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Biomedical subjects

J Kupersmith

Publications and source records attributed to J Kupersmith.

At least 91 records · Page 5Linked to original sources
PubMed1979

Regional effects of propranolol on intraventricular conduction in coronary artery disease.

In canines, propranolol slows conduction in acutely ischemic, but not in normal tissues. To determine propranolol effects on conduction in patients with coronary artery disease, we studied 7 patients after left anterior descending coronary artery bypass graft surgery. Bipolar electrodes were placed in the atrium, left ventricle (in the left anterior descending distribution), and right ventricle. On postoperative day 7, 3 mg propranolol were given intravenously. At a constant artrially paced rate, conduction intervals were measured from the earliest onset of the QRS in 3 simultaneously recorded surface electrocardiogram (ECG) leads to the major deflection of the electrogram recorded from each ventricle. Ten minutes after injection, conduction in the left ventricle was slowed by 4 +/- 0.3 msec (10 +/- 0.9%) and in the right ventricle by 0.4 +/- 0.3 msec (1 +/- 0.9%). QRS duration changed -1 msec (-0.8%). Stimulus to Q, a measure of propranol effect on A-V conduction, changed 16 +/- 2%. The difference in propranolol effects on left and right ventricles was significant (p less than 0.001). We suggest that in patients with coronary artery disease (1) propranolol has local anesthetic effects in slowing conduction; (2) the effects of propranolol vary with the region of ventricular myocardium; and (3) propranolol slows conduction more in the left than right ventricle. This difference may be due to potentiation of drug effects in left ventricular tissue that is abnormal due to chronic coronary artery disease.

Adult↗
PubMed1978

Shunt flow and pulmonary hemodynamics during labor and delivery in the Eisenmenger syndrome.

The Eisenmenger syndrome carries a high mortality rate in a women during delivery and the immediate postpartum period. It has been suggested that marked changes in shunt flow and pulmonary hemodynamics may be responsible. These functions were studied under various physiologic and pharmacologic conditions during labor and delivery in a patient with the Eisenmenger syndrome. Uterine contractions were associated with a decrease in the ratio of pulmonary to systemic blood flow (Qp/Qs) from 1.58 to 1.05. The Qp/Qs ratio also decreased (to 0.83) when forceps were applied during uterine contractions. Epidural anesthesia, oxytocin and the supine position did not adversely affect pulmonary hemodynamics or shunt flow. On the basis of these results, if pregnancy cannot be terminated in a patient with the Eisenmenger syndrome, it is recommended that the patient be given high concentration of oxygen and epidural anesthesia and that serial arterial blood gas determinations be performed to detect changes in shunt flow.

Adult↗
PubMed1978

Electrophysiologic effects of acute myocardial infarction in man.

Six patients undergoing surgery for ischemic heart disease were studied by means of epicardial electrodes affixed to the left ventricle. One patient who underwent triple coronary arterial bypass and plication of a left ventricular aneurysm had evidence of an acute myocardial infarction 1 day after operation. A surface electrocardiogram and a bipolar electrogram from the left ventricle were recorded before and after development of the infarction. The bipolar electrogram showed a marked loss of voltage and delay of conduction that were not present in the patients who underwent surgery but did not sustain an acute myocardial infarction. Thus, any acute myocardial infarction in conscious persons appears to be associated with areas of delayed epicardial action and diminution of local voltage. This observation suggests that the electrophysiologic mechanisms of infarction in man are similar to those of infarction in the dog.

Acute Disease↗
PubMed1977

Creating permanent complete heart block by indirect cauterization without atriotomy.

We created permanent complete heart block (CHB) in 11 dogs without atriotomy by means of indirect cauterization of the atrioventricular (A-V) bundle with a partially insulated wire placed through a small puncture in the atrial wall and guided by palpation. In six acute studies and five chronic studies, all dogs exhibited permanent CHB. To test the block, isoproterenol increased both atrial and ventricular rates 200%-400% without affecting the block. Atropine had no effect on ventricular rate or block.

Animals↗
PubMed1976

Ventricular paired pacing to control rapid ventricular heart rate following open heart surgery. Observations on ectopic automaticity. Report of a case in a four-month-old patient.

