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PubMed2003

Bispectral index in a 3-year old undergoing deep hypothermia and circulatory arrest.

We report a 3-year-old girl who presented with Scimitar syndrome and underwent hypothermic circulatory arrest for correction of anomalous pulmonary veins and an atrial septal defect. In this case the Bispectral Index (BIS) correlated significantly with the gradual onset of hypothermia and circulatory arrest. However, BIS remained low during the rewarming phase of cardiopulmonary bypass, in spite of adequate pump flows and stable haemodynamics. We postulate that this significant lag in BIS during the rewarming phase of deep hypothermic circulatory arrest may represent neuronal bewilderment or perhaps stunning, and differs from previous studies that show significant increase in BIS during rewarming from mild hypothermia.

Cardiopulmonary Bypass↗
PubMed2005

Monitoring oxygenator expiratory isoflurane concentrations and the bispectral index to guide isoflurane requirements during cardiopulmonary bypass.

OBJECTIVE: The purpose of this study was to measure the changes in isoflurane requirements during the rewarming phase of cardiopulmonary bypass with moderate hypothermia. DESIGN: An observational study. SETTING: University hospital, single center. PARTICIPANTS: Forty patients undergoing elective coronary artery bypass surgery with cardiopulmonary bypass. INTERVENTIONS: Isoflurane requirements were quantified by measuring the concentrations in the oxygenator expiratory gas. Anesthesia was guided by bispectral index monitoring. MEASUREMENTS AND MAIN RESULTS: Isoflurane concentrations required to maintain the bispectral index between 40 and 50 during the rewarming phase of cardiopulmonary bypass were measured. There was a progressive increase in expiratory isoflurane requirements during rewarming from 30 degrees C to 37 degrees C, with a Pearson correlation coefficient of 0.78. There was a significant difference in the concentration required at 30 degrees C (0.41% +/- 0.14%) compared with 37 degrees C (1.00% +/- 0.12%). CONCLUSION: Isoflurane requirements are reduced during hypothermic cardiopulmonary bypass. Monitoring anesthetic concentrations in the oxygenator expiratory gas may be a useful adjunct to monitoring the depth of anesthesia.

Anesthesia, Inhalation↗
PubMed2001

Desflurane pharmacokinetics during cardiopulmonary bypass.

OBJECTIVE: To describe the washin and washout of desflurane when first administered during cardiopulmonary bypass (CPB) for cardiac surgery. DESIGN: A single-arm prospective study. SETTING: University-affiliated hospital operating room. PARTICIPANTS: Ten adult patients presenting for cardiac surgery. INTERVENTIONS: Consenting patients presenting for cardiac surgery received anesthesia with midazolam and fentanyl. Patients were cooled to 32 degrees C on CPB, then desflurane 6% was administered and blood samples drawn repeatedly from the arterial and venous bypass cannulae as well as from the membrane oxygenator inlet and exhaust from 2 to 32 minutes of desflurane administration. Just before rewarming, final (maximum) washin samples were taken. On rewarming, desflurane was discontinued, and blood and gas samples were taken 2 to 24 minutes thereafter. MEASUREMENTS AND MAIN RESULTS: CPB time was 116 +/- 10 minutes, and ischemic time was 81 +/- 6 minutes. Mean pump flow was 4.49 +/- 0.03 L/min, and mean arterial pressure was 70.1 +/- 1 mmHg during the study period. Arterial washin of desflurane was initially rapid; arterial concentrations reached 50% of administered concentrations within 4 minutes, but then slowed, reaching 68% of inspired concentrations at 32 minutes (desflurane concentration 4.0% +/- 0.3%). Arterial washout of desflurane was more rapid; arterial concentrations fell to 18% of the maximum concentration reached within 4 minutes, and only 8% of the maximum arterial concentration was present in blood 20 minutes later. CONCLUSION: Desflurane showed rapid initial washin and washout on CPB when administration was started at 32 degrees C and stopped at time of rewarming.

Aged↗
PubMed2001

Cerebral effects of cold reperfusion after hypothermic circulatory arrest.

