Complete Bundle Branch Block Research Articles

Cardiovascular disease in the very elderly: Analysis of 40 necropsy patients aged 90 years or over

Clinical and necropsy observations are described in 40 patients (29 women) aged 90 years and older. The majority (21 patients [57%]) died during the 4 coldest months, and 12 (30%), during the 4 warmest months. At necropsy, 39 had ≥1 major cardiac abnormalities, the most frequent being calcific deposits in the major epicardial coronary arteries in 37 (92%). In 28 patients (70%), 1 or more of the 4 major arteries was narrowed 76 to 100% in cross-sectional area (XSA) by atherosclerotic plaques, an average of 1.9/4.0 per patient: the 12 patients with clinical events compatible with myocardial ischemia (angina pectoris or myocardial infarction) had an average of 2.2/4 and the other 28 patients an average of 1.0/4.0. In 36 patients, a histologic section was examined from each 5 mm long segment from each of the 4 major coronary arteries: of the 1,789 segments, only 6 (<1%) were narrowed 96 to 100% in XSA by plaques; 147 (8%), 76 to 95%; 339 (19%), 51 to 75%; 930 (52%), 26 to 50%, and 367 (21%), 0 to 25%. The average amount of XSA narrowing for the 1,789 segments was about 42%. In 10 patients with clinical evidence of myocardial ischemia, the average amount of narrowing per segment was approximately 55%; in the 26 patients without clinical ischemia, the average was about 38%. Of the 40 patients, 18 (45%) had left ventricular transmural foci of fibrosis or necrosis or both. Of 14 patients with transmural scars, only 1 had a clinical event compatible with acute myocardial infarction; of the 10 with acute myocardial infarction at necropsy, only 4 had typical clinical features of infarction. Calcific deposits were present in ≥1 aortic valve cusps in 22 patients (55%), causing aortic valve stenosis in 2, and in the mitral anulus in 19 (47%), probably causing mitral valve stenosis in 1. Amyloid deposits were present in the heart in at least 9 patients; they were grossly visible and caused fatal cardiac dysfunction in 4, and microscopically visible only in 5, causing no cardiac dysfunction. Eight patients (20%) had chronic congestive heart failure; 27 of 39 (69%) had either a history of systemic hypertension or blood pressure >140/90 mm Hg during their final year of life. Precordial murmurs were recorded in 25 (62%) patients—systolic only in 24 and both systolic and diastolic in 1. Data from electrocardiograms were available in 30 patients: 12 (40%) had atrial fibrillation; 12 (40%), abnormal axis; 12, complete bundle branch block; 1, criteria for left ventricular hypertrophy (despite increased cardiac mass in 67%); and 1, low voltage. All patients had fairly extensive atherosclerosis of the aorta, with aneurysmal formation in 5 with fatal rupture in 3. Five had strokes, which were fatal in 4. At least 5 had leg claudication. Two had massive pulmonary emboli superimposed on chronic obstructive pulmonary disease. Thus, cardiovascular disease was present at necropsy in 39 of our 40 patients, but frequently it was not diagnosed clinically.

Usefulness of the ajmaline test in patients with latent bundle branch block

Twelve patients were studied with intermittent bundle branch block whose conduction disturbance disappeared completely and could no longer be recorded even after provoked changes in heart rate. Premature atrial stimulation and atrial pacing at rapid rates were performed in nine patients; in none of these nine were these procedures able to evoke the complete bundle branch block pattern that all patients exhibited before the spontaneous normalization of conduction. In marked contrast, the administration of ajmaline (1 mg/kg body weight, intravenously in 90 seconds) caused the bundle branch block pattern to reappear in 10 (83.3 percent) of the 12 patients 30 to 120 seconds after the end of the injection, and in 11 patients (91.6 percent) when additional atrial stimulation was performed in 1 of the 2 “failures.” This pharmacologie test was much more rapid and simple than electrophysiologic testing and it was noninvasive. Results of this study suggest that some form of subclinical fascicular injury was present (or had persisted) at a time when intraventricular conduction was persistently normal even though no significant physiologic alteration could be demonstrated by the atrial stimulation techniques. The ajmaline test may become a valuable tool for uncovering cases of latent bundle branch block and furthering our knowledge of the early natural history of intraventricular block.

Alterations of surface electrocardiogram in 35 patients during upper fiberendoscopy.

