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PubMed1980

Urban accidental hypothermia: 135 cases.

We retrospectively reviewed 135 presentations (114 patients) of urban hypothermia treated at the discretion of the emergency department staff over a nine-year period from February 1971 to March 1980. Rewarming treatment options included passive external, active external, and heated oxygen aerosol administered by mask or intubation. The rates of rewarming were statistically similar for passive external (0.71 C/hr) and heated aerosol via mask (0.74 C/hr). The rate of rewarming for active external methods was 0.90 C/hr. Heated oxygen aerosol using intubation rewarmed the patient at a significantly greater rate than the passive external method (1.22 C/hr) (P < 0.01). The overall mortality rate for the series was 11.9%, but 47.9% when serious underlying disease was present. Individual mortality rates were 64.3% for active external (9/14), 7.67% for active core with a mask (1/13), 5.2% for passive external (4/68), and 5.0% for active core with a nasotracheal tube (2/40). Active core rewarming using intubation was selected more frequently with moderate and severe hypothermia (P < 0.001). The group of survivors had a higher mean arrival temperature (31.33 C) than did the non-survivors (27.55 C) (P = 0.01). Active core rewarming with heated aerosolized oygen via nasotraheal tube is a safe technique for the rapid rewarming of selected hypothermic patients. The arrival temperature and the presence of serious underlying disease, in addition to the method of rewarming, appear to be major determinants of prognosis.

Aerosols↗
PubMed1987

Multicenter hypothermia survey.

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.

Age Factors↗
PubMed2000

Effectiveness of forced air warming after pediatric cardiac surgery employing hypothermic circulatory arrest without cardiopulmonary bypass.

STUDY OBJECTIVE: To evaluate the effectiveness of forced-air warming compared to radiant warming in pediatric cardiac surgical patients recovering from moderate hypothermia after perfusionless deep hypothermic circulatory arrest. DESIGN: Prospective unblinded study. SETIING: Teaching hospitals. PATIENTS: 24 pediatric cardiac surgical patients. INTERVENTION: Noncyanotic patients undergoing repair of atrial or ventricular septal defects were cooled by topical application of ice and rewarmed initially in the operating room by warm saline lavage of the pleural cavities. On arrival at the intensive care unit (ICU), patients were warmed by forced air (n = 13) or radiant heat (n = 11). The time, heart rate, and blood pressure at each 0.5 degrees C increase in rectal temperature were measured until normothermia (36.5 degrees C) to determine the instantaneous rewarming rate. MEASUREMENTS AND MAIN RESULTS: Baseline characteristics were not different in the two groups. The mean (+/- SD) age was 5.6 +/- 3.4 years, weight was 20 +/- 8 kg, esophageal temperature for circulatory arrest was 25.7 +/- 1.3 degrees C, and duration of circulatory arrest was 25 +/- 11 minutes. The mean core temperature on arrival at the ICU was 29.9 +/- 1.3 degrees C and ranged from 26.1 to 31.5 degrees C. The mean rewarming rate for each 0.5 degrees C was greater (p < 0.05) for forced-air (2.43 +/- 1.14 degrees C/hr) than radiant heat (2.16 +/- 1.02 degrees C/hr). At core temperatures <33 degrees C, the rewarming rate for forced-air was 2.04 +/- 0.84 degrees C/hr and radiant heat was 1.68 +/- 0.84 degrees C/hr (p < 0.05). At core temperatures > or = 33 degrees C, the rewarming rate for forced air was 2.76 +/- 1.20 degrees C/hr and radiant heat was 2.46 +/- 1.08 degrees C/min (p = 0.07). Significant determinants of the rewarming rate in a multivariate regression model were age (p < 0.001), temperature (p < 0.05), time after arrival to the intensive care unit (p < 0.05), pulse pressure (p < 0. 05) and warming device (p < 0.001). The duration of ventilatory support and ICU length of stay was not different in the two groups. CONCLUSIONS: Both forced-air and radiant heat were effective for rewarming moderately hypothermic pediatric patients. When core temperature was less than 33 degrees C, the instantaneous rewarming rate by forced air was 21% faster than by radiant heat.

Adolescent↗
PubMed2002

Hypothermia.

