Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Rewarming”

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.

At least 91 records · Page 5Linked to original sources
PubMed1996

Preservation of alveolar epithelial fluid transport mechanisms in rewarmed human lung after severe hypothermia.

Although hypothermia abolishes alveolar fluid clearance in the in situ goat lung and in the ex vivo human lung, it is unknown whether alveolar fluid clearance resumes in lungs that are rewarmed after severe hypothermia. An isosmolar albumin solution was instilled into resected human lungs that were rewarmed to 37 degrees C after hypothermia (7 +/- 3 degrees C), and then alveolar fluid clearance was measured by the concentration of albumin in the alveolar fluid sample after 4 h. In control experiments in lungs that had not been cooled and rewarmed, alveolar fluid clearance was 11 +/- 2% over 4 h. In separate experiments, hypothermia completely abolished alveolar fluid clearance. However, alveolar fluid clearance resumed to a normal level of 12 +/- 1% over 4 h in the lungs that were rewarmed after hypothermia. Amiloride decreased alveolar fluid clearance by 47% in the rewarmed lungs. Terbutaline increased alveolar fluid clearance by nearly 300% in 2-h experiments in the rewarmed lungs (P < 0.05). The results of this study indicate that alveolar sodium-channel transport mechanisms are preserved in resected human lungs that are exposed to rewarming after hypothermia.

Aged↗
PubMed2006

Induction of monocytic tissue factor expression after rewarming from hypothermia in vivo is counteracted by heat shock in c-Jun-dependent manner.

OBJECTIVE: Triggering of tissue factor (TF)-mediated blood coagulation leads to the development of disseminated intravascular coagulation during rewarming from hypothermia. We studied post-rewarming TF levels, activity, and surface redistribution, along with the regulation of TF gene transcription in mononuclear cells (MNCs) obtained from an in vivo rat model. METHODS AND RESULTS: Rewarming after a 5-hour episode of 15 degrees C hypothermia caused an increase in TF activity, protein levels, and externalization of TF antigen in rat MNCs. This was accompanied by a dramatic elevation of c-Jun and JNK phosphorylation, and the absence of EGR-1 and NF-kappaB activation. To search for a stimulus to counteract c-Jun-mediated induction of TF activity in MNCs from rewarmed rats, we applied heat shock pretreatment one day before the hypothermia/rewarming experiment. This restored post-rewarming TF activity, protein levels, and surface-to-total TF ratio in rat MNCs to normothermic levels. Furthermore, in heat shock-pretreated animals, rewarming failed to increase phosphorylated c-Jun and JNK levels. We attribute this to the profound overexpression of heat shock protein 70 and inhibition of JNK. CONCLUSIONS: MNCs respond to rewarming from hypothermia by an induction of active TF antigen. This effect is dependent on c-Jun activation and is abolished by heat shock pretreatment.

Animals↗
PubMed2000

Inhalant corticosteroids inhibit hyperosmolarity-induced, and cooling and rewarming-induced interleukin-8 and RANTES production by human bronchial epithelial cells.

Inhaled corticosteroids are widely used for the treatment of bronchial asthma, and a long-term treatment with inhaled corticosteroids is effective in preventing exercise-induced bronchoconstriction (EIB). We have previously shown that hyperosmolarity, and cooling and rewarming induced interleukin-8 (IL-8) expression in human bronchial epithelial cells (BEC). However, the effect of inhalant corticosteroids on hyperosmolarity-induced, and cooling and rewarming-induced IL-8 and RANTES production has not been determined. To clarify these issues, we examined the effect of inhalant corticosteroids, beclomethasone dipropionate (BDP), and budesonide (BUD) on hyperosmolarity-induced, and cooling and rewarming-induced IL-8 and RANTES production. The results showed that BDP and BUD inhibited hyperosmolarity-induced, and cooling and rewarming-induced IL-8 and RANTES production. Because our previous studies have shown that p38 mitogen-activated protein (MAP) kinase and c-Jun-NH(2)-terminal kinase (JNK) regulate hyperosmolarity-induced, and cooling and rewarming-induced IL-8 and RANTES production, we examined the effect of BDP and BUD on p38 MAP kinase and JNK activation. The results showed that BDP and BUD did not inhibit hyperosmolarity-induced and cooling-induced p38 MAP kinase and JNK activation. These results indicated that inhalant corticosteroids inhibited hyperosmolarity-, and cooling and rewarming-induced IL-8 and RANTES production; however, the mechanism of inhaled corticosteroid-mediated inhibition of hyperosmolarity-induced, and cooling and rewarming- induced cytokine production remains to be clarified.

