Influence of temperature management on neurocognitive function in biological aortic valve replacement. A prospective randomized trial.

AIM: Aim of this study was to elucidate if postoperative neurocognitive function after biological aortic valve replacement (AVR) can be influenced by temperature management during cardiopulmonary bypass (CPB). METHODS: In this prospective randomized study, we measured the effect of mild hypothermic (32 °C, N.=30) vs. normothermic (37 °C, N.=30) CPB on neurocognitive function. All patients underwent elective isolated biological AVR (mean age 67 ± 8 years, mean additional EuroSCORE 5.6 ± 2.4). Neurocognitive function was objectively measured by means of objective P300 auditory-evoked potentials before surgery, one week and four months after surgery. Clinical data and outcome were monitored. RESULTS: P300 evoked potentials were comparable between patients operated with mild hypothermic (370 ± 30 ms) and normothermic CPB (373 ± 32 ms) before surgery (P=0.85). P300 peak latencies were prolonged (=impaired) in patients operated with normothermic (402 ± 29, P<0.0001) as well as with mild hypothermic CPB (405 ± 30 ms, P<0.0001) one week after surgery. Even four months after surgery, still impairment of P300 peak latencies could be documented in either patients operated with normothermic (394 ± 28 ms) and mild hypothermic CPB (400 ± 33 ms,) in repeated measures analysis of variance (P=0.042). Group comparison revealed no difference between patients operated with normothermic and mild hypothermic CPB at one week (P=0.54) and four months (P=0.67) after surgery. Clinical data as well as postoperative adverse events were comparable between the two groups. CONCLUSION: Normothermic temperature management during CPB is non-inferior to hypothermic in means of neuroprotection. Since patients after biological aortic valve replacement show a subclinical but measurable cognitive deficit up to four months after surgery, other factors have to be addressed to add further benefit to the extremely good results of open biological AVR.

Low-dose remifentanil to suppress haemodynamic responses to noxious stimuli in cardiac surgery: a dose-finding study.

BACKGROUND: High-dose remifentanil (1-5 microg kg-1 min-1), commonly used for cardiac surgery, has been associated with muscle rigidity, hypotension, bradycardia, and reduced cardiac output. The aim of this study was to determine an optimal lower remifentanil dose, which should be accompanied by fewer adverse events, that still effectively suppresses haemodynamic responses to typical stressful stimuli (i.e. intubation, skin incision, and sternotomy). METHODS: Total i.v. anaesthesia consisted of a target-controlled propofol (2 microg ml-1) and a remifentanil infusion. Forty patients were allocated to receive either a constant infusion of remifentanil at 0.1 microg kg-1 min-1 or up-titrations to 0.2, 0.3, or 0.4 microg kg-1 min-1, respectively, 5 min before each stimulus. Subsequently, changes in heart rate and mean arterial blood pressure were recorded for 8 min. Increases exceeding 20% of baseline were considered to be of clinical relevance. Patients who exhibited these alterations were termed responders. RESULTS: The number of responders was less with the two higher remifentanil dosages (P<0.05) while propofol target doses could either be kept at the same level or even be reduced without affecting the plane of anaesthesia. Although single phenylephrine bolus had to be applied more frequently in these two groups (P<0.05), no severe haemodynamic depression was observed. CONCLUSIONS: Remifentanil at 0.3 and 0.4 microg kg-1 min-1 in combination with a target-controlled propofol infusion in the pre-bypass period is well tolerated. It appears to mitigate potentially hazardous haemodynamic responses from stressful stimuli equally well as higher doses when compared with data from the literature.

Core and skin surface temperature course after normothermic and hypothermic cardiopulmonary bypass and its impact on extubation time.