Accidental hypothermia is defined as an unintentional decline in the core temperature below 35 degrees C. The population of patients at risk is very heterogeneous. Common thermal stressors include both primary exposures and secondary contributory diseases or injuries. As the core temperature progressively declines, the compensatory metabolic, adrenergic, and cardiovascular responses that attempt to maintain thermal homeostasis fail. At this juncture, therapeutic intervention must occur. An understanding of the pathophysiological variables impacting rewarming is critical. For example, the effects of cold on the coagulation system impact both the approach to cardiovascular resuscitation and the choice of rewarming technique. There are no randomized controlled trials that definitively establish the ideal rewarming strategy for each unique presentation. The resuscitative goal is to match the clinical presentation with the threshold temperatures at which various rewarming modalities and pharmacological interventions should occur. Identification of the indications for both noninvasive and invasive active rewarming techniques in patients requiring critical care is key. Poikilothermia, failure to rewarm, endocrinologic insufficiency, cardiovascular instability, traumatic or toxicological induced peripheral vasodilation, or the presence of major predisposing factors mandates active rewarming. The simultaneous or sequential use of the various rewarming techniques permits a versatile approach to therapy. Outcome remains problematic to predict because there may never be a validated prognostic neurological scale. The history, physical examination, and, ironically, the vital signs are routinely misleading. A tachycardia that is not proportionate to the degree of hypothermia suggests hypovolemia, hypoglycemia, or the presence of toxins. Given the decreased carbon dioxide production, persistent hyperventilation implies an underlying organic acidosis or central nervous system abnormality. Finally, toxic or traumatic or infectious impairment of the central nervous system may be obscured by hypothermia.

Journal Article↗
PubMed1982

Management of profound accidental hypothermia with cardiorespiratory arrest.

Complete recovery following rapid rewarming is described in three tourists who were admitted in a state of profound hypothermia with total cardiorespiratory arrest (rectal temperature ranging from 19 to 24 C). In all three patients, respiration and circulation had ceased during the rescue operation. Rapid core rewarming was achieved by thoracotomy and continuous irrigation of the pericardial cavity with warm fluids in one patient, whereas in the other two patients rewarming was accomplished with extracorporeal circulation using femoro-femoral bypass. In the first patient, the heart could not be defibrillated earlier than 90 minutes following thoracotomy; in the other patients rewarming was attained very rapidly, and within half an hour after institution of bypass, resuscitation of the heart was successful. The patients fully recovered their intellectual and physical abilities, despite the prolonged periods of circulatory arrest lasting from 2 1/2 to 4 hours. We conclude that rapid core rewarming is the adequate therapy for profound accidental hypothermia with circulatory arrest or low cardiac output. If feasible extracorporeal circulation represents the method of choice because it combines the advantage of immediate central rewarming with the benefit of efficient circulatory support, the heart is rewarmed before the shell, thus preventing the "rewarming shock" due to peripheral vasodilatation. Resuscitative efforts should be promptly initiated and vigorously pursued, even in the state of clinical death; in profound hypothermia neurologic examination is inconclusive regarding prognosis.

Accidents↗
PubMed1991

Effects of acute hypothermia and beta-adrenergic receptor blockade on serum potassium concentration in rats.

