Charles B. Hantler

Anesthesia awareness and the bispectral index.

BACKGROUND Awareness during anesthesia is a serious complication with potential long-term psychological consequences. Use of the bispectral index (BIS), developed from a processed electroencephalogram, has been reported to decrease the incidence of anesthesia awareness when the BIS value is maintained below 60. In this trial, we sought to determine whether a BIS-based protocol is better than a protocol based on a measurement of end-tidal anesthetic gas (ETAG) for decreasing anesthesia awareness in patients at high risk for this complication. METHODS We randomly assigned 2000 patients to BIS-guided anesthesia (target BIS range, 40 to 60) or ETAG-guided anesthesia (target ETAG range, 0.7 to 1.3 minimum alveolar concentration [MAC]). Postoperatively, patients were assessed for anesthesia awareness at three intervals (0 to 24 hours, 24 to 72 hours, and 30 days after extubation). RESULTS We assessed 967 and 974 patients from the BIS and ETAG groups, respectively. Two cases of definite anesthesia awareness occurred in each group (absolute difference, 0%; 95% confidence interval [CI], -0.56 to 0.57%). The BIS value was greater than 60 in one case of definite anesthesia awareness, and the ETAG concentrations were less than 0.7 MAC in three cases. For all patients, the mean (+/-SD) time-averaged ETAG concentration was 0.81+/-0.25 MAC in the BIS group and 0.82+/-0.23 MAC in the ETAG group (P=0.10; 95% CI for the difference between the BIS and ETAG groups, -0.04 to 0.01 MAC). CONCLUSIONS We did not reproduce the results of previous studies that reported a lower incidence of anesthesia awareness with BIS monitoring, and the use of the BIS protocol was not associated with reduced administration of volatile anesthetic gases. Anesthesia awareness occurred even when BIS values and ETAG concentrations were within the target ranges. Our findings do not support routine BIS monitoring as part of standard practice. (ClinicalTrials.gov number, NCT00281489 [ClinicalTrials.gov].).

Intrapatient reproducibility of the BISxp monitor

Background:The Bispectral Index (BIS) reportedly reflects anesthetic depth. It is recommended that anesthetic agents should be titrated to maintain the BIS between 40 and 60 arbitrary BIS units during anesthesia. For anesthesia providers to follow this recommendation, the monitor should be predictably affected by different anesthetic agents and have good interpatient and intrapatient reproducibility. The authors hypothesized that when two BISxp® devices (Aspect Medical Systems, Newton, MA) are placed concurrently on the same patient, their readings are concordant throughout the anesthetic period. Methods:Simultaneous BIS recordings from two BISxp® monitors were obtained during anesthesia at 5-s intervals from 12 participants. Results:In total 22,860 concurrent paired BIS readings were obtained. For 10.7% of the time, there were sustained periods of 30 s or greater where the readings suggested a different depth of anesthesia. For 6% of the time, there were sustained periods of 30 s or greater where the readings differed by 10 or more arbitrary BIS units. The regression coefficient (R2) for the two devices was 0.65 (range, 0.35–0.92). There was zero bias between the devices, and the 95% limits of agreement ranged between −18 and +17. Conclusion:A conflicting anesthetic management was suggested by the simultaneous BIS readings 10.7% of the time. These results suggest that BISxp® does not always provide a reproducible single number. Anesthesia providers should not rely exclusively on the BIS reading when assessing depth of anesthesia.

Congenital Long Qt Syndrome: Changes in Qt Interval during Anesthesia with Thiopental, Vecuronium, Fentanyl, and Isoflurane

Congenital long QT syndrome (LQTS) is a rare abnormality that can present at a young age with syncopal attacks (resulting from ventricular arrhythmias) or sudden death (1). It is thought that LQTS results from an asymmetrical adrenergic stimulus to the heart, which leads to delayed repolarization of the ventricle (manifested by a prolonged QT interval), lowering of the threshold for ventricular fibrillation, an increase in the duration of the vulnerable phase, and an increase in ventricular excitability (2). Untreated, these patients have a mortality of 70%, but treatment with beta-blockers shortens the QT interval and greatly decreases the mortality (1). There are 11 case reports describing the anesthetic management of these patients but only in two (3,4) were any measurements of the QT interval made perioperatively. Changes in the QT interval associated with surgery and anesthesia in patients with LQTS remain undocumented (5). This report documents the effect of thiopental, vecuronium, fentanyl, and isoflurane on the QT interval in a patient with LQTS during an uneventful anesthetic, in whom previous therapy with propran0101 failed to shorten the QT interval.

