The critical role of aprotinin in controlling haemostasis in conjunction with non-pharmacological blood-saving strategies during routine coronary artery bypass surgery.

OBJECTIVE: Aprotinin, a non-specific serine protease inhibitor, has been confirmed to be safe and effective in reducing intra- and postoperative blood drainage, transfusion requirements, and perioperative morbidity and mortality during coronary artery bypass surgery. It is the only one of the currently available haemo-static agents that is approved by the U.S. Food and Drug Administration (FDA) for use in cardiac surgery. However, one major weakness of currently available trials is the lack of information regarding the concomitant usage of aprotinin with blood-saving strategies that have been used more frequently in recent years. METHODS: Patients undergoing elective first-time coronary artery bypass grafting (n = 172) who were given systemic high-dose aprotinin (n = 85), combined systemic high-dose aprotinin and topical aprotinin (n = 27), or no aprotinin (n = 60) were reviewed retrospectively. The use of all blood-saving procedures was systematically taken in account. RESULTS: Postoperative blood drainage was significantly less in patients treated with aprotinin than controls (P < 0.0001). Concomitant use of topical aprotinin was accompanied by a postoperative blood loss reduction of 35% compared to systemic aprotinin use alone (P < 0.003). The intra- and postoperative donor blood requirements were dramatically reduced in both aprotinin-treated groups compared to controls, although patients received different blood saving strategies as appropriate (P < 0.0001). A trend of up to 20% lower postoperative blood drainage was noted in patients in whom intraoperative haemodilution and autologuos blood transfusions were used (P > 0.05). CONCLUSIONS: The present analysis demonstrates that the local and systemic administration of aprotinin is safe and effective in reducing intra- and postoperative blood drainage and transfusion requirements. In elective CABG procedures, aprotinin should still be used even if blood-saving strategies are employed.

[Assessment of psychiatric emergencies by physicians in the pre-hospital emergency medical system. A re-evaluation after 7 years]. / Psychiatrische Notfälle aus der Sicht von Notärzten. Eine Reevaluation nach 7 Jahren.

OBJECTIVE: In the German emergency medical system (EMS) psychiatric emergency situations (PES) are now responsible for up to 15% of all calls for the emergency physician (EP). A survey which was first conducted in 1996 to reveal knowledge about PES, reported a significant need for training. Seven years later it is interesting to investigate whether different conditions in the EMS may have changed assessments and attitudes. METHODS: The questionnaire of 1996 was modified to enable a comparison of PES and other frequent emergency situations with respect to the estimated number and the subjective stress. Open and multiple-choice questions or visual analogue scales were used to obtain the following data: demographic data, frequency of and stress by PES and other medical emergencies, own knowledge, and interest about training programs. RESULTS: Of the EPs 274 responded (male/female: 74/26%, mean age: 38 years, mean experience as an EP 6 years, anaesthesiologists 69%). The frequency of PES was estimated at 5% and 44% of EPs thought that there had been an increase in recent years. Personal knowledge was judged to be good by only 24%. The interest in training programs even increased slightly compared to the first survey; of particular interest was training in drug abuse disorders. Subsequent to internal, neurological and surgical emergencies, PES are considered to rank fourth in frequency, however the strain imposed by PES is significantly higher than for these other emergency situations. DISCUSSION: The results indicate an increase of relevance of PES in the German EMS, however, assessments made by the EP only changed marginally over the time period. The subjective awareness of the frequency of PES underestimates the reality in emergency medicine. The importance of training programs remains high to improve knowledge and to reduce feelings of incapability.

[Intracerebral hemorrhage after cesarean section under spinal anesthesia. Coincidence or causality?]. / Intrazerebrale Blutung nach Sectio ceasarea in SpinalanästhesieKoinzidenz oder Kausalität?