BACKGROUND AND METHODS: We hypothesized that beta-adrenergic receptor blockade would result in an increase in serum potassium concentration in hypothermic rats given a potassium load compared to non-beta-blocked, hypothermic, potassium-loaded rats. To test this hypothesis, we investigated the interaction between body temperature and beta-adrenergic receptor blockade on serum potassium concentrations in ureter-ligated rats with and without potassium loading. To achieve this goal, we performed three experiments. In the first experiment, serum potassium concentrations were determined in 16 rats as they were continuously cooled from 37 degrees C to 22 degrees C. In the second experiment, 12 ureter-ligated rats were cooled to 31 degrees C, after which they were rewarmed to 37 degrees C. Serum potassium concentrations were determined before and after cooling and on rewarming. Twelve other ureter-ligated rats were cooled to 31 degrees C, then given a potassium load until their serum potassium concentrations returned to their baseline values, after which they were rewarmed to 37 degrees C. Serum potassium concentrations were determined before and after cooling, during the potassium infusion, and on rewarming. In the third experiment, 14 rats were pretreated with propranolol and 14 rats served as controls. Half of the rats in each of these two groups were kept at 37 degrees C and half were cooled to 25 degrees C. All rats were then given a 690-mumol potassium chloride infusion. Serum potassium concentrations were determined before and after the potassium infusion. RESULTS: The rats developed hypokalemia with cooling, which spontaneously resolved in the rats without supplementation on rewarming to 37 degrees C. The hypothermic hypokalemic rats that had their serum potassium concentrations corrected to normothermic status (2.93 +/- 0.17 mmol/L) had marked increases in serum potassium concentrations (4.22 +/- 0.15 mmol/L) on rewarming. In the normothermic rats, potassium loading after beta-adrenergic receptor blockade resulted in even higher serum potassium concentrations (5.65 +/- 0.36 mmol/L) compared with non-beta-blocked rats given equal potassium loads (4.6 +/- 0.4 mmol/L). However, in hypothermic (25 degrees C) rats given the same potassium load, there was no difference in serum potassium concentrations in beta-blocked (6.5 +/- 0.35 mmol/L) and non-beta-blocked rats (6.63 +/- 0.3 mmol/L). CONCLUSIONS: These results suggest that acute hypothermia causes a decrease in serum potassium, probably secondary to redistribution, which is reversible on rewarming. Supplementation of potassium during hypothermia can cause a significant increase in serum potassium concentration on rewarming. Blocking beta-adrenergic receptors with propranolol did not effect hypothermia-induced hypokalemia, suggesting that the beta-adrenergic mechanism may not be functional in hypothermia.

Animals↗
PubMed1992

Hypothermic patients admitted to an intensive care unit: a fifteen year survey.

In the period 1975-1989, 620 (4.5%) of 13,645 patients admitted to the intensive care unit of a Danish university hospital were diagnosed as suffering from hypothermia. The aim of the retrospective survey carried out is to describe this group of patients and to evaluate the methods used for rewarming. The degree of hypothermia was mild in 554 of the patients, moderate in 60, and severe in six. The rewarming method used was passive rewarming with the use of endogenous heat production. Rewarming was established with a median temperature increment of 0.1 to 2.5 degrees centigrade. The mortality rate showed no relationship to the hypothermia. With the exception of extracorporal circulation, the rewarming and mortality rates did not differ from the results shown in studies carried out using active and invasive rewarming procedures. In conclusion, with the exception of extracorporal circulation, rewarming of hypothermic patients by preservation of the endogenous heat production seems as effective as active and invasive rewarming methods.

Adolescent↗
PubMed1978

Effect of altitude acclimatization on thermoregulation efficiency of man.

A study has been conducted on 20 sojourners (SJs) at a high altitude (HA) of 3500 m to evaluate the changes in thermoregulation efficiency (ThE) during acclimatization for 3 weeks, by observing the rate and pattern of rewarming of palm skin temperature (Tsk) after dipping the hand in water of 10 +/- 1 degrees C for 2 min (Tromp's water bath test). The ThE of the SJs was compared to that of 10 acclimatized lowlanders (ALs) staying at the same altitude for about 1 year and 10 high-altitude natives (HANs). In SJ, at sea level (SL), the effect of seasonal variation and ambient temperature on ThE was also studied. The initial Tsk of the palm (29.9 degrees C) was lower at altitude as compared to SL value (32.2 degrees C) in SJs inspite of similar ambient temperature (21 +/- 1 degrees C). There was a prolongation of rewarming time in all the subjects during stay at altitude. The rewarming curve showed a shift towards the right, indicating slower rewarming. The rewarming response of ALs and SJs was comparable at altitude. In HANs, the rewarming at altitude was faster and resembled those of SJs at SL. The rewarming improved in the season following cold months, and at higher ambient temperature in the same season, on the plains. It may be concluded that thermoregulation efficiency of man deteriorates at high altitude, and the peripheral vascular responses to local cold stress do not reach the level attained by natives even after 1 year of acclimatization. General cold acclimatization improves the rewarming response.

