Leena Lindgren

Epileptiform Electroencephalogram during Mask Induction of Anesthesia with Sevoflurane

BACKGROUND Sevoflurane is suggested as a suitable anesthetic agent for mask induction in adults. The authors recently found that hyperventilation during sevoflurane-nitrous oxide-oxygen mask induction is associated with cardiovascular hyperdynamic response. We tested the hypothesis that the hyperdynamic response can be explained by electroencephalography (EEG) findings. METHODS Thirty women were randomly allocated to receive sevoflurane-nitrous oxygen-oxygen mask induction using a single-breath method, followed by either spontaneous breathing (n = 15) or controlled hyperventilation (n = 15) for 6 min. EEG was recorded. Blood pressure and heart rate were recorded at 1-min intervals. RESULTS Epileptiform EEG activity (spikes or polyspikes) was seen in all patients with controlled hyperventilation, and in seven patients with spontaneous breathing (P < 0.01). Jerking movements were seen in three patients with controlled hyperventilation. In the controlled hyperventilation group, heart rate increased 54% from baseline at 4 min after induction (P < 0.001). Mean arterial pressure increased 17% (P < 0.05), peaking at 3 min. In the spontaneous breathing group, heart rate showed no change, and mean arterial pressure decreased by 14% (P < 0.01) at 6 min. Heart rate and mean arterial pressure differed significantly between the groups from 2 min after beginning of the induction to the end of the trial. An increase in heart rate of more than 30% from baseline always was associated with epileptiform EEG activity. CONCLUSIONS Sevoflurane mask induction elicits epileptiform EEG patterns. These are associated with an increase in heart rate in patients with controlled hyperventilation and also during spontaneous breathing of sevoflurane.

Effects of Halothane, Enflurane, and Isoflurane on Hypoxic Pulmonary Vasoconstriction in Rat Lungs In Vitro

Rat lungs were ventilated and perfused at a constant rate in vitro. The maximal hypoxic pulmonary vasoconstrictor (HPV) response was recorded by measuring the pulmonary artery pressure change when the inspired oxygen concentration was changed from 21% to 3% (with 5.5% carbon dioxide) in the absence of anesthetic vapor.In different experimental groups, the effects of halothane, enflurane, and isoflurane on HPV were examined. In random order the anesthetics were added to the inspired gas in concentrations of 0.25, 0.5, 1, 1.5, and 2 or 2.5 MAC units. The HPV pressor response to 3% oxygen in the presence of anesthetic agent was expressed as a per cent of the pressure response observed in the absence of anesthetic (R%MAX).All three agents depressed HPV in a dose-related manner. The concentrations in MAC units at which 50% depression of HPV (ED50) occurred was 0.47, 0.60, and 0.56 for halothane, isoflurane, and enflurane, respectively, and neither the ED50 values nor the slopes of these dose response curves were significantly different.It was concluded that these halogenated general anesthetics inhibit HPV with essentially the same potency.

Influence of Mixed Venous Oxygen Tension (PVO2) on Blood Flow to Atelectatic Lung

The influence of mixed venous oxygen tension (PVO2) on blood flow to the atelectatic left lung was studied at normal and reduced cardiac outputs (CO) using extracorporeal veno-venous bypass in six pentobarbital anesthetized, mechanically ventilated dogs. Aortic and left pulmonary artery flows; airway, left atrial, central venous, pulmonary, and systemic arterial pressures; hemoglobin, arterial, and mixed venous blood gases were measured. The blood flow reduction observed in atelectasis was altered by the PVO2. Approximately 50% of blood flow was diverted away from atelectatic lung when PVO2 was low (24 ± 2 mmHg) or normal (46 ± 2 mmHg) (mean left lung blood flow [VL] was 23.2 ± 4.6% with low PVO2 and 19.0 ± 3.4%, with normal PVO2). When PVO2I was increased to greater than 100 mmHg, diversion of blood flow away from atelectatic lung did not occur and VL% was nearly the flow expected for normoxic ventilated left lung (mean VL% = 40.4 ± 5.9%). Shunt (VS/VT%) was significantly greater when PVO2 was high than when it was normal or low (mean VS/VT% = 51.7 ± 5.6%, 31.0 ± 3.1%, 26.0 ± 3.4% with high, normal, and low PVO2, respectively). Mean PVO2 was significantly greater when PVO22 was high than when PVO2 was normal or low, despite the increase in VL% and VS/VT% (PVO2 = 327 ± 25 mmHg, 220 ± 32 mmHg, 115 + 21 mmHg with high, normal, and low PVO2, respectively). A 40% reduction in cardiac output significantly decreased transmural pulmonary artery pressure but did not affect PVO2, VS/VT%i or VL%- The mechanism of blood-flow reduction to atelectatic lung is therefore hypoxic pulmonary vasoconstriction, determined by the PVO2. The contribution of mechanical factors in reducing blood flow to atelectatic lung in the open chest is small