Administration, Inhalation↗
PubMed1996

Hypothermia and rewarming after hypothermic exposure alter venous relaxation.

Hypothermia has pathophysiological consequences on endothelial and smooth muscle cell function. This study investigates the impact on venous relaxation of hypothermia and rewarming following hypothermic exposure. In vitro isometric relaxation responses of norepinephrine precontracted rabbit external jugular veins to a panel of endothelium-dependent and -independent agonists were assessed in controls at 37 degrees C, and in an experimental group after cooling to 20 degrees C and after rewarming to 37 degrees C. On cooling, the endothelium-dependent responses to acetylcholine became multiphasic with initial contraction at low concentrations followed by relaxation at higher concentrations, the maximum of which was significantly diminished compared to controls. Incubation with indomethacin did not affect this response. Rewarming re-established a monophasic dose-dependent acetylcholine induced relaxation response but the maximal response was significantly augmented. This augmentation in relaxation on rewarming could be prevented by preincubation with indomethacin. The maximal response to calcium ionophore was reduced at 20 degrees C and augmented upon rewarming to 37 degrees C. All veins relaxed in a dose-dependent manner to the non-endothelium-dependent agonists forskolin and sodium nitroprusside; the maximal responses were significantly reduced at 20 degrees C and returned to normal upon rewarming. This study suggests that short-term exposure of venous tissue to hypothermia impairs the vessel's ability to produce endothelium-dependent relaxation. Rewarming does not re-establish normal endothelium-dependent relaxation but results in an enhanced, partially indomethacin-sensitive, response which appears to be independent of changes in non-endothelium-dependent mediated relaxation.

Analysis of Variance↗
PubMed1990

The relationship between body mass and rate of rewarming from hibernation and daily torpor in mammals.

1. Rewarming rate from torpor and body mass were inversely related in 86 mammals ranging in body mass between 2 and 8500 g. 2. Most of the mammalian taxa investigated showed a similar change of rewarming rate with body mass. Only the insectivores showed a more pronounced increase in rewarming with a decrease in body mass than did the other taxa. The rates of rewarming of marsupials were similar to those of placentals. 3. At low air temperature (Ta), the rate of rewarming of marsupials was not related to body mass, although a strong relationship between the two variables was observed in the same species at high Ta. 4. The slopes relating rewarming rates and body mass of the mammalian groups and taxa analysed here were similar to those obtained earlier for mass-specific basal metabolic rate (BMR) and body mass in mammals, suggesting that the rate of rewarming and BMR are physiologically linked.

Animals↗
PubMed1975

Accidental hypothermia: an experimental study of inhalation rewarming.

Inhalation rewarming of hypothermic humans with heated, humidified oxygen was compared to rewarming by immersion in a hot bath. In 10 subjects cooled to approximately 35 degrees C core temperature, there was no significant difference in the amount of temperature "afterdrop" with the two rewarming procedures. Inhalation rewarming provided rapid commencement of increase in tympanic and esophageal temperatures, indicating effective rewarming of critical core regions, especially heart and brain. This method of core rewarming avoids the physiological hazards associated with the peripheral vasodilation which accompanies external rewarming. Moverover the simplicity of application of this method suggests its greater use in both first-aid and hospital treatment of accidental hypothermia.

Accidents↗
PubMed1991

Hemodynamic and metabolic effects of hypothermia and rewarming.

There is a lack of detailed knowledge of the pathophysiologic mechanisms initiated during and after rewarming. To study cardiac function after rewarming from hypothermia sodium pentobarbital anesthetized open chest-dogs were cooled to 25 degrees C and rewarmed. Myocardial blood flow was measured at different temperatures, and blood samples were drawn from the aorta and the coronary sinus for metabolic measurements. Mean aortic blood pressure (AOP) and aortic blood flow were recorded. Compared to precooling, AOP and heart rate were both significantly reduced during hypothermia. During rewarming stroke volume (SV) decreased significantly. At the end of rewarming AOP and SV were significantly lower than before cooling and myocardial blood flow, as well as oxygen and lactate uptake were only 50% of precooling levels. The present study demonstrated that hypothermia and rewarming depress cardiovascular function. Changes in peripheral vascular function, myocardial metabolism and contractility, may lead to the observed reduction in recovery upon rewarming.