BACKGROUND AND OBJECTIVE: Cardiopulmonary bypass is associated with temperature pertubations that influence extubation time. Common extubation criteria demand a minimum value of core temperature only. The aim of this prospective study was to test the hypothesis that changes in core and skin surface temperature are related to extubation time in patients following normothermic and hypothermic cardiopulmonary bypass. METHODS: Forty patients undergoing cardiac surgery were studied; 28 patients had normothermic cardiopulmonary bypass (nasopharyngeal temperature >35.5 degrees C) and 12 had hypothermic cardiopulmonary bypass (28-34 degrees C). In the intensive care unit, urinary bladder temperature and skin surface temperature gradient (forearm temperature minus fingertip temperature: >0 degrees C = vasoconstriction, < or =0 degrees C = vasodilatation) were measured at 30-min intervals for 10 h postoperatively. At the same intervals, the patients were evaluated for extubation according to common extubation criteria. RESULTS: On arrival in the intensive care unit the mean urinary bladder temperature was 36.8 +/- 0.5 degrees C in the normothermic group and 36.4+/-0.3 degrees C in the hypothermic group (P = 0.014). The skin surface temperature gradient indicated severe vasoconstriction in the both groups. The shift from vasoconstriction to vasodilatation was faster in normothermic cardiopulmonary bypass patients (138+/-65 min) than in patients after hypothermic cardiopulmonary bypass (186+/-61 min, P = 0.034). There was a linear relation between the time to reach a skin surface temperature gradient = 0 degrees C and extubation time (r2 = 0.56, normothermic group; r2 = 0.82, hypothermic group). CONCLUSIONS: The transition from peripheral vasoconstriction to vasodilatation is related to extubation time in patients following cardiac surgery under normothermic as well as hypothermic cardiopulmonary bypass.

Magnesium moderately decreases remifentanil dosage required for pain management after cardiac surgery.

BACKGROUND: Magnesium is a calcium and an NMDA-receptor antagonist and can modify important mechanisms of nociception. We evaluated the co-analgesic effect of magnesium in the postoperative setting after on-pump cardiac surgery. METHODS: Forty patients randomly received either magnesium gluconate as an i.v. bolus of 0.21 mmol kg(-1) (86.5 mg kg(-1)) followed by a continuous infusion of 0.03 mmol(-1) kg(-1) h(-1) (13.8 mg kg(-1) h(-1)) or placebo for 12 h after tracheal extubation. After surgery, remifentanil was decreased to 0.05 microg kg(-1) min(-1) and titrated according to a pain intensity score (PIS, range 1-6) in the intubated, awake patient and a VAS scale (range 1-100) after extubation. If PIS was > or =3 or VAS > or =30, the infusion was increased by 0.01 microg kg(-1) min(-1); if ventilatory frequency was < or =10 min(-1) it was decreased by the same magnitude. RESULTS: Magnesium lowered the cumulative remifentanil requirement after surgery (P<0.05). PIS > or =3 was more frequent in the placebo group (P<0.05). Despite increased remifentanil demand, VAS scores were also higher in the placebo group at 8 (2 vs 8) and 9 h after extubation (2 vs 7) (P<0.05). Dose reductions attributable to a ventilatory frequency < or =10 min(-1) occurred more often in the magnesium group (17 vs 6; P<0.05). However, time to tracheal extubation was not prolonged. CONCLUSIONS: Magnesium gluconate moderately reduced the remifentanil consumption without serious side-effects. The opioid-sparing effect of magnesium may be greater at higher pain intensities and with increased dosages.

The use of the novel calcium sensitizer levosimendan in critically ill patients.

Levosimendan, a novel calcium sensitizer, enhances cardiac contractility by increasing myocyte sensitivity to calcium, and induces vasodilation. In this prospective observational study the haemodynamic effects of levosimendan in postoperative critically ill patients are reported. Twelve patients with the need for inotropic support were studied. One dose of levosimendan (12.5 mg) was administered at a rate of 0.1-0.2 microg kg(-1).min(-1), either alone or in addition to pre-existing inotropic therapy. Haemodynamic measurements were obtained at baseline, and at 3 h, 6 h, 12 h, and 24 h after the start of the levosimendan infusion. Levosimendan significantly increased cardiac output from (mean+/-SD) 4.3+/-0.91.min(-1) to 5.2+/-1.51 min(-1) after 24h (P=0.013), by increases in stroke volume (baseline 47+/-15 ml, after 24h 57+/-25 ml, P=0.05), as heart rate remained unchanged. Systemic vascular resistance decreased from 1239+/-430 dyn.sec.cm(-5) at baseline to 963+/-322 dyn.sec. cm(-5) at 24h (P<0.001). Pre-existing inotropic therapy present in ten patients remained unchanged or was reduced. In postoperative critically ill patients, infusion of levosimendan exerted favourable haemodynamic responses. Levosimendan increased cardiac output by increasing stroke volume, which might be attributed primarily to its inotropic properties. Due to its cyclic adenosine monophosphate independent positive inotropic effects, levosimendan may be of value as adjunctive therapy to other inotropic drugs in critically ill patients.

