Increase in prominence of electrocardiographic J waves after a single dose of propofol in a patient with early ventricular repolarisation.

J waves appear on an electrocardiogram as an elevation of the J point in the terminal portion of the QRS complex. J waves are often benign, but may be associated with malignant ventricular arrhythmias. In some cases, such problems appear to have been precipitated by propofol infusions. We observed a sudden increase in J waves and profound hypotension following a single intravenous dose of propofol in an 84-year-old woman with early repolarisation in the inferior ventricular wall. When early repolarisation (as shown by electrocardiographic J waves) is observed in the inferior ventricular wall pre-operatively, patients should be carefully monitored. Myocardial ischaemia and the use of drugs that might worsen J waves should be avoided.

Anaesthesia for a patient with paraneoplastic limbic encephalitis with ovarian teratoma: relationship to anti-N-methyl-D-aspartate receptor antibodies.

Paraneoplastic limbic encephalitis associated with ovarian teratoma has recently been related to the development of antibodies to specific heteromers of the N-methyl-d-aspartate receptor and exhibits various manifestations including psychiatric symptoms, hypoventilation, seizures and derangement of autonomic nervous system function. Although recovery can sometimes occur spontaneously, early tumour resection with immunotherapy facilitates earlier recovery. Herein, we describe anaesthetic management of a 20-year-old woman who developed general convulsions and decreased level of consciousness, whom we suspected of having paraneoplastic limbic encephalitis and was scheduled for left ovarian tumour resection. Anaesthetic management was successful with no complications but the case acts as focus of discussion for the potential interaction of N-methyl-D-aspartate receptors and anaesthetic sensitivity.

Dynamic QRS-complex and ST-segment monitoring by continuous vectorcardiography during carotid endarterectomy.

BACKGROUND: Many authors report a high incidence of cardiac events during carotid endarterectomy. The aim of the present study was to evaluate the usefulness of dynamic continuous on-line vectorcardiography for monitoring the occurrence of myocardial ischaemia during carotid endarterectomy. METHODS: We studied 21 patients undergoing carotid endarterectomy. Patients underwent general anaesthesia with isoflurane or sevoflurane. The vectorcardiogram was monitored continuously during carotid endarterectomy. Electrodes were placed according to the previously described lead system and connected to a computerized system for on-line vectorcardiography. Two trend variables were recorded: the QRS vector difference, which reflects changes in the shape of the QRS complex; and the ST vector magnitude, which represents deflection of the ST segment from the isoelectric level. The ST segment deflection was measured 60 ms after termination of the QRS complex. RESULTS: Vectorcardiography was successfully recorded in all 21 patients. Three patients showed intraoperative vectorcardiogram abnormalities. In one of these three patients, both ST vector magnitude and QRS vector difference increased after induction of anaesthesia and ST vector magnitude returned to baseline after administration of nitroglycerin. In the other two patients, both ST vector magnitude and QRS vector difference gradually increased after cross-clamping of the internal carotid artery and ST vector magnitude returned to baseline after unclamping. QRS vector difference remained elevated for several hours in all three patients. CONCLUSIONS: Monitoring ST vector magnitude and QRS vector difference by vectorcardiography may be useful for identifying myocardial ischaemia during carotid endarterectomy.

Effects of acute normovolemic hemodilution on ventriculoarterial coupling in dogs.