Animals↗
PubMed1987

Plasma catecholamine and metabolic changes during cooling and rewarming in dogs.

A slow and progressive fall in colonic temperature occurred in dogs immersed in cold water (8-16 degrees C) when heat production reached a maximum value (CVO2 max). When moderate hypothermic dogs were placed in air (21 degrees C), they continued to shiver and progressively recovered a normal core temperature. Plasma epinephrine (E) and norepinephrine (NE) concentrations, metabolic rate (VO2), arterial and venous blood gas, pH, saturation and oxygen content values were compared, for the same colonic temperature, during cooling and during rewarming. Plasma lactic acid, glucose and free fatty acid (FFA) concentrations, were also measured under both conditions. 1) VO2 was lower during rewarming than during cooling. 2) Plasma NE decreased from maximal value observed during cooling but was still significantly higher than precooling control. During rewarming as well as during cooling a correlation was found between plasma NE and mixed venous oxygen saturation and between plasma NE and mixed venous oxygen content. 3) As NE, plasma E was lower during rewarming than during cooling but was still significantly higher than precooling control. During cooling an acidosis was observed and plasma E was significantly correlated with venous and arterial pH. 4) During rewarming: arterial acidosis disappeared, plasma lactate and glucose concentrations were lower and FFA were higher than during cooling. These results suggest that for the same degree of moderate hypothermia there was less involvement of the sympathoadrenal system during rewarming than during cooling. The simultaneous decrease in metabolic rate and the variations observed in blood pH and in plasma substrate concentrations suggest a relationship between the level of plasma catecholamine concentrations and metabolic adjustments associated with rewarming from hypothermia.

Animals↗
PubMed1984

Hypothermia and electromagnetic rewarming in the rhesus monkey.

Five male rhesus monkeys (Macaca mulatta) were subjected, under ketamine anesthesia, to repeated hypothermia treatments that produced an average rectal temperature of 28.3 degrees C. Following hypothermia induction, the subjects were rewarmed using either a ventrally applied surgical heating pad supplied with 35 degrees C water or a radio-frequency (RF) induction coil operating at 13.56 MHz with an average specific absorption rate (SAR) calculated to be approximately 5.5 W X kg-1. A special temperature probe, nonperturbing to RF, was used in the RF rewarming experiments. Control experiments were also conducted in which only ketamine was administered over a 3-h period. RF rewarming to 35 degrees C typically required only 50 min; whereas, an average of 137 min was required for heating-pad rewarming. Analyses of blood serum collected during and up to 48 h after hypothermia treatments showed elevations at 24 h in creatine phosphokinase (CPK), lactic dehydrogenase (LDH), and glutamic oxaloacetic transaminase (GOT), and these elevations were highest for the ketamine controls and lowest for the RF rewarming experiments. The subjects have been periodically examined since these experiments, and all appear to be in good health. It is concluded that the careful application of RF energy to the central core of the body can successfully be used for rewarming purposes, is more effective than externally applied rewarming techniques, and is potentially useful in remote locations.

Animals↗
PubMed1994

Amelioration of rewarming ischemic injury of the pancreas graft during vascular anastomosis by increasing tissue ATP contents during preservation by the two-layer cold storage method.

