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Comparative effectiveness of hypothermia rewarming techniques: radio frequency energy vs. warm water.

The purpose of this study was to compare the rewarming effectiveness of a radio frequency coil (13.56 MHz) at a specific absorption rate (SAR) of 2.5 W/kg (RF) with warm water immersion (40 degrees C) (WW) and an insulated mummy-type insulating sack (IS) under simulated field conditions. Four male subjects, ages 24-35, were immersed in 10 degrees C water for up to 90 min or until their rectal temperatures (Tre) decreased to 35 degrees C. Each subject had 3 trials in which they were immersed. After each immersion, rewarming was accomplished with either RF, WW, or IS, so that each subject was rewarmed once with each method. Comparisons of the 3 rewarming methods were based on the rate of increase of Tre during rewarming (Tre/t), Tre 60 min after the start of rewarming (Tre60), the time-interval measured from extraction from the water to the end of afterdrop (tad), and the magnitude of any observed Tre afterdrop (Tad). WW had significantly greater Tre/t and Tre60 than either RF or IS (P < 0.03) and a smaller tad than IS (P < 0.05). IS had significantly greater Tad than either WW or RF (P < 0.05). No significant differences in Tre/t, Tre60, or tad were observed between IS and RF. The results of this study indicate that for mildly hypothermic individuals, active rewarming with RF at a SAR of 2.5 W/kg is less effective than WW and roughly equivalent to passive rewarming with IS.

Adult↗

Feasibility of a novel veno-veno circuit as a central rewarming method in a severely hypothermic canine model.

PURPOSE: Many victims of accidental hypothermia are successfully resuscitated, but questions remain regarding the optimum rewarming techniques. Most of the invasive warming techniques such as closed thoracic lavage, hemodialysis, peritoneal dialysis, and cardiopulmonary bypass require specialized personnel, equipment, and procedures that are not readily available in all facilities. The objective of this study was to investigate the technical feasibility of utilizing a novel veno-veno rewarming circuit to resuscitate severely hypothermic subjects. If this alternative invasive warming technique is successful, it could be available to treat hypothermic patients in virtually any emergency department setting. METHODS: The rewarming system consisted of a Baxter ThermaCyl warmer (Baxter Co., McGaw Park, IL), a roller pump, hemodialysis tubing, connectors, and 2 venous catheters. Blood was pumped from the body via the femoral vein, through the roller pump, into the warmer, and then returned to the body via the right jugular vein. Seven adult mongrel hounds of similar weights (20 to 25 kg) were anesthetized and instrumented for data collection. Temperature probes were placed in the rectum, the peritoneal cavity, and the esophagus to record core temperatures. Each animal was cooled by ice packing to a central core temperature of 29 degrees C and then rewarmed using the described veno-veno circuit. Vital signs, pulse oximetry, cardiac rhythm, and laboratory values were obtained prior to cooling the animals, and were repeated for every degree Celsius change once warming began. Christopher Haughn, MD, was the second place winner in the Basic Sciences Resident Competition at the Ohio American College of Surgeons meeting. RESULTS: Because of technical difficulties, data from 1 dog were not included in the results. Of the remaining 6 dogs, all were rewarmed from 29 degrees C to 37 degrees C. Adverse side effects included gross hematuria, acidemia (median pH decrease was 0.088), and decreases in haptoglobin (median decrease 13.5 g/dl), hemoglobin (median decrease 1.35 g/dl), and arterial pO(2) level (median decrease 167 mm Hg). Decreases in blood pressure and heart rate were also noted during the cooling process, but reversed upon rewarming. CONCLUSIONS: From this pilot study, we conclude that our novel veno-veno circuit rewarming is a feasible method of rewarming hypothermic subjects and warrants further investigation and comparison with other active warming methods.

Animals↗

Myointimal hyperplasia and sympathetic reinnervation following local cold injury and rapid rewarming in the rabbit central ear artery.