Blood pressure response to thermoregulatory vasoconstriction during isoflurane and desflurane anesthesia.

BACKGROUND: Mild perioperative hypothermia produces morbid cardiac outcomes that may result from sympathetically induced hypertension. However, volatile anesthetics produce vasodilatation that may reduce the hemodynamic response to hypothermia. We tested the hypothesis that the volatile anesthetics isoflurane and desflurane blunt the normal cold-induced hypertensive response. METHODS: We analyzed prospective data from three analogous studies: 1) 10 volunteers given desflurane (2.6 volume percentage) maintained in left-lateral position; 2) nine volunteers without anesthesia or anesthetized with various doses of desflurane; and 3) eight volunteers given various concentrations of isoflurane. Mean skin temperature was reduced to 31 C, which decreased core body temperature and triggered thermoregulatory vasoconstriction. Mean arterial pressures were determined before and after hypothermia provoked intense thermoregulatory vasoconstriction. RESULTS: The hemodynamic responses to thermoregulatory vasoconstriction were similar without anesthesia and at all concentrations of desflurane and isoflurane. On average, mean arterial pressure increased 14 (SD = 5) mmHg with and without anesthesia. CONCLUSION: We conclude that thermoregulatory vasoconstriction significantly increases arterial pressure with or without isoflurane or desflurane anesthesia.

Effects of epidural anesthesia on thermal sensation.

BACKGROUND AND OBJECTIVES: Epidural anesthesia decreases the core temperatures triggering vasoconstriction and shivering, presumably by increasing apparent (as opposed to actual) lower-body temperature. We therefore tested the hypothesis that epidural anesthesia also increases the overall perception of warmth. METHODS: We studied 8 volunteers in a randomized, cross-over protocol separated by at least 48 hours. On one day, epidural anesthesia was induced to a T11 sensory level; the other day was a control without anesthesia. Core temperature and upper-body skin temperatures (33 degrees C) were kept constant throughout. Lower-body skin temperature was set in a random order to 31 degrees C, 32 degrees C, 33 degrees C, 34 degrees C, 35 degrees C, and 36 degrees C and maintained by circulating water and forced air. At each temperature, the volunteers rated their thermal sensation with a visual analog scale (0 = cold, 100 = hot). Core temperature was 36.8 +/- 0.1 degrees C on the control day and 36.7 +/- 0.1 degrees C on the epidural day. RESULTS: Scores for thermal sensation on the epidural day were near 47 mm at each lower-body skin temperature. On the control day, visual analog scores at a lower-body skin temperature of 31 degrees C were 16 +/- 10 mm and increased linearly to 61 +/- 6 mm at 36 degrees C. Control thermal sensation scores thus equaled those during epidural anesthesia when lower-body skin temperature was near 34 degrees C. CONCLUSIONS: Thermal sensation with and without epidural anesthesia was comparable at a lower-body temperature near 34 degrees C, which is a normal leg skin temperature. This suggests that autonomic and behavioral thermoregulatory consequences of epidural anesthesia differ-or that the current explanation for reduced vasoconstriction and shivering thresholds during epidural anesthesia is incorrect.

Neither nalbuphine nor atropine possess special antishivering activity.

The special antishivering action of meperidine may be mediated by its kappa or anticholinergic actions. We therefore tested the hypotheses that nalbuphine or atropine decreases the shivering threshold more than the vasoconstriction threshold. Eight volunteers were each evaluated on four separate study days: 1) control (no drug), 2) small-dose nalbuphine (0.2 microg/mL), 3) large-dose nalbuphine (0.4 microg/mL), and 4) atropine (1-mg bolus and 0.5 mg/h). Body temperature was increased until the patient sweated and then decreased until the patient shivered. Nalbuphine produced concentration-dependent decreases (mean +/- SD) in the sweating (-2.5 +/- 1.7 degrees C. microg(-1). mL; r(2) = 0.75 +/- 0.25), vasoconstriction (-2.6 +/- 1.7 degrees C. microg(-1). mL; r(2) = 0.75 +/- 0.25), and shivering (-2.8 +/- 1.7 degrees C. microg(-1). mL; r(2) = 0.79 +/- 0.23) thresholds. Atropine significantly increased the thresholds for sweating (1.0 degrees C +/- 0.4 degrees C), vasoconstriction (0.9 degrees C +/- 0.3 degrees C), and shivering (0.7 degrees C +/- 0.3 degrees C). Nalbuphine reduced the vasoconstriction and shivering thresholds comparably. This differs markedly from meperidine, which impairs shivering twice as much as vasoconstriction. Atropine increased all thresholds and would thus be expected to facilitate shivering. Our results thus fail to support the theory that activation of kappa-opioid or central anticholinergic receptors contribute to meperidine's special antishivering action.