Rewarming ischemic injury during vascular anastomosis severely compromises posttransplant pancreas graft survival because the graft has already been subjected to warm and cold ischemia before vascular anastomosis. We examined whether preservation of the pancreas graft by the two-layer method ameliorates rewarming ischemic injury of the graft during vascular anastomosis and also investigated the energy metabolism of the pancreas graft before, during and after rewarming ischemic period. After flushing with cold University of Wisconsin solution (UW), the pancreas grafts were preserved by the two-layer (UW/perfluorochemical [PFC]) method (group 1) or simple cold storage in UW (group 2) for 24-hr and then autotransplanted. In control, the pancreas grafts were flushed out with cold UW and immediately autotransplanted without preservation (group 3). After completion of vascular anastomosis, vascular clamp was not released until 90, 120, or 150 min of rewarming ischemia, including anastomosis time, has elapsed. After 90 min of rewarming ischemia, graft survival rates were 5/5, 100%, 5/5, 100%, and 5/5, 100% in groups 1, 2 and 3, respectively. After 120 min, all the grafts in groups 2 and 3 failed (0/5, 0%, and 0/5, 0%, respectively), however, all the grafts in group 1 survived (5/5, 100%). Even after 150 min, 1 of 3 grafts in group 1 survived (1/3, 33%). After 24 hr preservation, tissue adenosine triphosphate (ATP) and total adenine nucleotides (TAN) levels of the grafts in group 1 were about 2-fold the reference values before harvesting and significantly higher compared with group 2(p < 0.05; p < 0.05). After 120 min of rewarming ischemia, tissue ATP levels in group 1 were 84% of the reference values and significantly higher compared with group 2(p < 0.05). TAN levels of group 1 were also significantly higher compared with group 2(p < 0.05). Two hours after reperfusion, ATP and TAN levels in group 1 were significantly higher than group 2(p < 0.05). There were no remarkable difference between group 1 and group 2 concerning adenosine diphosphate (ADP), adenosine monophosphate (AMP) levels. We conclude that the two-layer (UW/PFC) method ameliorates rewarming ischemic injury of the pancreas graft during vascular anastomosis by increasing tissue ATP concentration and TAN levels during preservation and maintaining tissue ATP and TAN levels during vascular anastomosis. Consequently, ATP levels are rapidly recovered after reperfusion and the graft survives.

Adenosine Triphosphate↗
PubMed1995

Splenic effects on hemodynamics induced by hypothermia and rewarming in miniature swine.

Central arterial hemodynamic changes were assessed during cooling, hypothermia, and rewarming in splenectomized (SPX, n = 4) and unsplenectomized (SP, n = 4) 8-10 month old male Yucatan miniature swine (34.0 +/- 1.4 kg). Under isoflurane anesthesia, and using circulating-water blankets, pigs were cooled to and then maintained for 2 h at a rectal temperature (Tre) of 27 +/- 1 degrees C; hypothermia was followed by rewarming to normothermia (37 +/- 1 degrees C). There were significantly (p < or = 0.05) greater changes in central arterial hematocrit and hemoglobin (delta HCT and delta HGB) from respective precooling baseline levels in the SP group during hypothermia and early rewarming (SP: delta HCTmax = 9-10%RBC, and delta HGBmax = 3.0-3.5 g/dl vs. SPX: delta HCTmax = 3-4%RBC, and delta HGBmax = 1.5-1.8 g/dl). By the end of rewarming, splenic resequestration and extravascular fluid shifts resulted in these values returning to baseline. In addition, cardiovascular instability was seen in the SPX group compared to the SP animals as evidenced by significant tachycardia and hypotension during rewarming. We have concluded from these studies that hypothermia causes significant hemoconcentration, and that splenic contraction is the major cause of this hemoconcentration during hypothermia and initial rewarming in miniature swine. A splenectomized design should be considered for swine studies that purport to pattern human pathophysiology, especially for modelling rewarming shock.

Analysis of Variance↗
PubMedDate not supplied

Influence of ethanol on circulation in surface-induced hypothermia and subsequent rewarming.