OBJECTIVES: This study was undertaken to explore whether an interval of cold reperfusion can improve cerebral outcome after prolonged hypothermic circulatory arrest. METHODS: Sixteen pigs (27-30 kg) underwent 90 minutes of circulatory arrest at a brain temperature of 20 degrees C. Eight animals were rewarmed immediately after hypothermic circulatory arrest (controls), and 8 were reperfused for 20 minutes at 20 degrees C and then rewarmed (cold reperfusion). Electrophysiologic recordings, fluorescent microsphere determinations of cerebral blood flow, calculations of cerebral oxygen consumption, and direct measurements of intracranial pressure (millimeters of mercury) were obtained at baseline (37 degrees C), before hypothermic circulatory arrest, after discontinuing circulatory arrest at 37 degrees C deep brain temperature, and at 2, 4, and 6 hours thereafter. Histopathologic features and percent brain water were determined after the animals were sacrificed. RESULTS: Cerebral blood flow and oxygen consumption decreased during cooling: cerebral oxygen consumption returned to baseline levels after 4 hours, but cerebral blood flow remained depressed until 6 hours in both groups. Cold reperfusion failed to improve electrophysiologic recovery or to reduce brain weight, but median intracranial pressure increased significantly less after cold reperfusion than in controls (P =.02). Although no significant difference in the incidence of histopathologic abnormalities between groups was found, all 3 animals with an intracranial pressure of more than 15 mm Hg after immediate rewarming had histopathologic lesions, and high intracranial pressure was more prevalent among all animals with subsequent histopathologic lesions (P =.03). CONCLUSIONS: Cold reperfusion significantly inhibited the rise in intracranial pressure seen in control pigs after 90 minutes of circulatory arrest at 20 degrees C, suggesting that cold reperfusion may decrease cerebral edema and thereby improve outcome after prolonged hypothermic circulatory arrest.

Animals↗
PubMed2001

Experimental study on the effect of antegrade cerebral perfusion on brains with old cerebral infarction.

OBJECTIVE: Patients with old cerebral infarction who undergo aortic arch operations are susceptible to postoperative neurologic dysfunction. To verify such susceptibility, we performed this experimental study. METHODS: A cerebral infarct model was created in mongrel dogs by means of injection of cylindrical silicone embolus through the internal carotid artery. The dogs that had obvious neurologic deficits 1 day later and survived for 4 weeks or more were included in the cerebral infarct model. One month after cerebral infarction was induced, deep hypothermia and selective cerebral perfusion were used in 14 mongrel dogs (infarct group, n = 7; control group, n = 7). During this procedure, serum glutamate concentration and venous-arterial lactate difference were measured. Histopathologic study of the brain was also performed. RESULTS: Changes in venous-arterial lactate difference in both groups were almost similar, except in the rewarming phase. At 32 degrees C during rewarming, the venous-arterial lactate difference in the infarct group was significantly higher than that in the control group (P =.006). Although pre-cooling concentrations of serum glutamate were similar in both groups, the values in the infarct group at the end of rewarming were significantly higher than those in the control group (P =.046). On histologic examination, the presence of old cerebral infarction with gliosis was confirmed in the infarct group, but neither new cerebral infarction nor destruction of the blood-brain barrier was found. CONCLUSION: We observed an accelerated anaerobic metabolism and an increased extracellular glutamate release in the infarct group. The brain with old cerebral infarction is more susceptible to ischemia during arch operation than noninfarcted brain.

Animals↗
PubMed1997

Calpain is a mediator of preservation-reperfusion injury in rat liver transplantation.