Intracerebral haemorrhage is a rare complication of spinal anaesthesia in obstetrics. A 37-year-old woman without any accompanying disease during a twin pregnancy, underwent an urgent caesarean section due to insufficiency of the placenta under spinal anaesthesia using hyperbaric bupivacain (0.5%) and a pencil-point spinal needle Sprotte 27 Gauge. The patient developed severe headache, a hemiparesis of the right upper limb and became somnolent and finally unconscious 80 min after the procedure. An immediately performed computed tomographic scan revealed a large acute intracerebral haemorrhage in the left hemisphere region with mass effect. The patient underwent temporoparietal craniotomy. No obvious cause of the haemorrhage, such as aneurysm or arteriovenous malformation was found. The patient fully recovered and was weaned from the respirator 32 h postoperatively. On postoperative day 7 the remaining neurologic deficits included aphasis and severe hemiparesis of the right upper limb and a right extensor plantar response. The neurologic status did not improve substantially until 6 months after the complication. The case and the recent literature are discussed.

Induced arterial hypotension for interventional thoracic aortic stent-graft placement: impact on intracranial haemodynamics and cognitive function.

BACKGROUND AND OBJECTIVE: The study investigated the impact of induced arterial hypotension for the facilitation of endovascular stent-graft placement in patients with thoracic aortic aneurysm on cerebral blood flow velocity and neurological/neurocognitive outcome. METHODS: In 27 ASA III patients, cerebral blood flow velocity was recorded during induced arterial hypotension for endovascular stent-graft placement using transcranial Doppler sonography and the Folstein Mini Mental State Examination and the National Institute of Health Stroke Scale were performed before and after the intervention. RESULTS: Mean arterial pressure was decreased <50 mmHg, and in 22 patients it was <40 mmHg. Diastolic cerebral blood flow velocity decreased by 59%. Postoperatively, six of 21 patients exhibited changes in the Folstein Mini Mental State Examination and four of these six patients in the National Institute of Health Stroke Scale as indices of new-found neurocognitive dysfunction, but there were no signs of stroke. Loss of the diastolic blood flow profile was detected in two of six patients with new-found neurocognitive dysfunctions and in 18 of 21 patients with no new-found neurocognitive dysfunction. Changes in the Folstein Mini Mental State Examination on postoperative day 1 were correlated to the pre-procedural Folstein Mini Mental State Examination, but not to the time spent with a mean arterial pressure <50 mmHg, <40 mmHg or with a loss of diastolic blood flow profile. CONCLUSIONS: Transcranial Doppler sonography visualizes the individual effect of induced hypotension and the period of intracranial circulatory arrest during aortic stent-graft placement. However, transient new-found neurocognitive dysfunctions occur independently of the transcranial Doppler data, and are in close correlation to the neurocognitive state before the procedure. The results suggest that induced arterial hypotension is not the major factor for postoperative new-found neurocognitive dysfunction.

[Heart rate variability in anesthesia]. / Herzfrequenzvariabilität in der Anästhesie.

Measurement of heart rate variability (HRV) in the perioperative period is not yet part of routine monitoring. Because of a lack of standardization, comparison of results of different investigations is difficult. Caution is needed in interpreting data of HRV measurements because of the complexity of autonomic control of the cardiovascular system. Moreover, confounding effects of multiple factors influencing HRV in the perioperative setting make interpretation of data difficult and limit this methodology, for example, as a depth-of-anaesthesia monitor. HRV reflects the response of the heart to a variety of influences. None of the parameters obtained, however, elucidates directly the mechanism or site of action of an anaesthetic drug. Knowledge of the pathophysiology underlying HRV is critical in order to understand the state of the autonomic nervous system and its relevance for patient management. Nevertheless, previous studies show that HRV can provide information about sympathetic and parasympathetic influences affecting the cardiovascular system in the perioperative period. Thus, HRV seems to be a useful tool for preoperative cardiovascular risk stratification. Of major concern in this context is the quality of the recording of the electrocardiogram when assessing HRV. Because of the ongoing progress in monitoring with regard to acquisition and computer-based analysis of HRV data, it seems at least possible to measure HRV routinely in the perioperative setting. However, the need for standardization requires large prospective and standardized trials. Depending on the results, the clinical relevance of HRV as a relatively simple and non-invasive perioperative monitoring has to be re-evaluated.

