SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
We describe 2 case reports dealing with accidental hypothermia in which continuous veno-venous haemofiltration and dialysis (CVVHD) in combination with hyperinfusion with heated crystalloids was used as a rewarming technique. In this way it also is possible to correct metabolic disturbances, even during cardiopulmonary resuscitation.
Brain protection is crucial during neonatal and pediatric cardiac surgery. The major methods for brain protection are the administration of steroids and deep hypothermia. Therefore, we have investigated the impact of methylprednisolone (MP) administration and deep hypothermia on neonatal mouse astrocytes, neurons and BV-2 microglia cells. Brain cells were pretreated with MP (100 mM) and incubated according to a deep hypothermia protocol mimicking temperature changes during cardiac surgery in children: deep hypothermia (2 h at 17 degrees C, phase 1), slow rewarming (2 h up to 37 degrees C, phase 2), and normothermia (20 h at 37 degrees C, phase 3). In all brain-related cell types cytotoxicity was investigated as well as the release of the pro-inflammatory cytokine interleukin-6 (IL-6), which plays a major role in neuroprotection and neuroregeneration. Deep hypothermia induces substantial cytotoxicity and the secretion of IL-6 by astrocytes, BV-2 microglia cells and neurons. MP administration has no influence on the cell survival and IL-6 release of normothermic astrocytes, BV-2 microglia cells and neurons, while hypothermia-induced cytotoxicity and IL-6 secretion are significantly suppressed by MP. These data suggest that MP increases cell survival after deep hypothermia but also suppresses important neuroprotective and regenerative processes induced by IL-6. Hence, more specific immune modulation than that provided by MP may be needed to protect the brain during neonatal and pediatric cardiac surgery.
To investigate the reversibility of neuronal functions during deep and mild hypothermia, we have examined changes in membrane properties of pyramidal neurons of the CA3 region of hippocampal slices during cooling and rewarming (8 approximately 37 degrees C) of the perfusion medium. Hypothermia reduced the excitatory postsynaptic potential (EPSP) slope in a temperature dependent manner, but the EPSP amplitude was enhanced transiently between 30 and 25 degrees C. In observing spikes generated by either orthodromic stimulation or by direct intracellular current injection, the critical threshold for spike generation was decreased transiently at a temperature of 30 degrees C. In addition, the numbers of spikes were increased transiently regardless of the progressive prolongation of spike duration and latency with cooling. The resting membrane potential was stable from 37 to 20 degrees C. However, this potential showed a depolarizing shift at 15 degrees C. The neuronal activities, including membrane properties, recovered fully when the temperature was raised to 35 degrees C even from a low of 15 degrees C. In addition, field population spikes (PS) recorded in the pyramidal cell layer showed a complete reversibility after long-term severe hypothermia (8 degrees C). These results suggest that synaptic function, neuronal excitability and membrane properties maintain reversibility during deep hypothermia, as well as in mild hypothermia.
We conducted a prospective, randomized trial of three methods of rewarming patients after hypothermic cardiopulmonary bypass. Patients underwent either coronary artery bypass grafting or first-time valve replacement and were cooled to 32 degrees C during bypass. No significant differences existed among the groups as regards operative or preoperative parameters including hemodynamics and blood use. The patients actively warmed with a convective (Bair Hugger system, 3 hours) or a conductive blanket (electric overblanket, 4 hours) reached normothermia more quickly than those warmed with the space blanket (7 hours). This was reflected in significantly earlier extubation in the former two groups: Bair Hugger system 10.8 +/- 0.6 hours, electric blanket 11.3 +/- 1.0 hours, and space blanket 14.8 +/- 0.8 hours. Patients warmed with the space blanket required a higher dosage of morphine over the first 12 hours than those warmed with the electric blanket (10.4 vs 6.5 mg; p = 0.004), which may account for some of the differences between these two groups. No differences could be demonstrated between the two active blankets. On economic grounds we therefore recommend the reusable electric blanket for routine use.
