Abnormal QRS Complexes Research Articles

Marked QRS complex abnormalities and sodium channel blockade by propoxyphene reversed with lidocaine.

The opiate analgesic propoxyphene produces cardiac toxicity when taken in overdose. We recently observed a patient with propoxyphene overdose in whom marked QRS widening was reversed by lidocaine. The reversal is apparently paradoxical as both agents block the inward sodium current (INa). We examined possible mechanisms of the reversal by measuring INa in rabbit atrial myocytes during exposure to propoxyphene and the combination of propoxyphene and lidocaine (60 and 80 microM, respectively). Propoxyphene caused use-dependent block of INa during pulse train stimulation. Block recovered slowly with time constants of 20.8 +/- 3.9 s. Block during lidocaine exposure recovered with time constants of 2-3 s. During exposure to the mixture, block recovered as a double exponential. The half time for recovery during exposure to the mixture was 1.6 +/- .9 s compared with a half-time of 14.3 +/- 2.9 s during exposure to propoxyphene alone. During pulse train stimulation, less steady-state block was observed during exposure to the mixture than during exposure to propoxyphene alone when the interval between pulses was greater than 0.95 s. Both drugs compete for a common receptor during the polarizing phase. The more rapid dissociation of lidocaine during the recovery period leads to less block during the mixture than during exposure to propoxyphene alone. The experiments suggest a mechanism for reversal of the cardiac toxicity of drugs which have slow unbinding kinetics.

ECG waveform analysis by significant point extraction: II. Pattern matching

From a set of significant points which characterizes the ECG waveform, the pattern matching algorithm detects and classifies QRS complexes. R waves are detected from the analysis of global curvature. Next, the morphology of the QRS complex is determined. QRS complexes with different morphologies are classified by a correlation algorithm. This method is sensitive to changes in shape, such as that of abnormal QRS complexes. The algorithm should be useful in automated analysis of waveforms, such as ECG signals recorded in clinical environments.

Electrocardiographic criteria for differentiating aberrancy and ventricular extrasystole in chronic atrial fibrillation: Validation by intracardiac recordings

Many electrocardiographic criteria have been proposed for the differentiation of ventricular extrasystole and supraventricular conduction with aberrancy in atrial fibrillation but the validity of these have not been confirmed by intracardiac studies. We recorded His bundle electrograms in nineteen patients (eleven men, eight women) referred for diagnosis of abnormal QRS complexes in the context of chronic atrial fibrillation. Of 1,068 wide QRS complexes analyzed, 91% proved to be of ventricular origin. Electrocardiographic criteria which were specific for ventricular extrasystole included: left bundle branch block morphology, right bundle branch block morphology with a monophasic R in lead V1 or an RS or QS pattern in lead V6, presence of a "compensatory pause", i.e., compensatory cycle (V2-V3) longer than the average cycle length of ten normally conducted beats preceding the abnormal complex (927 +/- 317 vs 780 +/- 199, mean +/- SD in msec. p less than 0.005), frontal QRS axis of the abnormal complex directed superiorly or to the right and the presence of a "short-long" cycle sequence. Right bundle branch morphology with a triphasic R in lead V1 or QRS pattern in V6 and concordant initial vector in lead V1 or in more than one ECG leads were very specific for supraventricular conduction with aberrancy. Analysis of coupling interval and Ashman's phenomenon, i.e., the long-short cycle sequence, were not specific for supraventricular conduction with aberrancy. We conclude that in digitalis-treated patients with chronic atrial fibrillation the majority of abnormal QRS complexes are of ventricular origin. The diagnosis of ventricular extrasystole or aberrancy can be made using a single ECG lead (V1) and applying a combination of easily applied criteria.

Cardiomyopathy in generalised glycogenosis type II in cattle.

The clinical, electrocardiographic and postmortem findings in five cattle affected by generalised glycogenosis type II are described. Three of the affected animals showed generalised muscle weakness for some months before being killed at 11, 15 and 16 months of age. Of the remaining two, one developed severe respiratory distress when 3 months old and died within 6 h of first being noticed to be ill. The other animal showed respiratory distress on exertion at 5 months of age, became recumbent and died when 7 months old. The sum of the QRS complex amplitudes in ECG leads I, II, a VR, aVL and aVF of the affected animals was significantly increased from the control or carrier animals, but only the two affected animals which showed clinical and pathological signs of congestive heart failure had increased heart weight to body weight, left and right ventricular weight to body weight ratios. In view of the lack of correlation between the increased QRS amplitudes and the presence of cardiac enlargement, it is suggested that the increased QRS amplitudes are a reflection of a conduction disorder. It is further suggested that QRS complex abnormalities in generalised glycogenosis in man, particularly in the late onset form may be due to a similar phenomenon.