BACKGROUND: Acute normovolemic hemodilution (ANH) causes a decrease in systemic vascular resistance. Similar to vasodilating drugs, ANH might modify ventriculoarterial coupling. Left ventricular elastance (Ees), effective arterial elastance (Ea), stroke work (SW), and pressure volume area (PVA) were used as indicators to examine the effects of ANH on this coupling. METHODS: After institutional approval eight dogs were anesthetized with isoflurane and subjected to measurements including aortic pressure, left ventricular (LV) pressure, and LV volume. Left ventricular volume was measured with a conductance catheter. Ees was determined as the slope of the end-systolic pressure-volume relationship. Ea was determined as the ratio of LV end-systolic pressure to stroke volume. Ventriculoarterial coupling was evaluated as the ratio of Ees to Ea. Mechanical efficiency, another criterion for ventriculoarterial coupling, was calculated as the ratio of SW to PVA. Data are expressed as mean+/-SD, and P<0.05 was considered significant. RESULTS: Normovolemic exchange of 50 ml kg-1 of blood for 6% hydroxyethyl starch (ANH50) reduced hemoglobin concentration from 12.8+/-3.0 g dl-1 to 6.4+/-1.3 g dl-1. Acute normovolemic hemodilution 50 did not change Ees significantly although it significantly decreased Ea. Left ventricular elastance/Ea did not change after ANH (1.0+/-0.4 at baseline and 1.2+/-0.5 at ANH50). Acute normovolemic hemodilution 50 significantly increased SW and PVA, preventing SW/PVA from changing significantly after ANH (0.57+/-0.10 at baseline and 0.62+/-0.14 at ANH50). CONCLUSION: Before ANH, ventriculoarterial coupling was so matched as to maximize SW at the expense of the work efficiency. This relation was preserved at ANH50.

Lidocaine and mexiletine inhibit mitochondrial oxidation in rat ventricular myocytes.

BACKGROUND: Accumulating evidence suggests that mitochondrial rather than sarcolemmal adenosine triphosphate-sensitive K+ (K(ATP)) channels may have an important role in the protection of myocardium during ischemia. Because both lidocaine and mexiletine are frequently used antiarrhythmic drugs during myocardial ischemia, it is important to investigate whether they affect mitochondrial K(ATP) channel activities. METHODS: Male Wistar rats were anesthetized with ether. Single, quiescent ventricular myocytes were dispersed enzymatically. The authors measured flavoprotein fluorescence to evaluate mitochondrial redox state. Lidocaine or mexiletine was applied after administration of diazoxide (25 microM), a selective mitochondrial K(ATP) channel opener. The redox signal was normalized to the baseline flavoprotein fluorescence obtained during exposure to 2,4-dinitrophenol, a protonophore that uncouples respiration from ATP synthesis and collapses the mitochondrial potential. RESULTS: Diazoxide-induced oxidation of flavoproteins and the redox changes were inhibited by 5-hydroxydecanoic acid, a selective mitochondrial K(ATP) channel blocker, suggesting that flavoprotein fluorescence can be used as an index of mitochondrial oxidation mediated by mitochondrial K(ATP) channels. Lidocaine (10(-3) to 10 mM) and mexiletine (10(-3) to 10 mM) reduced oxidation of the mitochondrial matrix in a dose-dependent manner with an EC50 of 98+/-63 microM for lidocaine and 107+/-89 microM for mexiletine. CONCLUSIONS: Both lidocaine and mexiletine reduced flavoprotein fluorescence induced by diazoxide in rat ventricular myocytes, indicating that these antiarrhythmic drugs may produce impairment of mitochondrial oxidation mediated by mitochondrial K(ATP) channels.

Bronchospasm induced by cardiopulmonary bypass.

Severe bronchospasm during cardiopulmonary bypass (CPB) is an unusual event. A 16-year-old girl with pulmonary stenosis who underwent reconstruction of the right ventricle outflow tract experienced severe bronchospasm following CPB. Just after the initiation of the partial CPB, high inspiratory airway pressure was suddenly recognized. The lung had become too stiff for the anesthetic circuit bag to be squeezed by hand. Tracheobronchial obstruction was ruled out by investigation with a fiberoptic bronchoscope. A presumptive diagnosis of severe bronchospasm was made, and aggressive bronchodilator therapy was instituted. The attack was successfully treated with aggressive bronchodilator therapy. Although the exact causes for bronchospasm in our case are not clear, CPB factors, such as the release of complements and allergic reactions might have induced the attack under relatively light anesthetic state.

Pulmonary arterial pressure can be estimated by transesophageal pulsed doppler echocardiography.

