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Biomedical subjects

B Surawicz

Publications and source records attributed to B Surawicz.

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

Coexistence of ventricular parasystole and ventricular couplets: mechanism and clinical significance.

In 78 consecutive patients with uniform ventricular ectopic complexes and without heart disease, ventricular couplets were present significantly more often when the coupling interval of ventricular ectopic complexes was variable than when it was fixed (P less than 0.04). In 69 consecutive patients with couplets, the prevalence of a variable coupling interval was significantly greater than that of (55 versus 14 cases; P less than 0.001). Among 55 patients with a variable coupling interval, ventricular parasystole was probable in 38 and possible in 17 patients. These results suggest that the association between ventricular couplets and parasystole is not coincidental. Of several possible mechanisms responsible for this association reentry within the parasystolic focus or its vicinity is the most probable. This may explain the observation that the couplets are seldom followed by consecutive ventricular ectopic complexes or ventricular tachycardia. If this hypothesis is correct, the clinical significance of ventricular couplets in the presence of ventricular parasystole may be similar to that of single reentrant ventricular ectopic complexes.

Electrocardiography↗
PubMed1979

Effects of K+ and K+-induced polarization on (dV/dt)max, threshold potential, and membrane input resistance in guinea pig and cat ventricular myocardium.

We studied the non-membrane potential-dependent effect of K+ on (dV/dt)max and threshold potential in guinea pig and cat ventricular myocardium. Membrane potential (MP) was changed uniformly in segments (length less than or equal to 1.0 mm) of papillary muscles by applying extracellular polarizing current pulses across a single sucrose gap. Control [K+]o was 5.4 mM and test [K+]o values were 2.0, 10.0, 11.5, 13.0, 16.2, 20, 22, and 24.0 mM. Each muscle was studied under four conditions: (1) control [K+]o and unaltered (control level) resting MP (Em); (2) one of the test [K+]o values and the unaltered (test level) Em; (3) the same test [K+]o and Em held at the control level; (4) control [K+]o and Em held at the test level. At all [K+]o greater than or equal to 11.5 mM, (dV/dt)max showed a decrease significantly (P less than 0.01) greater than the corresponding MP-dependent decrease in both guinea pig and cat myocardium. This non-MP-dependent decrease averaged 7.5% at 11.5 mM, 26.5% at 13.0 mM, 37.2% at 16.2 mM, and 22.7% at 20.0 mM. At [K+]o greater than or equal to 20.0 mM, (dV/dt)max was predominantly slow-channel-dependent; it was increased by hyperpolarization to -110 mV at [K+]o = 20 and 22 mM but not at [K+]o = 24mM. Threshold potential became progressively less negative with increasing [K+]o, but this effect was dependent only on MP. The membrane input resistance (rm) was determined by two opposing factors: at a given [K+]o, rm increased with depolarization; and at a given MP, rm decreased with increasing [K+]o. Our study shows that non-MP-dependent depression of (dV/dt)max in the ventricular myocardium occurs at [K+]o concentrations that may be encountered in vivo.

Action Potentials↗
PubMed1978

Exercise testing for detection of myocardial ischemia in patients with abnormal electrocardiograms at rest.

This review consists of two parts: (1) discussion of the electrophysiologic mechanisms that are believed to produce ventricular repolarization changes during the electrocardiographic stress test, and (2) clinical assessment of the electrocardiographic changes with stress in patients with an abnormal electrocardiogram at rest. In the first part, the mechanisms of S-T segment elevation, S-T segment depression, T wave changes and linked S-T and T wave changes are reviewed. In the second part, all electrocardiographic abnormalities at rest are grouped into four categories: (1) changes that mask the manifestations of ischemia, (2) changes that stimulate or exaggerate the manifestations of ischemia, (3) changes that have no important effect on the manifestations of ischemia, and (4) changes that reproduce the patterns of acute myocardial infarction after an apparent healing. The reported studies of electrocardiographic stress testing in patients who have abnormal electrocardiogram at rest are summarized.

Action Potentials↗
PubMed1978

Electrophysiologic and hemodynamic effects of verapamin. Correlation with plasma drug concentrations.