Proteases as well as alterations in intracellular calcium have important roles in hepatic preservation-reperfusion injury, and increased calpain activity recently has been demonstrated in liver allografts. Experiments were designed to evaluate (i) hepatic cytosolic calpain activity during different periods of cold ischemia (CI), rewarming, or reperfusion, and (ii) effects of inhibition of calpain on liver graft function using the isolated perfused rat liver and arterialized orthotopic liver transplantation models. Calpain activity was assayed using the fluorogenic substrate Suc-Leu-Leu-Val-Tyr-7-amino-4-methyl coumarin (AMC) and expressed as mean +/- SD pmol AMC released/min per mg of cytosolic protein. Calpain activity rose significantly after 24 hr of CI in University of Wisconsin solution and further increased with longer preservation. Activity also increased within 30 min of rewarming, peaking at 120 min. Increased durations of CI preceding rewarming resulted in significantly higher activity (P < 0.01). Calpain activity increased rapidly upon reperfusion and was significantly enhanced by previous CI (P < 0.01). Calpain inhibition with Cbz-Val-Phe methyl ester significantly decreased aspartate aminotransferase released in the isolated perfused rat liver perfusate (P < 0.05). Duration of survival after orthotopic liver transplantation using livers cold-preserved for 40 hr was also significantly increased (P < 0.05) with calpain inhibitor. In conclusion, calpain proteases are activated during each phase of transplantation and are likely to play an important role in the mechanisms of preservation-reperfusion injury.

Adenosine↗
PubMed1983

Centrioles as microtubule-organizing centers for marginal bands of molluscan erythrocytes.

The erythrocytes of blood clams (arcidae) are flattened, elliptical, and nucleated. They contain elliptical marginal bands (MBs) of microtubules, each physically associated with a pair of centrioles marginal bands (MBs) of microtubles, each physically associated with a pair of centrioles (Cohen, W., and I. Nemhauser, 1980, J. Cell Biol., 86:286-291). The MBs were found to be cold labile in living cells, disappearing within 1-2 h at 0 degrees C. After the cells had been rewarmed for 1-2 h, continuous MBs with associated centrioles were once again present. Time-course studies utilizing phase contrast, antitubulin immunofluorescence, and electron microscopy of cytoskeletons prepared during rewarming revealed structural evidence of centriole participation in MB reassembly. At the earliest stage of reassembly, a continuous MB was not present. Instead, relatively short and straight microtubules focused on a pointed centriolar "pole," and none were present elsewhere in the cytoskeleton. Thin continuous MBs then formed, still pointed in the centriolar region. Subsequently, the MBs regained ellipticity, with their thickness gradually increasing but not reaching that of controls even after several hours of rewarming. At these later time points, microtubules still radiated from the centrioles and joined the MBs some distance away. In the presence of 0.1 mM colchicines, MB reassembly was arrested at the pointed stage. Electron microscopic observations indicate that pericentriolar material is involved in microtubule nucleation in this system, rather than the centriolar triplets directly. The results suggest a model in which the centrioles and associated material nucleate assembly and growth of microtubules in diverging directions around the cell periphery. Microtubules of opposite polarity would then pass each other at the end of the cell distal to the centrioles, with continued elongation eventually closing the MB ellipse behind the centriole pair.

Animals↗
PubMed1965

CAT HEART MUSCLE IN VITRO. 8. ACTIVE TRANSPORT OF SODIUM IN PAPILLARY MUSCLES.

The cells of cat right ventricular papillary muscles were depleted of K and caused to accumulate Na and water by preincubation at 2-3 degrees C. The time courses of changes in cellular ion content and volume and of the resting membrane potential (V(m)) were then followed after abrupt rewarming to 27-28 degrees C. At physiological external K concentration ([K](o) = 5.32 mM) recovery of cellular ion and water contents was complete within 30 minutes, the maximal observable rates of K uptake and Na extrusion (Deltammol cell ion/(kg dry weight) (min.)) being 3.4 and 3.6, respectively. The recovery rate was markedly slowed at [K](o) = 1.0 mM. Rewarming caused V(m) measured in cells at the muscle surface to recover within from <1 to 9 minutes, but only slight restoration of cellular ion contents (measured in whole muscles) had occurred after 10 minutes. Studies of recovery in NaCl-free sucrose Ringer's solution made it possible to separate the ouabain-insensitive outward diffusion of Na as a salt from a simultaneous ouabain-sensitive Na extrusion which is associated with a net cellular K uptake. A hypothesis consistent with these observations is that rewarming may activate a ouabain-sensitive "electrogenic" mechanism, most probably the net active transport of Na out of the cell, from which net K uptake may then follow passively.