Prognostic differences in subgroups of patients with electrographic evidence of subendocardial or transmural myocardial infarction: The favorable outlook for patients with an initially normal QRS complex

To compare the prognostic significance of electrocardiographic descriptors of infarction, the hospital and follow-up course of 635 patients with acute myocardial infarction was evaluated. Patients were divided into two groups based on the initial electrocardiogram following the onset of symptoms: group I, a normal QRS complex; and group II, an abnormal QRS complex secondary to Q waves, bundle branch block or ventricular hypertrophy. Patients were further subdivided on the basis of serial electrocardiograms: A, no new Q waves; and B, the development of new Q waves. Patients in group IA had a lower incidence of atrial and ventricular arrhythmias, atrioventricular block and heart failure than patients in group IIA. There were no hospital deaths in group IA, compared with a 13 percent mortality in group IIA. The hospital mortality was significantly less for patients in group IB than in group IIB (8 percent versus 20 percent, p < 0.001). The mean duration of follow-up was 30 months. There was a significantly lower follow-up mortality in group IA (12 percent) than in group IIA (45 percent), p < 0.001), and in group IB (12 percent) than in group IIB (34 percent, p < 0.001). These data suggest that patients with either “subendocardial” or “transmural” infarctions can be subdivided into low and high risk categories regarding both hospital and long-term prognosis. Patients with a normal QRS complex initially have the greatest likelihood of a benign prognosis following an acute myocardial infarction.

Hiccups in infants: Characteristics and effects on ventilation

Twenty-seven polygraphic recordings of respiration were obtained on 20 infants, providing data on the frequency, distinguishing features, and medical significance of hiccupping episodes. Eight hiccupping episodes were recorded in seven subjects. The mean duration of the spells was 8.4 +/- 4.2 (SD) minutes. Unintubated subjects, not selected because they were hiccupping, hiccupped 2.5% of the time that they were monitored. Each hiccup was a brief, powerful inspiratory muscle contraction. In unintubated subjects, hiccups were marked by upper airway obstruction, whereas in intubated patients, hiccups were unobstructed inspirations. In unintubated subjects, hiccups were associated with an increase in obstructed eupneic breaths and with decreases in respiratory frequency and minute ventilation; in three subjects hiccups precipitated episodes of mixed apnea. In intubated patients, hiccupping spells were characterized by hyperventilation and respiratory alkalosis. Two types of ECG artifacts were seen with hiccups: high-frequency spikes, mimicking abnormal QRS complexes, and low-frequency waves. From these studies, it appears that hiccups occur frequently in young infants and may affect breathing in clinically significant ways.

Quantitative analysis of exercise electrocardiograms and left ventricular angiocardiograms in patients with abnormal QRS complexes at rest.

The ECG changes during exercise are described in 71 patients with a previous anteroseptal or anterolateral infarction (ANT-MI) and in 73 patients with an old posterior or inferior wall infarction (INF-MI). Left ventricular angiograms in 95 patients yielded a good correlation between areas of dyssynergy and the QRS pattern at rest. The ST changes in patients with coronary artery disease and a normal ECG at rest, and in normal subjects, were oriented toward the right, posteriorly and superiorly. In patients with INF-MI and inferior wall dyssynergy, the ST changes were more inferiorly oriented. Anteriorly-oriented ST changes were associated with anterior wall or apical dyssynergy and with ANT-MI. Thus the spatial direction of the ST changes during exercise is related to three independent factors: those factors which cause the ST changes in normal subjects, the degree of myocardial ischemia in that particular case, and the extent of dyssynergic areas in the wall of the left ventricle.

Familial atrioventricular heart block; an autosomal dominant trait.

A family of 28 individuals spanning four generations was investigated because of a finding of complete heart block in five members and the existence of a low degree of atrioventricular (A-V) heart block in a sixth member. The disorder was characterized by 1) adult onset in all, 2) complete A-V heart block in five and first degree A-V heart block in one, 3) sinus bradycardia in three, 4) atrial fibrillation in five, 5) abnormal QRS complex in five, 6) ventricular tachycardia in three, 7) left ventricular enlargement in all, and 8) mitral insufficiency in five. Proximal location of the A-V heart block was suggested by the fact that atropine caused acceleration of the ventricular rate and by the presence of a His bundle potential preceding the QRS complexes. Involvement of the distal conducting system was indicated by the widened QRS complex and a prolonged H-V interval. Pathologic examination in one case showed extensive sinus node fibrosis and interruption of the A-V node-His bundle connection. This disorder is probably due to an autosomal dominant trait.