BACKGROUND: Functional and pathological improvements following rapid rewarming in 42 degrees C water was compared with alterations following slow thawing at room temperature (22 degrees C) after frostbite (-9 degrees C, 15 minutes) in vivo of the rabbit central ear artery. METHODS: Following two to ten weeks of in vivo regeneration, vascular segments were tested in vitro. Maximal and dose-dependent isometric contractions were induced by exogenous noradrenaline. Sympathetic nerves in the vascular wall were stained with glyoxylic acid. Vascular ring segments were stained with haematoxylin and eosin. RESULTS: Following slow thawing, the total uptake, the K+ evoked and the spontaneous release of [3H]noradrenaline in the sympathetic nervous system were strongly reduced two weeks after freezing, with a subsequent increase to control level within 3-4 weeks. After rapid rewarming the total uptake, the spontaneous release and the K+ evoked release of [3H]noradrenaline commenced earlier such that after ten weeks the level was twice as high as following slow rewarming. The glyoxylic acid induced catecholamine fluorescence in sympathetic nerves, revealed an earlier regeneration after rapid rewarming. Haematoxylin and eosin-stained segments revealed less intimal hyperplasia three to 20 weeks after rapid rewarming than after slow thawing. CONCLUSION: Rapid rewarming of in vivo frozen arteries in warm water (42 degrees C) did not prevent immediate vasoparalysis and degeneration of sympathetic nerves. However, nerve regeneration occurred earlier and with higher tissue nerve densities as compared to tissue that had been slowly rewarmed. Myointimal hyperplasia was less pronounced after rapid rewarming. Abnormal sympathetic nerve function and myointimal hyperplasia, as observed in this study, may contribute to a greater understanding of sequelae in the human body following frostbite.

Adrenergic Fibers↗

Reduction of rewarming injury of the hepatic graft by a heat insulator.

BACKGROUND: The deleterious effect of rewarming in orthotopic liver transplantation is recognized. This study examined the significance of rewarming the hepatic allograft, and the possibility of using a heat insulator to reduce rewarming injury. METHODS: After total hepatectomy in rats with in situ perfusion by chilled (4 degrees C) lactated Ringer's solution, the livers were divided into four groups of ten each: group 1, 4-h preservation in chilled Ringer's solution and 15 min of rewarming; group 2, 6-h preservation in chilled Ringer's solution; group 3, 6-h preservation in chilled Ringer's solution and 15 min of rewarming; group 4, 6-h preservation in chilled Ringer's solution and 15 min of rewarming with a heat insulator. Glutamic-pyruvic transaminase (GPT) and N-acetyl-beta-glucosaminidase (NAG) concentrations in the final graft effluent, and the amount of adenosine 5'-triphosphate (ATP) in liver tissue after preservation, were measured. RESULTS: GPT and NAG concentrations in the final graft effluent of group 3 were higher than those of group 2 (P < 0.01), whereas values in group 4 were lower than those of group 3 (P < 0.05). The final ATP concentration in group 3 was significantly lower than that in group 2 (P < 0.01), whereas the value in group 4 was significantly higher than that of group 3 (P < 0.01). CONCLUSION: Rewarming diminishes the viability of a liver graft with degradation of ATP, and a heat insulator reduces rewarming injury.

Acetylglucosaminidase↗

Posttraumatic hypothermia followed by slow rewarming protects the cerebral microcirculation.

