Eugene Lepeschkin

The Measurement of the Q-T Interval of the Electrocardiogram

The sources of error in determination of the beginning of QRS and the end of T during measurement of the Q-T duration are analyzed. An important error is confusion of an elevated U wave with the T wave, resulting in the diagnosis of a prolonged Q-T. In such cases, some of the precordial leads usually show a notch or kink between T and U which indicates approximately the end of T. If these criteria are used, the true corrected Q-T duration in hypopotassemia without hypocalcemia is not prolonged, but normal or shortened, corresponding to an earlier appearance of the second heart sound.

Recommendations for Standardization of Leads and of Specifications for Instruments in Electrocardiography and Vectorcardiography

By COMMITTEE MEMBERS: CHARLES E. KOSSMANN, M.D., CHAIRMAN, DANIEL A. BRODY, M.D., GEORGE E. BURCH, M.D., HANs H. HECHT, M.D., FRANKLIN D. JOHNSTON, M.D., CALVIN KAY, M.D., EUGENE LEPESCHKIN, M.D., HUBERT V. PIPBERGER, M.D., AND by MEMBERS OF THE SUBCOMMITTEE ON INSTRUMENTATION: * HUBERT V. PIPBERGER, M.D., CHAIRMAN, GERHARD BAULE, PH.D., ALAN S. BERSON, M.S., STANLEY A. BRILLER, M.D., DAVID B. GESELOWITZ, Ph.D., LEO G. HORAN, M.D., AND OTTO H. SCHMITT, Ph.D.

Bilateral bundle branch block.

Abstract 1. 1. An electrocardiographic diagnosis of bilateral bundle branch block can be made in rare instances in which conduction in the branches is not completely interrupted and the degree of block in one of the branches is less than in the other on some occasions and greater on others; this allows the patterns of right and left bundle branch block to appear alternately or intermittently in the same patient, accompanied by changes of P-R. Two personal cases of this sort are reported and seven similar observations from the literature are discussed. 2. 2. While the incidence of bilateral bundle branch block in which this condition can be definitely proved is very small, the great incidence of unilateral bundle branch block makes it probable that many cases of complete A-V block, attributed to a conduction disturbance in the A-V node or the common stem of the bundle, are in reality caused by bilateral bundle branch block. 3. 3. In seven of the nine cases of definite bilateral bundle branch block, alternation of the right and left bundle branch block patterns was present at some time. The most probable explanation of this was considered to be 2:1 block in one of the branches in the presence of a constant prolongation of conduction in the other branch. 4. 4. Conduction in the branches behaves in the same way as in the rest of the A-V conduction system. In one of the cases (No. 1), all the possible forms of impaired conduction were demonstrated to be present in the left branch of the His bundle (simple prolonged conduction time, Wenckebach periods, 2:1 and 3:1 block, and transient complete interruption of conduction). 5. 5. True bilateral bundle branch block must necessarily prolong the A-V conduction time. The form of the ventricular complex is determined by the branch with the greater degree of block, while the conduction delay in the branch in which the block is less important determines the lengthening of the P-R interval. This must be so because the stimulus reaches the ventricules through the less affected branch. 6. 6. In true bilateral bundle branch block the intrinsicoid deflection of the ventricular complex is delayed only on the side of the chest corresponding to the more affected branch and is within normal limits on the opposite side. Cases in which the intrinsicoid deflection is delayed over both ventricles probably represent an association of true bundle branch block with an intraparietal conduction disturbance of the contralateral ventricle.

The electrocardiographic pattern of hypopotassemia with and without hypocalcemia.

Detailed analysis of the electrocardiogram in patients with hypopotassemia without hypocalcemia showed that the Q-U interval and its components (Q-oT, Q-aT, Q-T, and Q-aU) have essentially the same duration as in normal subjects for the same heart rate and sex. The typical hypopotassemia pattern is characterized by progressive depression of S-T, lowering and inversion of T and increase of U in left precordial leads. In hypopotassemia with hypocalcemia S-T and Q-T, but not Q-U, are prolonged, causing an increased degree of merging between T and U. Three methods of differentiation between completely merged T and U waves and true T waves of long Q-T duration are given.