ECG-monitor artifacts.

Comments and Corrections1 April 1973ECG-Monitor ArtifactsDOUGLAS R. HANSMANN, PH.D., JOSEPH J. SHEPPARD, PH.D.DOUGLAS R. HANSMANN, PH.D.Search for more papers by this author, JOSEPH J. SHEPPARD, PH.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-78-4-619 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The letter in the December 1972 issue "Artifacts in Portable ECG Monitoring" (Ann Intern Med 77:1004) described two malfunctions that may occur during the use of the Holter monitor, also known as dynamic electrocardiography (DCG). Two malfunctions were described: pseudotachycardia induced by an abnormally slow tape speed, which crowds the ECG complexes together; and apparently abnormal QRS complexes caused by improper erasure of a previously used DCG tape.With regard to the first malfunction, an artificial tachycardia can be manifested by either a worn-out motor or an insufficiently charged battery. In the case of a worn motor,... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByNicht-invasive Verfahren einschließlich Holter-MonitoringCar Wash TachycardiaC. RICHARD SMITH JR., D.O., DAVID ELBAUM, D.O.Unusual artifacts in electrocardiographic monitoringArtifacts in portable electrocardiographic monitoringInterference And Motion Artifact In Biopotentials 1 April 1973Volume 78, Issue 4Page: 619-619KeywordsElectrocardiographyTachycardia Issue Published: 1 April 1973 PDF DownloadLoading ...

ECG analysis no. 11. Supraventricular arrhythmias with abnormal QRS complex

Since all of the electrocardiographic manifestations of ventricular tachycardia may be mimicked, under certain circumstances, by supraventricular tachycardia, many exceptions must exist to the criteria that help to differentiate supraventricular arrhythmias with abnormal QRS complex from ventricular arrhythmias.^1-4For example, premature ventricular complexes that arise in the left ventricle (and, therefore, have a right bundle-branch block pattern) and conform to the rule of bigeminy may be difficult to differentiate from aberrantly conducted supraventricular complexes following a long-short cycle pattern²; functional bundle-branch block may occur within the left bundle-branch system^2,4; widened QRS complexes apparently introduced by a P wave may be due to coincident ventricular activity occurring independently (Fig 1). Often, a given arrhythmia with wide QRS complexes lacks distinct features that may characterize it as supraventricular or ventricular, or it may share features of both supraventricular and ventricular arrhythmias. In this final article of the series on

Supraventricular Arrhythmia With Abnormal QRS Complex

Thus far, the discussion of supraventricular arrhythmia with abnormal QRS complex has included preexisting conduction defects, the preexcitation syndrome (Wolff-Parkinson-White syndrome), and functional bundle-branch block due to sudden shortening of cycle length, often combined with prolongation of preceding cycle; the latter is popularly called the "Ashman phenomenon." We will now present examples of other causes of aberrancy for which the mechanistic explanations may not be as clearly delineated as for those entities previously presented. <h3>Aberrancy Occurring at Slow Rates</h3> The contour of QRS complexes which escape after long pauses may differ from the QRS complex inscribed during the normal dominant rhythm; yet, the duration of these escape systoles, which is less than 0.12 seconds, strongly, but not unequivocally, indicates an origin above the bifurcation of the bundle of His (Fig 1 and 2). Basically, four theories exist which attempt to explain the cause of such aberrantly conducted junctional escape beats.

Mobitz Type II Atrioventricular Block in a Newborn

Patients with congenital complete heart block and no other cardiac lesion usually are asvmptomatic and have a normal axis and QRS pattern on the electrocardiogram. The site of the block is usually in the region of the AV node. Another less common type of congenital AV block has an abnormal QRS complex on the electrocardiogram. Death from Stokes-Adams attack has been recorded in infancy in this group. Mobitz Type II block is very rare in infancy but may precede complete heart block which requires ventricular pacing. The purpose of this report is to illustrate Mobitz Type II heart block in a newborn which progressed to complete block.