Thirty-five patients with gastric complaints were analysed by continuous cardiac monitoring during routine upper fiberendoscopy (UFE); 15 of them showed previous electrocardiographic alterations. New alterations occurred in 8 patients during fiberendoscopy, all of them with previous changes of the electrocardiographic pattern: all these were slight and transient. Atrial and ventricular premature beats (more frequent and persistent in women), complete bundle branch block, atrial fibrillation, and ischemic T wave were detected, the latter in only one male patient. Generally the ECG alterations appear when the fiberscope passed the medium third of the esophagus and the cardia. The changes observed on withdrawal of the optic apparatus were irrelevant. Tachycardia was, as a rule, more frequent and persistent in women. Candidates to UFE shouid be previousiy submitted, at ieast, to screening standard ECG.

QT Prolongation and Ventricular Fibrillation in Acute Myocardial Infarction

Fourteen acute myocardial infarction (AMI) patients with early ventricular fibrillation (VF) were compared to 27 control patients without VF with regard to the corrected QT interval (QTc) and the QRS duration. Patients with complete bundle branch block (BBB) had been excluded. The QTc tended to be longer in the VF group than in the controls, but the difference, 13 msec, disappeared after exclusion of a further 5 VF patients and one control with QRS duration greater than 0.10 sec of other configurations than complete BBB. In the long QT syndrome of various types, VF is characteristically preceded by diastolic waves (DW) with larger amplitudes than the preceding T waves. None of the 5 AMI patients with an evaluable recording of the onset of VF, showed DWs preceding the arrhythmia. The results of this study do not support the opinion that VG is associated with a prolonged QT interval in AMI in the same way as in the long QT syndrome. The longer QT interval in patients with VF seems to be mainly secondary to the longer QRS duration.

Associated conduction disturbances in patients with symptomatic sinus node disease.

Electrophysiological investigations were performed in 30 patients with symptomatic sinus node disease (SND) to assess the extent and distribution of associated functional disturbances in the conduction system. The tests were performed before and after inhibition of autonomous tone with propranolol, 0.1 mg/kg, and atropine, 0.02 mg/kg. Surface ECG had shown bundle branch blocks (BBB) in 5 patients and fascicular blocks in 2. AV block I had been recorded in 4 patients, while none had shown high-degree AV block. Malfunction was most often detected in the AV junction, 17 patients showing a prolonged conduction time or an abnormal effective AV node refractory period. Intraventricular conduction delay was present in 7 patients, with a prolonged HV interval in 3 and a complete permanent BBB in the others. Rate-dependent BBBs were demonstrated in a further 4 patients. Long cardiac arrests following interruption of atrial pacing, suggesting impaired automaticity also of subsidiary escape pacemakers, were seen in 11 patients. Only 6 patients, 20%, showed no signs of associated malfunction of the conduction system. Thus, detailed electrophysiological assessment demonstrated associated conduction abnormalities in the majority of these SND patients. The results agree with histopathological studies and show that sinus node malfunction is often the clinically apparent manifestation of a widespread degenerative process in the cardiac conduction system.

Value of Treadmill Exercise Testing in Patients With Complete Bundle Branch Block

Exercise electrocardiography and selective coronary arteriography was performed in 24 consecutive patients with complete bundle branch block. The criteria for a positive exercise electrocardiogram (E-ECG) were a 1 mm depression or elevation in the J point from the control state, as well as in the ST-segment measured at 0.04 seconds from the J point. Eleven of 12 patients with complete left bundle branch block had a positive E-ECG. Nine of them had normal coronary arteriograms, except one with less than 50% lesions in two arteries. Two patients had severe three-vessel disease. Only one patient had a true negative exercise test. No patient had a false negative test. Nine of 12 patients with complete right bundle branch block had a positive E-ECG. One of these 9 had minimal nonobstructive disease, while the other 8 had severe two- or three-vessel coronary artery disease. Three of the 12 right bundle branch block patients had a negative E-ECG. Two of them had a true negative exercise test, and one a false negative test. Because of a high incidence of probably false positive results, E-ECG appears to be unreliable in detecting coronary artery disease in patients with complete left bundle branch block. But it can provide useful information in the noninvasive evaluation of coronary artery disease in patients with complete right bundle branch block.