Acclimatization↗
PubMed1997

Transcutaneous pacing in a hypothermic-dog model.

STUDY OBJECTIVE: To evaluate the hemodynamic response to transcutaneous pacing (TCP) during rewarming from hypothermia. METHODS: We conducted a prospective, controlled laboratory investigation using 20 mongrel dogs. The animals were anesthetized, intubated, and mechanically ventilated. Arterial pressure, core temperature, and cardiac rhythm were continuously monitored. All dogs were cooled to a core temperature of 27 degrees C; experimental animals were then subjected to TCP with active rewarming, and control animals underwent sham transcutaneous pacing and rewarmed in the same manner. Serial hemodynamic measurements, time to rewarming, and cardiac isoenzyme concentrations were analyzed. RESULTS: Rewarming was accomplished significantly faster in the paced group (171.5 +/- 31.5 minutes) than in the control group (254 +/- 55.9 minutes, P < .05). After rewarming, the mean cardiac index in the paced dogs returned to 84% of baseline, compared with 63% of baseline in the nonpaced group (P < .05). None of the paced animals demonstrated significant hemodynamic deterioration, potentially lethal arrhythmias, or other evidence of myocardial injury. CONCLUSION: TCP is safe, effective and easily implemented in dogs. In this small series of dogs, TCP restored and maintained hemodynamic stability and allowed the hypothermic animals to rewarm in half the time required by their nonpaced counterparts.

Animals↗
PubMed1996

Influence of cooling on mesenteric vascular reactivity.

OBJECTIVES: Cardiopulmonary bypass has been shown to cause hypoperfusion of certain vascular beds leading to multiple system organ failure. It has been reported that the gut may be an important trigger. The underlying mechanism is not fully known, but vascular changes, particularly those due to cooling, could play a role. METHODS: We examined the effect of cooling (28 degrees C) and subsequent rewarming (37 degrees C) on the vascular reactivity of the rabbit mesenteric artery and abdominal aorta to a range of vasoactive substances using an in vitro organ bath apparatus. Cumulative concentration-responses of the agonists (noradrenaline, histamine, dopamine and potassium chloride) were examined at 37 degrees C, then repeated at 28 degrees C and then subsequently repeated after rewarming to 37 degrees C. RESULTS: All agonists were capable of inducing a constrictor response on the mesenteric artery and abdominal aorta. The results represent means +/- SEM. There was an increase in potency of noradrenaline at the lower temperature [from 5.6 +/- 0.1 (37 degrees C) to 6.0 +/- 0.1 (28 degrees C); Bonferroni-corrected P < 0.05; n = 10], which returned to normal [5.6 +/- 0.1 (37 degrees C)] following rewarming in the mesenteric artery. In contrast, there was a decrease in potency of noradrenaline in the aorta on cooling [6.5 +/- 0.1 (37 degrees C) to 6.2 +/- 0.1 (28 degrees C); Bonferroni-corrected P < 0.05; n = 8]. Neither histamine or dopamine showed any difference in potency at 28 degrees C or at 37 degrees C following rewarming in the mesenteric artery or aorta. There was no difference in the efficacy of the response of the mesenteric artery to noradrenaline as indicated by the maximum responses. However, the response to the highest dose of dopamine was increased on rewarming to 37 degrees C compared to control responses at 37 degrees C before cooling in the aorta [7.23 +/- 1.48 g vs 3.6 +/- 0.6 g; Bonferroni-corrected P < 0.05; n = 14]. Histamine contractions were attenuated at 28 degrees C and following rewarming to 37 degrees C in the mesenteric artery [5.5 +/- 0.5 g (37 degrees C) vs 2.2 +/- 0.2 g (28 degrees C); Bonferroni-corrected P < 0.05; n = 18], [5.5 +/- 0.5 g (37 degrees C) vs 2.32 +/- 0.5 g (37 degrees C rewarming); Bonferroni-corrected P < 0.05; n = 18]. CONCLUSIONS: We conclude that cooling elicits a heterogeneous responsiveness of the rabbit mesenteric artery and abdominal aorta to noradrenaline and dopamine which could have important implications for blood flow to mesenteric vascular beds during hypothermic cardiopulmonary bypass.