Normothermic cardiopulmonary bypass is beneficial for cognitive brain function after coronary artery bypass grafting--a prospective randomized trial.

BACKGROUND: Hypothermic and normothermic cardiopulmonary bypass (CPB) have resulted in apparently contradictionary cardiac and neurologic outcome. Cerebrovascular risk and cognitive dysfunction associated with normothermic CPB still remain uncertain. MATERIALS AND METHODS: In a prospective randomized study, we measured the effects of mildly hypothermic (32 degrees C, n=72) vs. normothermic (37 degrees C, n=72) CPB on cognitive brain function. All patients received elective coronary artery bypass grafting (mean age 62.1+/-6.3 years, mean ejection fraction 60.4+/-13%). Cognitive brain function was objectively measured by cognitive P300 auditory-evoked potentials before surgery, 1 week and 4 months after surgery, respectively. Additionally, standard psychometric tests ('trailmaking test A', 'mini-mental state') were performed and clinical outcome was monitored. RESULTS: Patients, operated with mild hypothermia, showed a marked impairment of cognitive brain function. As compared with before surgery (370+/-45 ms), P300 evoked potentials were prolonged at 1 week (385+/-37 ms; P<0.001) and even at 4 months (378+/-34 ms, P<0.001) after surgery, respectively. In contrast, patients operated with normothermic CPB, did not show an impairment of P300 peak latencies (before surgery 369+/-36 ms, 1 week after surgery 376+/-38 ms, n.s.; 4 months after surgery 371+/-32 ms, n.s.). Group comparison revealed a trend towards prolonged P300 peak latencies in the patient group undergoing mildly hypothermic CPB (P=0.0634) 1 week after surgery. Four months postoperatively, no difference between the two groups could be shown (P=n.s.) Trailmaking test A and mini mental state test failed to discriminate any difference. Five patients died (mild hypothermia n=3, normothermia n=2) postoperatively (cardiac related n=3, sepsis n=2). None of the patients experienced major adverse cerebrovascular events. CONCLUSIONS: Objective cognitive P300 auditory evoked potential measurements indicate, that subclinical impairment of cognitive brain function is more pronounced in patients undergoing mildly hypothermic CPB as compared with normothermic CPB for CABG.

Core cooling by central venous infusion of ice-cold (4 degrees C and 20 degrees C) fluid: isolation of core and peripheral thermal compartments.

BACKGROUND: Central venous infusion of cold fluid may be a useful method of inducing therapeutic hypothermia. The aim of this study was to quantify systemic heat balance and regional distribution of body heat during and after central infusion of cold fluid. METHODS: The authors studied nine volunteers, each on two separate days. Anesthesia was maintained with use of isoflurane, and on each day 40 ml/kg saline was infused centrally over 30 min. On one day, the fluid was 20 degrees C and on the other it was 4 degrees C. By use of a tympanic membrane probe core (trunk and head) temperature and heat content were evaluated. Peripheral compartment (arm and leg) temperature and heat content were estimated with use of fourth-order regressions and integration over volume from 18 intramuscular thermocouples, nine skin temperatures, and "deep" hand and foot temperature. Oxygen consumption and cutaneous heat flux estimated systemic heat balance. RESULTS: After 30-min infusion of 4 degrees C or 20 degrees C fluid, core temperature decreased 2.5 +/- 0.4 degrees C and 1.4 +/- 0.2 degrees C, respectively. This reduction in core temperature was 0.8 degrees C and 0.4 degrees C more than would be expected if the change in body heat content were distributed in proportion to body mass. Reduced core temperature resulted from three factors: (1) 10-20% because cutaneous heat loss exceeded metabolic heat production; (2) 50-55% from the systemic effects of the cold fluid per se; and (3) approximately 30% because the reduction in core heat content remained partially constrained to core tissues. The postinfusion period was associated with a rapid and spontaneous recovery of core temperature. This increase in core temperature was not associated with a peripheral-to-core redistribution of body heat because core temperature remained warmer than peripheral tissues even at the end of the infusion. Instead, it resulted from constraint of metabolic heat to the core thermal compartment. CONCLUSIONS: Central venous infusion of cold fluid decreases core temperature more than would be expected were the reduction in body heat content proportionately distributed. It thus appears to be an effective method of rapidly inducing therapeutic hypothermia. When the infusion is complete, there is a spontaneous partial recovery in core temperature that facilitates rewarming to normothermia.