STUDY OBJECTIVE: To investigate the efficacy of warmed, humidified inspired oxygen (O(2)) for the treatment of mildly hypothermic postoperative patients. DESIGN: Prospective, randomized, unblinded clinical trial. SETTING: Postanesthesia care unit in a tertiary care hospital. PATIENTS AND INTERVENTIONS: 30 ASA physical status I, II, and III patients following intraabdominal surgical procedures were randomly assigned to receive either routine O(2) therapy (control group, n = 15), or warmed (42 degrees C) humidified O(2) (treatment group, n = 15) for the initial 90 postoperative minutes. MEASUREMENTS: Core (tympanic) temperature, dry mouth score and shivering score. MAIN RESULTS: Tympanic temperature was similar in both groups on admission ( approximately 35.8 degrees C). Rewarming rate in the first postoperative hour was greater in the treatment group (0.7 +/- 0.1 degrees C. hr(-1)) compared to the control group (0.4 +/- 0.1 degrees C. hr(-1)) (p = 0.03). Patients receiving the warmed, humidified O(2) had a lower incidence of dry mouth compared to the control group (p = 0.03). The incidence of shivering was low and similar in both groups. CONCLUSIONS: Warming and humidifying inspired O(2) hastens recovery from hypothermia in postoperative patients.
The influence of moderate hypothermia induced by surface cooling was studied on haemodynamic variables and whole-body oxygen consumption in a 43-yr-old female undergoing clipping of multiple cerebral aneurysms. Decreasing oesophageal temperature to 32 degrees C lowered the whole-body oxygen consumption by about 40%. The decrease in oxygen consumption was matched by a proportional decrease in cardiac output. During the rewarming phase, there was a progressive increase in oxygen consumption, which was matched by a proportional increase in cardiac output. This resulted in a constant oxygen extraction ratio, as evidenced by oxyhaemoglobin saturation which remained constant at different body temperatures. While the temperature-corrected PVO2 decreased progressively with cooling, the temperature-uncorrected PVO2 remained constant at all body temperatures. Thus the use of temperature-uncorrected PO2 during hypothermia may simplify clinical interpretation because of our familiarity with normothermic PO2 values and the normothermic oxyhaemoglobin dissociation curve.
OBJECTIVE: To determine the effects of hypothermia and rewarming on changes in the villus microcirculation induced by intestinal ischemia-reperfusion (I/R). SUMMARY BACKGROUND DATA: The small intestine is extremely sensitive to I/R injury, and although hypothermia can reduce cellular injury, its capacity to influence the villous microcirculation after intestinal I/R is unclear, especially after the return to normothermic conditions. METHODS: Core body temperature of PVG rats was maintained at either 36 degrees to 38 degrees C (n = 12) or 30 degrees to 32 degrees C (n = 24) and then subjected to 30 minutes of intestinal ischemia. A subgroup of hypothermic animals (n = 12) were returned to normothermic conditions 120 minutes after clamp removal. The mucosal surface was visualized in an exteriorized ileal segment and macromolecular leak (MML) and leukocyte adhesion were monitored using in vivo microscopy (n = 6 in each group). MML from individual villi and numbers of adherent leukocytes within villi were determined for 2 to 4 hours after clamp removal. Heart rate and mean blood pressure were monitored in all animals. Control animals underwent sham surgery (n = 12). RESULTS: Ten of 12 normothermic animals failed to survive the reperfusion period, whereas all hypothermic animals and 11 of 12 of the hypothermic animals that were returned to normothermic conditions survived. MML was significantly increased in all animals subjected to I/R, although leakage was more marked in animals subjected to continuous normothermia. Enhanced leukocyte adhesion and decreased blood flow were observed only in normothermic animals. CONCLUSIONS: Hypothermia might prove to be an effective strategy for preventing adverse side effects in clinical settings in which intestinal I/R can be predicted.
Hyperkalemic cardioplegic arrest (HCA) and rewarming evokes postoperative myocyte contractile dysfunction, a phenomenon of particular importance in settings of preexisting left ventricular (LV) failure. Caspases are intracellular proteolytic enzymes recently demonstrated to degrade myocardial contractile proteins. This study tested the hypothesis that myocyte contractile dysfunction induced by HCA could be ameliorated with caspase inhibition in the setting of compromised myocardial function. LV myocytes were isolated from control pigs (n = 9, 30 kg) or pigs with LV failure induced by rapid pacing (n = 6, 240 bpm for 21 days) and were randomized to the following: (1) normothermia (2003 myocytes), incubation in cell culture medium for 2 hours at 37 degrees C; (2) HCA only (506 myocytes), incubation for 2 hours in hypothermic HCA solution (4 degrees C, 24 mEq K); or (3) HCA + z-VAD, incubation in hypothermic HCA solution supplemented with 10 microM of the caspase inhibitor z-VAD (z-Val-Ala-Asp-fluoromethyl-ketone, 415 myocytes). Inotropic responsiveness was examined using beta-adrenergic stimulation (25 nM isoproterenol). Ambient normothermic myocyte shortening velocity (microm/s) was reduced with LV failure compared with control values (54 +/- 2 versus 75 +/- 2, respectively, P < 0.05). Following HCA, shortening velocity decreased in the LV failure and control groups (27 +/- 5 and 45 +/- 3, P < 0.05). Institution of z-VAD increased myocyte shortening velocity following HCA in both the LV failure and control groups (49 +/- 5 and 65 +/- 5, P < 0.05). Moreover, HCA supplementation with z-VAD increased beta-adrenergic responsiveness in both groups compared with HCA-only values. This study provides proof of concept that caspase activity contributes to myocyte contractile dysfunction following simulated HCA. Pharmacologic caspase inhibition may hold particular relevance in the execution of cardiac surgical procedures requiring HCA in the context of preexisting LV failure.