Adrenergic alpha-Agonists↗
PubMed1997

Outcome of survivors of accidental deep hypothermia and circulatory arrest treated with extracorporeal blood warming.

BACKGROUND: Cardiopulmonary bypass has been used to rewarm victims of accidental deep hypothermia. Unlike other rewarming techniques, it restores organ perfusion immediately in patients with inadequate circulation. This study evaluated the long-term outcome of survivors of accidental deep hypothermia with circulatory arrest who had been rewarmed with cardiopulmonary bypass. METHODS: Deep hypothermia (core temperature, <28 degrees C) with circulatory arrest was found in 46 of 234 patients with accidental hypothermia. In 32 of the 46 patients, rewarming with cardiopulmonary bypass was attempted, resulting in 15 long-term survivors. In most of these patients, deep hypothermia developed after mountaineering accidents or suicide at tempts. After an average (+/-SD) of 6.7+/-4.0 years of follow-up, we obtained the patients' medical histories and performed neurologic and neuropsychological examinations, neurovascular ultrasound studies, electroencephalography, and magnetic resonance imaging of the brain. RESULTS: The average age of the patients was 25.2+/-9.9 years; seven were female and eight were male. The mean interval from discovery of the patient to rewarming with cardiopulmonary bypass was 141+/-50 minutes (range, 30 to 240). At follow-up there were no hypothermia-related sequelae that impaired quality of life. Neurologic and neuropsychological deficits observed in the early period after rewarming had fully or almost completely disappeared. One patent had cerebellar atrophy on magnetic resonance imaging with mild clinical signs, a condition that may have been caused by hypothermia. Other clinical abnormalities were either preexisting or due to injuries not related to hypothermia CONCLUSIONS: This clinical experience demonstrates that young, otherwise healthy people can survive accidental deep hypothermia with no or minimal cerebral impairment, even with prolonged circulatory arrest. Cardiopulmonary bypass appears to be an efficacious rewarming technique.

Accidents↗
PubMed1994

Treatment of mild immersion hypothermia by direct body-to-body contact.

Body-to-body contact is often recommended for rewarming mildly hypothermic victims in the field. This procedure involves a euthermic individual donating heat to the recipient by direct contact in an insulated bag. However, this technique has not been critically evaluated and may not be beneficial because there is limited direct contact between recipient and donor, peripheral vasoconstriction may impair heat transfer to the core, skin warming may blunt the recipient's shivering response, and cold stress to the donor may be excessive. The present study was designed to evaluate whether donation of heat by a donor would be sufficient to enhance rewarming of a hypothermic subject (recipient). Six pairs of recipients (5 men, 1 woman) and donors (2 men, 4 women) participated in the study. Esophageal and skin temperatures, cutaneous heat flux, and oxygen consumption were measured. Recipients were immersed in 8 degrees C water until esophageal temperature decreased to a mean of 34.6 +/- 0.7 degrees C (SD). They then were rewarmed by one of three methods: rewarming by the endogenous heat generated by shivering only (SH), body-to-body rewarming (BB), or rewarming with a constant-heat source manikin (MAN). Mean afterdrop for the three conditions was 0.54 +/- 0.2, 0.54 +/- 0.2, and 0.57 +/- 0.2 degrees C for SH, BB, and MAN, respectively (NS), and the rate of rewarming was 2.40 +/- 0.8, 2.46 +/- 1.1 and 2.55 +/- 0.9 degrees C/h for SH, BB, and MAN, respectively (NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1997

Effects of hypothermia on energy metabolism in rat and Richardson's ground squirrel hearts.

Glycolysis, glucose oxidation, palmitate oxidation, and cardiac function were measured in isolated working hearts from ground squirrels and rats subjected to a hypothermia-rewarming protocol. Hearts were perfused initially for 30 min at 37 degrees C, followed by 2 h of hypothermic perfusion at 15 degrees C, after which hearts were rewarmed to 37 degrees C and further perfused for 30 min. Functional recovery in ground squirrel hearts was greater than in rat hearts after rewarming. Hypothermia-rewarming had a similar general effect on the various metabolic pathways in both species. Despite these similarities, total energy substrate metabolic rates were greater in rat than ground squirrel hearts during hypothermia despite a lower level of work being performed by the rat hearts, indicating that rat hearts are less efficient than ground squirrel hearts during hypothermia. After rewarming, energy substrate metabolism recovered completely in both species, although cardiac work remained depressed in rat hearts. The difference in functional recovery between rat and ground squirrel hearts after rewarming cannot be explained by general differences in energy substrate metabolism during hypothermia or after rewarming.