In the clinical and laboratory setting, multiple reports have suggested the efficacy of hypothermia in blunting the damaging consequences of traumatic brain injury (TBI). With the use of posttraumatic hypothermia, it has been recognized that the time of initiation and duration of hypothermia are important variables in determining the degree of neuroprotection provided. Further, it has been recently recognized that the rate of posttraumatic rewarming is an important variable, with rapid rewarming exacerbating neuronal/axonal damage in contrast to slow rewarming which appears to provide enhanced neuroprotection. Although these findings have been confirmed in the brain parenchyma, no information exists for the cerebral microcirculation on the potential benefits of posttraumatic hypothermia followed by either slow or rapid rewarming. In the current communication we assess these issues in the pial circulation using a well-characterized model of TBI. Rats were prepared for the placement of cranial widows for direct assessment of the pial microcirculation prior to and after the induction of impact acceleration injury followed by moderate hypothermia with either subsequent slow or rapid rewarming strategies. The cranial windows allowed for the measurement of pial vessel diameter to assess ACh-dependent and CO2 reactivity in the chosen paradigms. ACh was applied topically to assess ACh-dependent dilation, while CO2 reactivity was assessed by changing the concentration of the inspired gas. Through this approach, it was found that posttraumatic hypothermia followed by slow rewarming maintained normal arteriolar vascular responses in terms of ACh-dependent dilation and CO2 reactivity. In contrast, arterioles subjected to TBI followed by normothermia or hypothermia and rapid rewarming showed impaired vasoreactivity in terms of their ACh-dependent and CO2 responses. This study provides additional evidence of the benefits of posttraumatic hypothermia followed by slow rewarming, demonstrating for the first time that the previously described neuroprotective effects extend to the cerebral microcirculation.

Acetylcholine↗

Pharmacological vasodilatation improves efficiency of rewarming from hypothermic cardiopulmonary bypass.

An afterdrop in core temperature after hypothermic cardiopulmonary bypass (CPB) is related to inadequate peripheral rewarming. We proposed that pharmacological vasodilatation during rewarming on bypass would improve peripheral rewarming and reduce the degree of afterdrop. Fifty-nine of 120 patients were randomized to receive a sodium nitroprusside (SNP) infusion during the rewarming stage of hypothermic CPB. Mean systemic vascular resistance (SVR) during the rewarming phase of CPB was 1129 dyne s-1 cm-5 in the control group and 768 dyne s-1 m-5 in the SNP group (P < or = 0.001). Patients receiving SNP rewarmed to 37.0 degrees C faster (299 min vs 376 min; P = 0.003) and were extubated earlier (490 min vs 621 min; P = 0.001). Patients receiving SNP had a warmer mean peripheral temperature (MPT) (32.9 degrees C vs 32.4 degrees C; P = 0.05) on termination of CPB. Postoperative core temperature fell less in the SNP group (35.6 degrees C vs 35.2 degrees C; P = 0.01) as did MPT (31.8 degrees C vs 31.2 degrees C; P = 0.004). SNP-induced vasodilatation during rewarming from hypothermic CPB improves peripheral rewarming, reduces the degree of postoperative core and peripheral hypothermia and reduces time to extubation.

Aged↗

Body morphology and the speed of cutaneous rewarming.

BACKGROUND: Infants and children cool quickly because their surface area (and therefore heat loss) is large compared with their metabolic rate, which is mostly a function of body mass. Rewarming rate is a function of cutaneous heat transfer plus metabolic heat production divided by body mass. Therefore, the authors tested the hypothesis that the rate of forced-air rewarming is inversely related to body size. METHODS: Isoflurane, nitrous oxide, and fentanyl anesthesia were administered to infants, children, and adults scheduled to undergo hypothermic neurosurgery. All fluids were warmed to 37 degrees C and ambient temperature was maintained near 21 degrees C. Patients were covered with a full-body, forced-air cover of the appropriate size. The heater was set to low or ambient temperature to reduce core temperature to 34 degrees C in time for dural opening. Blower temperature was then adjusted to maintain core temperature at 34 degrees C for 1 h. Subsequently, the forced-air heater temperature was set to high (approximately 43 degrees C). Rewarming continued for the duration of surgery and postoperatively until core temperature exceeded 36.5 degrees C. The rewarming rate in individual patients was determined by linear regression. RESULTS: Rewarming rates were highly linear over time, with correlations coefficients (r2) averaging 0.98+/-0.02. There was a linear relation between rewarming rate (degrees C/h) and body surface area (BSA; m2): Rate (degrees C/h) = -0.59 x BSA (m2) + 1.9, r2 = 0.74. Halving BSA thus nearly doubled the rewarming rate. CONCLUSIONS: Infants and children rewarm two to three times faster than adults, thus rapidly recovering from accidental or therapeutic hypothermia.