Protamine pretreatment attenuation of hemodynamic and hematologic effects of heparin-protamine interaction: A prospective randomized study in human beings undergoing aortic reconstructive surgery

Hemodynamic and hematologic responses to protamine sulfate reversal of heparins anticoagulant effects were studied in 15 consecutive randomized patients undergoing aortic reconstructive surgery. In a double-blinded manner, patients were pretreated with either normal saline solution (n = 8) or protamine (0.75 mg/kg/3 min, n = 7) 5 minutes before heparinization (150 IU/kg). After aortic grafts were placed, protamine (1.5 mg/kg/3 min) was administered intravenously to reverse the heparin. Arterial blood pressure, heart rate, pulmonary artery and capillary wedge pressure, central venous pressure, and cardiac output were monitored, as were platelet count, white blood cell count, activated clotting time, total hemolytic complement levels, and C3a levels. Calculated parameters included systemic vascular resistance and pulmonary vascular resistance. Pretreatment with protamine compared with saline solution prevented the hypotension (+6 vs. -16 mm Hg, p less than 0.05) and declining pulmonary artery pressure (+1 vs. -7 mm Hg, p less than 0.01) observed with protamine reversal of heparin. Significant differences between the two groups in central venous pressure and pulmonary vascular resistance were of less clinical relevance. Protamine pretreatment lessened the thrombocytopenia found during reversal compared with saline-pretreated patients although the difference was not statistically significant. Minimal hypotension occurring after protamine pretreatment alone was not accompanied by hemodynamic or hematologic changes, other than decreased heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Suppression of Ventricular Arrhythmias by Volatile Anesthetics in a Canine Model of Chronic Myocardial Infarction

Ventricular tachycardia likely secondary to a reentrant mechanism may be reliably induced by programmed electrical stimulation in dogs 4-6 days after creating a 2-h experimental, occlusion-reperfusion myocardial infarction. The effects of 1.1 and 1.8 MAC halothane, isoflurane, and enflurane on pacing-induced arrhythmias were studied in this model. The ease of initiation of ventricular tachycardia was measured in both awake and anesthetized dogs (n = 18). Excitation thresholds, conduction times, and refractory periods in both normal and infarcted myocardium were also determined to understand changes in the ease of induction of the arrhythmias secondary to anesthetic exposure. Halothane and enflurane administration suppressed the induction of ventricular tachycardia compared with the unanesthetized control (P less than 0.01 for both). During isoflurane anesthesia, there was a trend that was not statistically significant for pacing-induced ventricular tachycardia to be less frequent than during the conscious state (P = 0.11). Halothane and enflurane prolonged refractory periods in both normal and infarcted myocardium, whereas isoflurane had that effect only in normal myocardium. In addition, halothane and enflurane tended to increase refractory periods more than isoflurane in both regions. Conduction times and excitation thresholds were not altered by anesthetic administration. It is concluded that halothane and enflurane suppress inducible ventricular arrhythmias secondary to a prior myocardial infarction. In addition, the increased efficacy of halothane and enflurane as antiarrhythmic agents compared with isoflurane in this model may be related to their greater prolongation of refractory periods.