Animals↗
PubMed1988

Treatment of experimental frostbite with urokinase.

An experimental model of frostbite using a standard cold injury in rats was used to test the therapeutic usefulness of the fibrinolytic agent urokinase. Control groups included rapid rewarming, slow rewarming, and slow rewarming followed by saline infusion. Urokinase was administered through an intra-arterial catheter 30 minutes after cold injury and slow rewarming. Optimum results were obtained with rapid rewarming of the extremity at 43 degrees C. However, with rewarming at room temperature eventual tissue loss was significantly decreased with the infusion of urokinase compared with either no treatment or saline infusion. In the clinical situation where the patient with frostbite is seen after slow rewarming, we believe that clinical trials of the use of a fibrinolytic agent are warranted.

Animals↗
PubMed1996

Developmental differences in myocyte contractile response after cardioplegic arrest.

Although developmental differences in left ventricular function after cardioplegic arrest and rewarming have been postulated, whether differences exist at the level of the myocyte remains unexplored. This project tested the hypothesis that there is a differential effect of hypothermic hyperkalemic cardioplegic arrest with subsequent rewarming on contractile function of immature compared with adult ventricular myocytes. Myocytes were isolated from the left ventricular free wall of five immature and five adult rabbits and incubated for 2 hours in hyperkalemic modified Ringer's solution at 4 degrees C (cardioplegia) or for 2 hours in cell culture medium at 37 degrees C (normothermia). Myocytes were resuspended ("rewarmed") in 37 degrees C cell culture medium after the incubation protocol. Normothermic baseline contractile performance was lower in immature, compared with adult, myocytes. Specifically, myocyte shortening velocity was 62 +/- 4 microm/sec in immature and 112 +/-6 microm/sec in adult myocytes (p < 0.01). After cardioplegia and rewarming, immature myocyte contractile function was unchanged, whereas adult myocyte contractile function was significantly diminished. For example, myocyte shortening velocity was 65 +/- 4 microm/sec in immature and 58 +/- 3 microm/sec in adult myocytes (p < 0.01 versus normothermic). Myocyte surface area, which reflects myocyte volume, was increased after cardioplegia and rewarming in adults (3582 +/- 55 versus 3316 +/- 46 microm2, p < 0.01), but remained unchanged in immature myocytes (2212 +/- 27 versus 2285 +/- 28 microm2, P = not significant). These unique findings demonstrate a preservation of myocyte contractile function and volume regulation in immature myocytes after cardioplegic arrest and rewarming. Thus this study directly demonstrates that developmental differences exist in myocyte responses to hypothermic hyperkalemic cardioplegic arrest with subsequent rewarming.

Animals↗
PubMed1994

In vitro investigations of the effects of nonfreezing low temperatures on lesioned and uninjured mammalian spinal neurons.

This two-part investigation explored the parameters and mechanisms of: (1) injury to spinal cord (SC) neurons by nonfreezing low temperatures, and (2) hypothermic protection of SC neurons subjected to a defined, physical injury (dendrite transection). Conclusions from the studies of hypothermic injury were: (1) morphologic and ultrastructural signs of stress developed in SC neurons as the temperature was decreased below 17 degrees C; (2) most neurons showing stress during cooling died upon rewarming to 37 degrees C; (3) spontaneous SC network activity was not significantly changed by cooling to 17 degrees C for 2 hours and rewarming, but cooling to 10 degrees C for 1 hour caused a reduction of burst frequency after rewarming, and cooling to 10 degrees C for 2 hours resulted in electrical silence after rewarming; and (4) application of N-methyl-D-aspartate (NMDA) antagonists before cooling prevented neuronal death, ultrastructural damage, and loss of activity upon rewarming, but application after cooling (before rewarming) was not protective. Conclusions from the studies of hypothermic protection were: (1) cooling at 17 degrees C for 2 hours followed by rewarming to 37 degrees C significantly increased lesioned neuron survival, but protection was lost when the period at 17 degrees C was increased to 6 hours; (2) NMDA blockade under normothermic (37 degrees C) or hypothermic (17 degrees C or 10 degrees C for 2 hours) conditions was not more protective of lesioned neurons than cooling to 17 degrees C (no NMDA antagonist); and (3) 200 microM thiopental or 100 microM pentobarbital increased lesioned neuron survival to a degree comparable to cooling for 2 hours at 17 degrees C.