Topography of clonidine-induced electroencephalographic changes evaluated by principal component analysis.

BACKGROUND: Principal component analysis is a multivariate statistical technique to facilitate the evaluation of complex data dimensions. In this study, principle component analysis was used to reduce the large number of variables from multichannel electroencephalographic recordings to a few components describing changes of spatial brain electric activity after intravenous clonidine. METHODS: Seven healthy volunteers (age, 26 +/- 3 [SD] yr) were included in a double-blind crossover study with intravenous clonidine (1.5 and 3.0 microg/kg). A spontaneous electroencephalogram was recorded by 26 leads and quantified by standard fast Fourier transformation in the delta, theta, alpha, and beta bands. Principle component analysis derived from a correlation matrix calculated between all electroencephalographic leads (26 x 26 leads) separately within each classic frequency band. The basic application level of principle component analysis resulted in components representing clusters of electrodes positions that were differently affected by clonidine. Subjective criteria of drowsiness and anxiety were rated by visual analog scales. RESULTS: Topography of clonidine-induced electroencephalographic changes could be attributed to two independent spatial components in each classic frequency band, explaining at least 85% of total variance. The most prominent effects of clonidine were increases in the delta band over centroparietooiccipital areas and decreases in the alpha band over parietooccipital regions. Clonidine administration resulted in subjective drowsiness. CONCLUSIONS: Data from the current study supported the fact that spatial principle component analysis is a useful multivariate statistical procedure to evaluate significant signal changes from multichannel electroencephalographic recordings and to describe the topography of the effects. The clonidine-related changes seen here were most probably results of its sedative effects.

[Interactions of intravenous anesthetics with cerebral alpha-2-adrenoceptors]. / Interaktionen intravenöser Anästhetika mit zerebralen alpha 2-Adrenozeptoren.

OBJECTIVE: Up to date the exact mechanisms of action of anaesthetics on structures of the central nervous system have not been elucidated. Agents acting on central alpha 2-adrenoceptors have been demonstrated to possess potent sedative properties. Beside the classical agonists, general anaesthetics that are currently in clinical use e.g. etomidate have also been shown to act on alpha 2-adrenoceptors. Thus, the aim of this study was to study the effect of the intravenous anaesthetic agents propofol and ketamine on the binding of the specific alpha 2-adrenoceptor agonist paraiodoclonidine at cerebral alpha 2 adrenoceptors. METHODS: After approval of the local animal care committee brain tissue of six Wistar rats was removed and frozen at -80 degrees C. The tissue was sectioned in 15-20 microns thick slices. After washing in TRIS-buffer (pH = 7.5) the slices were incubated with 2.5 nM 125I-paraiodoclonidine (PIC) for determination of specific binding. Unspecific binding was determined in presence of 200 microM unlabeled clonidine. Displacement experiments were performed in presence of propofol (11-530 microM) and ketamine (52-1100 microM) and evaluated autoradiographically. Average exposure time was three days. All films were then analysed by densitometry. Statistical significance calculated by Student's t-test was assumed at a level of p < 0.05. RESULTS: Only at the highest concentration of propofol and ketamine an effect on PIC binding was noticeable. Neither propofol nor ketamine was able to displace PIC completely from cerebral alpha 2-adrenoceptors. CONCLUSION: In contrast to other anaesthetics such as etomidate which was demonstrated to displace PIC completely from alpha 2-adrenoceptors, propofol and ketamine exerted only minor effects on the binding of PIC even at concentrations that exceeded clinical concentrations. These data suggest that an additional site of action of these anaesthetics at cerebral alpha 2-adrenoceptors beside the known actions on GABA receptors or NMDA receptors is unlikely.

[Effect of remifentanil on clinical and electroencephalographic parameters of depth of anesthesia in balanced anesthesia with propofol, enflurane or isoflurane]. / Einfluss von Remifentanil auf klinische und elektroenzephalographische Parameter der Narkosetiefe während balanzierter Anästhesie mit Propofol, Enfluran oder Isofluran.