Adult↗

Efficacy of forced-air and inhalation rewarming by using a human model for severe hypothermia.

We recently developed a nonshivering human model for severe hypothermia by using meperidine to inhibit shivering in mildly hypothermic subjects. This thermal model was used to evaluate warming techniques. On three occasions, eight subjects were immersed for approximately 25 min in 9 degrees C water. Meperidine (1.5 mg/kg) was injected before the subjects exited the water. Subjects were then removed, insulated, and rewarmed in an ambient temperature of -20 degrees C with either 1) spontaneous rewarming (control), 2) inhalation rewarming with saturated air at approximately 43 degrees C, or 3) forced-air warming. Additional meperidine (to a maximum cumulative dose of 2.5 mg/kg) was given to maintain shivering inhibition. The core temperature afterdrop was 30-40% less during forced-air warming (0.9 degree C) than during control (1.4 degrees C) and inhalation rewarming (1.2 degrees C) (P < 0.05). Rewarming rate was 6- to 10-fold greater during forced-air warming (2.40 degrees C/h) than during control (0.41 degree C/h) and inhalation rewarming (0.23 degree C/h) (P < 0.05). In nonshivering hypothermic subjects, forced-air warming provided a rewarming advantage, but inhalation rewarming did not.

Adult↗

Cardiovascular effects of epinephrine during rewarming from hypothermia in an intact animal model.

Rewarming from accidental hypothermia is often complicated by "rewarming shock," characterized by low cardiac output (CO) and a sudden fall in peripheral arterial pressure. In this study, we tested whether epinephrine (Epi) is able to prevent rewarming shock when given intravenously during rewarming from experimental hypothermia in doses tested to elevate CO and induce vasodilation, or lack of vasodilation, during normothermia. A rat model designed for circulatory studies during experimental hypothermia and rewarming was used. A total of six groups of animals were used: normothermic groups 1, 2, and 3 for dose-finding studies, and hypothermic groups 4, 5, and 6. At 20 and 24 degrees C during rewarming, group 4 (low-dose Epi) and group 5 (high-dose Epi) received bolus injections of 0.1 and 1.0 microg Epi, respectively. At 28 degrees C, Epi infusion was started in groups 4 and 5 with 0.125 and 1.25 microg/min, respectively. Group 6 served as saline control. After rewarming, both CO and stroke volume were restored in group 4, in contrast to groups 5 and 6, in which both CO and stroke volume remained significantly reduced (30%). Total peripheral resistance was significantly higher in group 5 during rewarming from 24 to 34 degrees C, compared with groups 4 and 6. This study shows that, in contrast to normothermic conditions, Epi infused during hypothermia induces vasoconstriction rather than vasodilation combined with lack of CO elevation. The apparent dissociation between myocardial and vascular responses to Epi at low temperatures may be related to hypothermia-induced myocardial failure and changes in temperature-dependent adrenoreceptor affinity.

Adrenergic alpha-Agonists↗

Hemodynamics among neonates with hypoxic-ischemic encephalopathy during whole-body hypothermia and passive rewarming.

