1465 98

A 62-year-old man suffered out-of-hospital cardiac arrest and was treated with mechanical compression-decompression during transport to the hospital. In the emergency department, 28 min after cardiac arrest, spontaneous circulation returned briefly but the patient rapidly became asystolic and mechanical compression-decompression was again applied. After further resuscitation a spontaneous circulation returned and the patient was transferred, deeply comatose, to the coronary intervention laboratory while therapeutic hypothermia was induced. In the laboratory the heart arrested again and coronary angiography was performed during manual CPR revealing a left main stem occlusion. After successful reperfusion of the heart the patient was transferred to the intensive care unit with an intra-aortic balloon pump. The patient was treated with hypothermia for 24 h and awoke without neurological sequelae after a sustained intensive care period of 13 days. The present case is an example of how modern resuscitation principles implementing new clinical and experimental findings may strengthen the chain of survival during resuscitation.
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PMID:Successful resuscitation with mechanical CPR, therapeutic hypothermia and coronary intervention during manual CPR after out-of-hospital cardiac arrest. 1579 84


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