Biological Transport↗
PubMed1998

Moderate hypothermia for 48 hours after temporary epidural brain compression injury in a canine outcome model.

In a previous study with this dog model, post-insult hypothermia of 31 degrees C for 5 h prevented secondary intraventricular pressure (IVP) rise, but during 35 degrees C or 38 degrees C, one-half of the dogs developed delayed IVP rise to brain death. We hypothesized that 31 degrees C extended to 48 h would prevent brain herniation. Using epidural balloon inflation, we increased contralateral IVP to 62 mm Hg for 90 min. Controlled ventilation was to 72 h and intensive care to 96 h. Group 1 dogs (n = 10) were normothermic controls (37.5 degrees C). Group 2 dogs (n = 10) were surface-cooled from 15 to 45 min of balloon inflation and maintained at moderate hypothermia (31 degrees C) to 48 h. Rewarming was from 48 to 72 h. Four additional dogs of hypothermia Group 2 had to be excluded from analysis for pneumonia and/or bleeding diathesis. After balloon deflation, IVP increased to 20 mm Hg or greater at 154 +/- 215 (range 15-720) min following the insult in Group 1 and at 1394 +/- 1191 (range 210-3420) min in Group 2 (p = 0.004), still during 31 degrees C but without further increase during hypothermia. Further IVP rise led to brain death in Group 1 in 6 of 10 dogs at 44 +/- 18 (range 21-72) h (all during controlled ventilation); and in Group 2, in 6 of 10 dogs at 87 +/- 11 (range 72-96) h (p = 0.001), all after rewarming, during spontaneous breathing. Survival to 96 h was achieved by 4 of 10 dogs in Group 1, and by 7 of 10 dogs in Group 2 (NS). Three of the six brain deaths in Group 2 occurred at 96 h. The macroscopically damaged brain volume was only numerically smaller in Group 2. The vermis downward shift was 6.8 +/- 3.5 mm in Group 1, versus 4.7 +/- 2.2 mm in Group 2 (p = 0.05). In an adjunctive study, in 4 additional normothermic dogs, hemispheric cerebral blood flow showed post-insult hypoperfusion bilaterally but no evidence of hyperemia preceding IVP rise to brain death. In conclusion, in this model, moderate hypothermia during and for 48 h after temporary epidural brain compression can maintain a low IVP during hypothermia but cannot prevent lethal brain swelling after rewarming and may cause coagulopathy and pulmonary complications.

Animals↗
PubMed1987

Effects of hypothermia on somatosensory evoked responses in man.

Somatosensory evoked responses after median nerve stimulation were recorded in 21 patients during hypothermic cardiopulmonary bypass. During hypothermia a significant linear correlation (P less than 0.001) was found between evoked potential latency and temperature. Correlation was best for tympanic membrane temperature during cooling and for perfusate temperature (arterial, venous) during rewarming. The increase in latency was more pronounced for middle latency components (N2, N3) and for the early cortical N1 than for the cervical N0 and central conduction time. In all patients N1 was detectable at 26 degrees C, with slightly reduced amplitude. In the rewarming period the changes occurred in the reverse order and pre-bypass values were achieved at normothermia. The slopes of the regression lines were different during cooling and rewarming, when latencies were related to patient (tympanic, nasopharyngeal, rectal) temperature, but identical when arterial or venous blood temperature was used as the reference. No correlation was found between latency and perfusion pressure. We conclude that sophisticated temperature measurement is required to aid the interpretation of evoked responses used during hypothermia.

Aged↗
PubMed1995

Tracheal tube cuff pressure during cardiac surgery using cardiopulmonary bypass.