OBJECTIVE: To assess changes in cardiac performance, with Doppler echocardiography, among newborns with hypoxic-ischemic encephalopathy during mild therapeutic hypothermia and during rewarming. METHODS: For 7 asphyxiated neonates (birth weight: 1840-3850 g; umbilical artery pH: 6.70-6.95) who received mild whole-body hypothermia, the following hemodynamic parameters were determined immediately before rewarming (33 degrees C) and during passive rewarming (35 degrees C and 37 degrees C): heart rate, systolic and diastolic blood pressure, core and peripheral temperatures, left ventricular ejection time, mean velocity of aortic flow, stroke volume, and cardiac output. RESULTS: Heart rate decreased during hypothermia. Bradycardia, with heart rates below 80 beats per minute, did not occur. The median difference between core and peripheral temperatures decreased from 2.0 degrees C (range: 0-6.2 degrees C) during hypothermia to 0.7 degrees C (range: 0.4-1.9 degrees C) at normothermia. Cardiac output was reduced to 67% and stroke volume to 77% of the posthypothermic level. The median heart rate was 129 beats per minute before rewarming and increased to 148 beats per minute during complete rewarming. Before and during passive rewarming, hypotension was not observed. Before, during, and at the end of rewarming, the following parameters increased: mean velocity of aortic flow (median: 44, 55, and 58 cm/second, respectively), stroke volume (median: 1.42, 1.55, and 1.94 mL/kg, respectively), and cardiac output (median: 169, 216, and 254 mL/kg per minute, respectively). Left ventricular ejection time remained unchanged. CONCLUSIONS: Whole-body hypothermia resulted in reduced cardiac output, which reached normal levels at the end of passive rewarming, at normothermia. Physiologic cardiovascular mechanisms seemed to be intact to provide sufficient tissue perfusion, with normal blood lactate levels.

Asphyxia Neonatorum↗

Rewarming from hypothermia leads to elevated plasma lipopolysaccharide concentrations.

Rewarming victims of hypothermia such as divers or immersion victims, participants in winter sports and military operations, and surgical patients on cardiopulmonary bypass (CPB) may lead to vascular instability, multiorgan failure, shock, and even death. While the causes of these rewarming symptoms are unknown, they may be related to bacterial lipopolysaccharide (LPS) translocated from the intestines into the circulation due to splanchnic ischemia. We have determined LPS during the cooling (to 31.5 degrees-34.0 degrees C) and rewarming phases of hypothermic surgery in 11 patients at the Stanford University Medical Center. During rewarming, there was an LPS spike in 6/11, in one more patient there was an LPS spike during surgery but not during rewarming, and in 4/11 there was no rise in LPS, i.e., a temporary endotoxemia occurred in 7/11 (63.6%) patients, usually at the commencement of rewarming. All four patients with no LPS spike received dexamethasone for at least 7 days before surgery. We propose that hypothermia reduced splanchnic blood flow (BF), causing ischemic damage to the gut wall and translocation of LPS from the gut into the vascular space. Upon rewarming, splanchnic BF is restored, the translocated LPS transits from the splanchnic to the systemic circulations as a bolus, and the gut wall is healed. No sequelae occurred in these patients because of their adequately functioning immune systems. However, had they been immunocompromised, symptoms might have occurred. Rewarming of accident victims probably also incurs a similar risk of endotoxemia, and dexamethasone may have protected the gut wall. Further studies are indicated.

Body Temperature↗

Rewarming cardiac surgical patients: warm water vs warm air.