Hypothermia and ethanol are often closely linked and in hypothermic accidents ethanol is often a contributing factor. To study the effects of ethanol on the circulation in hypothermic conditions, cardiac catheterization was carried out on 18 anaesthetized beagle dogs. They were divided into two groups. One gram of ethanol/kg of b.wt. diluted in saline was infused into the vena cava superior within 30 min to seven dogs. The dogs were then cooled between ice bags until the blood temperature in the ascending aorta was 25 degrees C and they were then rewarmed. The control group of 11 dogs was cooled and rewarmed without ethanol infusion. The heart rate first increased when cooling down to 33 degrees C and decreased thereafter in the control group. In the ethanol group heart rate increased during the ethanol infusion and remained high when cooling down to 33 degrees C and decreased thereafter. Heart rate was higher in the ethanol group throughout the experiments, and during rewarming the difference was significant. In the control group cardiac output first increased until a body temperature of 33 degrees C was achieved but then decreased. In the ethanol group cardiac output started to decrease after ethanol infusion. During rewarming there was a significantly higher cardiac output in the ethanol group, probably due to the higher heart rate. In the cardiac cycle the systolic period prolonged significantly (p < 0.001) in both groups when the body temperature decreased from 37 degrees C to 25 degrees C whereas the diastolic period remained quite stable. The contraction phase was also affected by the cooling. The changes in contraction force cannot be seen in dP/dt alone because dP/dt values first increased significantly when cooling from 37 degrees C to 33 degrees C but then decreased. Ejection fraction, systolic period, and the systemic vascular resistance increased despite the reduction of the dP/dt and thus we conclude that the contraction force is augmented in hypothermia. In the ethanol group the myocardium seems to be depressed due to ethanol. In the early phase of cooling heart rate increased but cardiac output decreased in the ethanol group, indicating the decreased ability of the heart to respond to cooling in the presence of ethanol. The time constant of exponential pressure fall (tau) increased linearly with cooling from 37 degrees C to 25 degrees C and recovered with rewarming in both groups. Changes in negative dP/dt coincided with the changes in the time constant of exponential isovolumic pressure fall. Ethanol did not influence relaxation. All the parameters we checked recovered to normal during rewarming.

Animals↗
PubMed2000

Biologically variable pulsation improves jugular venous oxygen saturation during rewarming.

BACKGROUND: Conventional pulsatile (CP) roller pump cardiopulmonary bypass (CPB) was compared to computer controlled biologically variable pulsatile (BVP) bypass designed to return beat-to-beat variability in rate and pressure with superimposed respiratory rhythms. Jugular venous O2 saturation (SjvO2) below 50% during rewarming from hypothermia was compared for the two bypass techniques. A SjvO2 less than 50% during rewarming is correlated with cognitive dysfunction in humans. METHODS: Pigs were placed on CPB for 3 hours using a membrane oxygenator with alpha-stat acid base management and arterial filtration. After apulsatile normothermic CPB was initiated, animals were randomized to CP (n = 8) or BVP (roller pump speed adjusted by an average of 2.9 voltage output modulations/second; n = 8), then cooled to a nasopharyngeal temperature of 28 degrees C. During rewarming to stable normothermia, SjvO2 was measured at 5 minute intervals. The mean and cumulative area for SjvO2 less than 50% was determined. RESULTS: No between group difference in temperature existed during hypothermic CPB or during rewarming. Mean arterial pressure, arterial partial pressure O2, and arterial partial pressure CO2 did not differ between groups. The hemoglobin concentration was within 0.4 g/dL between groups at all time periods. The range of systolic pressure was greater with BVP (41 +/- 18 mm Hg) than with CP (12 +/- 4 mm Hg). A greater mean and cumulative area under the curve for SjvO2 less than 50% was seen with CP (82 +/- 96 versus 3.6% +/- 7.3% x min, p = 0.004; and 983 +/- 1158 versus 42% +/- 87% x min; p = 0.004, Wilcoxon 2-sample test). CONCLUSIONS: Computer-controlled BVP resulted in significantly greater SjvO2 during rewarming from hypothermic CPB. Both mean and cumulative area under the curve for SjvO2 less than 50% exceeded a ratio of 20 to 1 for CP versus BVP. Cerebral oxygenation is better preserved during rewarming from moderate hypothermia with bypass that returns biological variability to the flow pattern.

Animals↗
PubMed2003

Rapid rewarming after mild hypothermia accentuates the inflammatory response after acute volume controlled haemorrhage in spontaneously breathing rats.