Left Anterior Hemiblock in Acute Myocardial Infarction

The incidence of intraventricular conduction defects was examined retrospectively in 449 consecutive patients with acute myocardial infarction (AMI). The incidence of left anterior hemiblock (LAH), right bundle branch block (RBBB), left bundle branch block (LBBB) and RBBB+LAH was 12.2, 4.2, 3.8 and 2.5%, respectively. At least 24 patients (5.8%) developed LAH as a result of the AMI. LAH was present in 20% (33/164) of patients with anterior infarction, in 14% (18/131) of those with infarction of undetermined localization, and in 3% (4/143) of patients with diaphragm infarction. The incidence of complete atrioventricular (AV) block in patients with LAH was 6% and in patients with no intraventicular conduction defects 7%. In patients with RBBB, RBBB+LAH and LBBB, the incidence of complete AV block was 37, 45 and 18%, respectively. Severe pump failure occurred with the same low incidence in patients with LAH as in patients without intraventricular conduction defects, but was much more common in patients with complete bundle branch block (BBB). The mortality rate for patients with LAH was 22% and for patients with no intraventricular conduction defects 21%. In patients with RBBB, RBBB+LAH and LBBB, the mortality rates were 53, 55 and 53%, respectively. Patients with complete BBB had a higher age and a higher incidence of previous AMI than the others. Compared to patients with no intraventricular conduction defects, the presence of LAH did not increase the mortality rate, or the risk of developing severe heart failure or complete AV block, in contrast to the serious prognosis in patients with complete BBB.

Sarcoidosis of the heart: A clinicopathologic study of 35 necropsy patients (group I) and review of 78 previously described necropsy patients (group II)

Certain clinical and morphologic observations are described in 35 necropsy patients with cardiac sarcoidosis (group IA and IB), and similar observations are summarized in 78 previously described necropsy patients with cardiac sarcoidosis (group IIA and IIB). All patients had non-necrotic (“hard”) granulomas in lymph nodes and either sarcoid granulomas in the heart (108 patients) or transmural myocardial scarring (five patients) unassociated with coronary arterial narrowing, i.e., healed granulomas. The 113 patients (groups I and II) whose data are analyzed also were divided into those in whom cardiac dysfunction clearly was the result of sarcoid granulomatous infiltration of the heart (89 patients) (groups IA and IIA), and those in whom cardiac dysfunction, if present, was clearly not the result of sarcoid involvement of the heart (24 patients) (groups IB and IIB). Analysis of the 89 patients in groups IA and IIA disclosed that death was sudden (arrhythmia) in 60 (67 per cent), secondary to progressive congestive cardiac failure in 20 (23 per cent), from recurring pericardial effusion in three (3 per cent) and from other or unknown causes in six (7 per cent). Sudden death was the initial manifestation of sarcoidosis in 10 (17 per cent) of the 60 patients who died suddenly. Other than premature ventricular beats, ventricular tachycardia was the most common arrhythmia (17 patients), and complete heart block was the most common conduction disturbance (25 patients). Complete bundle branch block occurred in 21 patients. Ventricular aneurysm (eight patients) and papillary muscle dysfunction (possibly 16 patients) were other cardiac disturbances observed. Although corticosteroid therapy tends to cause fibrous replacement of myocardial sarcoid granulomas, a possible consequence of this medication is the development of ventricular aneurysm. Most patients with cardiac sarcoidosis causing dysfunction (groups IA and IIA) presented initially with manifestations related to the heart. Furthermore, most patients with cardiac sarcoidosis have little or no clinical evidence of dysfunction of an organ system other than the heart. Usually the course in patients with extensive cardiac sarcoidosis is not prolonged.

Tachyarrhythmias and Ectopic Beats With Aberrant Intraventricular Conduction in Children

Ectopic foci associated with aberrant intraventicular conduction (AIVC) may either be ventricular foci or supraventricular foci. The electrocardiogram may not help in this differentiation. Knowledge of the site of origin is essential to determine appropriate therapy for patients who develop sustained tachycardias and may be of prognostic value in those who have frequent premature contractions. To determine the site of the ectopic focus, His bundle electrograms were performed in seven children whose conventional ECGs showed arrhythmias with frequent premature ectopic beats and runs of bigeminy with AIVC. In two patients the focus was in the supraventricular area while the other five had a ventricular focus. Incomplete right bundle branch block was noted in one patient with a supraventricular focus but complete bundle branch block occurred in both patients with both ventricular and supraventricular foci.

Contribution of the his bundle recording to the diagnosis of bilateral bundle branch conduction defects.