The duration of the Q-U interval and its components in electrocardiograms of normal persons☆

Abstract 1. 1. In fifty normal men and fifty normal women the synchronous standard limb and precordial leads as well as the heart sounds were registered at rest. The following intervals were measured: the intervals from the beginning of the QRS complex to the end of this complex (QRS), to the origin of the T wave (Q-oT), to the apex of the T wave (Q-aT) to the end of the T wave (Q-T), to the “halfway point of T” (Q-T/2), to the apex of the U wave (Q-aU), and to the end of the U wave (Q-U). The origin of the T wave or the end of the RS-T segment was defined as the point most distant from a straight line connecting the RS-T junction with the apex of T. The relation of the beginning of the second heart sound to the apex and end of T and to the apex of U was also studied. All values were correlated with the heart rate and the age and sex, and in some cases also with the body height. 2. 2. The QRS duration, when measured from the earliest to the latest points in synchronous leads, is greater than when measured in separate limb leads. It increases slightly with decreasing heart rate but shows the greates relation to the body size. Men have a greater QRS duration than women, but in the same height groups the values were equal for both sexes. The upper limit for a height up to 5 feet 6 inches was 0.10 second, that for a height from 5 feet 6 inches to 6 feet was 0.11 second, and that for a height from 6 feet to 6 feet 6 inches was 0.12 second. Of nine persons over 6 feet tall, seven had a QRS exceeding 0.11 second. 3. 3. The Q-T duration increases with decreasing heart rate; at all heart rates women had on the average a 7 per cent longer Q-T duration than men. The components of Q-T (Q-oT and Q-aT) showed the same dependence on the heart rate as the entire Q-T interval. When expressed as a percentage of the Q-T interval expected for the heart rate, Q-oT ranged between 49 and 63 per cent, while Q-aT ranged between 62 and 92 per cent, independently of the heart rate and sex. Of all the components of Q-T, the RS-T segment was the most elastic, showing the greatest differences between the sexes and at high and low heart rates. QRS was the most rigid component. 4. 4. The interval from the end of T to the apex of U was practically independent of the heart rate and sex; it averaged 0.10 second. The Q-aU interval expected for a certain heart rate can be easily determined, therefore, by adding 0.10 second to the Q-T interval expected for this rate. The interval from the apex to the end of U was influenced by the heart rate more than any other interval, but as the determination of the end of U especially at high heart rates was difficult, this observation should be interpreted with caution. 5. 5. The second heart sound began within 0.03 second before or after the end of the T wave, 0.06 to 0.12 after the apex of T and 0.04 to 0.14 second before the apex of the U wave. At lower heart rates it tended to begin up to 0.01 second earlier. 6. 6. The electrocardiogram of women is characterized not only by a longer duration of Q-T and its components Q-oT and Q-aT but also by a longer and more horizontal RS-T segment than that of men. The point when the T wave reaches one-half of its final amplitude is situated nearer to the apex of T in women than in men. These characteristics make it possible, in most normal cases, to distinguish the electrocardiogram of a woman from that of a man.

Catecholamine-induced myocardial hypoxia in the presence of impaired coronary dilatability independent of external cardiac work∗☆

Abstract Surface electrocardiograms were taken in vagotomized cats over areas of the left ventricle. An adjustable nonoccluding restriction device prevented part of the coronary arterial supply from dilating. Under these circumstances, brief stimulation of the cardiac sympathetic nerves or reflex stimulation of the adreno-sympathetic system through electrically induced muscular “exercise,” or intravenous injection of catecholamines (epinephrine, norepinephrine) caused regularly marked elevations of the S-T segment and the T wave, even if concomitant augmentation of cardiac mechanical work was only minimal. Identical electrocardiographic changes were elicited by exogenous anoxia (breathing 100 per cent nitrogen), and by more complete coronary constriction. By contrast, no S-T displacement occurred despite coronary restriction when heavy work loads were imposed upon the heart by noncatecholamine influences, namely, tachycardia produced by electrical stimulation of the right atrium, or high rises of the blood pressure produced by intravenous injection of angiotensin II , or both combined. Neurogenic and blood-borne catecholamines cause severe regional myocardial hypoxia when the normal compensatory coronary dilatation is impaired. Such catecholamine-induced myocardial hypoxia is not caused by the concomitant augmentation of cardiac mechanical work which these neurohormones usually elicit, but by their specific biochemical oxygen-wasting properties. Our findings agree with the clinical experience that in patients with coronary sclerosis attacks of angina pectoris are ordinarily triggered by sympathetic-stimulating, catecholamine-liberating conditions (exercise, emotions and other stresses), and prevented by various antiadrenergic measures. Contrary to traditional belief, it is suggested that anginal symptoms do not occur because “the heart works harder” but because certain areas of the myocardium whose coronary vessels have lost the ability for compensatory dilatation are exposed to the biochemical hypoxiating influence of acute catecholamine discharges accompanying various stresses. Except in cases of far advanced coronary sclerosis, the term “coronary insufficiency” is to be understood as meaning inability of the coronary circulation to compensate by adequate dilatation for sympathogenic (catecholamine-induced) excessive myocardial oxygen losses.