Accidental hypothermia is a common companion of trauma/haemorrhage, and several clinical studies have identified reduced body temperature as an independent risk predisposing to increased morbidity and mortality. Accordingly, the majority of trauma care guidelines prescribe early and aggressive rewarming of hypothermic patients. Enzyme reactions are generally downregulated at temperatures below 37 degrees C, including most of those responsible for the inflammatory response. The rationale for adhering to these recommendations uncritically may therefore be questioned. In a rat model of mild hypothermia and haemorrhagic shock we wanted to compare the influence of rapid rewarming with persistently reduced temperature on the synthesis of early inflammatory mediators and organ function. Thirty-four male albino Sprague-Dawley rats were studied. Withdrawal of 2.5 ml blood/100 g body weight was performed over 10 min, with simultaneous reduction of body temperature to 32.5-33.5 degrees C. Seventy-five minutes after initiation of bleeding, two-thirds of the shed blood was retransfused. One group (n=17) was rewarmed to normothermia, the other (n=17) was kept hypothermic. The study was terminated after an observation period of 2 h. At the end of the study the rewarmed animals had a significantly lower mean arterial pressure, higher heart rate, higher synthesis of reactive oxygen species from peritoneal phagocytes, increased circulating levels of nitric oxide, and higher values of the organ markers aspartate aminotransferase and urea. The pro-inflammatory cytokines TNF-alpha and IL-6, the anti-inflammatory cytokine IL-10, the organ markers alanine aminotransferase, alpha-glutathione S-transferase and creatinine, as well as organ injury scores were equal in both groups. Three rewarmed rats died prematurely, versus one hypothermic animal. In conclusion, the results suggest that during the early stages after haemorrhagic shock, rapid rewarming from mild hypothermia may have unfavourable effects both on basic haemodynamic variables, and on the internal inflammatory environment of cells and tissues.

Animals↗
PubMed1999

The effects of two rewarming strategies on heat balance and metabolism after coronary artery bypass surgery with moderate hypothermia.

BACKGROUND: Postoperative hypothermia is common in cardiac surgery with hypothermic cardiopulmonary bypass (CPB). This trial was designed to evaluate whether rewarming over the normal bladder temperature (over 37 degrees C) at the end of hypothermic CPB combined with passive heating methods after CPB might result in a better heat balance, lower energy expenditure (EE) and decrease of disturbances in oxygen balance compared to only rewarming the patients to a bladder temperature of 35-37 degrees C. METHODS: A prospective, randomized controlled clinical study was performed in 38 patients scheduled for elective coronary artery bypass surgery. Twenty patients (group C) were rewarmed to a bladder temperature of 35-37 degrees C at the end of hypothermic (28 degrees C) CPB. Eighteen patients (group W) were rewarmed to a bladder temperature of 37-38.5 degrees C. RESULTS: At the end of CPB, the bladder temperature was 36.2+/-0.7 degrees C (mean+/-SD) in group C and 37.9+/-0.5 degrees C in group W. After half an hour's stay in the ICU, the mean body temperature (MBT) was 35.1+/-0.6 degrees C in group C and 36.6+/-0.7 degrees C in group W. During the following five hours, MBT increased to 37.4+/-0.8 degrees C in group C and to 38.0+/-0.6 degrees C in the other group. The peak value of EE in the ICU was 1.73+/-0.44 (group C) vs 1.35+/-0.29 (W/kg) (group W) (P=0.003). EE was significantly (P=0.044) higher in group C than in the other group between 1.5 and 5.5 h in the ICU. The increased energy expenditure due to heat production was associated with an increase in O2 consumption (VO2) 61.6+/-30.4% vs 25.2+/-24.1%, (peak values) compared to the basal values of the two groups measured before anesthesia (between groups P<0.001). Between 1.5 and 5.5 h in the ICU, group C had significantly higher VO2 (P=0.026), CO2 production (P=0.017), venous pCO2 (P<0.001) and minute ventilation (p=0.014) than group W. Venous pH was lower (P<0.001) in group C. The peak value of oxygen extraction was also higher (P=0.045) in group C. On the other hand, the lowest value of venous oxygen saturation was higher (P=0.04) in group W. CONCLUSION: With rewarming the patients at the end of CPB to a bladder temperature of over 37 degrees C combined with passive heating methods after CPB, it was possible to decrease EE and VO2 compared to the control group (rewarmed to bladder temperature of 35-37 degrees C) after coronary artery bypass surgery with moderate hypothermia.

Body Temperature↗
PubMed1996

[Effect of arterial blood pressure on cerebral vein oxygen saturation in the rewarming phase of extracorporeal circulation].