We examined whether pulmonary arterial pressure can be estimated on the basis of pulmonary arterial flow velocity determined via intraoperative pulsed Doppler transesophageal echocardiography (TEE) in 20 patients undergoing cardiac surgery. Standard pulmonary artery measurements were taken as well. Measurements were taken before sternotomy, after pericardiotomy, after cardiopulmonary bypass, and after sternum closure. The variables obtained by TEE included preejection period (PEP), acceleration time (AT), right ventricular ejection time (RVET), and R-R interval (RR). Five ratios were calculated as indices of pulmonary arterial pressure--PEP/AT, PEP/RVET, AT/RVET, PEP/ square root of RR, and AT/ square root of RR--and were compared with pulmonary artery catheterization findings, i.e., systolic pulmonary arterial pressure (sPAP), log sPAP, mean PAP (mPAP), and log mPAP. Before sternotomy, PEP/AT, PEP/ square root of RR, and AT/ square root of RR showed significant correlation with all pulmonary artery catheterization values. AT/RVET showed correlation with all pulmonary artery values except log mPAP. PEP/AT showed the closest correlation with sPAP (r = 0.771) and log sPAP (r = 0.789). PEP/AT also showed close correlation with mPAP (r = 0.764) and log mPAP (r = 0.777). Significant agreement between sPAP and mPAP values calculated from a regression equation and values measured via pulmonary artery catheter was observed by plotting the differences against the mean values of the two measurements. We therefore conclude that noninvasive estimation of pulmonary arterial pressure is feasible via intraoperative TEE when sternotomy is not involved.

Intraoperative evaluation of pulmonary artery flow during the Fontan procedure by transesophageal Doppler echocardiography.

After the Fontan procedure, pulmonary artery (PA) flow is maintained without right ventricular pump function. We evaluated intraoperative PA flow velocity patterns using transesophageal Doppler echocardiography (TEE) immediately after cardiopulmonary bypass (CPB) in patients during Fontan or hemi-Fontan procedures. We studied 10 patients with single-ventricle physiology (age range, 5 mo to 3 yr 1 mo). Anesthesia was induced and maintained with fentanyl. After induction of anesthesia, a pediatric TEE probe was inserted into the esophagus. All patients had surgical repair involving direct anastomosis of the right atrium to the PA. Immediately after completion of CPB, adequacy of the atriopulmonary anastomosis was assessed and PA flow velocity was recorded. In all patients, the atriopulmonary anastomosis was clearly defined using a single-plane TEE probe, and PA flow recording was completed successfully. Intraoperative PA flow velocities showed two distinct patterns. Biphasic forward flows with peak velocities during systole and diastole were observed in six patients. The remaining four patients showed forward flows with flow reversals. The four patients demonstrating flow reversals showed significantly reduced fractional shortening (26.5+/-2.1% vs. 35.5+/-6.3%) and larger pressure gradient between the right atrium and left atrium (10.8+/-1.3 mm Hg vs 8.0+/-0.9 mm Hg) when compared to those without reverse flow. Two patients with reverse flow required reoperation because of hypotension. Because PA flow is influenced by pulmonary vascular resistance and left ventricular function, TEE assessed intraoperative PA flow should be further evaluated as a useful predictor of surgical outcome after a Fontan procedure.

Transesophageal echocardiographic assessment of pulmonary arterial and venous flow during high-frequency jet ventilation.

