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Biomedical subjects

B Bui-Xuan

Publications and source records attributed to B Bui-Xuan.

35 records · Page 2Linked to original sources
PubMed1988

A case of sotalol poisoning with fatal outcome.

The case of a 58 year old woman who died after ingestion of 14.4 g of sotalol and 50 mg of triazolam is described. Despite medical treatment, intracardiac pacing and hemodialysis, cardiovascular failure persisted and became irreversible. High sotalol concentrations were observed in plasma (65 micrograms/ml) and in post mortem tissues samples. Tissue to plasma ratios ranged from 2.5 to 6. The high drug concentration found in heart tissue (104.4 micrograms/g) explains the difficulties experienced in the sotalol poisoning.

Chromatography, High Pressure Liquid↗
PubMed1986

[Continuous measurement of gas exchange during artificial ventilation].

A system for on-line measurement of respiratory gas exchange in patients undergoing artificial ventilation is described. Fractional concentrations were measured by a mass spectrometer and expired flow by a pneumotachometer; signals processing was carried out by a microcomputer. The accuracy of the measurement of the burning methanol RQ was within 1.6% at FIO2 lower or equal to 0.4. When compared to a reference method (the Douglas bag method), correlation was found to be excellent. The major problem in measuring gas exchange in a ventilated patient is that physiological signals are contaminated by artefacts which may lead to erroneous computations. An algorithm was developed in order to identify and disregard artefacted periods or ventilatory unsteady state in the patients. The technique used for data processing gave reliable continuous measurements of respiratory gas exchange for periods up to 24 h, without interfering with the nursing of the ventilated patients.

Algorithms↗
PubMed1979

[A fast transient osmotic method. Simultaneous in vivo determination of the reflexion coefficient and of the permeability/filtration coefficient ratio of the pulmonary capillary endothelium in the dog].

Thermodynamic variables characterizing the transport of water and urea across Dog pulmonary capillary membrane were obtained in vivo by means of a pulse transient osmotic method. Results were inconsistent with the hypothesis of a homoporous membrane. When data were interpreted in terms of an exclusive water channel and of a shared pore pathway, the value of the pore reflexion coefficient was close to zero for urea.

Animals↗
PubMed1979

[The anesthesiologist and the hemodynamic effect of anti-arrhythmic agents (excluding beta blockers)].

On the basis of a haemodynamic study involving the intravenous administration of disopyramide, a review is undertaken of the haemodynamic action of various anti-arrhythmics likely to be used pre- or peroperatively by the anaesthetist. All anti-arrhythmic agents have possible haemodynamic properties which may prove troublesome for the anaesthetist: --all (with the possible exception of bretylium tosylate) have negative inotropic properties; --all (with the exception of disopyramide) decrease peripheral resistance. These effects are as a rule slight in the healthy subject but may give rise to difficulties during anaesthesia of a patient with a damaged myocardium.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

[Sudden death during anesthesia: human error, drug related or cardiac death?].

We carried out a retrospective analysis of 1500 forensic autopsies following sudden unexpected cardiac death. This analysis showed a group of 43 cases that could have been related to surgery and/or anaesthesia. Pathological examination revealed the existence of cardiac lesions in 40 cases: arrhythmogenic right ventricular cardiomyopathy (14 cases), coronary artery disease (9 cases), cardiomyopathy (8 cases), structural abnormalities of the His bundle (7 cases), mitral valve prolapse (1 case) and acute myocarditis (1 case). These disorders are compatible with a paroxysmal (rhythmic) phenomenon at the origin of the cardiac arrest. Identification of the cause of death in a patient who was presumed to be at low risk may provide major relief to the patient's family and the medical staff.

Adolescent↗
PubMedDate not supplied

[Cardiotoxicity of 5-fluorouracil: report of 6 cases].

5-fluorouracil (5-FU), a fluoropyrimidine antimetabolite, is widely used in the treatment of cancers of the digestive tract and breast. The clinical cardiotoxicity of 5-FU was first reported in 1975. Adverse cardiac effects include coronary disorders, heart failure and sudden death of suspected cardiac origin. Six new cases are reported, including 5 cases of angina and one of heart failure. The patients, 4 males and 2 females, were 26 to 71 years of age (mean: 56.2). They had no medical history of heart failure, myocardial ischemia or electrocardiographic anomalies prior to 5-FU treatment. Three patients had hypertension of whom one had had type-II diabetes mellitus for the past 20 years. Clinical symptoms included chest pain in 4 patients and heart failure in one, whereas the last patient had ECG changes with no associated clinical symptoms. Clinical symptoms of angina totally disappeared after the cessation of 5-FU administration, but heart failure was alleviated only after the introduction of digitalis, a converting-enzyme inhibitor and a diuretic. It has been estimated that 1.6% of patients treated with 5-FU develop adverse cardiac effects. Patients at greater risk are those with a history of ischemic cardiac disease, thoracic radiotherapy or high-dose 5-FU therapy. The mechanism involved is not clearly elucidated. Spasms of the coronary arteries or toxic inflammation of the myocardium have been suspected. These 6 new cases confirm the potential for cardiotoxicity of 5-FU and the need for careful cardiac monitoring of treated patients.

Adult↗
PubMedDate not supplied

Influence of the restoration of vagal tone by intracisternal injection of dextromoramide on the cardiac effects of the antiarrhythmic drugs.