UNLABELLED: This study concerns the effects of elevated mean arterial blood pressure (MAP) on decreases in jugular bulb oxygen saturation (SjO2) using fiberoptic jugular bulb oximetry and on cerebral blood flow velocity measured by transcranial Doppler sonography (TCD) during cardiopulmonary bypass (CPB) for coronary artery bypass graft (CABG). METHODS: 27 ASA III patients undergoing CABG were studied. Anaesthesia was maintained with fentanyl, midazolam and continuous infusion of etomidate. CPB was managed according to alpha-stat conditions under moderate hypothermia (27 degrees C). SjO2 (%) and jugular bulb temperature were measured using a fiberoptic catheter placed in the right jugular bulb via the right internal jugular vein. TCD recordings of middle cerebral artery mean blood flow velocity (Vmean, cm/s) were taken during the investigation period. Data were recorded continuously before and for 40 min following start of rewarming. In group 1 (n = 17) MAP was kept between 55 and 65 mmHg, in group 2 (n = 10) MAP was maintained above 70 mmHg using norepinephrine infusion during rewarming of CPB. RESULTS: Following rewarming MAP was statistically significant elevated in group 2 compared to group 1. In groups 1 and 2, Vmean was increased and SjO2 was decreased to a similar extent during rewarming of CPB. Decreases in SjO2 below 50% were seen in both groups. CONCLUSION: The present data show decreases in Sjo2 during rewarming regardless to the level of arterial blood pressure (range 55-80 mmHg). This suggests that desaturation during rewarming of CPB is not a function of decreases in MAP since CBF autoregulation appears to be maintained within this pressure range.

Adult↗
PubMed1995

Differential age effects of mean arterial pressure and rewarming on cognitive dysfunction after cardiac surgery.

Central nervous system dysfunction is a common consequence of otherwise uncomplicated cardiac surgery. Many mechanisms have been postulated for the cognitive dysfunction that is part of these neurologic sequelae. The purpose of our investigation was to evaluate the effects of mean arterial pressure (MAP) during cardiopulmonary bypass (CPB) and the rate of rewarming on cognitive decline after cardiac surgery. Two hundred thirty-seven patients completed preoperative and predischarge neuropsychologic testing. MAP and temperature were recorded at 1-min intervals using an automated anesthesia record keeper. MAP area less than 50 mm Hg (time and degree of hypotension), as well as the maximal rewarming rate, were determined for each patient. Multivariable linear regression revealed that the rate of rewarming and MAP were unrelated to cognitive decline. However, interactions significantly associated with cognitive decline were found between age and MAP area less than 50 mm Hg on one measure, and between age and rewarming rate in another, identifying susceptibility of the elderly to these factors. Although MAP and rewarming were not the primary determinates of cognitive decline in this surgical population, hypotension and rapid rewarming contributed significantly to cognitive dysfunction in the elderly.

Aged↗
PubMed2003

Use of a centrifugal vortex blood pump and heparin-bonded circuit for extracorporeal rewarming of severe hypothermia in acutely injured and coagulopathic patients.

BACKGROUND: Standard rewarming methods for posttraumatic hypothermia are ineffective or require systemic heparinization. Centrifugal vortex blood pumps (CVBPs), heparin-bonded circuits, and, potentially, percutaneous access techniques, facilitate the institution of an extracorporeal circulation by noncardiac surgeons. METHODS: Seven severely hypothermic patients requiring emergent operative intervention were rewarmed intraoperatively using the CVBP with heparin-bonded circuitry. RESULTS: Patients were critically ill (average Injury Severity Score of 43.5 [SD, 13.6] for the traumatized patients). The mean temperature before rewarming was 31.5 degrees C (SD, 1.6 degrees C). The CVBP outflow site was the common femoral vein in all patients, with the inflow into the superficial femoral artery (n = 2), contralateral common femoral vein (n = 2), and internal jugular vein (n = 3). The mean time to rewarm to 37 degrees C was 73.3 (SD, 30.5) minutes. All patients survived the initial operation, although the ultimate survival was 43%. CONCLUSION: Noncardiac surgeons can effectively use an extracorporeal rewarming strategy incorporating a heparin-bonded CVBP to rapidly rewarm hypothermic coagulopathic patients undergoing surgery.

Adult↗