INTRODUCTION: We report two drowning victims with hypothermic circulatory arrest who were resuscitated with the use of extracorporeal circulation (ECC). The first patient developed severe post-bypass pulmonary oedema and inspired us to use a leucocyte-depletion filter in the second patient to attenuate leucocyte-mediated pulmonary reperfusion injury. METHODS: In the first patient, a standard extracorporeal circuit was used. In the second patient, systemic leucocyte depletion was applied using leucocyte-depletion filters (Pall RS 1, Pall, Portsmouth, UK), in the venous side of the extracorporeal circuit. Circulating leucocyte counts were measured and arterial blood gas analysis and chest X-rays were performed. RESULTS: Both patients showed a decrease of the circulating leucocyte counts during rewarming and had nearly similar leucocyte counts on arrival at the intensive care unit (ICU). The first patient developed severe pulmonary oedema, with poor arterial blood gases, whereas the second patient, who had leucocyte-depletion by filtration, did not develop severe pulmonary oedema, and had good arterial blood gases. CONCLUSION: Profound leucocyte-depletion by means of filtration may have contributed to limit leucocyte-mediated pulmonary reperfusion injury.
Malignant hyperthermia (MH) is a rare hypermetabolic disorder of skeletal muscle that can be fatal if not recognized and treated aggressively. We describe a patient with a suspected family history of MH who developed hyperpyrexia, acidosis, and hypermetabolism after cardiac surgery despite a nontriggering anesthetic. No drugs were identified as being causative and we theorize that systemic rewarming was the inciting cause of MH in this MH-susceptible individual via a mechanism similar to heat stroke.
This case report demonstrates successful cardiopulmonary and cerebral resuscitation (CPCR) of a young male explored 15 hours following a suicide attempt (carbamazepine intoxication) in deep hypothermia (19 degrees C) with circulatory arrest. An extracorporeal circuit was used to rewarm the patient's blood. Weaning from extracorporeal circulation (ECC) was successful and without complications as was recovery from multiorgan dysfunction, severe rhabdomyolysis and carbamazepine intoxication. An excellent outcome was achieved without any neurological deficit at the time of discharge from the hospital.
Successful cryopreservation of whole organs may require electromagnetic (EM) heating at much faster warming rates than those at which thermal relaxation can smooth out nonuniform power distribution or suppress hot spots which become unstable due to an increase of power absorbtion with temperature in the material being heated. Calculations of the heating distribution for a uniform spherical workpiece in a resonant EM applicator show that the size of a workpiece for which there will be good uniformity of heating has a sharp upper limit given D < or = 0.3 lambda m, where D is the workpiece diameter and lambda m is the EM wavelength in the material. We also introduce three stability factors which indicate whether thermal runaway can occur; they are dependent solely on the material's dielectric properties and the geometry and orientation of any irregularities. These factors provide clear guidelines to the choice of source frequency and applicator geometry that are favorable for intrinsic control of thermal runaway. Experimental results are presented for spherical phantom workpieces of 36- and 45-mm diameter, rewarmed from -90 to above 0 degrees C in 30 to 150 s, in a 434-MHz resonant cavity applicator. The observed spatial temperature distributions for different E-field configurations clearly indicate the effectiveness of the stability factors in predicting uniformity of temperature, and the significance of the workpiece size limit, in practical EM heating situations.
Helium-cold hypothermic hamsters, colonic temperature (Tc) 7 to 11 degrees C, injected with acetylcholine (ACH) at a preoptic-anterior hypothalamic (AHPOA) site responded with a rise in colonic temperature while remaining in a cold environmental chamber. The He-Cold hamster does not thermoregulate at these body temperatures. In contrast to central ACH-elicited responses, the injection of alpha and beta adrenergic drugs into the systemic circulation of the He-Cold hamster did not elicit a rise in colonic temperature. The data describe a different animal model of rewarming than has previously been described that is under pharmacologic control by the experimenter. The use of exogenous neurotransmitter provides the potential to understand the mechanisms of thermoregulation in deep experimental hypothermia.