Verapamil was administered intravenously to 30 open-chest dogs and the electrophysiologic and hemodynamic effects of the drug were correlated with the corresponding plasma concentrations. At concentrations below 152 ng/ml, verapamil prolonged the A-H interval, abolished ventriculoatrial conduction, but did not significantly change sinus rate, cardiac output, left ventricular dp/dt, of systemic vascular resistance. Concentrations above 200 ng/ml were associated with slowing of the sinus rat, high degree atrioventricular block during atrial pacing, 24% decrease in mean aortic pressure, and decreased cardiac output and left ventricular dp/dt. Sinus arrest, high degree atrioventicular block during sinus rhythm, decreased systemic vascular resistance and increased left ventricular end-diastolic pressure occurred when plasma verapamil concentrations exceeded 400 ng/ml. These results show that plasma verapamil concentrations reliably reflect the electrophysiologic and hemodynamic actions of the drug, and that "therapeutic" drug effects can be achieved at plasma concentrations at which myocardial depressant effects are unlikely.

Animals↗
PubMed1978

The effects of verapamil and lidocaine on the automatic depolarizations in guinea-pig ventricular myocardium.

Rhythmic automatic depolarizations (RAD) were produced in guinea-pig papillary muscles depolarized to membrane potentials at which depolarizations depend on membrane currents passing through the slow channel. Verapamil depressed the RAD and decreased their overshoot. These verapamil effects were dependent on its concentration either in the bath (in vitro) or in plasma and myocardium (in vivo). Increase in [Ca++] counteracted the effects of verapamil on RAD. Lidocaine concentrations ranging from 4 to 16 mg/l had no effect on overshoot and only a slight effect on the rate of RAD. We conclude that RAD are more sensitive to nonlethal and presumably therapeutic concentrations of verapamil than to high, presumably toxic, concentrations of lidocaine.

Animals↗
PubMed1977

Electrocardiographic exercise test in patients with abnormal T waves at rest.

The results of submaximal ECG exercise test were evaluated in six leads recorded simultaneously in two groups of patients with T-wave abnormalities in one or more of Leads I, II, and V4-6. Group I included 185 patients with documented ischemic heart disease (IHD) and Group II 28 patients in whom IHD appeared unlikely. The test was positive in 88 per cent of patients in Group I and in 4 per cent of patients in Group II. In the majority of patients in both groups the T wave either did not change or became more positive or less negative after exercise. The pattern of exercise-induced T-wave changes was similar in patients with and without IHD, and was influenced predominantly by the physiologic effects of exercise. T-wave normalization after exercise occurred frequently in patients with and without IHD, and in patients with positive and negative exercise tests. Our results suggest that T-wave abnormalities, not caused by hypertrophy, conduction disturbances, drugs, or electrolyte imbalance, do not modify the results of submaximal ECG stress test, and that behavior of T wave after exercise does not alter the interpretation of the postexercise ECG. The independent behavior of the S-T segment and T wave after exercise in consistent with the theory that the S-T segment and the T wave are generated by different components of the ventricular action potential.

Adult↗
PubMed1976

Ventricular monophasic action potential changes associated with neurogenic T wave abnormalities and isoproterenol administration in dogs.

Changes in the duration of monophasic action potentials on the anterior and posterior walls of the dog ventricle were correlated with changes in T wave polarity and duration of the Q-T interval after (1) left stellate ganglion transection, (2) right stellate ganglion stimulation, and (3) administration of isoproterenol before or after these procedures. Left stellate ganglion transection and right stellate ganglion stimulation produced similar changes in T wave polarity, but the former prolonged and the latter shortened the Q-T interval. All procedures changed the duration of the monophasic action potential and the Q-T interval in the same direction. The reversal of T wave polarity induced by left stellate ganglion transection, right stellate ganglion stimulation or administration of isoproterenol after left stellate ganglion transection was associated with an average change of 13 to 17 msec in the difference between the monophasic action potential durations on the anterior and posterior ventricular walls. Isoproterenol restored to normal the neurogenic T wave abnormalities produced by left stellate ganglion transection and right stellate ganglion stimulation. The drug shortened the previously prolonged monophasic action potential more than the normal monophasic action potential, and the normal monophasic action potential more than the previously shortened monophasic action potential. This study confirms that the T wave is a sensitive indicator of relatively small changes (less than 20 msec) in the sequence of ventricular repolarization and explains the mechanism by which isoproterenol "normalizes" the primary T wave abnormalities.

Action Potentials↗