73 research outputs found

    Value of a specific bradycardic agent in cardiac surgery compared to placebo

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    The effects of alinidine on systemic and pulmonary haemodynamics and the ECG were studied in 8 patients early after open heart surgery as a double-blind cross-over comparison between alinidine and placebo. Placebo had no effect on any of the measured variables. Alinidine given as an i.v. bolus (10 mg) followed by an infusion (10 mg h−1) was associated with alinidine plasma levels of 172 ± 17 and 114 ± 13, respectively, (±SE, ng ml−1) and decreased heart rate (−12%) and rate-pressure product (−14%) in all patients. While stroke volume index tended to increase, there were no changes in arterial, pulmonary and atrial pressures, cardiac index, and systemic and pulmonary vascular resistances. PR and QRS intervals of the ECG remained unaffected, and the QTC interval transiently decreased. Alinidine appears to be a suitable drug for control of inappropriate sinus tachycardia in patients with heart disease undergoing surger

    Behavioral Theory of Timing Applied to a DRL-Limited Hold Procedure

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    The behavioral theory of timing (Killeen & Fetterman, 1988) holds that animals use behavioral tasks, called adjunctive behaviors, to aid them in timing intervals. Several studies have supported this theory, however the majority of these studies have been correlational. The present study used an experimental approach to manipulate the presence of adjunctive behavior. Rats responded on two DRL limited-hold procedures in which subjects must wait a certain time interval before responding; early responses were not reinforced and reset the clock. In addition, the animal had a specific interval of time in which to make a response; late responses were not reinforced and also reset the clock. The opportunity for adjunctive behavior was manipulated with a chew block which was provided for half of the sessions. The results show that the presence of the chew block did not have an effect on timing ability. In fact very little chewing occurred, and when chewing did occur it interfered with timing ability. This violates the predictions of BeT that chewing would improve timing ability. However, the low rates of chewing show that perhaps this is not an appropriate test for BeT. In addition, it is possible that other adjunctive behaviors were occurring during the experimental sessions. Future studies should include more subjects, run more sessions, and examine all behavior during each session

    CARDIOVASCULAR EFFECTS OF DILTIAZEM IN THE DOG

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    SUMMARY The effects of two bolus injections (0.2 mg kg−1) and two infusion rates (0.2 mg min−1 and 0.4 mg min−1) ofdiltiazem on global and regional left (LV) and right ventricular (RV) performance (ultrasonic dimension technique), on coronary (electromagnetic flow meters) and systemic haemodynamics, and on electrophysiology (PR, QRS, QTC intervals) were studied in eight open-chest dogs anaesthetized with droperidol and fentanyl. The two bolus injections of diltiazem resulted in plasma concentrations of 688 ± 115 and 650 ± 85 ng ml−1 (means ± SE), respectively, and caused substantial decreases in systemic and coronary vascular resistances, and in aortic pressure, and increases in LV segment shortening, stroke volume and aortic flow. Electro -physiological variables were little affected. At the low infusion rate (plasma concentration 140 ± 23 ng ml−1) coronary and systemic vaso-dilatation occurred, but global and regional RV and LV performance were little affected. PR interval increased by 15%. At the higher infusion rate (plasma concentration 282 ± 33 ng ml−1) coronary and systemic vasodilatation were maintained. Aortic pressure decreased slightly. Whereas LV end-diastolic and end-systolic dimensions remained unchanged, they increased in the RV. In addition, the PR interval increased by 35%, and three animals developed atrio-ventricular block type I. The data indicate that diltiazem is a potent coronary and systemic vasodilator with little effect on global RV and L V performance. However, at a higher infusion rate RV dimensions clearly tend to increase, and conduction abnormalities develo

    Spinal anaesthesia in a patient with Takayasu's disease

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    We report the successful anaesthetic management of therapeutic abortion under spinal anaesthesia in a 32-yr-old woman with Takayasu's disease. The pathology and pathophysiology of this syndrome and their impact on anaesthesia are discussed. (Br. J. Anaesth. 1994; 72: 129-132

    Use of myocardial tissue Doppler imaging for intraoperative monitoring of left ventricular function

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    Background. Detection of myocardial ischaemia during surgery is usually by assessment of regional wall motion using two‐dimensional transoesophageal echocardiography (TOE). Tissue Doppler imaging (TDI) may assist this assessment and improve its accuracy. Methods. We measured peak myocardial velocities in the anterior mid‐wall of the left ventricle by TOE and pulsed‐wave TDI in addition to transmitral flow velocity, two‐dimensional echocardiography and cardiovascular variables. We studied 42 patients before and after coronary bypass surgery with left internal mammary artery grafts. Results. Peak systolic and early and late diastolic velocity measurements of the anterior mid‐wall were obtained in all patients. Variation between and within observers was small (<6%). Peak systolic thickening velocity correlated with visual assessment of anterior wall motion score, fractional area change of the left ventricle and left ventricular systolic wall stress. Because of the wide overlap of systolic velocity between the segments with normal and abnormal wall motion, it was not possible to separate normal from abnormal segments on the basis of TDI‐derived velocity alone. The diastolic velocity in the anterior wall reflected the transmitral filling pattern. After surgery, the peak systolic and late diastolic anterior wall velocities increased (from 4.2 (95% confidence interval 4.0, 4.7) to 5.7 (4.8, 6.3) cms-1 and from 3.5 (3.2, 3.9) to 6.0 (5.1, 6.9) cms-1 respectively), while the ratio of early to late diastolic velocity decreased from 1.5 (1.2, 1.7) to 1.0 (0.8, 1.2). TDI changes characteristic of new myocardial ischaemia were not seen in any patient. Conclusion. Intraoperative measurement of TDI in the anterior wall of the left ventricle is feasible and provides additional quantitative information on both regional and global systolic and diastolic function. We found changes in myocardial velocities indicating improvement in the systolic and impairment in the diastolic function of the anterior wall of the left ventricle immediately after mammary artery grafting. Br J Anaesth 2003; 91: 473-8

