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Biomedical subjects

M M Scheinman

Publications and source records attributed to M M Scheinman.

At least 289 records · Page 16Linked to original sources
PubMed1976

Disposition kinetics of quinidine.

The disposition kinetics of quinidine in 12 hospitalized patients in whom oral quinidine therapy was to be initiated is described. Quinidine in doses of 2.6 to 5.2 mg/kg base were infused intravenously over 22 min. Plasma samples were collected during the postinfusion for 24 hr and analyzed by a specific and sensitive assay procedure. In the 12 hr after administration, postinfusion plasma quinidine concentration decay was described by a biexponential equation. Attempts to include the 24-hr data point in the fitting procedures resulted in poorer agreements between the theoretical and experimental curves. A 2-compartment open model is proposed to describe the disposition of quinidine. The volume of the central pool (Vc) and steady-state volume of distribution (Vdss) were 0.91 +/- 0.11 L/kg and 3.03 +/- 0.25 L/kg, respectively, and indicate that quinidine distribution is predominantly extravascular. Quinidine distribution was quite rapid (t1/2alpha = 7.19 +/- 0.70 min), while the apparent elimination half-life (t1/2beta) was considerably longer, 6.333 +/- 0.47 hr. Total body plasma clearance ranged from 1.49 to 7.15 ml/min/kg (mean 4.70) and is primarily associated with nonrenal mechanisms of drug elimination. Urine specimens collected for 48 hr indicated that 17% of the dose is excreted intact and that urinary excretion was essentially complete within 24 hr. Renal clearance (Clr) was 0.80 +/- 0.18 ml/min/kg. The study demonstrated that there is substantial interpatient variability with respect to quinidine disposition.

Adult↗
PubMed1976

Atrial pacing in patients with sinus node dysfunction.

Sinus nod recovery time (SNRT) at paced atrial rates of 100 (SNRT100) and 120 (SNRT120) beats/min, atrial effective refractory periods at spontaneous heart rates (AERP) and at paced rates of 100 (AERP100) and 120 (AERP120) beats/min, and premature atrial stimulation were among the studies in evaluating 33 patients with symptomatic sinus node disease and 42 normal subjects. Although mean SNRT100 and SNRT120 were statistically significantly greater in patients than in control subjects, there was a significant overlap between patient and control groups, and SNRT100 or SNRT120 was associated with a 30.3 per cent false-negative and 5 per cent false-positive incidence. Correction for heart rate (SNRT-spontaneous cycle length) failed to improve the sensitivity or specificity of this test. There was no significant difference in mean AERP, AERP100 or AERP120, or in sinoatrial conduction time in patients compared with control subjects. Analyses of curves derived from plots of test and return cycles showed abnormal curves in only five of the 24 patients studied by progressively premature atrial stimulation. Two of these five patients showed normal zone I and II phenomena followed by a progressive linear increase in the return cycle that was thought to be due to abnormal refractoriness of the perinodal fibers.

Adult↗
PubMed1976

Precise "one line" measurement of intracardiac electrograms.

Atrioventricular nodal (A-H) and infranodal (H-Q) conduction times were determined in 22 patients undergoing intracardiac electrophysiologic studies. These measurements were determined independently both on line from a digital oscilloscope and from paper recordings at a rate of 100 mm/sec. There was no significant difference and excellent correlation between mean A-H (91.39 +/- 29 versus 95.44 +/- 32 msec) and H-Q (53.48 +/- 14 versus 50.52 +/- 15 msec) intervals determined by these two methods. The digital oscilloscope enables virtually instantaneous highly accurate (+/- 1 msec) timing of intracardiac events and rapid and more efficient processing of data. Potential applications during electrophysiologic studies include precise monitoring of drug effects on atrioventricular conduction and refractoriness, on line analyses of complex rhythm disturbances, and ready storage of data for computer retrieval and analyses.

Arrhythmias, Cardiac↗
PubMed1976

Right atrial versus left atrial echo zones: a proposed new criterion for determining the atrial site of retrograde preexcitation.