Increases in hemodynamic variables and catecholamine levels after rapid increase in isoflurane concentration

Background:Ventilation of the lungs with isoflurane in nitrous oxide and oxygen has been shown to increase the plasma concentration of norepinephrine. Whether this increase is related to the tachycardia and increased arterial blood pressures, seen following a sudden increase in the concentration of isoflurane, was tested in humans. Methods:Twenty-two healthy patients in whom the trachea was intubated were given 15 min of stable isoflurane-O2-air anesthesia [end-tidal concentration of isoflurane (ETISO) of 1.3%] (baseline). Patients were then randomly allocated to one of two groups. For 13 “IsoHigh,” patients, the inspired concentration of isoflurane was increased abruptly. In those patients, the F.TISO was kept at 2.6% for 10 min, i.e., until the end of the study, after which the depth of anesthesia was reduced. For nine “IsLOW” control patients, the ETITO level of 1.3% was continued until the end of the study. Heart rate, arterial pressures, catecholamine levels, and end-tidal concentration of CO2 were recorded at baseline and at 1, 1.5, 2, 4, 6, and 10 min after increase in isoflurane. Results:Isomgh, patients showed significant increases in heart rate (40%, from 84.6 to 118.1 beats/min), systolic arterial pressure (SAP, 23%, from 96.4 to 118.3 mmHg), and diastolic arterial pressure (DAP, 30%, from 53.9 to 70.0 mmHg); all three variables peaked at 2 min. Significant increases occurred also in norepinephrine levels (80%, from 0.342 to 0.615 ng/ml) and in end-tidal concentration of CO2 (from 4.22% to 4.43%), both of which peaked at 4 min. Epinephrine levels did not increase significantly, although significant differences were seen between Isomgh, and IsoLow patients during the trial. IsoLow patients had no changes in these variables. Conclusions:A sudden Increase in isoflurane concentration is associated with a transient but clinically significant increase in heart rate, arterial pressures, and noreplnephrine concentration.

Pulmonary Blood Pressure and Flow during Atelectasis in the Dog

The purpose of the study was to measure the time course, direction, and magnitude of the hypoxic pulmonary vasoconstriction (HPV) response to atelectasis. Six dogs were anesthetized with pentobarbital. With the chest open, each lung was ventilated separately, Pulmonary blood flow was measured with electromagnetic flow probes. Pulmonary arterial, left atrial, and systemic arterial pressures were measured via indwelling catheters. The right lung was ventilated continuously with 100% O2, while the left lung was either ventilated with 100% O2, (control phase), unventilated (4 hours of atelectasis), or ventilated with a gas mixture containing 4% O2, 3% CO2, and 93% N2 (hypoxia phase). Left lung atelectasis resulted in a reduction of the per cent left lung blood flow from 43 ± 4% (mean ± SE) to 25 ± 7% at 15 min and to 12 ± 1% at 60 min which persisted for the remaining four-hour period. The per cent left lung blood flow was significantly lower (8 ± 1%) and the Pao2 significantly higher (356 ± 38 mmHg) during the maximal response to atelectasis as compared to 15 min of hypoxic ventilation (23 ± 5%; 211 ± 21 mmHg). With atelectasis or hypoxic ventilation, pulmonary perfusion pressure was increased significantly from the control value of 7.9 ± 0.8 mmHg to approximately 11 mmHg.The present study demonstrated that in the open chest model without systemic hypoxemia, the response to acute atelectasis is a regional increase in pulmonary vascular resistance which develops quickly (15 min) and is maximal by 60 min and is maintained thereafter. As a result, there is a sustained diversion of blood flow away from the atelectatic lung and a generalized increase of pulmonary perfusion pressure.

QT dispersion after subarachnoid hemorrhage.

Subarachnoid hemorrhage (SAH) causes a stress response with increased concentrations of plasma catecholamines and serious cardiac arrhythmias. Increased QT dispersion has been shown to predispose to cardiac arrhythmias. In SAH patients, QT dispersion has not been studied previously. QT dispersion was analyzed in 26 patients with SAH and in 16 patients (control group) scheduled for ligation of a nonruptured cerebral aneurysm. In 15 patients with SAH, the plasma concentrations of catecholamines were analyzed, and an 18-hour continuous electrocardiogram (ECG) recording was obtained. In the other 11 patients, electrocardiography was repeated daily for up to 9 days for analysis of QT dispersion. The median (25th and 75th percentiles) QT dispersion in all SAH patients was 78 milliseconds (50 and 109 milliseconds, respectively), and in control patients, it was 25 milliseconds (15 and 33 milliseconds, respectively) (P < .001). There was a positive correlation with QT dispersion and the plasma concentration of DHPG, a metabolite of norepinephrine (P < .05). All patients had episodes of cardiac arrhythmia during the 18-hour recording period. In conclusion, increased QT dispersion is a common finding after SAH and may be a result of high plasma concentrations of catecholamines in these patients.