The participation of intraventricular conduction defects in the AV delays and blocks has been investigated by His bundle electrogram recording in 239 patients with different degrees of AV blocks and QRS enlargement (greater than 0.12 sec). In absence of PR prolongation, the His bundle electrogram can demonstrate intraventricular conduction delay (HV superior to 55 msec) with an increasing frequency in right bundle branch block and right bundle branch with left axis deviation, left bundle branch block and right bundle block with right axis deviation. In cases of first-degree AV block (PR greater than 0.20 sec) delay within the His bundle is present in 20% of the cases and HV prolongation, isolated or associated with an upper conduction defect is demonstrated in 66% of the cases. Second-degree AV block with QRS enlargement in the conducted beats is due to a subnodal lesions of the conducting tissue in 80% of the cases. Wenckebach phenomenon and bundle branch block is as frequent above as below the site of His bundle electrogram recording. Möbitz II block has always an infranodal localization. Third-degree AV block with wide QRS complexes is the consequence of a lesion within the His bundle in 11% and of a complete bilateral bundle branch block in 78% of the cases. Exploration of the AV conduction in acute myocardial infarction with AV block confirms the usual bilateral bundle branch lesion in anterior myocardial necrosis and the AH localization of the AV block in posterior myocardial infarction even in presence of enlarged QRS complexes. Unidirectional block occurs in 19 of the 82 cases of complete anterograde bilateral bundle branch block, with retrograde conduction to the atria in 11 and concealed retrograde conduction in 8 cases.

Conduction disorders in the canine proximal His-Purkinje system following acute myocardial ischemia. II. The pathophysiology of bilateral bundle branch block.

The evolution of bilateral bundle branch block (BBB) was studied in ten anesthetized dogs by recording electrical activity from the bundle of His (Hb), right (Rb) and left bundles (Lb) for precise localization and characterization of the conduction disorder. Records were obtained before and at intervals up to 8 hours after ligation of the anterior septal artery. Forty to 140 min after ligation conduction was impaired in either the Rb or Lb showing complete BBB both at rapid heart rates (tachycardia-dependent) and slow rates (bradycardia-dependent) with normal QRS or incomplete BBB at control rates. Later complete BBB became constant at all heart rates. When both bundles were significantly involved, various combinations of intraventricular and atrioventricular conduction disorders occurred. Unequal delay in both bundles (unequal 1° bilateral BBB) gave rise to prolonged H-V interval and a QRS pattern of incomplete or complete bundle branch block corresponding to the branch in which the conduction delay was greater. Equal delay in both bundles gave rise to a narrow QRS with prolonged H-V interval. Second degree block in one bundle and complete (3°) block in the other manifested as 2:1, Mobitz type II, or Wenckebach A-V conduction disturbance. Unequal and asynchronous 2° bilateral BBB gave rise to complex patterns of alternating BBB associated with alteration in the H-V interval of 25-35 msec. In two experiments showing alternating BBB, longitudinal dissociation and asynchronous conduction in the distal Hb was suggested.

Complete Heart Block Occurring during Cardiac Catheterization in Patients with Preexisting Bundle Branch Block

A case of catheter-induced complete heart block in a patient with preexistent left bundle branch block is documented by His bundle recordings. It is recommended that a temporary pacemaker catheter on demand should be placed in the right ventricular apex in all patients with complete bundle branch block undergoing cardiac catheterization. In the coronary care units catheters should never be passed blindly to the right heart chambers in patients with left bundle branch block.

Coronary disease in staveley, derbyshire with an international comparison with three towns in marion county, west virginia

A survey of coronary disease has been carried out in a sample of men aged 35–74 living in Staveley, United Kingdom. The prevalence of cardiac pain based on standard questions and the frequency of certain electrocardiographic abnormalities was compared in miners and exminers, foundry and exfoundry workers, mixed dust and other exposure groups, and men who had never worked in dust or fumes. The findings have been compared with a similar survey conducted in three communities in Marion County, West Virginia, United States. No striking occupational differences were found, though the prevalence of probable cardiac pain was slightly less in miners and exminers than in the other occupational groups. The prevalence of cardiac pain was twice as high in the United States as in the United Kingdom population. T wave inversion and left complete bundle-branch block occurred more frequently in the U.S. group. But abnormal Q waves, flat T waves, ST depression and other E.C.G. changes were equally common in each country. The American men were nearly 5 cm taller and 5 kg heavier than the British men. Of the etiological factors examined, weight and smoking were associated to a small amount with coronary disease. But the most striking association was with blood pressure. Systolic blood pressure was roughly 20 mm Hg higher and diastolic blood pressure 10 mm Hg higher in the coronary compared with the other group.

Prognostic factors in acute myocardial infarction treated in a coronary care unit.