The effects of four antiarrhythmic drugs, quinidine, procainamide, amiodarone and verapamil were studied on sinus rate, conduction time and, when possible, effective refractory period (ERP) in atrioventricular node (AV node), and finally atrial muscle ERP. This study was made under two types of conditions, vagal tone being absent or present after restoration in the anesthetized dog by a new technique, the intracisternal injection of dextromoramide. Quinidine and procainamide which tend to slow down sinus rate and conduction in the former case accelerate them considerably in the latter by opposing the effects of acetylcholine released by vagal endings. The prolongation of atrial ERP also induced by these drugs results from both this process and their own capacity. Amiodarone and verapamil, usually responsible for bradycardia, notable delay in AV node conduction and lengthening of AV node ERP are, however, liable to elicit opposite effects, especially amiodarone when vagal tone is very high. The reduction of vagal influence is, in the case of these drugs, the only factor in the prolongation of atrial ERP. In any case, the response of both specialized and common tissue of the heart to antiarrhythmic drugs should not be interpreted unless the degree of vagal tone is known.

Amiodarone↗
PubMedDate not supplied

Disappearance with ischaemic depolarization of the antifibrillatory activity in a sodium channel blocker and appearance in calcium channel blocker.

Results obtained in the prevention of ventricular fibrillation secondary to myocardial ischaemia are unexpected. Profibrillatory properties might be manifested by Class I antiarrhythmic drugs, normally antifibrillatory. Clear antifibrillatory properties might be manifested by calcium channel blockers, the antifibrillatory effects of which are normally questionable. Therefore, the action of a Class I antiarrhythmic drug, flecainide, and of a calcium channel blocker, verapamil, on the vulnerability to ischaemic ventricular fibrillation was assessed in anaesthetized, open-chest pigs by ventricular fibrillation threshold. Ventricular fibrillation threshold was determined with trains of diastolic stimuli of 100 msec duration, delivered at a rate of 180 beats/min (near that of the ventricular tachycardia), by a subepicardial electrode inserted into the area that could be subjected to ischaemia. Before determining this threshold, ventricles were paced at the same rate, particularly during the ischaemic periods. Ischaemia was produced by complete occlusion of the left anterior descending coronary artery, either at its origin or half-way from it, over increasing periods. The monophasic action potential and conduction time were recorded in the ischaemic area. Before ischaemia, flecainide was adapted to rais the ventricular fibrillation threshold, in spite of a lengthening of the conduction time. Verapamil was devoid of any influence on these parameters. The antifibrillatory effect of flecainide disappeared with ischaemia, which reduced the ventricular fibrillation threshold down to near 0 mA, with triggering of the spontaneous fibrillation at this level: this reduction was no longer counteracted and even hastened by flecainide, becomes finally profibrillatory. Verapamil, on the contrary, delayed the fall in ventricular fibrillation threshold, maintained far from 0 mA, with prevention of fibrillation, unless the occlusion was maintained over a much longer period. Verapamil similarly delayed the shortening of the monophasic action potential duration and the lengthening of the conduction time, preceding fibrillation and leading to it. Consequently, ischaemic depolarization is apparently responsible for the loss of antifibrillatory activity in a sodium blocker, such as flecainide, and the development of antifibrillatory activity in a calcium blocker, since the sodium channel is activated only at high potentials, whereas the calcium channel is activated at lower potentials.

Animals↗
PubMedDate not supplied

Prevention by calcium antagonists of profibrillatory effects of class I antiarrhythmic drugs in acute myocardial ischemia: study in pig heart in situ.

Class I antiarrhythmic drugs do not decrease, but increase, the risk of ventricular fibrillation in the ischemic myocardium. On the contrary, vulnerability to fibrillation related to ischemia appears to be substantially reduced by calcium antagonists. We assessed whether the calcium antagonist diltiazem (0.50 mg/kg bolus plus 0.02 mg/kg/min infusion) could prevent the profibrillatory effect or even partially restore the antifibrillatory effect of a class I antiarrhythmic drug, flecainide (1 mg/kg bolus plus 0.04 mg/kg/min infusion) in the ischemic myocardium of anesthetized, open-chest pigs. Ischemia was obtained by completely occluding the left anterior descending coronary artery near its origin. Vulnerability to fibrillation was assessed by electrical fibrillation threshold (EFT), measured with diastolic impulses of 100 msec duration delivered at a rate of 180 beats/minute. Diltiazem did not oppose the rise in EFT induced by flecainide in the absence of ischemia (6.8 +/- 1.2 to 9.9 +/- 0.9 mA, p<0.001). It limited the fall in EFT observed under the dual influence of ischemia and flecainide (4.2 +/- 0.9 vs 1.3 +/- 0.6 mA, p<0.001). By reducing calcium entry into myocardial fibers, diltiazem delayed ischemic depolarization, as evidenced by reduced shortening of the monophasic action potential duration from 215 +/- 7 to 200 +/- 4 msec, instead of 178 +/- 6 (p<0.001), and reduced lengthening of intraventricular conduction time from 33 +/- 5 to 43 +/- 4 msec, instead of 53 +/- 4 (p<0.01). Therefore, diltiazem is likely to prevent the loss and even the reversal of the antifibrillatory properties of flecainide due to myocardial ischemia in dosages that do not adversely affect myocardial contractility or atrioventricular conduction to a large extent.

Animals↗