This study utilized microvascular corrosion casting techniques to evaluate changes in the microvascular patency of rat hindpaws cooled to four different subzero temperatures. Left hindpaws of anesthetized rats in group 1 were cooled to -5 degrees C, in group 2 to -15 degrees C, in group 3 to heat of fusion (HOF), and in group 4 to HOF and then to -15 degrees C. Although freezing did not take place in the hindpaws of groups 1 and 2, initiation of freezing in the tissues, as indicated by HOF, did occur in groups 3 and 4. Cooled hindpaws were rapidly rewarmed. Right hindpaws served as controls. Microvascular corrosion casts were made from the left and right hindpaws of all animals. There was no significant difference when the mean cast weights of cooled hindpaws from groups 1, 2, and 3 were compared to the mean cast weights of their respective control hindpaws. In group 4, there was a significant difference (P less than 0.05) when the mean cast weight of the cooled hindpaws (47.69 +/- 9.05, mg +/- SEM) was compared to that of the control hindpaws (80.63 +/- 12.23). Since, in this acute experiment, a loss of vascular integrity occurred when the hindpaws in group 4 were cooled to -15 degrees C after reaching HOF, the initiation of freezing alone was not sufficient to reduce mean cast weight.
We describe a UHF rewarming system which has been used to measure warming rates, and particularly the uniformity of warming on three orthogonal axes, in a rabbit kidney phantom 36 mm in diameter. The stabilizing effect is demonstrated of using an E-field directed along the temperature gradient (or normal to any surface of dielectric discontinuity). One hot spot remains unaccounted for. The average warming rates and power dissipation are related to the volumetric heat capacity of the phantom material at -30 degrees C.
Thirty-three patients undergoing elective myocardial revascularization were prospectively randomized into two study groups (Group S and Group P) to permit evaluation of the effects of shivering on oxygen consumption per minute (VO2), carbon dioxide production per minute (VCO2), and hemodynamic performance. Group S was allowed to shiver during the postoperative rewarming period, and Group P received hourly injections of pancuronium bromide and Metubine (metocurine) sulfate with sedation to block the shivering response. Group S demonstrated significantly higher increases in VO2 and VCO2, lower systolic blood pressure and mixed venous oxygen saturation, and a greater use of inotropic support than the patients in Group P. Suppression of the shivering response minimized increases in VO2 and VCO2, improved hemodynamic stability, and resulted in a decreased need for inotropic support.
In 12 rabbits hypothermia and rewarming were induced with temperature-controlled circulating peritoneal dialysis in combination with temperature-controlled hypoxic and hypercapnic gas mixtures. The average cooling time necessary for the esophageal temperature to decrease from 37.7 degrees +/- 0.7 to 20.6 degrees +/- 1.0 degrees C was 81 +/- 34 minutes with a range of 41 to 150 minutes. The average warming time for esophageal temperature to increase from 20.6 degrees +/- 1.0 degrees C to 35.2 degrees +/- 1.8 degrees C was 90 +/- 35 minutes. Time of cooling was related to the proportions of inspired carbon dioxide and oxygen. In contrast to surface and bypass methods, esophageal and muscular temperatures agreed very closely, suggesting an absence of regional temperature gradients.
OBJECTIVES: To measure the effect of ice slurry topical cooling on brain surface temperature during deep hypothermic circulatory arrest. DESIGN: This was a prospective, controlled experiment. SETTING: Animal laboratory at a university hospital. PARTICIPANTS: Five control lambs, five treatment (ice slurry) lambs. INTERVENTIONS: Animals were studied in two groups: the study group had topical cooling of the head with ice slurry started immediately before circulatory arrest and continued throughout the period of circulatory arrest; control group lambs received no supplemental topical cooling. MEASUREMENTS AND MAIN RESULTS: Brain surface temperature, scalp, nasopharyngeal, and rectal temperatures were measured at 5-minute intervals during 45 minutes of circulatory arrest. Lambs receiving topical cooling of the head with ice slurry had a statistically significant decrease in brain surface temperature of 2.2 +/- 1.2 degrees C during circulatory arrest, whereas brain surface temperature increased 1.2 +/- 0.3 degrees C, in control lambs. Equilibration of temperature between the scalp and brain in control lambs produced rewarming of the brain surface. CONCLUSIONS: Topical cooling of the head with ice slurry in newborn lambs lowers brain surface temperature during deep hypothermic circulatory arrest. Surrogate temperature monitoring locations such as nasopharyngeal and rectal temperatures varied significantly and do not accurately reflect changes in brain surface temperature.