Pulsatility does not change cerebral oxygenation during cardiopulmonary bypass.

BACKGROUND: To determine the effect of pulsatility during cardiopulmonary bypass (CPB) on cerebral oxygenation, we measured oxyhaemoglobin (HbO2), deoxyhaemoglobin (Hb) and oxidised cytochrome aa3 (CtO2) with near-infrared spectroscopy (NIRS) in 14 patients electively scheduled for cardiac surgery. METHODS: Cerebral oxygenation was measured during steady state CPB at a core temperature of 32 degrees C. Non-pulsatile flow and pulsatile flow were performed for 10 min each. RESULTS: After 14 min of CPB, HbO2, Hb and CtO2 were significantly below prebypass values. HbO2 and CtO2 did not alter with changing flow patterns. Hb significantly increased both during the period of nonpulsatile (median: -0.7 vs. 0.25 micromol/l; P<0.05) and pulsatile flow (median: 0.25 vs. 0.5 micromol/l; P<0.001). This increase was independent of flow pattern. CONCLUSIONS: Neither oxygenated haemoglobin, nor intracellular oxygenation, represented by CtO2, indicated a beneficial effect of pulsatile perfusion during hypothermic CPB. These results, however, are only valid for short time effects within 10 min before rewarming from CPB and patients without flow-limiting stenoses of the carotid artery.

Resistive heating is more effective than metallic-foil insulation in an experimental model of accidental hypothermia: A randomized controlled trial.

STUDY OBJECTIVE: We study a resistive-heating blanket in a volunteer model of severe accidental hypothermia to evaluate differences in rates of rewarming, core temperature afterdrop, and body heat content and distribution during active and passive rewarming. METHODS: Eight volunteers participated in a crossover design on 2 days. The volunteers were anesthetized and cooled to 33 degrees C (91.4 degrees F); anesthesia was subsequently discontinued, and shivering was prevented with meperidine. On one randomly assigned day, the volunteers were rewarmed passively with reflective foil (passive insulation), whereas on the other they were covered with a carbon fiber-resistive heating blanket set to 42 degrees C (107.6 degrees F; active rewarming). Trunk and head temperature and heat content were calculated from core (tympanic membrane) temperature. Peripheral (arm and leg) tissue temperature and heat content were estimated by using fourth-order regressions and integration over volume from 30 tissue and skin temperatures. RESULTS: Core heat content increased 73+/-14 kcal (mean+/-SD) during 3 hours of active warming, but only 31+/-24 kcal with passive insulation, a difference of 41+/-20 kcal (95% confidence interval [CI] 27 to 55 kcal; P <. 001). Peripheral tissue heat content increased linearly by 111+/-16 kcal during active warming but only by 38+/-31 kcal during passive warming, a difference of 74+/-34 kcal (95% CI 50 to 97; P <.001). Consequently, total body heat increased 183+/-22 kcal during active warming but only 68+/-54 kcal with passive insulation, a difference of 115+/-42 kcal (95% CI 86 to 144 kcal; P <.001). Core temperature increased from 32.9 degrees C+/-0.2 degrees C to 35.2 degrees C+/-0. 4 degrees C during 3 hours of active warming, a difference of 2.3 degrees C+/-0.4 degrees C. In contrast, core temperature with foil insulation only increased from 32.9 degrees C+/-0.2 degrees C to 33. 8 degrees C+/-0.5 degrees C, a difference of only 0.8 degrees C+/-0. 4 degrees C. The difference in the core temperature increase between the two treatments was thus 1.5 degrees C+/-0.4 degrees C (95% CI 1. 2 degrees C to 1.7 degrees C; P <.001 between treatments). Active warming was not associated with an afterdrop, whereas the afterdrop was 0.2 degrees C+/-0.2 degrees C and lasted a median of 45 minutes (interquartile range, 41 to 64 minutes) with passive insulation. CONCLUSION: Resistive heating more than doubles the rewarming rate compared with that produced by reflective metal foil and does so without producing an afterdrop. It is therefore likely to be useful in the prehospital setting.

Inhaled nitric oxide reduces pulmonary vascular resistance more than prostaglandin E(1) during heart transplantation.