An unusual case is presented in which an atrioventricular (A-V) junctional tachycardia at a rate of 285 beats/min developed in the immediate postoperative period following surgical repair (a Mustard procedure) of transposition of the great vessels in a four-month-old infant. With that heart rate the systolic blood pressure bacame 35-40 mm Hg and urinary output ceased. Ventricular paired pacing was employed successfully to halve the mechanically effective ventricular rate. This resulted in a clinically effective blood pressure and return of normal urinary output. The clinical course of the A-V junctional tachycardia, plus its response to several interventions, suggested that the mechanism of the A-V junctional tachycardia was automatic rather than re-entrant. The study demonstrates that ventricular paired pacing for the control of cardiac arrhythmias is a useful clinical technique in selected cases.

Atrioventricular Node↗
PubMed1976

Electrophysiological and antiarrhythmic effects of propranolol in canine acute myocardial ischemia.

To correlate the antiarrhythmic and electrophysiological effects of propranolol in acute myocardial ischemia, we examined the effects of temporary (15-minute) ligations of the left anterior descending coronary artery in studies on 15 dogs. We recorded bipolar electrograms and monophasic action potentials from the ischemic and normal zones and measured the intervals from the onset of QRS in a standard electrocardiogram lead to the major deflection of electrograms recorded from the ischemic and normal zones. We also determined monophasic action potential duration (APD) and effective refractory period (ERP). Data for control ligations were compared to those during which propranolol, 40 mug/kg, was administered intravenously immediately after ligation. Propranolol reduced the mean number of ventricular beats per minute (from 15 to 6) (P less than 0.01). Propranolol slowed conduction in the ischemic zone (by 10 msec at peak effect, P less than 0.01) and had no or only a very slight effect (by 1-msec at 15 minutes, P less than 0.05) on conduction in the normal zone. Propranolol also prolonged APD in the ischemic (32-msec) and normal (14-msec) zones (P less than 0.01), prolonged ERP in the ischemic (41-msec) and normal (20-msec) zones (P less than 0.01), and reduced the APD/ERP ratio in the ischemic (1.62 to 1.47) (P less than 0.01) and normal (1.62 to 1.55) (P less than 0.05) zones. During the control ligation, APD in the ischemic zone was 25 msec shorter than in the normal zone (P less than 0.01), but with propranolol the difference was not significant. The effects of propranolol in slowing conduction in the ischemic zone, in prolonging refractoriness, in reducing APD/ERP, and in reducing the disparity in APD between ischemic and normal zones may explain its demonstrated antiarrhythmic effects in acute myocardial ischemia.

Action Potentials↗
PubMed1975

In vivo electrophysiological effects of lidocaine in canine acute myocardial infarction.

Lidocaine was administered as a rapid intravenous bolus injection followed by a constant-rate intravenous infusion to nine dogs with 2-hour-old myocardial infarctions. Bipolar electrograms were recorded from and effective refractory periods were determined in the infarcted and normal zones of the heart. Intervals (Q-EG) were measured from the onset of the QRS complex in a standard electrocardiogram limb lead to the major deflection of the recorded electrograms from the normal and infarcted zones. QRS duration and serum lidocaine concentration were also determined. At serum concentrations considered to be therapeutic, lidocaine prolonged the Q-EG intervals in the infarcted zones of the heart 17-26% at peak effect (P less than 0.01), but it had no effect on the Q-EG intervals in the normal zone except for a slight (1.5%) prolongation shortly after the initial intravenous bolus injection. Lidocaine also had no effect on QRS duration. Similarly, lidocaine prolonged the effective refractory period of the infarcted zone 23% (P less than 0.01) at peak effect but had no effect on the effective refractory period of the normal zone. Prior to lidocaine administration, the mean effective refractory period of the normal zone was 26 msec longer than that of the infarcted zone, but at peak drug effect the disparity in refractoriness was reduced to 1 msec. The present study thus shows that lidocaine has different effects in infarcted and normal zones of the heart. In delaying activation and prolonging the effective refractory period of the infarcted zone of the heart, lidocaine has local anesthetic actions which might explain its effectiveness in curtailing ventricular arrhythmias after acute myocardial infarction.

Animals↗