In a patient whose electrocardiogram (ECG) initially (1966) showed a Type A Wolff-Parkinson-White pattern, recurrent supraventricular tachycardia (SVT) developed but never subsequently showed antegrade bypass conduction. Intracardiac pacing studies (1975) revealed that premature high right atrial (induced 250-450 msec after atrial depolarization) or coronary sinus depolarization (250-550 msec) resulted in SVT. Late coronary sinus depolarization resulted in SVT without A-H prolongation. During SVT, P wave morphology changed and the coronary sinus atrial electrogram preceded that from the low right atrium; retrograde ventriculoatrial conduction time was 240 msec. Neither pacing the high right atrium or coronary sinus up to rates of 200 beats/min nor progressive atrial premature depolarizations from the high right atrium or coronary sinus resulted in antegrade bypass conduction. Failure of antegrade bypass conduction does not preclude SVT due to retrograde preexcitation and must be distinguished from atrioventricular (A-V) nodal reentry. Atrial effective refractory period (200 msec) was shorter than the minimal time required for an atrial impulse to return to the atrium (380 msec), suggesting concealed antegrade bypass conduction. Stimulation of the atrium linked to the A-V bypass results in earlier bypass activation and recovery and explains the differing high right atrial vs coronary sinus echo zones.

Adult↗
PubMed1976

Analysis of secondary pauses following termination of rapid atrial pacing in man.

The first ten cycles following cessation of atrial pacing were evaluated in 44 control subjects (mean age 52.9 +/- 14.88 yr) and 39 patients (mean age 62.9 +/- 15.41 yr) suspected of having sinus node dysfunction (SND). The maximal cycle length for each postpacing cycle following several pacing periods in each control subject was determined, and was normalized by dividing it by the subject's mean spontaneous control cycle length (SCL). Using the control group, a normalized maximal post-pacing response pattern (mean and SD) was derived. For each SND patient, a composite SD for each post-pacing cycle was calculated by adding the patient's SCL variance to the variance determined for each post-pacing cycle in the control group. Two composite SD above the mean value for each post-pacing cycle was selected as the upper limit of the normal recovery response and used to identify abnormal post-pacing responses in the 39 SND patients. Abnormally prolonged cycle lengths subsequent to the first escape cycle (secondary pauses) were found in 16/39 (41.0%) patients, of whom 11/39 (28.2%) had a prolonged SNRTmax. Of importance, 11/12 (91;7%) patients with documented SA block or sinus pauses prior to electrophysiologic study, demonstrated secondary pauses, while only 7/12 (58.3%) had a prolonged SNRTmax. Criteria are derived for the identification of secondary pauses during the postpacing period, and a close association between secondary pauses and the presence of spontaneous SA block or sinus pauses prior to electrophysiologic study is demonstrated.

Aged↗
PubMed1976

Ankylosing spondylitis with complete heart block.

A patient with complete heart block due to ankylosing spondylitis exhibited an unusually brisk increase in ventricular rate with exercise. Despite broad ventricular (QRS) complexes, His bundle electrograms demonstrated a His deflection before each QRS complex and thus established the level of atrioventricular (A-V) block to be proximal to or localized to the His bundle. A junctional pacemaker accounted for the brisk response to exercise, atropine, or isoproteronol. Left bundle branch block pattern and prolongation of infranodal conduction time (H-Q) suggested additional disease involving the His bundle and/or right fascicle. Wide-spread disease affecting A-V nodal and infranodal conduction was compatible with pathologic changes seen in this disease. Because the pacemaker was able to respond to stress promptly and with appropriate increase in heart rate, the patient appeared not to warrant pacemaker implantation in his present state.

Atropine↗
PubMed1975

Use of atropine in patients with acute myocardial infarction and sinus bradycardia.

Fifty-six patients with acute myocardial infarction complicated by sinus bradycardia (SB) were treated with intravenous atropine and monitored in a coronary care unit. Atropine decreased or completely abolished premature ventricular contractions (PVCs) and/or bouts of accelerated idioventricular rhythm in 27 of 31 patients (87%) and brought systemic blood pressure up to normal in 15 of 17 patients (88%) with hypotension. In addition, atropine administration was associated with improved atrioventricular conduction in 11 of 13 patients (85%) with acute inferior myocardial infarction associated with 2 degrees or 3 degrees atrioventricular block. Seven patients developed ten significant adverse effects: ventricular tachycardia or fibrillation in three, sustainedsinus tachycardia in three, increased PVCs in three, and toxic psychosis in one. These major adverse effects correlated with either a higher initial dose of atropine (i.e., 1.0 mg aa compared with the usual 0.5 or 0.6 mg) or a total cumulative dose exceeding 2.5 mg over 21/2 hours. Atropine is the drug of choice for management of patients with SB and hypotension and is effective in the treatment of ventricular arrhythmias as well as conduction disturbances in patients with inferior myocardial infarction. Serious adverse effects, however, preclude use of atropine without careful medical supervision.

Acute Disease↗