UNLABELLED: Heart transplantation in patients with increased pulmonary vascular resistance is often associated with postbypass right heart failure. We therefore compared the abilities of prostaglandin E(1) (PGE(1)) and inhaled nitric oxide to reduce pulmonary vascular resistance during heart transplantation. Patients undergoing orthotopic heart transplantation for congestive heart failure were randomly assigned to either a PGE(1) infusion at a rate of 8 ng. kg. (-1)min(-1) starting 10 min before weaning from cardiopulmonary bypass (CPB) (n = 34) or inhalation of 4 ppm nitric oxide starting just before weaning from CPB (n = 34). Both treatments were increased stepwise, if necessary, and were stopped 6 h postoperatively. Hemodynamic values were recorded after the induction of anesthesia, 10 and 30 min after weaning from CPB, and 1 h and 6 h postoperatively. Immediately after weaning from CPB, pulmonary vascular resistance was nearly halved in the nitric oxide group but reduced by only 10% in the PGE(1) group. Pulmonary artery pressure was decreased approximately 30% during nitric oxide inhalation, but only approximately 16% during the PGE(1) infusion. Six hours after surgery, pulmonary vascular resistance and pulmonary artery pressure were similar in the two groups. The ratio between pulmonary vascular resistance and systemic vascular resistance was significantly less in the nitric oxide patients at all postbypass times. In contrast, the pulmonary-to-systemic vascular resistance ratio increased approximately 30% in the patients given PGE(1). Cardiac output, heart rate, mean arterial pressure, right atrial pressure, and pulmonary wedge pressure did not differ between the groups. Weaning from CPB was successful in all patients assigned to nitric oxide inhalation; in contrast, weaning failed in six patients assigned to PGE(1) (P = 0.03). IMPLICATIONS: Nitric oxide inhalation selectively reduces pulmonary vascular resistance and pulmonary artery pressure immediately after heart transplantation which facilitates weaning from cardiopulmonary bypass.

Efficacy of two methods for reducing postbypass afterdrop.

BACKGROUND: Afterdrop, defined as the precipitous reduction in core temperature after cardiopulmonary bypass, results from redistribution of body heat to inadequately warmed peripheral tissues. The authors tested two methods of ameliorating afterdrop: (1) forced-air warming of peripheral tissues and (2) nitroprusside-induced vasodilation. METHODS: Patients were cooled during cardiopulmonary bypass to approximately 32 degrees C and subsequently rewarmed to a nasopharyngeal temperature near 37 degrees C and a rectal temperature near 36 degrees C. Patients in the forced-air protocol (n = 20) were assigned randomly to forced-air warming or passive insulation on the legs. Active heating started with rewarming while undergoing bypass and was continued for the remainder of surgery. Patients in the nitroprusside protocol (n = 30) were assigned randomly to either a control group or sodium nitroprusside administration. Pump flow during rewarming was maintained at 2.5 l x m(-2) x min(-1) in the control patients and at 3.0 l x m(-2) x min(-1) in those assigned to sodium nitroprusside. Sodium nitroprusside was titrated to maintain a mean arterial pressure near 60 mm Hg. In all cases, a nasopharyngeal probe evaluated core (trunk and head) temperature and heat content. Peripheral compartment (arm and leg) temperature and heat content were estimated using fourth-order regressions and integration over volume from 18 intramuscular needle thermocouples, nine skin temperatures, and "deep" hand and foot temperature. RESULTS: In patients warmed with forced air, peripheral tissue temperature was higher at the end of warming and remained higher until the end of surgery. The core temperature afterdrop was reduced from 1.2+/-0.2 degrees C to 0.5+/-0.2 degrees C by forced-air warming. The duration of afterdrop also was reduced, from 50+/-11 to 27+/-14 min. In the nitroprusside group, a rectal temperature of 36 degrees C was reached after 30+/-7 min of rewarming. This was only slightly faster than the 40+/-13 min necessary in the control group. The afterdrop was 0.8+/-0.3 degrees C with nitroprusside and lasted 34+/-10 min which was similar to the 1.1+/-0.3 degrees C afterdrop that lasted 44+/-13 min in the control group. CONCLUSIONS: Cutaneous warming reduced the core temperature afterdrop by 60%. However, heat-balance data indicate that this reduction resulted primarily because forced-air heating prevented the typical decrease in body heat content after discontinuation of bypass, rather than by reducing redistribution. Nitroprusside administration slightly increased peripheral tissue temperature and heat content at the end of rewarming. However, the core-to-peripheral temperature gradient was low in both groups. Consequently, there was little redistribution in either case.