STUDY OBJECTIVE: To evaluate high-frequency jet ventilation (HFJV) effects on pulmonary arterial and venous flow compared to those of intermittent positive-pressure ventilation (IPPV) by using pulsed Doppler transesophageal echocardiography. DESIGN: Prospective clinical study. SETTING: University-affiliated hospital operating room. PATIENTS: 13 ASA physical status I and II patients undergoing lower abdominal or lower extremity surgery. INTERVENTIONS: PATIENTS had total IV anesthesia with propofol and fentanyl. After anesthesia induction, a transesophageal echocardiography probe was inserted into the esophagus. IPPV (TV, 8-10 mL/kg; respiratory rate, 10-12 cycles/min; I/E ratio, 1:2; FIO(2), 1.0) and HFJV (driving pressure, 0.5-0.6 kgf/cm(2); frequency,3 Hz; I/E ratio, 1:1; FIO(2), 1.0) were performed under hemodynamically stable conditions. MEASUREMENTS: Pulmonary-arterial-flow velocity, pulmonary-venous-flow velocity, left ventricular short-axis view, and airway-pressure curve were recorded simultaneously. Parameters measured were: hemodynamic variables, arterial blood gases, inspiratory airway pressure; [from pulmonary-arterial-flow velocity] pre-ejection period (PEP), acceleration time (AT), right ventricular ejection time (RVET), and their ratios (PEP/AT, AT/RVET); [from pulmonary-venous-flow velocity] time-velocity integral of the first systolic wave (S1), second systolic wave (S2), and diastolic wave (D), and systolic fraction (integral S1 + S2/S1+ S2 + D); [from M-mode] left-ventricular-end systolic volume, left-ventricular-end diastolic volume (LVEDV), stroke volume, cardiac output, and ejection fraction, using Teichholz's method. MAIN RESULTS: Peak inspiratory airway pressure during HFJV was significantly lower than that during IPPV. HFJV significantly decreased PEP/AT, correlating positively with pulmonary arterial pressure, and significantly increased AT and AT/RVET, correlating negatively with pulmonary arterial pressure. Systolic fraction, correlating negatively with left atrial pressure, increased significantly during HFJV, as did LVEDV, stroke volume, cardiac output, and ejection fraction. CONCLUSIONS: Our results suggest that, in comparison to IPPV, HFJV significantly decreases pulmonary arterial pressure and left atrial pressure, resulting in significant increases in cardiac output and ejection fraction in healthy anesthetized adults.

Cyclic variation of integrated ultrasound backscatter in the left ventricle during the early neonatal period.

BACKGROUND: Significant changes in the contractility and histologic structure of the ventricular myocardium occur during the early neonatal period. Cyclic variation (CV) of ultrasonic integrated backscatter (IBS) reflects myocardial contractile performance. The aim of this study was to define normal values of and its serial changes in CV of IBS in the left ventricle of normal neonates. METHODS AND RESULTS: We recorded long-axis IBS images in 169 healthy neonates within 14 days after birth (mean 4.6 +/- 4.2 days) and in 84 infants and children (mean age 8.7 +/- 5.2 years). For each, we obtained CV of IBS in the interventricular septum (CV(IVS)) and the posterior wall (CV(PW)). In neonates, there was a significant linear correlation between CV and date after birth in measurements of both the interventricular septum and the posterior wall (r = 0.57 and 0. 60, respectively). In infants and children, there was no significant relation between age and CV(IVS) or CV(PW). In neonates >4 days after birth, the magnitude of CV(IVS) was not significantly different from that in infants or children. By contrast, the magnitude of CV(PW) was still significantly decreased in neonates >9 days after birth compared with that in infants and children (P <. 005). The ratio of CV(IVS) to CV(PW) (CV(IVS)/CV(PW)) was significantly higher in neonates than in infants and children (0.99 +/- 0.29 vs 0.80 +/- 0.22, P <.001). CONCLUSIONS: Both CV(IVS) and CV(PW) in neonates gradually increase after birth, indicating developmental maturation of the left ventricle. High values of CV(IVS)/CV(PW) might reflect the remnant of relatively high contractile performance in the right ventricle during fetal life.

Nitric oxide does not play a major role in the regulation of systemic hemodynamic responses to acute normovolemic hemodilution.

BACKGROUND: The mechanisms of cardiovascular changes following acute normovolemic hemodilution (ANH) have not been fully elucidated. We tested the hypothesis that inhibition of nitric oxide synthesis attenuates ANH-induced cardiovascular responses. METHODS: We observed the effects of N(omega)-nitro-L-arginine methyl ester (L-NAME) pretreatment on ANH-induced cardiovascular responses and compared these effects with those elicited by phenylephrine (PHE). Twenty dogs anesthetized with isoflurane were divided into two groups: one group was pretreated with L-NAME and the other with PHE. Both groups were normovolemically hemodiluted using 6% hydroxyethyl starch to reduce the hemoglobin concentration to approximately 50% of the pretreatment value. RESULTS: Pretreatment with either L-NAME or PHE caused a significant increase in mean aortic blood pressure (MAP) and systemic vascular resistance (SVR) with a significant decrease in cardiac output (CO) and stroke volume (SV). However, no remarkable differences in these variables were seen between groups. In both groups ANH produced increases in heart rate, CO, SV, and maximal left ventricular dP/dt with a significant decrease in SVR. No significant differences in these variables were apparent after ANH except that MAP was decreased in the PHE group but not in the L-NAME group. CONCLUSION: Our results suggest that nitric oxide does not play a major role in mediation or modulation of the systemic vascular responses to ANH.

