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Biomedical subjects

B Befeler

Publications and source records attributed to B Befeler.

At least 55 records · Page 3Linked to original sources
PubMed1975

Electrophysiologic effects of the antiarrhythmic agent disopyramide phosphate.

The electrophysiologic effects of the antiarrhythmic agent disopyramide phosphate given intravenously were studied in 10 patients with cardiac disease. Studies included determinations of sinus recovery time and refractoriness of the atria, the atrioventricular (A-V) node and the His-Purkinje system. Measurements were performed at rest and 15 and 30 minutes after administration of disopyramide. Serum drug levels were measured at these times. Sinus recovery time was shortened at both 15 and 30 minutes, with an average decrease of 39.5 and 146.2 msec, respectively (P less than 0.01). Atrial refractoriness was not altered significantly, but tended to be reduced; the mean effective refractory period was 289.5 msec before administration of disopyramide and 259 and 270 msec 15 and 30 minutes, respectively, after administration. The functional refractory period of the atrioventricular (A-V) node was definitely prolonged in seven patients 15 minutes after administration of disopyramide. The relative refractory period of the His-Purkinje System was not altered. Although this study does not elucidate the mechanism by which disopyramide acheives its antiarrhythmic effects, animal work has shown that it is similar to that of quinidine. In the doses used the drug does not seem to cause first, second or third degree A-V block or fascicular or bundle branch block; it did not increase the severity of first degree A-V block in the three patients with this disturbance. The drug may be particularly useful when arrhythmias are associated with slow sinus rates.

Adult↗
PubMed1975

Atrioventricular block after reciprocating atrioventricular junctional tachycardia.

Short runs of symptomatic atrioventricular (A-V) block occurred after spontaneous cessation of reciprocating A-V junctional tachycardia in a patient with right bundle branch block, normal H-V interval and sinus nodal dysfunction. These episodes were characterized by long (more than 1 sec) P-P intervals during which the A deflections were not followed by His bundle electrograms. Three possible explanations are: (1) a posttachycardia-induced period of abnormally prolonged A-V nodal refractoriness; (2) pseudo-A-V block produced by concealed A-V junctional tachycardia, or (3) bradycardia-dependent (phase 4) A-V block at the "upper" His bundle, above the site from which the H deflection was recorded.

Atrioventricular Node↗
PubMed1975

Effect of intrarenal furosemide on renal function and intratenal hemodynamics in acute renal failure.

The ability of short-term furosemide administration to alter intrarenal hemodynamics and to modify the clinical course of acute renal failure was assessed in six patients 2 to 9 days after the onset of acute renal failure. Following renal arterial catheterization, the intraarterial administration of furosemide at a dose of 9.6 mg/min for 30 minutes failed to improve renal function as assessed either by an increase in urine output or a decrease in serum creatinine during the 4 days after administration in the five oliguric patients. In a sixth patient with nonoliguric acute renal failure, urine volume increased with a gradual decrease in blood urea nitrogen and creatinine during the week after study. Furosemide failed to alter either mean renal blood flow or its intrarenal distribution as determined at intervals of 3 to 40 minutes after its infusion. These studies demonstrate that the short-term administration of furosemide in large doses does not improve renal hemodynamics or alter the clinical course of patients with established acute oliguric renal failure.

Acute Kidney Injury↗
PubMed1975

Measurements of conduction times with catheter electrodes during pacing from different ventricular sites.

Filtered bipolar catheter electodes, I mm apart, were used to pace and record from the high right atrium, right ventricular apex, right ventricular outflow tract, right ventricular inflow tract, middle cardiac vein, great cardiac vein, and endocardium of the left ventricular septal surface. Right ventricular apex to middle cardiac vein and the middle cardiac vein to right ventricular apex conduction intervals gave a rough estimate of anteroposterior and posteroanterior "transseptal plus free left ventricular wall" conduction times, respectively. On the other hand, the right ventricular apex to left ventricular septal surface and left ventricular septal surface to right ventricular apex intervals represented pure "transseptal" conduction times, since both sets of electrodes were in contact with the respective septal surface. During stimulation of the intermediately located right ventricular inflow tract propagation to the right ventricular apex and right ventricular outflow tract was longer than between these two sites. Moreover, conduction was almost as delayed to the right ventricular apex and right ventricular outflow tract as it was to the left ventricular septal surface. These findings were attributed to the peculiar electrophysiological behaviour of the right ventricular inflow tract muscle. Pacing from different segments of the great cardiac vein produced QRS morphologies and arrival of excitation patterns consistent with the relation between the anatomical location of this structure and the recording electrodes. However, from this study no inferences could be drawn regarding the conduction velocity or specific conduction pathways used by the stimulus in its journey from stimulating to recording areas.

Arrhythmias, Cardiac↗
PubMed1975

Mechanisms determining the ventricular rate in wolff-parkinson-white arrhythmias.

In patients with WPW syndrome the maximal ventricular rate attained during ectopic rapid supraventricular thythms depended on the type of arrhythmia as well as on the physiological properties of the AP. During reciprocating tachycardias the impulse is almost invariably conducted to the ventricles through the AV node. Therefore, the maxiaml ventricular rate is a function of the AV nodal ERP. On the other hand, when atrial flutter or atrial fibrillation were present the ventricular rate could be moderately elevated (when the ERP of the AP was longer than that of the AV node) or very rapid where the ERP of the AP was significantly short. Therefore, from the electrophysiological viewpoint, the AP appears to behave as His-Purkinje tissue in some cases and as ordinary artrial muscle in other patients. These assumptions await further documentation.