Relative contribution of skin and core temperatures to vasoconstriction and shivering thresholds during isoflurane anesthesia.

BACKGROUND: Thermoregulatory control is based on both skin and core temperatures. Skin temperature contributes approximately 20% to control of vasoconstriction and shivering in unanesthetized humans. However, this value has been used to arithmetically compensate for the cutaneous contribution to thermoregulatory control during anesthesia--although there was little basis for assuming that the relation was unchanged by anesthesia. It even remains unknown whether the relation between skin and core temperatures remains linear during anesthesia. We therefore tested the hypothesis that mean skin temperature contributes approximately 20% to control of vasoconstriction and shivering, and that the contribution is linear during general anesthesia. METHODS: Eight healthy male volunteers each participated on 3 separate days. On each day, they were anesthetized with 0.6 minimum alveolar concentrations of isoflurane. They then were assigned in random order to a mean skin temperature of 29, 31.5, or 34 degrees C. Their cores were subsequently cooled by central-venous administration of fluid at approximately 3 degrees C until vasoconstriction and shivering were detected. The relation between skin and core temperatures at the threshold for each response in each volunteer was determined by linear regression. The proportionality constant was then determined from the slope of this regression. These values were compared with those reported previously in similar but unanesthetized subjects. RESULTS: There was a linear relation between mean skin and core temperatures at the vasoconstriction and shivering thresholds in each volunteer: r2 = 0.98+/-0.02 for vasoconstriction, and 0.96+/-0.04 for shivering. The cutaneous contribution to thermoregulatory control, however, differed among the volunteers and was not necessarily the same for vasoconstriction and shivering in individual subjects. Overall, skin temperature contributed 21+/-8% to vasoconstriction, and 18+/-10% to shivering. These values did not differ significantly from those identified previously in unanesthetized volunteers: 20+/-6% and 19+/-8%, respectively. CONCLUSIONS: The results in anesthetized volunteers were virtually identical to those reported previously in unanesthetized subjects. In both cases, the cutaneous contribution to control of vasoconstriction and shivering was linear and near 20%. These data indicate that a proportionality constant of approximately 20% can be used to compensate for experimentally induced skin-temperature manipulations in anesthetized as well as unanesthetized subjects.

Tissue heat content and distribution during and after cardiopulmonary bypass at 17 degrees C.

UNLABELLED: We measured afterdrop and peripheral tissue temperature distribution in eight patients cooled to approximately 17 degrees C during cardiopulmonary bypass and subsequently rewarmed to 36.5 degrees C. A nasopharyngeal probe evaluated trunk and head temperature and heat content. Peripheral tissue temperature (arm and leg temperature) and heat content were estimated using fourth-order regressions and integration over volume from 30 tissue and skin temperatures. Peripheral tissue temperature decreased to 19.7+/-0.9 degrees C during bypass and subsequently increased to 34.3+/-0.7 degrees C during 104+/-18 min of rewarming. The core-to-peripheral tissue temperature gradient was -5.9+/-0.9 degrees C at the end of cooling and 4.7+/-1.5 degrees C at the end of rewarming. The core-temperature afterdrop was 2.2+/-0.4 degrees C and lasted 89+/-15 min. It was associated with 1.1+/-0.7 degrees C peripheral warming. At the end of cooling, temperatures at the center of the upper and lower thigh were (respectively) 8.0+/-5.2 degrees C and 7.3+/-4.2 degrees C cooler than skin temperature. On completion of rewarming, tissue at the center of the upper and lower thigh were (respectively) 7.0+/-2.2 degrees C and 6.4+/-2.3 degrees C warmer than the skin. When estimated systemic heat loss was included in the calculation, redistribution accounted for 73% of the afterdrop, which is similar to the contribution observed previously in nonsurgical volunteers. IMPLICATIONS: Temperature afterdrop after bypass at 17 degrees C was 2.2+/-0.4 degrees C, with approximately 73% of the decrease in core temperature resulting from core-to-peripheral redistribution of body heat. Cooling and rewarming were associated with large radial tissue temperature gradients in the thigh.

Tissue heat content and distribution during and after cardiopulmonary bypass at 31 degrees C and 27 degrees C.