Effects of differing rates of protamine reversal of heparin anticoagulation

BACKGROUND Protamine sulfate reversal of heparin anticoagulation may be associated with adverse cardiovascular side effects. The purpose of this study was to determine whether diminished systemic oxygen consumption and hemodynamic changes were more likely to accompany rapid versus slow protamine administration. METHODS Fifteen patients undergoing abdominal aortic aneurysm resection in a prospective randomized double-blinded study received intravenous protamine (1.5 mg/kg) rapidly during a 3-minute period (group I, n = 7) or slowly during a 15-minute period (group II, n = 8). Systemic oxygen consumption (VO2) and hemodynamic parameters were assessed for up to 20 minutes after protamine administration began. RESULTS Blood pressure declines (millimeters of mercury) were greatest in group I with rapid protamine administration (-19 systolic and -9 diastolic) compared with group II with slow protamine administration (-12 systolic and -1 diastolic). Heart rate fell markedly in both groups I and II. Cardiac output (CO) declined in group I at virtually all time periods. Similar CO declines in group II occurred 10 minutes after protamine infusion had begun and persisted for 3 minutes after protamine administration was complete. Maximum VO2 decreases were -16% (60 seconds into protamine infusion) and -13% (1.5 minutes after protamine infusion) in groups I and II, respectively, with statistically significant declines (p < 0.05) occurring only in group I compared with baseline values. Statistically significant differences (p < 0.01), however, were found when mean declines during and after protamine infusion were compared with controls for both CO and VO2 in both groups. CONCLUSIONS Significant declines in systemic VO2 and hemodynamic perturbations accompany protamine reversal of heparin anticoagulation during aortic surgery. Rapid protamine administration increases the magnitude of these adverse responses.

Effects of isoflurane on myocardial blood flow, function, and oxygen consumption in the presence of critical coronary stenosis in dogs.

Because isoflurane has been reported to produce coronary steal, we studied 12 open chest, anesthetized (pentobarbital) dogs with critical stenosis (CS) of the left circumflex coronary artery (LCA). Son micrometers were implanted to measure systolic watt thickening, myocardial Hood flow (MBF) was measured with microspheres (15 μm diameter), and regional venous sampling was performed to estimate regional oxygen extraction and myocardial oxygen consumption (MVO2). Anesthetic concentrations of isoflurane reduced arterial blood pressure dramatically, resulting in a maldistribution of MBF distal to the CS consistent with the pattern characterizing a transmural coronary steal effect. Elevation of arterial blood pressure with phenylephrine during high concentration is oflurane (1.7 ± 0.1%) augmented MBF, but the maldistribution distal to the CS persisted. Despite the maldistribution, however, there was no indication of ischemia in the LCA region because systolic wall thickening, oxygen extraction, and MVo2 were not significantly different between the LCA and left anterior descending coronary artery (LAD) (control) areas. Because wall thickening, oxygen extraction, and MVo2 were markedly reduced by isoflurane in both the LCA and control areas, it was concluded that isoflurane substantially reduced myocardial oxygen requirements by inducing myocardial depression, reducing heart rate, and decreasing afterload. Consequently, the apparent maldistribution of LCA blood flow (coronary steal) was due to the hemodynamic and vasodilatory effects of isoflurane, but did not result in ischemia because the level of blood flow was at or above the requirements of the myocardium.

Perioperative Management of the Patient Undergoing Automatic Internal Cardioverter-Defibrillator Implantation

I T HAS BEEN ESTIMATED that 400,000 people die annually from sudden cardiac arrest in the United States.’ Various treatment modalities have been tried in patients at high risk for sudden death from ventricular fibrillation, but delivery of an electrical countershock of sufficient energy remains the only reliable treatment.* The automatic internal cardioverterdefibrillator (AICD) has dramatically changed the treatment of patients at high risk for sudden death. The first clinical trial was by Mirowski et al3 in 1980. The implantation of AICDs has greatly increased since the Food and Drug Administration approved the device in 1985. There have been more than 3,000 AICDs inserted since 1982, at greater than 200 centerse4 The results of conventional treatment are not optimal. The l-year sudden-cardiac-death rate for survivors of an episode of cardiac arrest receiving empiric drug therapy is 20% to 50%.5-9 The l-year sudden-cardiac-death rate for patients with electrophysiologic or Holter-monitorguided therapy is 2% to 1 5%.5,6Y9 The results from a number of series of patients with AICDs, however, have been very encouraging. The lyear sudden-cardiac-death rate of AICD patients has been reported to be about 2%.‘@14

Effects of the volatile anesthetic agents on sinus node function and atrioventricular conduction in dogs: a comparison with chloralose anesthesia