Vibration stimulus induced EEG bursts in isoflurane anaesthesia

The EEG and heart rate reactions to vibration stimulus were studied in 14 patients during moderately deep surgical isoflurane anaesthesia, at a level when EEG showed a burst suppression pattern. Vibration applied to the palm of the hand induced bursts in EEG in 12 patients, usually with a latency of about 0.5 sec from the onset, or from the end of the 3 sec stimulus. Increases in heart rate were seen at bursts related to both vibration onset and offset, as well as at spontaneous bursts. With spontaneous bursts, an initial positive wave was frequently seen. In 6 patients the vibration induced bursts were different in shape from the spontaneous bursts; no initial positive wave was seen before the negative DC shift in Cz-Fz recording. We conclude that EEG bursts can be evoked by a non-noxious stimulus such as vibration in patients during isoflurane anaesthesia.

Poor Antibacterial Effect of Ropivacaine Comparison with Bupivacaine

ROPIVACAINE (1-propyl-29,69-pipecoloxylidide) is a long-acting aminoamide local anesthetic that has been introduced into clinical use in the last few years, largely as a replacement for bupivacaine. Bupivacaine has been reported to possess a significant antibacterial effect. Because data regarding ropivacaine are not available, we compared the antibacterial effects of clinically appropriate concentrations of ropivacaine and bupivacaine in a laboratory setting.

The effect of amrinone on recovery from severe bupivacaine intoxication in pigs.

Cardiovascular collapse following intravascular bupivacaine may be resistant to treatment. The effect of amrinone on recovery from bupivacaine-induced severe cardiovascular depression was evaluated in 20 pigs (13-26 kg) in a placebo-controlled randomized double-blind study. Under 0.7% isoflurane anesthesia at FIO2 0.21, 0.5% bupivacaine 2 mg.kg-1.min-1 was infused until mean arterial pressure was 40% of the baseline. Cardiac output and heart rate decreased 75% and 50% from the baseline, respectively. The total dose of bupivacaine was 17 +/- 6 (SD) mg.kg-1 in the control and 19 +/- 5 mg.kg-1 in the amrinone group, resulting in mean plasma concentrations of 42 +/- 6 and 53 +/- 19 micrograms.ml-1, respectively. A bolus of amrinone 4 mg.kg-1 (n = 10) was given immediately after cardiovascular depression, followed by an infusion of 0.6 mg.kg-1.min-1. The control animals received corresponding volumes of physiologic saline (n = 10). After cardiovascular depression, the lungs were ventilated with FIO2 1.0 without anaesthetics or sympathomimetic support. Electric activity of the heart ceased in all control animals in 3.9 +/- 2 min after cardiovascular depression despite atropine and external cardiac compression. All animals in the control group and 5 of 10 animals in the amrinone group were given atropine (P less than 0.01). The animals receiving amrinone survived without cardiac compression (P less than 0.0001). During bupivacaine infusion, all animals developed burst suppression in the electroencephalogram. At the time of cardiovascular depression, in 8 of 10 control and in 6 of 10 amrinone animals, the electroencephalogram was isoelectric.(ABSTRACT TRUNCATED AT 250 WORDS)

Transient hyperdynamic response associated with controlled hypocapneic hyperventilation during sevoflurane-nitrous oxide mask induction in adults.

UNLABELLED We assessed hemodynamic variables during sevoflurane face mask anesthetic induction in female ASA physical status I or II patients. Anesthesia was induced with a single-breath inhalation method with 8% sevoflurane in 50% nitrous oxide in oxygen. Thirty patients were randomized either to breathe spontaneously (SB group, n = 15) or to receive controlled ventilation (CV group, n = 15) for 6 min after the loss of consciousness. Noninvasive blood pressure and heart rate (HR) were recorded at 1-min intervals. Mean +/- SD HR increased from 83+/-18 to 112+/-24 bpm at 4 min in the CV group (P < 0.001 between groups and within group compared with baseline). Mean arterial pressure increased from 97+/-9 to 106+/-26 mm Hg at 4 min in the CV group, which was significantly higher than that in the SB group (P < 0.01). In the SB group, mean arterial pressure decreased significantly, from 96+/-8 to 78+/-13 mmHg, at 6 min (P < 0.001), and HR remained unchanged. Therefore, hyperventilation should be avoided during the induction of sevoflurane anesthesia via a mask. IMPLICATIONS In this randomized, prospective study, we found that controlled hypocapneic hyperventilation delivered manually during sevoflurane/ N2O/O2 mask induction was associated with a significant transient hyperdynamic response. This kind of hemodynamic arousal can be detrimental to many patients and can be avoided by conducting sevoflurane mask induction with unassisted spontaneous breathing.