BACKGROUND: Afterdrop following cardiopulmonary bypass results from redistribution of body heat to inadequately warmed peripheral tissues. However, the distribution of heat between the thermal compartments and the extent to which core-to-peripheral redistribution contributes to post-bypass hypothermia remains unknown. METHODS: Patients were cooled during cardiopulmonary bypass to nasopharyngeal temperatures near 31 degrees C (n=8) or 27 degrees C (n=8) and subsequently rewarmed by the bypass heat exchanger to approximately 37.5 degrees C. A nasopharyngeal probe evaluated core (trunk and head) temperature and heat content. Peripheral compartment (arm and leg) temperature and heat content were estimated using fourth-order regressions and integration over volume from 19 intramuscular needle thermocouples, 10 skin temperatures, and "deep" foot temperature. RESULTS: In the 31 degrees C group, the average peripheral tissue temperature decreased to 31.9+/-1.4 degrees C (means+/-SD) and subsequently increased to 34+/-1.4 degrees C at the end of bypass. The core-to-peripheral tissue temperature gradient was 3.5+/-1.8 degrees C at the end of rewarming, and the afterdrop was 1.5+/-0.4 degrees C. Total body heat content decreased 231+/-93 kcal. During pump rewarming, the peripheral heat content increased to 7+/-27 kcal below precooling values, whereas the core heat content increased to 94+/-33 kcal above precooling values. Body heat content at the end of rewarming was thus 87+/-42 kcal more than at the onset of cooling. In the 27 degrees C group, the average peripheral tissue temperature decreased to a minimum of 29.8 +/-1.7 degrees C and subsequently increased to 32.8+/-2.1 degrees C at the end of bypass. The core-to-peripheral tissue temperature gradient was 4.6+/-1.9 degrees C at the end of rewarming, and the afterdrop was 2.3+/-0.9 degrees C. Total body heat content decreased 419+/-49 kcal. During pump rewarming, core heat content increased to 66+/-23 kcal above precooling values, whereas peripheral heat content remained 70+/-42 kcal below precooling values. Body heat content at the end of rewarming was thus 4+/-52 kcal less than at the onset of cooling. CONCLUSIONS: Peripheral tissues failed to fully rewarm by the end of bypass in the patients in the 27 degrees C group, and the afterdrop was 2.3+/-0.9 degrees C. Peripheral tissues rewarmed better in the patients in the 31 degrees C group, and the afterdrop was only 1.5+/-0.4 degrees C.

Acute normovolaemic haemodilution does not aggravate gastric mucosal acidosis during cardiac surgery.

OBJECTIVE: Acute normovolaemic haemodilution with subsequent autologous blood transfusion after surgery is widely used to reduce homologous blood requirements during cardiac surgery. The hypothesis tested was whether a low intraoperative haematocrit (Hct) resulting from haemodilution decreases gastric mucosal pH (pHi). DESIGN: Prospective clinical investigation. SETTING: University Hospital of Vienna, Austria. PATIENTS: 16 consecutive patients scheduled for elective cardiac surgery. INTERVENTIONS: The patients were randomly assigned to one of two groups: In 10 patients (group 1), 500 ml of blood was withdrawn and stored after anaesthesia induction. An equal amount of 6% hydroxyethyl starch was simultaneously infused. After discontinuation of cardiopulmonary bypass (CPB), the autologous blood unit was transfused. Six patients (group 2), who were not subjected to haemodilution and autologous blood transfusion served as controls. In all patients, a gastric tonometry probe was inserted. MEASUREMENTS AND RESULTS: Measurements of pHi and Hct were performed before and after acute normovolaemic haemodilution, during pulsatile hypothermic (30-32 degrees C) CPB, after rewarming, and 30 min after autologous blood transfusion in group 1, and at corresponding time intervals in group 2. Repeated measures analysis of variance and the Mann-Whitney U test were used for statistical analysis. Data are presented as means +/- standard error of the mean. Haemodilution in group 1 caused a significant and persistent decrease in Hct (after haemodilution in group 1 34 +/- 1 vs 40 +/- 1% in group 2). In both groups, pHi decreased during rewarming and after termination of CPB. However, in group 1, pHi was better preserved than in group 2 (rewarming: 7.44 +/- 0.02 vs 7.34 +/- 0.04; after CPB: 7.38 +/- 0.03 vs 7.28 +/- 0.02; p < 0.05). CONCLUSIONS: Acute normovolaemic haemodilution does not aggravate gastric mucosal acidosis during cardiac surgery.