To determine the effects of cardiopulmonary bypass (CPB) on tracheal cuff pressure, we have measured intracuff pressure (ICP) in 29 consecutive patients undergoing cardiac surgery with CPB. Premedication comprised hyoscine and, after induction of anaesthesia with diazepam and fentanyl, followed by vecuronium, the trachea was intubated using a Portex Profile tracheal tube. Anaesthesia was maintained with high-dose fentanyl and 100% oxygen. ICP was measured with a transducer and the ICP was adjusted to 20 mm Hg. CPB was used with mild to deep hypothermia and blood-gas tensions were regulated according to alpha-stat (temperature uncorrected) pH management. Before CPB, ICP was significantly reduced from the mean baseline value of 20 (SEM 0.2) to 16.7 (0.6) mm Hg (P < 0.01). ICP changed significantly during CPB, decreasing to 8.0 (1.0) mm Hg before rewarming (P < 0.01 vs immediately before CPB) and increasing to 17.0 (0.6) mm Hg after the start of rewarming (P < 0.01 vs before rewarming). After CPB, ICP did not differ significantly from that immediately before CPB. We conclude that the decrease in ICP during the hypothermic phase of CPB may protect the tracheal mucosa against hypotensive ischaemic injury.

Adult↗
PubMed1999

Time course of neurone-specific enolase and S-100 protein release during and after coronary artery bypass grafting.

Serum neurone-specific enolase (NSE) and S-100 protein are well established as markers of cerebral injury, and have been used as markers of neuronal and glial cell damage, respectively, after cardiac surgery with cardiopulmonary bypass (CPB), but the speed of their increase during CPB has not been studied. Therefore, we have investigated the time course of NSE and S-100 release during and after CPB. We studied 18 adult patients undergoing elective coronary artery bypass grafting (CABG). Standard hypothermic (32 degrees C) pulsatile bypass with membrane oxygenation was used. Blood samples were obtained at induction, before bypass, before rewarming, at the end of rewarming, 10 min, 1 h and 8 h after bypass and 1, 2 and 3 days after surgery. NSE and S-100 were assayed using immunoradiometric assay kits (Sangtec Medical). NSE and S-100 release followed similar time courses. Both increased sharply during bypass, reached peak concentrations at the end of rewarming (mean 25.55 (SEM 2.79) and 1.65 (0.23) microgram litre-1, respectively), had decreased significantly by the end of operation and returned to pre-bypass concentrations by the second day after surgery. No patient developed a major neurological deficit. When using NSE and S-100 assays to study cerebral dysfunction in relation to CPB, postoperative samples miss peak (end-bypass) concentrations, and studies should be designed to include intraoperative samples.

Adult↗
PubMed1999

Oxygenator exhaust capnography as an index of arterial carbon dioxide tension during cardiopulmonary bypass using a membrane oxygenator.

We have studied the relationship between the partial pressure of carbon dioxide in oxygenator exhaust gas (PECO2) and arterial carbon dioxide tension (PaCO2) during hypothermic cardiopulmonary bypass with non-pulsatile flow and a membrane oxygenator. A total of 172 paired measurements were made in 32 patients, 5 min after starting cardiopulmonary bypass and then at 15-min intervals. Additional measurements were made at 34 degrees C during rewarming. The degree of agreement between paired measurements (PaCO2 and PECO2) at each time was calculated. Mean difference (d) was 0.9 kPa (SD 0.99 kPa). Results were analysed further during stable hypothermia (n = 30, d = 1.88, SD = 0.69), rewarming at 34 degrees C (n = 22, d = 0, SD = 0.84), rewarming at normothermia (n = 48, d = 0.15, SD = 0.69) and with (n = 78, d = 0.62, SD = 0.99) or without (n = 91, d = 1.07, SD = 0.9) carbon dioxide being added to the oxygenator gas. The difference between the two measurements varied in relation to nasopharyngeal temperature if PaCO2 was not corrected for temperature (r2 = 0.343, P = < 0.001). However, if PaCO2 was corrected for temperature, the difference between PaCO2 and PECO2 was not related to temperature, and there was no relationship with either pump blood flow or oxygenator gas flow. We found that measurement of carbon dioxide partial pressure in exhaust gases from a membrane oxygenator during cardiopulmonary bypass was not a useful method for estimating PaCO2.