    Effects of halothane, sevoflurane and propofol on left ventricular diastolic function in humans during spontaneous and mechanical ventilation

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    Background. There is limited knowledge of the effects of anaesthetics on left ventricular (LV) diastolic function in humans. Our aim was to evaluate these effects in humans free from cardiovascular disease. Methods. Sixty patients (aged 18-47 yr) who had no history or signs of cardiovascular disease were randomized to receive general anaesthesia with halothane, sevoflurane or propofol. Echocardiography was performed at baseline and during spontaneous respiration at 1 minimum alveolar concentration (MAC) of the inhalational agents or propofol 4 ”g ml−1 (step 1), and repeated during positive-pressure ventilation with 1 and 1.5 MAC of the inhalational agents or with propofol 4 and 6 ”g ml−1 (steps 2a and 2b). Analysis of echocardiographic measurements focused on heart rate corrected isovolumic relaxation time (IVRTc) and early diastolic peak velocity of the lateral mitral annulus (Ea). Results. IVRTc decreased from baseline to step 1 in the halothane group (82 [95% CI, 76-88] ms and 74 [95% CI, 68-80] ms respectively; P=0.02), remained stable in the sevoflurane group (78 [95% CI, 72-83] ms and 73 [95% CI, 67-81] ms; n.s.) and increased in the propofol group (80 [95% CI, 74-86] ms and 92 [95% CI, 84-102] ms; P=0.02). Ea decreased in the propofol group only (18.8 [95% CI, 16.5-19.9] cm s−1 and 16.0 [95% CI, 14.9-17.9] cm s−1; P=0.003). From step 2a to step 2b, IVRTc increased further in the propofol group (109 [95% CI, 99-121] ms and 119 [95% CI, 99-135] ms; P=0.04) but remained stable in the other two groups. Ea did not change from step 2a to step 2b. Conclusions. Halothane and sevoflurane did not impair LV relaxation, whereas propofol caused a mild impairment. However, the impairment by propofol was of a magnitude that is unlikely to cause clinical diastolic dysfunctio

    Effects of sevoflurane and propofol on left ventricular diastolic function in patients with pre-existing diastolic dysfunction

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    Background. The effects of anaesthetics on left ventricular (LV) diastolic function in patients with pre-existing diastolic dysfunction are not well known. We hypothesized that propofol but not sevoflurane will worsen the pre-existing LV diastolic dysfunction. Methods. Of 24 randomized patients, 23 fulfilled the predefined echocardiographic criterion for diastolic dysfunction. They received general anaesthesia with sevoflurane 1 MAC (n=12) or propofol 4 ÎŒg ml−1 (n=11). Echocardiographic examinations were performed at baseline and in anaesthetized patients under spontaneous breathing and under positive pressure ventilation. Analysis focused on peak early diastolic velocity of the mitral annulus (Ea). Results. During spontaneous breathing, Ea was higher in the sevoflurane than in the propofol group [mean (95% CI) 7.0 (5.9-8.1) vs 5.5 (4.7-6.3) cm s−1; P<0.05], reflecting an increase of Ea from baseline only in the sevoflurane group (P<0.01). Haemodynamic findings were similar in both groups, but the end-tidal carbon dioxide content was more elevated in the propofol group (P<0.01). During positive pressure ventilation, Ea was similarly low in the sevoflurane and propofol groups [5.3 (4.2-6.3) and 4.4 (3.6-5.2) cm s−1, respectively]. Conclusions. During spontaneous breathing, early diastolic function improved in the sevoflurane but not in the propofol group. However, during positive pressure ventilation and balanced anaesthesia, there was no evidence of different effects caused by the two anaesthetic

    Volatile anaesthetics and positive pressure ventilation reduce left atrial performance: a transthoracic echocardiographic study in young healthy adults

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    Background Animal and in vitro studies suggest that volatile anaesthetics affect left atrial (LA) performance. We hypothesized that human LA pump function and dimensions are altered by volatile anaesthetics in vivo. Methods We performed transthoracic echocardiographic (TTE) measurements in 59 healthy subjects (aged 18-48 yr) undergoing minor surgery under general anaesthesia. The unpremedicated patients were randomly assigned to anaesthesia with sevoflurane, desflurane, or isoflurane. TTE examinations were performed at baseline and after induction of anaesthesia and upon placement of a laryngeal mask during spontaneous breathing. After changing to intermittent positive pressure ventilation (IPPV), an additional TTE was performed. The study focused on the velocity-time integral of late peak transmitral inflow velocity (AVTI) and maximum LA volume. Results We found no evidence for relevant differences in the effects of the three volatile anaesthetics. AVTI decreased significantly from 4.1 (1.2) cm at baseline to 3.2 (1.1) cm during spontaneous breathing of 1 minimum alveolar concentration of volatile anaesthetics. AVTI decreased further to 2.8 (1.0) cm after changing to IPPV. The maximum LA volume was 45.4 (18.6) cm3 at baseline and remained unchanged during spontaneous breathing but decreased to 34.5 (16.7) cm3 during IPPV. Other parameters of LA pump function and dimensions decreased similarly. Conclusions Volatile anaesthetics reduced active LA pump function in humans in vivo. Addition of IPPV decreased LA dimensions and further reduced LA pump function. Effects in vivo were less pronounced than previously found in in vitro and animal studies. Further studies are warranted to evaluate the clinical implications of these findings. Clinical trial registration NCT002445
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