Supraventricular Arrhythmia With Abnormal QRS Complex

Thus far, the discussion of supraventricular arrhythmia with abnormal QRS complex has included preexisting conduction defects, the preexcitation syndrome (Wolff-Parkinson-White syndrome), and functional bundle-branch block due to sudden shortening of cycle length, often combined with prolongation of preceding cycle; the latter is popularly called the "Ashman phenomenon." We will now present examples of other causes of aberrancy for which the mechanistic explanations may not be as clearly delineated as for those entities previously presented. Aberrancy Occurring at Slow Rates The contour of QRS complexes which escape after long pauses may differ from the QRS complex inscribed during the normal dominant rhythm; yet, the duration of these escape systoles, which is less than 0.12 seconds, strongly, but not unequivocally, indicates an origin above the bifurcation of the bundle of His (Fig 1 and 2). Basically, four theories exist which attempt to explain the cause of such aberrantly conducted junctional escape beats.

Experimental bigeminal arrhythmia in the dog

Ventricular bigeminal rhythm was successfully induced in 26 of 34 vagotomized dogs. Induction was accomplished through bilateral carotid artery occlusion, constriction of the thoracic aorta, or a combination of both. The following observations were made:o1.This arrhythmia appears to depend on some combination of high systemic arterial pressure and increased heart rate. It can be induced under conditions in which sympathetic discharge to the heart is inhibited.2.Sinoatrial firing rate during the bigeminal rhythm is usually regular. The PR interval is always shorter and QRS duration longer in the abnormal complex of a bigeminal pair.3.Delta waves are commonly present in the initial portion of QRS complexes of abnormal beats. These complexes have the general characteristics associated with ventricular pre-excitation (WPW).4.Mean frontal QRS vector angles in normal beats of bigeminal pairs were in the range of 23°–76°. Vector angles for abnormal mean frontal QRS complexes were widely distributed in a range of 137°–357°.5.The experimental data do not provide a positive basis for classifying the abnormal complexes as ventricular pre-excitation or coupled late ventricular ectopic beats. In either case, it appears that the site of initial ventricular activation in abnormal complexes is widely dispersed in this group of animals. This arrhythmia appears to depend on some combination of high systemic arterial pressure and increased heart rate. It can be induced under conditions in which sympathetic discharge to the heart is inhibited. Sinoatrial firing rate during the bigeminal rhythm is usually regular. The PR interval is always shorter and QRS duration longer in the abnormal complex of a bigeminal pair. Delta waves are commonly present in the initial portion of QRS complexes of abnormal beats. These complexes have the general characteristics associated with ventricular pre-excitation (WPW). Mean frontal QRS vector angles in normal beats of bigeminal pairs were in the range of 23°–76°. Vector angles for abnormal mean frontal QRS complexes were widely distributed in a range of 137°–357°. The experimental data do not provide a positive basis for classifying the abnormal complexes as ventricular pre-excitation or coupled late ventricular ectopic beats. In either case, it appears that the site of initial ventricular activation in abnormal complexes is widely dispersed in this group of animals.

Atrioventricular Conduction Defects in Patients with Sinus Bradycardia

A-V conduction was analyzed in 75 patients (mean age, 73 years) with sinus bradycardia (SB) by His bundle (BH) recordings. Forty-five of these patients had normal QRS complexes (≦0.10 sec) and 30 had abnormal QRS complexes (≧0.12 sec). The conduction times through the atrium (P-A), A-V node (A-H), and His-Purkinje system (H-V) were measured during normal sinus rhythm and transient right atrial pacing up to rates of 150/min. The normal range of conduction times through various regions is: P-A = 25 to 45 msec; A-H = 50 to 120 msec, and H-V = 35 to 45 msec. Overall A-V conduction was completely normal only in 25 (33%) patients. Of these 25 patients, 20 had a narrow QRS complex and five had an abnormal QRS complex. The remaining 50 patients showed abnormal A-V conduction in one or more regions (P-A in 10, A-H in five, BH in six, H-V in 10, and mixed in 19). In some patients despite normal ECGs, the H-V time was abnormal and 1:1 A-V conduction was present during atrial pacing up to 150/min. An abnormal H-V time in association with a normal QRS complex is suggestive of delay in the His bundle. Fourteen patients were restudied at intervals of 6 months to 2 years. Three of these 14 patients showed prolongation of conduction times over 1½ to 2 years. Our data demonstrate that SB is often (67%) associated with A-V conduction abnormalities. A-V conduction was abnormal in 56% of patients with normal and 83% with abnormal QRS complexes. The ECG and atrial pacing are of limited value in assessing A-V conduction. The BH recordings in symptomatic patients with sinus bradycardia may be of clinical significance in the selection of site for pacemaker implantation, that is, atrial or ventricular.