UNLABELLED: Electrophysiological parameters are well-suited to detect changes in cerebral function. The present study investigates whether balanced anaesthesia with remifentanil during nociceptive stimulation is associated with changes in clinical and electrophysiological parameters indicating inadequate depth of anaesthesia. Following IRB approval and written informed consent, 23 patients (ASA: I; age: 36 +/- 11) scheduled for elective gynaecological laparoscopy were included in the study. Without any premedication, anaesthesia was induced with remifentanil (1.0 microgram/kg bolus injection), propofol (0.5 mg/kg added by repetitive (10 mg) bolus injections every 10 s until unconciousness) and vecuronium (0.1 mg/kg). Following endotracheal intubation (normoventilation: PetCO2: 36 bis 38 mmHg), remifentanil infusion was started with continuous doses of 0.5 microgram/kg/min over 5 minutes and maintained with 0.25 microgram/kg/min during surgery. Remifentanil was randomly combined with propofol (group 1: 100 micrograms/kg/min; n = 7), enflurane (group 2: 0.5 MAC; n = 8) or isoflurane (group 3: 0.5 MAC; n = 8). Monitoring included: heart rate (beats/min), mean arterial pressure (mmHg), oxygen saturation (%), endtidal CO2 (mmHg) and endtidal enflurane and isoflurane (%). EEG: 2-channel recordings of Fz versus mastoid and ECG (artefact control) during steady-state anaesthesia and surgery. Following fast-fourier-transformation (4 s; 256/s; 0.5 to 35.0 Hz), spectral power densities were calculated for the selected frequency bands. Auditory evoked potentials (AEP; middle latency) were registered simultaneously after binaural stimulation via head-phones click-stimulation (6 Hz; 75 dB above hearing threshold; 512 stimulations per average). Bandpass was 0.01 to 2.0 kHz. ANALYSIS: Na, Pa, Nb (latencies; ms) and peak-to-peak amplitudes (NaPa, PaNb; microV). EEG and AEP recording technique [15]. The study protocol included baseline values from pre-intubation, pre-surgery, the respective post-stimulation values (1 min, 3 min, 5 min) and all data at five-minute intervals during surgery until emergence from anaesthesia. During steady-state study conditions with defined remifentanil applications, mean data indicate that in response to nociceptive stimuli no changes in clinical or electrophysiological parameters were observed. In contrast to other studies using different anaesthetic techniques, the present data from remifentanil indicate very stable haemodynamic and electrophysiological parameters (EEG, AEP) during noxious stimulations. Adjustable and with no plasma accumulation, remifentanil demonstrates potent antinociceptive effects resulting in signs of adequate anaesthesia.

The effect of remifentanil on cerebral blood flow velocity.

UNLABELLED: In the present study, we investigated the effect of remifentanil on cerebral blood flow velocity (CBFV). We investigated 20 patients (ASA physical status III) scheduled for elective coronary artery bypass graft surgery. Anesthesia was induced with remifentanil 5 microg/kg IV (Group 1, n = 10) or 2 microg/kg IV (Group 2, n = 10) and was maintained with 3 microg x kg(-1) x min(-1) IV (Group 1) or 1 microg x kg(-1) x min (-1) IV (Group 2). Pancuronium (0.1 mg/kg IV) was administered for muscle relaxation. Assisted ventilation followed by controlled ventilation via a mask was performed with the PaCO2 kept constant. Mean cerebral blood flow velocity (Vmean) was measured in the middle cerebral artery using a transcranial Doppler sonography system. Mean arterial pressure (MAP) was kept constant by the IV administration of norepinephrine. Measurements were made at baseline and every minute after remifentanil infusion for 10 min. Data were analyzed by using analysis of variance and a post hoc t-test (P < 0.05). Heart rate, MAP, and PaCO2 did not change over time in either group. Vmean did not change in Group 2. In contrast, there was a 31% decrease of Vmean in Group 1 (P < 0.05). The results show that large-dose, but not moderate-dose, remifentanil reduces CBFV unrelated to any changes in systemic hemodynamics in isocapnic cardiac patients. IMPLICATIONS: Transcranial Doppler sonography was used to monitor remifentanil-induced changes in cerebral perfusion. We found that large doses of remifentanil reduced cerebral blood flow velocity despite constant perfusion pressure. This may implicate a central mechanism for cerebral hemodynamic effects of remifentanil.