Blockade of adenosine triphosphate-sensitive potassium channels by thiamylal in rat ventricular myocytes.

BACKGROUND: The adenosine triphosphate (ATP)-sensitive potassium (KATP) channels protect myocytes during ischemia and reperfusion. This study investigated the effects of thiamylal on the activities of KATP channels in isolated rat ventricular myocytes during simulated ischemia. METHODS: Male Wistar rats were anesthetized with ether. Single, quiescent ventricular myocytes were dispersed enzymatically. Membrane currents were recorded using patch-clamp techniques. In the cell-attached configuration, KATP channel currents were assessed before and during activation of these channels by 2,4-dinitrophenol and after administration of 25, 50, and 100 mg/l thiamylal. The open probability was determined from current-amplitude histograms. In the inside-out configuration, the current-voltage relation was obtained before and after the application of thiamylal (50 mg/1). RESULTS: In the cell-attached configuration, 2,4-dinitrophenol caused frequent channel opening. 2,4-Dinitrophenol-induced channel activities were reduced significantly by glibenclamide, suggesting that the channels studied were KATP channels. Open probability of KATP channels was reduced by thiamylal in a concentration-dependent manner. KATP channels could be activated in the inside-out configuration because of the absence of ATP. Thiamylal inhibited KATP channel activity without changing the single-channel conductance. CONCLUSIONS: The results obtained in this study indicate that thiamylal inhibits KATP channel activities in cell-attached and inside-out patches, suggesting a direct action of this drug on these channels.

Recurrent laryngeal nerve palsy after cardiovascular surgery: relationship to the placement of a transesophageal echocardiographic probe.

OBJECTIVE: To examine the relationship between the incidence of recurrent laryngeal nerve palsy after cardiovascular surgery and the placement of a transesophageal echocardiographic probe. DESIGN: A prospective clinical study. SETTING: A single-institutional study in a university hospital. PARTICIPANTS: One hundred sixteen patients undergoing cardiovascular surgery. INTERVENTIONS: All patients were assigned into one of two groups: 64 patients in whom transesophageal echocardiography (TEE) was performed and 52 patients in whom TEE was not performed during surgery. The incidence of recurrent laryngeal nerve palsy was examined and compared between the two groups. MEASUREMENTS AND MAIN RESULTS: Five of 64 patients (7.8%) in whom TEE was monitored and 3 of 52 patients (5.8%) in whom TEE was not monitored were diagnosed with recurrent laryngeal nerve palsy postoperatively. There was no statistically significant difference between the incidence of recurrent laryngeal nerve palsy in patients with intraoperative TEE monitoring, and patients without it. The durations of surgery, anesthesia, and cardiopulmonary bypass were significantly longer in patients with nerve palsy than those without it. CONCLUSION: These results suggest that placement of the transesophageal echocardiographic probe is not responsible for postoperative recurrent laryngeal nerve palsy. It seems likely that surgical manipulation itself and the durations of surgery, cardiopulmonary bypass, and tracheal intubation are related to the incidence of laryngeal nerve palsy.

The feasibility of gastrothoracic ventricular pacing during transesophageal echocardiography.

