Robert E. Edmands

T wave alternans: An association with abrupt rate change

Abstract A case of alternation of T wave with reversal of polarity, independent of any changes of the QRS but apparently greatly influenced by abrupt cycle length change, is presented. Evidence suggests that this phenomenon is indicative of severe myocardial disturbance.

The Relation of Contractile Enhancement to Action Potential Change in Canine Myocardium

Simultaneous recordings of contractile tension and transmembrane potentials from canine ventricular tissue yielded a consistent correlation of action potential (AP) alteration with contractile change associated with abrupt rate change. The AP terminating a relative prolongation of the cycle-length manifested shortening of phase 2 with lengthening of phase 3 and was associated with potentiation of contractile force. Conversely, the AP terminating a relative abbreviation of cycle-length displayed a broader phase 2 with a more precipitous phase 3, while the associated contraction was less forceful than the control. In each circumstance, the relative magnitude of cycle-length change correlated with the extent of both AP change and contractile alteration. Changes in AP configuration may reflect changes in transmembrane flux of K+ during repolarization consistent with the findings of prior workers who have related K+ efflux to increased contractility. Mechanical alternans, in addition, was frequently observed in association with abrupt rate change and was consistently associated with an electrical alternans manifested by action potentials with alternately wide and narrow plateaus (phase 2). As above, the more forceful contractions were associated with action potentials which displayed a narrower phase 2. Mechanical alternans initiated by abrupt rate change may represent an adaptive phenomenon prior to the establishment of a stable contractile state, as reflected by a stable AP configuration.

Complete atrioventricular block due to potassium.

Intravenous infusion of KC1 at a rate of 1.22 or 2.45 mEq per minute to anesthetized dogs frequently resulted in complete A-V block at a time when P waves were still recorded in the ECG. Furthermore, some of the observations suggest that in hyperkalemia a regular idioventricular rhythm may not be essential for the diagnosis of complete atrioventricular (A-V) block. Thus, with complete A-V block induced during a rapidly changing plasma K+, the ventricular pacemaker may be irregular. In addition, evidence was obtained that some parts of the atrial tissue, the automatic ventricular focus and the ventricular myocardium, are more resistant to K+ than is the A-V conduction tissue. The relative sensitivity of the various tissues of the heart seems to depend, among other factors, on the rate of KCl infusion.

An Electrophysiologic Correlate of Ouabain Inotropy in Canine Cardiac Muscle

Action potentials were recorded via intracellular microelectrodes, together with recordings of isometric-contractile tension, from isolated trabecular muscles of canine ventricle. The effects of administration of ouabain solution in concentrations varying from 1.7 × 10−7 to 5 × 10−4 M were recorded. The early inotropic effects of ouabain (increase in contractile force) were accompanied by changes in configuration of the action potential identical to those associated with interval-dependent potentiation in the control state, that is, abbreviation of phase 2 and lengthening of phase 3, without significant change in duration of the action potential. The progressive administration of ouabain, while associated with contractile enhancement of the regularly stimulated contraction was also accompanied by a loss of the contractile increment associated with poststimulation potentiation; this loss of interval-dependent potentiation corresponds to a loss of interval-dependent alteration of the action potential. Thus, both interval-dependent contractile potentiation and ouabain inotropy correlate consistently with phase 2 abbreviation of the accompanying action potentials.

The effect of change in cycle length on the ventricular action potential in man.

Abstract Electrophysiologic studies of human papillary fibers disclosed a characteristic alteration in the configuration of action potential, associated with abrupt change in the cycle length. After a relative prolongation of the cycle, phase 2 was abbreviated and phase 3 lengthened. Conversely, a relative abbreviation of the cycle was terminated by an action potential with a more sustained phase 2 and a more precipitous phase 3. In either case the total duration of the action potential remained unchanged. The physiologic mechanism underlying these changes in action potential, although obscure, may represent a primary alteration in repolarization possibly caused by time-dependent changes in membrane permeability to K + . This pattern of change in action potential, associated with abrupt alteration in rate, is clearly at variance with the conventional concept of a direct relation between duration of phase 2, the total action potential and the length of the preceding diastole. The latter relation appears to hold true only if the preparation is driven at a constant rate. It is suggested that this interval-dependent alteration in repolarization may account for the so-called change in post-extrasystolic T wave that is occasionally observed in the surface electrocardiogram. The absence of such T wave changes in normal subjects suggests that these changes in repolarization may be of insufficient magnitude in the normal subject to be recorded in the surface electrocardiogram. A temporal relation has been observed between the magnitude of contractility and morphology of the human action potential. Similar observations have been made in the dog. Whether the parallel between morphology of action potential and potentiation of contractility reflects a causal relation between inotropic phenomena and membrane permeability remains to be seen.

The postextrasystolic T wave change

Abstract Microelectrophysiologic studies of canine and human ventricular myocardium demonstrate characteristic changes in the configuration of the transmembrane action potential upon abrupt rate change. Additional studies have shown also that these action potential changes, involving cellular repolarization (phase 2 and phase 3), correlate closely with the magnitude of the concurrent postextrasystolic contractile changes. Further experiments in normal anesthetized dogs demonstrate that the postextrasystolic T wave change relates significantly to the magnitude of the postextrasystolic contractile potentiation. In addition, depression of the contractile state by pentobarbital enhanced the relative magnitude of postextrasystolic contractile change, whereas enhancement of the contractile state by acetylstrophanthidin yielded a lessening of the relative magnitude of postextrasystolic contractile potentiation. However, the associated T wave relation persists, as a result of which the postextrasystolic T wave change is more prominent in the presence of myocardial depression of contractility. It has therefore been suggested that the postextrasystolic T wave change is basically a normal phenomenon correlating with the magnitude of postextrasystolic contractile change. The observed association of the postextrasystolic T wave change with myocardial disease may reflect the relatively greater postextrasystolic contractile change associated with depression of the contractile state. A review of clinical electrocardiograms appears to corroborate this contention, demonstrating that when other variables are excluded exhibition of the postextrasystolic T wave change relates significantly to the closeness of the coupling of the premature complex and the magnitude of the base line T wave.

The electrocardiographic effects of elevated cerebrospinal fluid pressure: Wolff-Parkinson-White type of conduction disturbance

Abstract Cerebrospinal fluid pressure was elevated in 14 dogs and an ECG was recorded before elevation of CSF pressure, 5 and 10 minutes after CSF pressure elevation to 100 mm. Hg, 5 and 10 minutes after CSF pressure elevation to 200 mm. Hg, and 10 minutes after CSF pressure returned to control levels. In 10 of the 14 studies, the ECG exhibited what appeared to be anomalous A-V conduction with a short P-R and widened QRS. This usually occurred in alternate complexes but occasionally a phasic, cyclical pattern was observed with progressive shortening of P-R and widening of QRS. With the short P-R, the QRS consistently assumed a left axis deviation with rightward directed terminal forces and distinct delta waves were inscribed in the anomalous left precordial complexes. Systemic blood pressure, heart rate, and serum glucose were significantly elevated during CSF pressure of 200 mm. Hg. These data suggest that WPW-like anomalous conduction may result from neurohumoral factors and need not be dependent on abnormal anatomical pathways.