SPATIAL MAGNITUDE, ORIENTATION, AND VELOCITY OF THE NORMAL AND ABNORMAL QRS COMPLEX.

Curves of spatial magnitude, orientation, and velocity of the QRS complex were obtained by digital computation from 252 normal and 328 abnormal orthogonal electrocardiograms (Frank system). An attempt was made to evaluate the diagnostic usefulness of this type of spatial data display. Because of interindividual variability in QRS duration it was not possible to compare accurately individual records with normal standards. Normalization in time was, therefore, necessary by dividing each QRS complex in time in 10 equal parts. Mean curves were computed for the normal control group and eight pathologic entities. Although differences in configuration between the various groups became evident, a large overlap between the various ranges prevented an efficient classification for diagnostic purposes. A point-by-point separation between normal ranges and individual curves showed high recognition rates for abnormalities without specific diagnostic classification. The highest information content appeared to be present in curves of spatial orientation. Since time-normalization and numerical statistical analysis of multiple points are not feasible with presently available analog computers, the question is raised whether digital computation is not more efficient in diagnostic classification of electrocardiograms.

Differentiation of supraventricular and ventricular tachycardias

Summary o 1. Problems encountered in the differential diagnosis of supraventricular and ventricular tachycardias are reviewed and exemplified by representative electrocardiograms. 2. In supraventricular, as well as in ventricular, types of rapid ectopic rhythms, the action of the ventricles may be very rapid or only moderately accelerated, regular or irregular, the QRS duration may be normal or prolonged, and the atria may beat independently or follow the action of the ventricles. Clinical and electrocardiographic criteria based on one or several of these aspects are, therefore, inconclusive and deceptive. 3. When an ectopic tachycardia presents abnormal and/or prolonged QRS complexes, its supraventricular or ventricular origin can be established, though not in every instance, on the basis of: (a) a comparison with single conducted (supraventricular) impulses, or single premature beats, recorded before, after, or during the tachycardia; (b) the occurrence of ventricular fusion beats and (c) a consideration of the type of QRS widening and the mode of its onset and/or disappearance.

Acetyl strophanthidin sensitivity in dogs with congestive heart failure

Fifteen normal dogs and five dogs with experimental congestive heart failure were given standard doses of acetyl strophanthidin on the basis of ascites-free weight. Four animals with cardiac failure developed persistent atrioventricular dissociation with abnormal QRS complexes, whereas no normal dog showed a serious arrhythmia. The normal dogs demonstrated a greater rise in the concentration of serum potassium after acetyl strophanthidin than did the animals with congestive failure. Analysis of the electrocardiograms suggests that atrioventricular dissociation may occur as a result of simultaneous slowing of the sinus node, slowed conduction velocity in intraventricular conduction tissue, and increased rhythmicity of one or more foci in this tissue or in ordinary myocardial fibers. The available evidence suggests that physical, nervous, and chemical factors operating on the failing heart could explain its increased sensitivity to digitalis-like compounds. It is also possible that the congested liver makes a larger fraction of administered drug available to the heart and is incapable of producing the normal rise in the concentration of serum potassium after digitalis has been administered.

Muscular dystrophy; catheterization studies indicating latent congestive heart failure.

In an attempt to explain the electrocardiographic and other cardiac abnormalities in patients with muscular dystrophy, hemodynamic studies by right heart catheterization were done on 12 patients with muscular dystrophy. The study indicated the presence of latent congestive failure in some patients. An attempt to explain the abnormal QRS complexes and leads from the right side of the precordium in some of those patients is also made.

Cancellation of the abnormal QRS complex of heart disease

1. 1. Mirror patterns were found on the body surface for normal and abnormal QRS complexes in sixty-two patients, using a precision cancellation technique. Cancellations were 85 per cent or better in 90 per cent of the patients; the poorest cancellation was 81 per cent. 2. 2. Existence of mirror patterns of QRS complexes indicates the dipolar nature of the electrical behavior of the heart during the period of ventricular depolarization. 3. 3. In a patient with right bundle branch block locations and amplitudes of the mirror patterns were predictable from a model with a properly located dipole. 4. 4. Localized electrocardiographic QRS patterns on the chest wall are not due to localized currents from subadjacent myocardium, but rather to alteration of the equivalent heart dipole.