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Biomedical subjects

L S Gettes

Publications and source records attributed to L S Gettes.

At least 73 records · Page 4Linked to original sources
PubMed1982

Factors related to vulnerability to arrhythmias in acute myocardial infarction.

Ion-selective electrodes designed in our laboratory have been employed to determine the characteristics of the changes in extracellular K+ and pH associated with acute coronary artery ligation and release. These studies have defined major inhomogeneities in the rate and magnitude of change of extracellular K+ and pH not only at the lateral margin of the ischemic zone but also between the subepicardium and subendocardium, between the subendocardium and endocardium, and even between closely spaced electrodes throughout the ischemic zone. The inhomogeneities during reperfusion were as great as or greater than those induced by coronary ligation. We have used papillary muscles of guinea pigs to determine the effect of the various combinations of extracellular pH and K+ observed at any point in time in an intact heart to study the anticipated changes in conduction and have found both a speeding and a slowing of conduction, which can be expected to occur simultaneously in an intact heart. These results indicate that significant inhomogeneities exist in the ionic and electrical consequences of acute coronary artery ligation and release and that these inhomogeneities can be expected to result in disorders of conduction leading to reentry.

Animals↗
PubMed1982

Multiformity if induced unifocal ventricular premature beats in human subjects: electrocardiographic and angiographic correlations.

Single ventricular premature responses induced by strength-interval pacing were elicited at multiple sites in 30 patients undergoing cardiac catheterization to determine if and under what circumstances unequivocally unifocal stimulated ventricular premature beats could manifest multiformity of the QRS configuration. Multiformity was defined as unifocal responses whose mean frontal axes differed by greater than 15 degrees with or without associated morphologic differences in the horizontal leads. Multiformity occurred in 12 (40 percent) of 30 patients. A statistically significant association was found between multiformity and the presence of a quantitatively defined left ventricle wall motion abnormally (p less than 0.01), prior myocardial infarction (p less than 0.01) and a left ventricular election fraction of less than 0.60 (p less than 0.05). Twelve (67 percent) of the 18 patients without multiformity had coronary artery disease, but only 4 of those 12 had a left ventricular wall motion abnormally or prior myocardial infarction, or both. Multiformity was also dependent on the site of stimulation and on the degree of prematurity. The results of this study indicate that the QRS configuration of early premature beats cannot be relied on as a predictor of their site of origin and multiformity is not necessarily synonymous with multifocality.

Adult↗
PubMed1982

Atrial excitability and conduction in patients with interatrial conduction defects.

Prolongation of P-wave duration is an accepted indicator of an interatrial conduction disturbance and may predispose patients to atrial arrhythmias. This study was performed to monitor electrophysiologic characteristics of the atria in patients with a prolonged P-wave duration. Atrial excitability and conduction times were compared in 7 patients with a P-wave duration of less than 115 ms (Group I), and 13 patients with a duration of greater than of equal to 115 ms (Group II). In contrast of the Group I patients, most of the 13 patients in Group II had atrial arrhythmias, including sinus nodal dysfunction (3 patients) and a history of atrial fibrillation or ectopic atrial tachycardia (6 patients). Electrophysiologic differences between the 2 groups included a higher late diastolic threshold in Group II (0.8 +/- 0.2 mA versus 1.3 +/- 0.2 mA; p less than 0.005), and a greater increase in intraatrial conduction time (5 +/- 10 ms versus 30 +/- 20 ms; p less than 0.005) and interatrial conduction time (5 +/- 15 ms versus 30 +/- 15 ms; p less than 0.05) of early premature responses. There were no differences between the 2 groups in refractory periods, shape of the strength interval curve, or conduction times of premature responses occurring late in diastole. These abnormalities in conduction time and excitability found in patients with a prolonged P-wave duration may predispose to the initiation of certain atrial tachyarrhythmias.

Adult↗
PubMed1982

Interaction of acidosis and increased extracellular potassium on action potential characteristics and conduction in guinea pig ventricular muscle.

We studied the individual and combined effects of extracellular acidosis and increases in extracellular potassium on action potential characteristics and conduction in order to gain a better understanding of the effects of acute ischemia. At each level of potassium between 2.7 and 17 mm, acidosis induced by increasing Pco2 (respiratory acidosis) and by decreasing HCO3- (metabolic acidosis) decreased resting membrane potential, the maximum rate of rise of the action potential upstroke (Vmax), and slowed conduction. Metabolic acidosis consistently and significantly lengthened the steady state action potential duration whereas respiratory acidosis did not. Respiratory acidosis caused changes in resting membrane potential, Vmax, and conduction velocity; which occurred more rapidly and were of greater magnitude than the changes induced by metabolic acidosis. The changes in Vmax induced both types of acidosis were due to a change in the resting membrane potential-Vmax relationship as well as to the changes in the resting membrane potential. The conduction slowing induced by acidosis was greater when potassium was 9 and 13 mM than when potassium was 5.4 mm. Our results suggest that acidosis causes important changes in the electrophysiological properties of ventricular fibers and that many of the known electrophysiological effects of acute ischemia can be mimicked by the combined effects of extracellular acidosis and an increase in extracellular potassium.

Acidosis↗
PubMed1980

Effect of acute coronary artery occlusion on local myocardial extracellular K+ activity in swine.