Adult↗
PubMed1975

Double accessory pathways in Wolff-Parkinson-White syndrome.

Intracardiac electrophysiological studies were performed in two patients with Wolff-Parkinson-White (WPW) syndrome. Atrial pacing at increasing rates or shorter coupling intervals produced inscription of the forward His bundle deflection at progressively longer intervals after the onset of ventricular depolarization. There was an associated increase in QRS duration without any change in the P-R (or St-V) interval. This response was consistent with a Kent bundle. Case 1 also had a short A-H interval which did not show the expected prolongation with stimulation at progressively faster rates. This suggested the presence of a James bundle in addition to the Kent bundle. In case 2 beats conducted exclusively through the atrioventricular (A-V) node had a short H-V interval but a delta wave was not inscribed. Absence of an initial slurring was attributed to the existence of an infra-His bundle bypass of the Mahaim type causing only slight pre-excitation, which was not of sufficient magnitude to be recorded by body surface leads. However, the existence of a congenitally short anterosuperior division of the left bundle could nt be excluded.

Bundle of His↗
PubMed1975

Mitral valve prolapse and coronary artery disease. Clinical, hemodynamic, and angiographic correlations.

Among 95 patients with angina pectoris and angiographically documented coronary artery disease (CAD), prolapse of the scallops of the posterior leaflet of the mitral valve (PLMV) was noted in 30 patients. Left ventriculograms in the right anterior oblique (RAO) projection revealed isolated prolapse of the posteromedial commissural scallop (PMCS) in 12 patients and the anterolateral commissural scallop (ALCS) in two patients. Seven patients had prolapse of both PMCS and ALCS, three had prolapse of the PMCS and middle scallop (MS), and six had prolapse of all three scallops of the PLMV. Left ventricular dilatation with increase trabeculations was observed in 19 patients. Contractility determined in a quantitative fashion by segmental motion analysis was markedly impaired in 29 patients. None of the patients had angiographic evidence of mitral insufficiency. Left ventricular dysfunction was documented in 28 patients by either elevated left ventricular end-diastolic pressure (LVEDP), low cardiac index (CI) or decreased ejection fraction (EF). In two patients in whom left ventricular contractility improved after aortocoronary by pass, previously prolapsed scallops could not be identified in the postoperative ventriculogram. Prolapsed PLMV is a frequent angiographic finding in patients with angiographically observed CAD. Impaired contractility of the ventricular myocardium and papillary muscles, left ventricular dilatation, and hypertrophy appear to play a significant role in the pathogenesis of this abnormality through distortion of the directional axis of the papillary muscles, asynergic contraction of the related free wall of the left ventricle, and changes in the normal spatial alignment necessary for mitral valve closure. The syndrome of papillary muscle dysfunction in patients with coronary artery disease represents a wider clinical spectrom than previously described.

Adult↗
PubMed1975

Situs inversus totalis associated with subaortic and subpulmonic stenosis.

The unusual occurrence of total situs inversus and idiopathic hypertrophic subaortic stenosis with the demonstration of right and left heart dynamic obstruction in one patient is presented. The fact that the patient was known to have a rare abnormality (total situs inversus) and the presenting symptom being angina pectoris, may have obscured the diagnosis of IHSS and emphasized the value of comprehensive evaluation of patients. The documentation of right ventricular dynamic obstruction, in addition to obstruction of the left side of the heart, was facilitated by the use of simultaneous pressure recordings in the pulmonary artery and in the body of the right ventricle. The angina-like pain was secondary to left ventricular outflow obstruction, rather than to coronary disease.

Adult↗
PubMed1975

Electrophysiologic studies in a patient with atrial flutter and 1:1 atrioventricular conduction.

Intracardiac electrophysiologic studies were performed in a patient having paroxysms of atrial flutter with 1:1 atrioventricular (A-V) conduction. Although duration of conduction intervals was normal during sinus rhythm, the atrio-His (A-H) interval did not show the expected increase when the atria were stimulated at progressively higher rates. The results of pacing with the extrastimulus technique also indicated that the refractory periods of the A-H tissues were shorter than normal. Yet, intravenously administered ouabain produced a significant increase in these refractory periods. The findings in the case are compatible with a partial A-V nodal bypass with a shorter refractory period than the A-V node or with an A-V node with unusual capacity for rapid conduction. The response to ouabain therapy was that of A-V nodal tissues.

Adult↗
PubMed1975

Syndrome of short P-R, narrow QRS and repetitive supraventricular tachyarrhythmias: the possible occurrence of the R-on-T phenomenon and the limits of this syndrome.

The R-on-T phenomenon was observed in two patients with narrow QRS complexes and repetitive supraventricular tachyarrhythmias. Case 1 had a typical Lown-Ganong-Levine syndrome in which the shortening of the P-R interval was due to a reduction of the A-H interval. In Case 2 the P-R interval (140 msec) was not short but the A-H interval was at the lower limits of normal (50 msec) and the P-A interval at the upper limits of normal (40 msec). Both patients showed the R-on-T phenomenon during periods of 1:1 A-V conduction occurring during atrial stimulation at a rate of 200/min (Case 1) and atrial flutter with a rate of 300/min (Case 2). Although total A-V conduction time was prolonged, the magnitude of this prolongation appeared to have been less than that occurring in normal subjects. This was attributed to the presence of an accessory pathway bypassing the area where the most significant delay occurred at the A-V node. The findings in Case 2 suggest, but do not prove, that a similar bypass might be operative in patients with atrial flutter with periods of 1:1 conduction, regardless as to whether the R-on-T phenomenon is, or is not, present.

Arrhythmias, Cardiac↗