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

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

[Electrophysiologic arousal reactions during sufentanil-/isoflurane anesthesia]. / Elektrophysiologische Arousalreaktionen während Sufentanil-/Isofluran-Anästhesien.

PURPOSE: There is controversy about relevant EEG signal changes indicating adequate or inadequate anaesthesia. Differences of drug-induced and nociceptive mediated signal changes have not been studied in detail. The present study investigates whether signal changes during decreases of depth of anaesthesia due to surgical stimulation depend on different isoflurane concentrations during sufentanil anaesthesia. METHODS: Following IRB approval and written informed consent 28 patients (ASA: I; age 43 +/- 11 y) scheduled for elective abdominal surgery were included in the study. Anaesthesia: propofol (2.0 mg/kg) and sufentanil (1.0 micrograms/kg). Following endotracheal intubation (vecuronium 0.1 mg/kg) patients were normoventilated (P(ET)CO2: 36-38 mmHg). Randomly assigned to steady-state anaesthesia (group 1: P(ET)Isoflurane 0.2%, (14n); group 2: P(ET)Isoflurane 0.6%, (14n) during the start of surgery. Monitoring: heart rate (HF), mean arterial blood pressure (MAP), P(ET)CO2, arterial oxygen saturation and rectal temperature. EEG (16 channels referenced to Cz; CATEEM, Medisyst, Linden) recorded 5 min before until 10 min after the start of surgery. EEG-analysis (FFT: 4s, 256/s, 0.45-35.0 Hz): topographical distribution of power spectral densities (delta, theta, alpha 1, and alpha 2). Artifact control: ECG and EOG. RESULTS: Surgical stimulation resulted in increases of MAP in both groups (p < 0.05 vs BL), whereas HR was only slightly affected in group 2 when compared with BL. Other variables except of EEG data did not change over time. In group 1 (0.2% isoflurane) surgical stimulation resulted in decreases of delta over the whole cortex (F2, C3, P3, O1) and in marked increases of alpha predominantly at central leads (C3)(p < 0.05 vs BL). In group 2 (0.6% isoflurane) nociceptive stimulation was associated with decreases of faster waves (alpha: F3)(p < 0.05 vs BL) and increases in delta at fronto-central areas (F3, C3)(p < 0.05 vs BL). CONCLUSIONS: EEG recordings are useful in assessing pharmacodynamic drug effects. In contrast, intraoperative EEG recordings have a low correlation to clinical signs of changes in the anaesthetic state. Previous studies demonstrate paradoxical EEG-arousal reactions during isoflurane anaesthesia. The present data suggest that classical or even paradoxical EEG arousal due to nociceptive stimulation may depend on the isoflurane concentration. It seems reasonable that the ascending reticular formation is functionally blocked by isoflurane in a dose-dependent manner.

Physostigmine prevents postanesthetic shivering as does meperidine or clonidine.