Effect of epinephrine and norepinephrine on the electrocardiogram of 100 normal subjects

Abstract Electrocardiograms were registered during infusions of epinephrine and norepinephrine, 0.2 to 0.3 μg. per kg. per minute, in 100 normal young adults. Epinephrine caused increase of heart rate (a decrease occurred when the hypertensive effect was great), lower voltage of the T wave, elevation and earlier appearance of the U wave, and depression of the S-T segment. Inversion of the T wave in lead II and sometimes also in leads V 4 to V 6 occurred in about 10 per cent of the subjects, while in about 10 per cent the elevated U waves showed fusion with the T waves, resulting in a combination wave which resembled a wide, elevated T wave. This effect is explained on the basis of change in repolarization velocity seen in ventricular action potentials. Norepinephrine infusion caused decrease of heart rate and usually elevation of the T wave, but after atropine was given its effect became similar to that of epinephrine. Ectopic rhythms appeared after norepinephrine administration only at high blood pressure levels and at low heart rates, while after epinephrine administration they appeared at all rates. The differences between the effects of these two substances are attributed largely to partial counteraction of the direct effect of norepinephrine on the heart by reflex vagal excitation and sympathetic inhibition originating in the pressoreceptor areas.

The Effect of Ventricular Systole on Auricular Rhythm in Auriculoventricular Block

In some cases of complete A-V block the curve of the duration of P-P intervals showed a sudden dip with a gradual return, during or after the T wave. This positive chronotropic (accelerating) effect of ventricular systole is probably caused by the traction exerted on the right auricle by the contracting ventricle. Other cases showed a sudden rise in the curve of P-P intervals late in diastole, followed by a gradual return. This negative chronotropic (slowing) effect is probably caused by a vagal reflex precipitated by stimulation of the arterial pressoreceptors by the pulse wave. The interplay of these two effects determines whether the P-P intervals containing QRS will be shorter than those not containing it, or whether the relation is reversed (paradox effect).

Effect of Body Build on the QRS Voltage of the Electrocardiogram in Normal Men Its Significance in the Diagnosis of Left Ventricular Hypertrophy

Various sets of QRS voltages that are used in the diagnosis of left ventricular hypertrophy were determined from the electrocardiograms of 300 normal men judged to be free from cardiopulmonary disease, and these were correlated to body build expressed in terms of ponderal index. A correlation was found for all voltages studied and a highly significant correlation was found for the criteria “RI + SIII” “greatest R + greatest S in the precordial leads” and “greatest R + S ina single precordial lead.” Age or activity did not appear to be specific factors in the population studied. Graphs were constructed for the latter three sets of voltages defining upper limits of normal for various values of the ponderal index. By using these sets of voltage criteria in conjunction with this index, one would hopefully improve both accuracy and specificity in the electrocardiographic diagnosis of early left ventricular hypertrophy.

Low and High Magnesium Concentrations at Various Calcium Levels Effect on the Monophasic Action Potential, Electrocardiogram, and Contractility of Isolated Rabbit Hearts

Electrocardiograms, ventricular monophasic action potentials registered with suction and intracellular microelectrodes, and pressure curves were recorded simultaneously in isolated rabbit hearts perfused with oxygenated Krebs-Henscleit solution containing varying calcium/magnesium ratios. The duration of the action potential and Q-T interval was not affected by low and high magnesium concentrations unless calcium was omitted or significantly reduced. When Mg was completely absent, solutions free of calcium or with one-sixteenth of the “normal” Ca concentration caused a progressive prolongation of the action potential and Q-T interval until they occupied the entire cardiac cycle. When Mg concentration was low (0.075 to 0.6 mM/L.), the prolongation occurred at a slower rate and was less pronounced. With higher Mg concentrations (1.2 to 19.2 mM/L.), the initial lengthening of the action potential and Q-T interval was followed by a gradual shortening. The higher the Mg concentration employed, the shorter was the period of the initial lengthening, and the more pronounced was the subsequent shortening. These observations can be best explained by assuming that calcium-like action of Mg on the plateau of the action potential becomes apparent only when Ca is absent or significantly decreased. The depression of contractility by calcium deficiency proceeded at the same rate at all studied Mg concentrations. The findings are discussed in relation to the electrocardiographic patterns encountered in clinical cal cium and magnesium deficiency.