Adult↗
PubMed1988

Role of red blood cells in the coronary microcirculation during cold blood cardioplegia.

The role of red blood cells during cold blood cardioplegia was studied using an intravital microscope in 13 isolated canine hearts perfused with diluted blood containing potassium chloride. The coronary microcirculation on the left ventricular epicardial surface was observed while the perfusate temperature was varied between 37 degrees C and 10 degrees C. Considerable sludging of red blood cells occurred during hypothermia. The percentage of capillaries perfused by red blood cells (percentage change) significantly decreased as perfusate temperature was reduced (100, 56, and 31% at 37, 20, and 10 degrees C respectively). This was caused by occlusion of microvessels due to sludging and by functional closure due to hypothermia. There was incomplete recovery of perfusion of capillaries at the end of rewarming (60%). The diameters of venules were reduced to 76% of control value at 10 degrees C because of the decrease in the numbers of feeding capillaries, but this value returned to 91% at the end of rewarming. Coronary vascular resistance (mmHg.ml-1.min-1 (kPa.s.litre-1] significantly decreased from 2.0(0.2) at 37 degrees C to 1.2(0.12) at 10 degrees C, but it increased to 2.4(0.24) at the end of rewarming. The finding in this study that sludging occurred which was slow to clear is a definite disadvantage of perfusion with red blood cells during hypothermia.

Animals↗
PubMed2000

A placebo-controlled study of the effects of dopexamine on gastric mucosal perfusion in infants undergoing hypothermic cardiopulmonary bypass.

We used a laser Doppler probe to measure gastric mucosal blood flow (flux) and a paediatric tonometer to intermittently calculate gastric-arterial PCO2 difference (PrCO2-PaCO2 gap) in 50 infants aged 0.3-52 weeks who required hypothermic cardiopulmonary bypass (CPB). During CPB, patients in group 2 (n = 25) were given dopexamine 1.0 mg kg-1 over 5 min, followed by an infusion of 2 micrograms kg-1 min-1. Patients in group 1 (n = 25) received an equal volume of saline. Drug allocation was random and blinded. Measurements of flux, PrCO2-PaCO2 gap and mean femoral arterial pressure (MAP) were made over 5 min during steady state before and after cooling on CPB to 18-24 degrees C. MAP and blood lactate concentrations were similar in both groups throughout CPB. Mean flux decreased from 182 (SD 60) at the beginning of CPB to 158 (51) after rewarming on CPB in group 1, whereas it increased from 180 (56) to 196 (49) in group 2. This post-rewarm flux was significantly greater in group 2 than in group 1 (P = 0.01). Similarly, mean PrCO2-PaCO2 gap increased significantly from 3.6 (6.3) to 8.2 (6.7) in group 1 (P = 0.01) compared with a significant decrease from 5.8 (5.5) to 2.1 (5.5) in group 2 (P = 0.02). Mean PrCO2-PaCO2 gap after rewarming in group 2 was significantly higher than that in group 1 (P = 0.001). These data indicate that dopexamine may be useful in maintaining normal gut perfusion in infants requiring hypothermic CPB.

Adrenergic beta-Agonists↗
PubMed1996

Cardiovascular responses to an acute volume load in deep hypothermia.

Intravenous administration of warm fluids is used clinically as first aid either alone or as a contributing method, to rewarm hypothermic patients back to normal body temperature. The aim of this study was to determine the effects of an acute volume load in hypothermic conditions on the canine circulatory system. Cardiac catheterization was performed on 18 anaesthetized beagle dogs. Eleven of them were cooled and at a body temperature of 25 degrees C they received 40 ml.kg-1 dextran administered intravenously. The control group received dextran at normal body temperature. During cooling the body from 37 degrees C down to 25 degrees C most of the volume load escaped from the circulation due to extravazation. During rewarming, the opposite effect could be seen and the volume load persisted up to 29 degrees C and signs of cardiac decompensation were observed. According to these results, the intravenous administration of warm fluids to rewarm hypothermic patients should not be used routinely when hypovolaemia is the only result of hypothermia.