BACKGROUND: Postanesthetic shivering develops in as many as one half of patients recovering from isoflurane anesthesia. Cholinergic stimulation of the hypothalamic-pituitary-adrenal axis and adrenal medulla by physostigmine enhances secretion of arginine vasopressin, epinephrine, and norepinephrine. Because the hypothalamus is the dominant thermoregulatory controller in mammals, and these neurotransmitters may be involved in body temperature control, physostigmine administration may influence the incidence of shivering. Accordingly, the authors tested the hypothesis that physostigmine administration inhibits postanesthetic shivering. Its efficacy was compared with that of saline (negative control) and meperidine and clonidine (positive controls). METHODS: Sixty patients having surgery of the ear or nose were tested. General anesthesia was induced with 2 mg/kg propofol, 0.1 mg/kg vecuronium, and 1.5 microg/kg fentanyl and maintained with isoflurane (1.5 +/- 0.4%) in 70% nitrous oxide. At the end of surgery, the patients were randomly assigned to receive an intravenous bolus of 0.04 mg/kg physostigmine, isotonic saline, 0.5 mg/kg meperidine, or 1.5 microg/kg clonidine. Heart rate, mean arterial blood pressure, oxygen saturation, visual analog pain score, temperature, and postanesthetic shivering were measured during recovery. RESULTS: Postanesthetic shivering occurred in 6 of 15 (40%) patients given saline. In contrast, postanesthetic shivering was significantly reduced in physostigmine-treated patients (1 of 15, or 7%) and was absent in patients given clonidine or meperidine. CONCLUSIONS: Physostigmine inhibited shivering as well as did two established treatments, meperidine and clonidine. These data suggest that cholinergic systems contribute to the genesis and control of postanesthetic shivering.

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

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

Transmyocardial laser revascularization induces cerebral microembolization.

BACKGROUND: Transmyocardial laser revascularization may vaporize fluid in the left heart, allowing bubbles to form. This study aimed to determine whether the laser pulse resulted in cerebral emboli and to examine changes in middle cerebral artery flow velocity and jugular bulb oxygen saturation (SjO2) during transmyocardial laser revascularization. METHODS: Twelve patients (American Society of Anesthesiologists physical status III) were studied after the authors received institutional review board approval and the patients' informed consent. Monitored variables included mean arterial blood pressure (measured in millimeters of mercury), heart rate (measured as beats/min), and partial pressure of carbon dioxide (measured in millimeters of mercury). A 5-MHz transesophageal-sonography system was used to record intraventricular events after laser injection. Mean blood flow velocity (Vmean; measured in centimeters per second) was monitored in the middle cerebral artery using transcranial Doppler sonography, and SjO2 (expressed as a percentage) was measured using a fiberoptic thermodilution catheter placed in the right jugular bulb. Data were recorded before, during, and for 4 min after laser injection. RESULTS: After laser injection, intraventricular echogenic contrast was seen in transesophageal-sonography, and 2-4 s later high-intensity signals (microemboli) appeared in the transcranial Doppler sonography spectra. As long as mean arterial pressure remained stable during the observation period, Vmean and SjO2 did not change. CONCLUSIONS: These data show that microemboli can be detected after laser injection in the middle cerebral artery, although they do not effect Vmean and SjO2. The results suggest that these microemboli do not induce a global oxygen imbalance.

The effects of fentanyl and sufentanil on cerebral hemodynamics.

Our study investigated the effects of moderate doses of fentanyl and sufentanil versus high-dose sufentanil on cerebral hemodynamics by using transcranial Doppler ultrasonography (TCD). Thirty American Society of Anesthesiologists (ASA) II and III patients scheduled for elective coronary artery bypass graft (CABG) were studied after Institutional Review Board (IRB) approval and informed consent. The evening before surgery, all patients received oral flurazepam (1 mg/kg), Atropine (0.4 mg/70 kg s.c.) and a combination of droperidol (70 micrograms/kg s.c.) plus fentanyl (1.5 micrograms/kg s.c.) were given as preanesthetic medication 1 h before induction of anesthesia. Anesthesia was induced with either 25 micrograms/kg fentanyl i.v. (group 1, n = 10), 3 micrograms/kg sufentanil i.v. (group 2, n = 10) or 6 micrograms/kg sufentanil i.v. (group 3, n = 10). All patients received 100 micrograms/kg pancuronium i.v. With the induction of respiratory depression, assisted ventilation was performed followed by controlled ventilation to maintain normoxia and normocapnia (FiO2, 1.0). Cerebral blood flow velocity (CBFV, cm/s) was measured continuously in the middle cerebral artery by using a bidirectional 2-MHz TCD system. Monitoring included heart rate (HR, beats/min), direct mean arterial blood pressure (MAP, mm Hg), and PaCO2. Physiologic variables including arterial blood gases were measured at baseline, 5 min, and 10 min after infusion of fentanyl or sufentanil. In all patients, HR, MAP, end-tidal carbon dioxide tension (PetCO2), and PaCO2 were constant over time and did not differ between groups. CBFV did not change with moderate doses of fentanyl (group 1) or sufentanil (group 2). In contrast, infusion of high-dose sufentanil (group 3) was associated with 27 to 30% decreases in CBFV (p < 0.05). Our results suggest that sufentanil decreases CBFV in a dose-related fashion with a threshold effect. Increases in CBFV and CBF seen in previous studies may be related to an increasing PaCO2 when maintenance of normocarbia is based on only real-time capnography with a constant PetCo2 rather than additional arterial blood gas monitoring.