BACKGROUND: Hypothermia is experienced by 60% to 90% of adult patients after surgery. The detrimental physiological consequences of prolonged hypothermia are a significant risk for cardiac surgical patients. OBJECTIVE: To compare the effect of a warmed convective-air blanket with that of a warmed circulating-water blanket on the rates of increase in skin and core temperatures and on total rewarming time in patients with hypothermia after cardiac surgery. METHODS: A quasi-experimental, repeated-measures design was used to study rewarming in 76 adult patients who were hypothermic after cardiac surgery. Subjects were randomized to two groups: 40 were warmed with a convective-air blanket; 36, with a circulating-water blanket. Skin and core temperatures were recorded every 15 minutes until the subject's pulmonary artery temperature reached 37 degrees C. Total time required for rewarming was the period between time of placement of the blanket and time of removal. The effects of 13 other variables on the time required for rewarming were also determined. RESULTS: Both skin and core temperatures increased more rapidly in patients treated with the warm circulating-water blanket than in those treated with the convective-air blanket. The mean time required for rewarming was 45 minutes shorter in the group treated with the circulating-water blanket. The patient's age, volume of i.v. fluids received, length of anesthesia, starting core temperature, and treatment method had significant effects on the time required for rewarming. CONCLUSIONS: The data suggest that rewarming with a circulating-water blanket produces normothermia more rapidly than rewarming with a warm convective-air blanket in adult patients who are hypothermic after cardiac surgery.

Adult↗

Prolonged rewarming after hypothermic cardiopulmonary bypass does not attenuate reduction of jugular bulb oxygen saturation.

OBJECTIVE: This study investigates the effects of rapid versus graded rewarming on decreases in jugular bulb oxygen saturation (SjO2) during cardiopulmonary bypass (CPB) in a prospective nonrandomized and nonblinded design. SETTING AND PARTICIPANTS: At the Department of Anesthesiology (University Hospital Eppendorf, Germany), 28 patients (ASA III) undergoing coronary artery bypass graft were investigated. INTERVENTION: CPB was managed according to alpha-stat conditions during moderate hypothermia (27 degrees C). In group 1 (n = 17), rewarming was performed by increasing the perfusate temperature to 36 degrees C within 7 minutes, in group 2 (n = 11) within 15 minutes. MEASUREMENTS AND MAIN RESULTS: SjO2 was measured by a fiberoptic catheter placed in the right jugular bulb. Data were recorded before and 40 minutes after the start of rewarming every 5 minutes. During rewarming of CPB, SjO2 was decreased to 43 +/- 7% in group 1 and to 44 +/- 4% in group 2. In groups 1 and 2, the maximum reduction of SjO2 occurred 17 minutes and 30 minutes after start of rewarming, respectively. The delayed reduction of SjO2 in group 2 correlated strongly with the prolonged increase in jugular bulb temperature. CONCLUSION: The current data show that slow rewarming does not attenuate reductions of SjO2. This suggests that the reduction of SjO2 during rewarming of CPB is not a function of the rewarming speed but is strongly correlated with the increase in jugular bulb temperature, with a maximum effect just before reaching normothermia of the brain.

Adult↗

Comparison of the effects of sodium nitroprusside and isoflurane during rewarming on cardiopulmonary bypass.

OBJECTIVES: Afterdrop in core temperatures after discontinuation of cardiopulmonary bypass (CPB) is reported to be a sign of inadequate total body rewarming on CPB. The purpose of this study was to compare the effects of three different drug regimens on hemodynamic stability and the uniformity of rewarming during the rewarming period of CPB. DESIGN: This prospective randomized study was performed in the Anesthesiology Department of the University of Istanbul. PARTICIPANTS: Sixty-six patients undergoing uncomplicated valve replacement and aortocoronary bypass grafting surgery were studied. INTERVENTIONS: Anesthesia was maintained with isoflurane and fentanyl infusion during the prebypass and the postbypass periods. Patients were allocated into three groups by the initiation of CPB. Group 1 (n = 22): fentanyl infusion + diazepam + sodium nitroprusside (SNP) in the rewarming period), group 2 (n = 22): fentanyl infusion + isoflurane, group 3, control (n = 22): fentanyl infusion + diazepam. Rectal, esophageal, and forearm temperatures were monitored throughout the study. MEASUREMENTS AND MAIN RESULTS: None of the durational and temperature data showed significant differences between groups 1 and 2. In the control group, afterdrop in esophageal temperature was significantly higher than groups 1 and 2 (group 1: -1.4 +/- 0.9 degrees C, group 2: -1.44 +/- 0.8 degrees C, group 3: -2.1 +/- 0.65 degrees C). In group 1, the number of patients whose mean arterial pressure (MAP) decreased below 45 mmHg was significantly higher than group 2 (p = 0.002). Mean SNP infusion rate and mean isoflurane concentration during the rewarming period were calculated as 1.55 +/- 0.8 micrograms/kg/min and 0.775 +/- 0.27%, respectively. CONCLUSIONS: Isoflurane produced more stable hemodynamic conditions than SNP during the rewarming period, improved the uniformity of rewarming, and permitted earlier extubation in the intensive care unit (ICU). It is concluded that isoflurane alone is capable of fulfilling the anesthesia needs during hypothermia and the rewarming period of CPB.