Cell Death↗
PubMed1993

Absence of nonshivering thermogenesis in anesthetized adult humans.

BACKGROUND: Typically, core temperature rapidly decreases after induction of anesthesia, but reaches a stable plateau after several hours. This plateau typically occurs in conjunction with the onset of thermoregulatory vasoconstriction. Decreased heat loss, caused by vasoconstriction, may not be sufficient to establish thermal steady state without a concomitant increase in heat production. Accordingly, the authors tested the hypothesis that nonshivering thermogenesis contributes to thermal steady state during anesthesia. Rewarming from hypothermia is often associated with an afterdrop (a further reduction in core temperature, despite cutaneous warming). Because total body heat content increases during cutaneous warming, heat storage during afterdrop must reflect increased temperature and heat content of the peripheral tissue mass. Thermal balance was measured during rewarming to estimate the thermal capacity of the peripheral tissues. METHODS: Five volunteers were anesthetized with isoflurane and paralyzed with vecuronium. Oxygen consumption was measured during cooling to a core temperature at least 1 degree C less than that which triggered vasoconstriction. Volunteers were subsequently rewarmed using a circulating-water blanket and forced-air warmer. Oxygen consumption and cutaneous heat flux were measured to assess thermal balance and peripheral tissue heat storage during rewarming. RESULTS: The core temperature threshold for vasoconstriction was 35.2 +/- 0.8 degrees C. Oxygen consumption decreased 9 +/- 5%/degrees C during active cooling before vasoconstriction and 9 +/- 3%/degrees C after vasoconstriction. After the start of rewarming, core temperature continued to decrease for an additional 32 +/- 8 min. The magnitude of this afterdrop was 0.6 +/- 0.1 degree C. Peripheral tissue heat storage measured from the start of rewarming until the first net increase in core temperature was 144 +/- 60 kcal, which approximately equals 2 h of resting metabolic heat production. CONCLUSIONS: The authors concluded that nonshivering thermogenesis is not an important thermoregulatory response in adults anesthetized with isoflurane. Afterdrop and delayed core temperature recovery during rewarming reflect the large heat storage capacity of peripheral tissues.

Adult↗
PubMed1986

A model for the treatment of accidental severe hypothermia.

Central to the controversy that surrounds the treatment of accidental severe hypothermia is the question of how the method of rewarming affects myocardial performance, and therefore survival. We induced severe hypothermia and cardiac arrest in 15 mongrel dogs. Each dog was rewarmed by one of three methods: partial cardiac bypass (Group I); peritoneal dialysis (Group II); or external rewarming with a fluid-circulated blanket (Group III). The cardiac arrest state was supported by partial cardiac bypass in Group I and by standard mechanical cardiopulmonary resuscitation (CPR) in Groups II and III. In all dogs, the hypothermically depressed myocardial performance returned to normal upon rewarming. Groups I and II had similar rewarming times and required similar volumes of crystalloid and bicarbonate solutions to maintain adequate cardiac filling pressures and arterial pH. However, Group III had a significantly slower rewarming time and required significantly greater volumes of crystalloid and bicarbonate solutions. The sole procedural death occurred in Group III. Our results show that partial cardiac bypass, peritoneal dialysis, and the fluid-circulated blanket are equally effective in rewarming severely hypothemic dogs with cardiac arrest, provided that the cardiac arrest is relieved by partial cardiac bypass or standard mechanical CPR and that physiologic levels of intravascular volume, oxygenation, and pH are maintained.

Accidents↗