Administration of sufentanil and nitrous oxide blunts cardiovascular effects of desflurane but does not prevent an increase in middle cerebral artery blood flow velocity.

Desflurane has been reported to cause tachycardia and hypertension during induction of anaesthesia. The aim of this study was to determine the effects of desflurane on cerebral blood flow (CBF) velocity using transcranial Doppler ultrasonography in a setting that closely resembled usual clinical practice. In two groups (n = 9 in each) ASA Grade I or II patients, anaesthesia was induced with etomidate and vecuronium intravenously (i.v.), sufentanil (0.3 microgram kg-1 i.v.) was added in the second group. Patients were ventilated by facemask for 2 min before desflurane was administered in steps of 0.5 MAC min-1 until 1.5 MAC was reached and maintained for 7 min. Haemodynamic variables and CBF velocity in the middle cerebral artery (MCA) were monitored throughout the study period. In group 1 heart rate increased to 108 +/- 2 b.p.m. (37% increase) whereas MAP increased to 114 +/- 6 mmHg after administration of desflurane (33% increase). CBF velocity increased to 86 +/- 7 cm s-1 (69% increase). In group 2 no significant changes in systemic haemodynamic responses were measured after desflurane administration; however, CBF velocity increased to 73 +/- 5 cm s-1 (59% increase). The results indicate that desflurane increases CBF velocity concurrently with induction of tachycardia and hypertension. Although sufentanil and N2O attenuate the systemic haemodynamic alterations caused by desflurane, the CBF velocity increases. These data suggest that the abrupt addition of desflurane may have adverse consequences in patients at risk for intracranial hypertension.

Jugular bulb oxygen saturation and middle cerebral blood flow velocity during cardiopulmonary bypass.

This study investigates changes of jugular bulb oxygen saturation (SjO2) measured by fiberoptic jugular bulb oximetry and changes of intracranial hemodynamics using transcranial Doppler sonography (TCD) during cardiopulmonary bypass (CPB) for coronary artery bypass graft (CABG) in 17 ASA III patients. Anesthesia was maintained with fentanyl, midazolam, and continuous infusion of etomidate. Hypothermic CPB (27 degrees C) was managed according to alpha-stat conditions. SjO2 (%) was measured by a fiberoptic catheter (Opticath F 5.5; Abbott Critical Care Systems) placed in the right jugular bulb via the right internal jugular vein. Mean blood flow velocity (Vmean, cm/s) was measured in the middle cerebral artery using a bidirectional 2-MHz TCD system (Transpect, Medasonics). Data were recorded continuously from the beginning to the end of the CPB. During cooling and hypothermia (27 degrees C); SjO2 and Vmean did not change compared with values at the start of CPB. However, with the beginning of rewarming, Vmean was increased 65% compared with stable hypothermia (27 degrees C). This increase in Vmean was associated with a 25% decrease in SjO2. Maximum desaturation occurred at a 36 degrees C jugular bulb temperature. During cooling and stable hypothermia, global oxygen balance and intracerebral perfusion seemed to be maintained. However, a major alteration in the balance of the cerebral oxygen supply and demand may occur in response to rewarming despite increases in Vmean. Findings suggest inadequate increases in CBF to meet cerebral metabolic demand. Further investigations need to validate these findings with biochemical techniques and neuropsychological tests.