Adolescent↗

Cold-preservation-induced sensitivity of rat hepatocyte function to rewarming injury and its prevention by short-term reperfusion.

With increasing time of cold preservation, levels of high-energy nucleotides in the liver are reducing. The authors hypothesized that cold preservation sensitizes hepatocyte function to ischemic injury occurring during graft rewarming and that the injury can be prevented by short-term reperfusion. Rat livers were cold-preserved in University of Wisconsin solution for 0 to 18 hours and ischemically rewarmed for 0 to 45 minutes to simulate the implantation stage of transplantation. Hepatobiliary function was assessed using a blood-free perfusion model. In comparison with controls, neither 18-hour preservation nor 45-minute ischemic rewarming significantly influenced hepatocyte function. Compared with livers subjected to 45-minute ischemic rewarming, livers subjected to 9-hour preservation and 45-minute rewarming, and livers subjected to 18-hour preservation and 45-minute rewarming exhibited, respectively: 3.8 and 24 times reduced bile production, 4.3- and 116-fold decreased taurocholate excretion, and 3.1 and 42 times depressed bromosulfophthalein excretion. Thirty-minute oxygenated warm reperfusion after 9- and 18-hour preservation nearly completely blunted sensitization of hepatocyte function to rewarming ischemia. The authors found that short-term oxygenated reperfusion restored adenine nucleotides in liver tissue to the values found before organ preservation and that reperfusion with energy substrate containing solutions increased tissue adenosine triphosphate concentration to a higher level than that found before preservation. In conclusion, sensitization of hepatocyte function to rewarming ischemia increases disproportionally with storage time, suggesting that this phenomenon may play a role in graft dysfunctions with increasing liver preservation time. Short-term oxygenated reperfusion of the liver may protect hepatocyte functions against warm ischemic insult, even after extended preservation.

Adenosine↗

Rapid rewarming causes an increase in the cerebral metabolic rate for oxygen that is temporarily unmatched by cerebral blood flow. A study during cardiopulmonary bypass in rabbits.

BACKGROUND: Jugular venous hemoglobin desaturation during the rewarming phase of cardiopulmonary bypass is associated with adverse neuropsychologic outcome and may indicate a pathologic mismatch between cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2). In some studies, rapid rewarming from hypothermic cardiopulmonary bypass results in greater jugular venous hemoglobin desaturation. The authors wished to determine if rewarming rate influences the temperature dependence of CBF and CMRO2. METHODS: Anesthetized New Zealand white rabbits, cooled to 25 degrees C on cardiopulmonary bypass, were randomized to one of two rewarming groups. In the fast group (n = 9), aortic blood temperature was made normothermic within 4 min. In the slow group (n = 9), aortic blood temperature was made normothermic over 25 min. Cerebral blood flow (microspheres) and CMRO2 (Fick) were determined at baseline (25 degrees C), and at brain temperatures of 28 degrees, 31 degrees, 34 degrees, and 37 degrees C during rewarming. RESULTS: Systemic physiologic variables appeared similar between groups. At a brain temperature of 28 degrees C, CMRO2 was 47% greater in the fast rewarming group than in the slow group (2.2 +/- 0.5 vs. 1.5 +/- 0.2 ml O2.100 g-1. min-1, respectively; P = 0.01), whereas CBF did not differ (48 +/- 18 vs. 49 +/- 8 ml.100 g-1.min-1, respectively; P = 0.47). Throughout rewarming, CBF increased as a function of brain temperature but was indistinguishable between groups. Cerebral metabolic rate for oxygen differences between groups decreased as brain temperatures increased. CONCLUSIONS: Cerebral venous hemoglobin desaturation with rapid rewarming is caused by an increase in CMRO2 that is temporarily greater than the increase in CBF. This mismatch may indicate a transient abnormality in flow-metabolism coupling, or the effect of temperature gradients on oxygen transfer from hemoglobin to brain.