UNLABELLED: We evaluated whether ventricular pacing is possible using pacing electrodes attached to a transesophageal echocardiography (TEE) probe in 20 patients undergoing elective cardiovascular surgery. A bipolar pacing lead was fixed with silicone adhesive anteriorly to the TEE probe with the distal electrode 25 mm from the TEE probe tip. The TEE probe was positioned to obtain a transgastric short-axis view of the left ventricle. The distal or proximal electrode on the TEE probe was the cathode; the chest electrode placed at the V5 lead position was the anode. Gastrothoracic ventricular pacing (GVP) was performed at 100 bpm at 30- or 50-ms pulse duration. Transgastric ventricular pacing (TVP) was also attempted using both TEE probe electrodes alternately as cathode/anode. Maximal generator output was 32 mA. GVP with the distal electrode as cathode was successful in 75% and 80% of patients at 30- and 50-ms pulse durations and 23.3+/-5.8 mA and 22.6+/-5.8 mA threshold currents, respectively. However, success rates (20% and 25%, respectively) were significantly lower with the proximal electrode as cathode using the same pulse durations and 14.4+/-5.3 mA and 16.7+/-6.8 mA threshold currents. The TVP success rate was significantly lower than that for GVP. With optimization, this system could become an available technique for intraoperative emergency ventricular pacing. IMPLICATIONS: Using an endocardial pacing lead attached to a transesophageal echocardiography probe, gastrothoracic ventricular pacing can be performed successfully without complications in 75%-80% of patients undergoing cardiovascular surgery.

[Changes of arterial blood pressure and heart rate during induction of anesthesia with propofol--efficacy of propofol titration using bispectral index as an indicator].

Bispectral index (BIS) is a processed EEG parameter that measures the hypnotic effects of anesthetic and sedative agents on the brain. We studied whether propofol titration using BIS allows us to prevent hemodynamic changes during induction of anesthesia and endotracheal intubation. Thirty patients without hypertension and obesity were studied. In the titration group (n = 15), BIS was maintained at 40 during induction of anesthesia with propofol. In the bolus group, anesthesia was induced with a bolus infusion of propofol 2 mg.kg-1 (n = 15). Arterial blood pressure and heart rate were recorded before induction of anesthesia, during induction of anesthesia, immediately after, and 1 min, 2 min, and 3 min after intubation. Diastolic blood pressure and heart rate increased significantly after endotracheal intubation in both groups. Systolic blood pressure significantly increased immediately after intubation in the bolus group, but was unchanged in the titration group. These results suggest that BIS is useful to prevent significant increases in systolic blood pressure associated with endotracheal intubation during induction of anesthesia with propofol.

Effects of sevoflurane on regional myocardial blood flow distribution: quantification with myocardial contrast echocardiography.

BACKGROUND: Using myocardial contrast echocardiography, the authors tried to determine whether sevoflurane causes myocardial blood maldistribution in humans and dogs. METHODS: In animal experiments, 15 mongrel dogs were organized into dipyridamole (n = 6) and sevoflurane (n = 9) groups. Sonicated albumin was infused into the left main coronary artery. The peak gray level corrected for background was analyzed at the following intervals: (1) at baseline, (2) after stenosis of the left circumflex coronary artery (blood flow reduced by 40%), (3) after administration of dipyridamole (1 mg/kg given intravenously) or sevoflurane (1 minimum alveolar concentration) during stenosis, and (4) after phenylephrine during stenosis and administration of dipyridamole or sevoflurane. In human studies, nine patients undergoing coronary artery bypass grafting were studied. During partial extracorporeal circulation, the peak gray level was analyzed before and 20 min after sevoflurane (1 minimum alveolar concentration). RESULTS: In animal experiments, dipyridamole decreased significantly the inner:outer ratio of the peak gray level in the ischemic area and the ischemic:normal ratio of the peak gray level. After arterial pressure was restored with phenylephrine, neither the inner:outer ratio nor the ischemic:normal ratio improved. In contrast, after sevoflurane administration, the inner:outer ratio and the ischemic:normal ratio remained unchanged, but these increased with phenylephrine. In human studies, sevoflurane did not change the inner:outer ratio in the area supplied by the most stenotic coronary artery. CONCLUSION: These results suggest that dipyridamole, a potent coronary vasodilator, produces maldistribution of coronary blood flow in our dog models, whereas sevoflurane does not do this in animal or human studies.