Animals↗
PubMed1998

Pharmacologic electroencephalographic suppression during cardiopulmonary bypass: a comparison of thiopental and isoflurane.

UNLABELLED: In this study, we examined the cerebral oxygenation effects of two methods of pharmacologic burst suppression during cardiopulmonary bypass (CPB) in valvular heart surgery patients. Patients were randomly entered into one of three groups: control (n = 13, fentanyl and midazolam), control plus burst suppression doses of thiopental (n = 15), or control plus burst suppression doses of isoflurane (n = 16). Burst suppression (80% suppression) was accomplished in the thiopental and isoflurane groups 15 min before aortic cannulation and was maintained through aortic decannulation. Cerebral physiologic measurements were made during hypothermia (27-28 degrees C) and on rewarming to 36 degrees C. During hypothermia, burst suppression produced significant (P < 0.005) differences with regard to cerebral vascular resistance (P = 0.003), cerebral arterial venous oxygen difference [C(a-v)O2] (P = 0.032), cerebral blood flow (CBF) (P = 0.009), and cerebral oxygen delivery (P = 0.027). There was a similar pattern on rewarming, with groups differing significantly (P < 0.05) with respect to CBF (P = 0.016), cerebral vascular resistance (P = 0.008), oxygen delivery (P = 0.004), C(a-v)O2 (P = 0.043), and cerebral oxygen extraction (P = 0.046). Rewarming rates were similar among groups. There was no difference in neurologic outcome or requirement for inotropic support among groups. The time to awakening was increased (P = 0.0005) in the thiopental group. The thiopental group had lower cerebral oxygen delivery, but not lower cerebral metabolic rate of oxygen consumption, compared with the control group, resulting in widening C(a-v)O2 during CPB. This lack of coupling of oxygen delivery and consumption suggests that pharmacologic neuroprotective mechanisms are complex and involve more than an improvement in the ratio of global cerebral oxygen supply to demand. IMPLICATIONS: This study demonstrates that the balance of cerebral oxygen delivery to consumption during cardiopulmonary bypass is altered differently by thiopental and isoflurane. As others have noted, it seems that cerebral protection is more complex than a simple improvement in the balance of oxygen delivery and consumption.

Adult↗
PubMed1998

Propofol does not ameliorate cerebral venous oxyhemoglobin desaturation during hypothermic cardiopulmonary bypass.

UNLABELLED: Reductions in cerebral venous oxyhemoglobin saturation (SjO2) occur during the rewarming phase of hypothermic cardiopulmonary bypass (CPB). We prospectively investigated the effects of propofol on these reductions in SjO2 (SjO2 <50%). Fiberoptic jugular bulb catheters were inserted in 30 patients undergoing coronary artery bypass grafting. Patients were randomly allocated to a test or control group. Test group patients (n = 15) received a propofol IV infusion titrated to electroencephalographic burst suppression during CPB. No significant differences in SjO2 <50% were found between the groups either by blood sampling and bench oximetry or fiberoptic oximetry. The arteriovenous difference in lactate concentration became negative in 59 of 120 samples. Propofol was associated with an increased incidence of hypotension (mean arterial pressure <50 mm Hg) (P = 0.023), an increased requirement for vasoconstrictor therapy (P = 0.025), and increases in the lactate oxygen index (P < 0.01). Propofol, when administered in doses that produce electroencephalographic burst suppression, does not attenuate the frequency or extent of reductions of SjO2 below 50% during rewarming from hypothermic CPB. However, it is associated with arterial hypotension and an increase in cerebral anaerobic metabolism. IMPLICATIONS: Reductions in cerebral venous oxyhemoglobin saturation during the rewarming phase of cardiopulmonary bypass may be related to brain injury. When administered in doses sufficient to produce electroencephalographic burst suppression, propofol did not attenuate the frequency or extent of such reductions in cerebral venous oxyhemoglobin saturation.

Aged↗