Animals↗

Hypercapnia prevents jugular bulb desaturation during rewarming from hypothermic cardiopulmonary bypass.

UNLABELLED: BACKGROUND. The rewarming period of hypothermic cardiopulmonary bypass (CPB) is associated with reduced jugular bulb venous oxygen saturation (SjO2). This study investigates the effects of normocapnia vs. hypercapnia on changes in SjO2 during rewarming from hypothermic CPB for coronary artery bypass graft in patients classified as American Society of Anesthesiologists physical status 111. METHODS: Anesthesia was induced and maintained with fentanyl, midazolam, and continuous infusion of etomidate. Hypothermic CPB (27 degrees C) was managed according to alpha-stat conditions. The SjO2 percentage was measured using a fiberoptic catheter placed in the right jugular bulb via the right internal jugular vein. Data were recorded before and during the rewarming period. Patients were assigned to a normocapnic (PaCO2: 36-40 mmHg, n = 10) or hypercapnic (PaCO2: 45-50 mmHg, n = 10) PaCO2 regimen during rewarming. RESULTS: The maximum reduction of SjO2 occurred during rewarming with the jugular bulb temperature at 35-36 degrees C. In contrast, SjO2 did not change during rewarming from hypothermia in hypercapnic patients. CONCLUSIONS: These results show that mild hypercapnia prevents the desaturation of SjO2 seen with the normocapnic group during the rewarming period from hypothermic CPB. These data suggest that mild hypercapnia during rewarming from CPB is associated with a better balance between cerebral oxygen supply and demand.

Aged↗

Plasma catecholamines in rats during rewarming from induced hypothermia.

The present study sought to quantitate the levels of plasma catecholamines [norepinephrine (NE), epinephrine (E), and dopamine (DA)] during induction and rewarming from hypothermia. Male rats (317 +/- 8 g) were made hypothermic by exposure to 0.9% halothane at -10 to -15 degrees C while blood pressure (carotid artery), heart rate, and colonic temperature (Tc) were monitored. Anesthesia was discontinued when Tc reached 28 degrees C. Tc continued to fall but was held at 20-20.5 degrees C for 30 min. Rewarming was then initiated by raising ambient temperature to 22 degrees C. Arterial blood samples were taken 1) before cooling, 2) just before rewarming, 3) when Tc reached 22 degrees C during rewarming, and 4) when Tc reached 27 degrees C during rewarming. Plasma was assayed radioenzymatically for catecholamines using both phenylethanolamine-N-methyltransferase and catechol-O-methyltransferase procedures, and hypothermic induction resulted in significant increases in NE, E, and DA above control levels (P less than 0.01). With rewarming to Tc = 22 degrees C, all catecholamines increased above the level observed during hypothermia (P less than 0.01), and NE and DA increased still further (P less than 0.01) when Tc reached 27 degrees C. The levels of plasma catecholamines observed during hypothermia and during the rewarming phase indicate a role of the sympathoadrenal medullary system in the metabolic adjustments associated with hypothermia and recovery. During rewarming, the levels of E and NE attained exceed those at which both substances may be expected to act as circulating hormones.

Adaptation, Physiological↗