The effects of equipotent concentrations (1.5 times minimum alveolar concentration) of the inhalational agents halothane, enflurane, and isoflurane on sinus node function, and atrioventricular (A-V) conduction and refractoriness were compared with chloralose anesthesia in 49 mongrel dogs. Sinus node function was assessed using corrected sinus node recovery time. Atrial-His and His-ventricular conduction times were measured at paced heart rates of 150, 180, and 200 beats/min, and A-V refractoriness was assessed by Wenckebach periodicity. There was no evidence that sinus node function was impaired by any of the inhalational agents. Enflurane anesthesia was associated with a significant prolongation of atrial-His conduction at paced heart rates of 180 and 200 beats/min when compared to chloralose anesthesia and the other two inhalational agents (P < .001). Atrioventricular refractoriness was impaired by enflurane (P < .001) and halothane (P < .05), but not isoflurane, when compared with chloralose anesthesia. Ventricular-His conduction was not altered by any of the agents. The authors conclude that enflurane is associated with a greater impairment of A-V conduction and refractoriness than halothane or isoflurane, and that these changes are related to the anesthetic agent and not the anesthetic state.

Case report: Inferior vena-cava right atrial anastomotic stenosis after bicaval orthotopic heart transplantation

PurposeThis case report describes the occurrence of acute postoperative liver and renal failure after bicaval orthotopic heart transplantation (OHT) due to stenosis of the inferior vena cava (IVC)-right atrial (RA) anastomosis. We also discuss the role of measuring femoral venous pressure and transesophageal echocardiography (TEE) in establishing the diagnosis.Clinical featuresA 42-yr-old female patient with idiopathic dilated cardiomyopathy underwent an OHT, using the bicaval anastomotic technique. During the first 12 hr postoperatively she developed unexplained kidney and liver failure. Her left and right ventricular functions were excellent and the right and left sided filling pressures were normal. The femoral pressure was elevated while the RA pressure was normal. An emergent TEE showed colour-flow and Doppler characteristics consistent with IVC-RA anastomotic stenosis. Emergent surgical re-exploration was undertaken; a hemostatic suture was found at the RA cannulation site that had caused the constriction of the IVC-RA anastomosis.ConclusionsAcute liver and renal failure after OHT can have multiple causes including ischemia due to a low flow state. This case demonstrates the importance of doing a detailed intraoperative TEE after OHT, and the importance of repeating the intraoperative examination after any hemostatic sutures are placed. Femoral venous pressure monitoring can be a useful diagnostic tool in detecting IVC-RA stenosis.RésuméObjectifDécrire l’occurrence d’insuffisance hépatique et rénale aiguës, survenant après une transplantation cardiaque orthotopique (TCO) bicave, causée par la sténose de l’anastomose entre la veine cave inférieure (VCI) et l’oreillette droite (OD). Discuter aussi du rôle de la mesure de la pression veineuse fémorale et de l’échocardiographie transœsophagienne (ETO) dans l’établissement du diagnostic.Éléments cliniquesUne femme de 42 ans, atteinte de cardiomyopathie dilatée, a subi une TCO selon la technique anastomotique bicave. Pendant les 12 premières heures postopératoires, une insuffisance rénale et hépatique inexpliquée s’est développée. La fonction des ventricules gauche et droit était excellente, les pressions de remplissage étaient normales des deux côtés. La pression fémorale était élevée, celle l’OD était normale. Un examen d’ETO d’urgence a montré des caractéristiques de débit chromatique et Doppler compatibles avec une sténose anastomotique VCI-OD. Une ré-exploration chirurgicale urgente a révélé la présence d’une suture hémostatique, au site de canulation de l’OD, causant la constriction de l’anastomose VCI-OD.ConclusionL’insuffisance hépatique et rénale aiguës suivant une TCO peut avoir de multiples causes dont l’ischémie provoquée par un bas débit. Le présent cas démontre l’importance de faire une ETO peropératoire détaillée après la TCO et de répéter cet examen après la mise en place de toute suture hémostatique. Le monitorage de la pression veineuse fémorale peut aider à détecter la sténose VCI-OD.M