We studied the time course, magnitude and homogeneity of the change in extracellular myocardial potassium activity after acute ligation of the left anterior descending coronary artery in pigs using potassium-sensitive electrodes made from a valinomycin-polyvinyl chloride matrix membrane. We also studied the relationship between the changes in potassium activity and the simultaneous changes in ventricular activation using the reference barrel of the K+ electrode to record ventricular electrograms. We found that the K+ rose sooner, more rapidly and to higher levels than previously reported. The K+ changes occurred in three phases: a phase of rapidly rising K+ that began within seconds of the ligation and lasted 5-15 minutes, a plateau phase that lasted approximately 15 minutes and a phase of slowly rising K+ that extended throughout the longest occlusion (60 minutes) used in this study. The K+ changes were reversed by release of the occlusion during the rapidly rising and plateau phases, but were not reversed by release of the occlusion during the phase of slowly rising K+. Inhomogeneities in the K+ rise appeared between the center and lateral margins of the midmyocardial ischemic zone, between the subendocardium and the subepicardium in the center of the ischemic zone, and between closely spaced electrodes located in the midmyocardial center of the ischemic zone. Thus, the change in K+ activity, as recorded by our electrodes, can be considered an excellent marker of ischemia. Changes in ventricular activation paralleled the K+ rise, the inhomogeneities of K+ rise and the reversal of the K+ rise after release but could not be entirely explained by the change in K+.

Animals↗
PubMed1979

Effects of verapamil on rapid Na channel-dependent action potentials of K+-depolarized ventricular fibers.

We studied the effects of 1 to 3 micrograms/ml of verapamil on Vmax and plateau duration in guinea-pig papillary muscles depolarized from -90 to -55 mV by increasing extracellular potassium from 5.4 to 20 mM. Under the conditions of our experiments, we found that verapamil did not influence the steady-state or recovery characteristics of Vmax at any of the studied K levels even when Vmax was less than 20 V/sec. Thus in the absence of rapid sodium channel blockade, the value of Vmax cannot be used to identify slow channel-dependent action potentials. Verapamil caused no shortening of plateau or total action potential duration when potassium was less than 7.5 mM. Above this level, verapamil caused progressive shortening of plateau and total action potential duration, due to the increase in potassium and not the associated decrease in resting membrane potential. Increasing extracellular calcium shortened plateau duration at all levels of potassium before verapamil but lengthened plateau duration in the high K, verapamil-treated fibers. These results, which can be explained by known effect of verapamil on the slow outward as well as slow inward currents, provide a mechanism whereby verapamil may increase Vmax of K-depolarized but rapid sodium current-dependent premature action potentials.

Action Potentials↗
PubMed1978

Flexible valinomycin electrodes for on-line determination of intravascular and myocardial K+.

Flexible electrode systems capable of monitoring in vivo changes in venous and myocardial extracellular potassium activity were constructed using valinomycin-polyvinyl chloride matrix membrane and polyvinyl chloride tubing. Electrode impedance was 1--30 Momega, time constant 10--200 ms, drift less than 1 mV/h, and shelf life approximately 3 days (intramyocardial electrode) and approximately 6 wk (venous electrode). In vitro and in vivo accuracy were determined in 5 dogs and 18 pigs, anesthetized with sodium pentobarbital (35 mg/kg iv), with normal and elevated K+ levels. Serum and venous K+ concentration, determined using a K+ electrode with tip diameter of 1.5 mm, correlated well to serum K+ values determined by flame photometry (r = 0.997). Steady-state myocardial extracellular K+ concentration determined using double-barrel electrodes with total tip diameter of 0.6 mm also correlated well to the serum K+ concentration (r = 0.992). These electrode assemblies permit on-line, virtually instantaneous in vivo determination of intravascular and local myocardial extracellular K+ activity, a capability not previously available.

Animals↗
PubMed1976

Combined effects of rate membrane potential, and drugs on maximum rate of rise (Vmax) of action potential upstroke of guinea pig papillary muscle.

We studied the effect of increasing the rate of stimulation on the maximum rate of rise of the action potential upstroke (Vmax) in guinea pig papillary muscles at various resting membrane potentials and after the addition of quinidine and lidocaine to the perfusate. Increasing rate caused a decrease in Vmax due to interaction of three factors: (1) a metabolic factor, presumably resetting of the Na-K pump, which caused a decrease in Vmax at all levels of resting potential between -90 and -60 mV, (2) a transient decrease in resting potential which influenced Vmax when the resting potential was less negative than approximately -80 mV, and (3) the recovery characteristics of Vmax which contributed to the decrease in this variable when rate was faster than 5/sec. As a result of these factors the steady state curve relating membrane potential to Vmax was itself rate-dependent. Lidocaine and quinidine exaggerated the rate-dependent decrease in Vmax; however, their effects differed. The effect of quinidine was consistent with its known depressant effect on the Na-K pump. The lidocaine effect was consistent with a slowing of recovery of Vmax. Our results help to explain the effects of an increase in rate on Vmax and conduction velocity in normal, partially depolarized, and drug-treated fibers

Action Potentials↗
PubMed1976

Painless ST-segment depression in patients with angina pectoris. Correlation with daily activities and cigarette smoking.

Ambulatory electrocardiographic monitoring was employed in 33 patients with angina pectoris and abnormal stress tests to determine the frequency with which myocardial ischemia manifested by painless ST-segment depression occurred during normal activity. ST-segment depression occurred in 24 patients during the monitoring period; and in 21, it occurred either solely in the absence of pain or both with and without pain. Of 109 recorded episodes of ST-segment depression, 61 percent were painless. The frequency of painless ST-segment depression was independent of activity other than automobile driving, during which all episodes were painless. In patients who smoked cigarettes, ST-segment depression was more common while smoking, but the incidence of painless ST-segment depression was not altered. The study indicates that ST-segment depression occurs more commonly in the absence than in the presence of chest pain and that ambulatory electrocardiographic monitoring is a useful method of determining the frequency of myocardial ischemia during normal daily activity.

Adult↗