Summary: Prognostic factors in 269 cases of acute myocardial infarction treated in a coronary unit were analysed using a computer. The mortality rate was significantly higher in the elderly (≤60 years) and those with extensive infarction, shown by prolonged cardiac pain (>4 hours) or high serum enzyme levels (SGOT> 200 Sigma-Frankel units/ml; LDH> 2,000 Berger-Broida units/ ml). It was high also with tachycardia (sinus, supraventricular or ventricular), complete heart block, and complete bundle branch block. It increased progressively with severity of myocardial failure. Secondary cardiac arrect had a high mortality. Clinical signs of catecholamine hypersecretion (sinus tachycardia, pallor, sweating), hypoxaemia (central cyanosis), or low cardiac output (peripheral cyanosis, cold extremities, oliguria) greatly increased the mortality rate. Radiological cardiomegaly and pulmonary congestion each doubled it. An insignificant mortality increase accompanied ventricular and supraventricular ectopics, atrial fibrillation, incomplete heart block, and previous myocardial infarction, angina, and hypertension. There was no significant relationship between mortality and admission delay, sex, tobacco consumption, diabetes, or family history of ischaemic disease or diabetes. Only one patient died of primary cardiac arrest. Sinus bradycardia was a good prognostic sign. Analysis of the literature showed its lower mortality rate to be significant. Since intravenous atropine may cause arrhythmias, it should be reserved for sinus bradycardia with hypotension. It was suggested that patients with adverse prognostic signs short of extreme myocardial decompensatiqn should be monitored longer. Younger patients without severe infarction had a low mortality rate. Investigation of these may reveal a group which can be discharged safely from hospital soon after the completion of monitoring.

Complete bundle-branch block complicating acute myocardial infarction.

Bundle-branch block complicated 68 out of 806 cases of acute myocardial infarction managed in a coronary-care unit and was associated with a mortality of 56 per cent. Twenty-five out of 48 patients with right-bundle-branch block, and 13 of 20 patients with left-bundle-branch block died. In 21 of the 68 patients complete heart block subsequently developed, and in 13 of these an idioventricular pacemaker failed to emerge. Bilateral bundle-branch block preceded the onset of complete heart block in 15 patients. Transvenous pacing electrodes were inserted prophylactically in the last 31 consecutive cases of bundle-branch block. This procedure was associated with a high proportion of life-threatening arrhythmias, and pacing did not reduce subsequent mortality in the nine patients in whom complete heart block developed.

Chronic left complete bundle-branch block. Phonocardiographic and mechanocardiographic study of 30 cases.

Chronic left complete bundle-branch block. Phonocardiographic and mechanocardiographic study of 30 cases.

An epidemiological assessment of bundle-branch block.

Complete bundle-branch block was found in 57 of 1,560 (3.7%) electrocardiograms routinely recorded on members of a retirement community. Of this number, 19 were identified as left bundle-branch block (LBBB), while 38 fulfilled the criteria for right bundlebranch block (RBBB). Individuals with LBBB were found to have cardiomegaly more frequently than did individuals with normal electrocardiograms. Individuals with RBBB, regarded as a homogeneous group, also demonstrated a greater prevalence of cardiomegaly than did the control group, but the difference from normals was less striking than in the case of LBBB. Neither LBBB nor RBBB was significantly associated with hypertension, as defined in the text. When the common, uncomplicated RBBB was regarded as a separate entity, the prevalences of hypertension and cardiomegaly were indistinguishable from those of a control group with normal electrocardiograms. The RBBB variant, regarded as a possible manifestation of left ventricular disease secondary to hypertrophy or myocardial infarction, was found to be frequently associated with hypertension, cardiomegaly, and the need for digitalis therapy. RBBB with left axis deviation, regarded as a complication of the common RBBB due to left ventricular hypertrophy or myocardial infarction, was similarly associated with a high prevalence of cardiovascular disease. None of the 38 cases of RBBB fulfilled the criteria for classic RBBB. It is suggested, therefore, that the chronic uncomplicated RBBB in the adult may indeed bear a less ominous portent than has previously been ascribed to it. This is suggested only in relation to the parameters evaluated, however; prospective evaluation is clearly necessary to assess the validity of such an inference.

The electrocardiogram in diphtheritic myocarditis

Hospital records of 229 children with diphtheria revealed evidence of myocarditis affecting 47 (20 per cent), both by physical signs and abnormal electrocardiograms. The 437 electrocardiograms taken on the 47 patients were analyzed by the conventional and the electrovectorcardiographic method of Grant, and the QRS-T spatial angles were evaluated. A high predictability of survival from diphtheria is afforded by the electrocardiogram. Cases were grouped according to their most severe ECG abnormalities. If only the P-R interval was prolonged (Group A), or the T vector was shifted (Group B), causing the QRS-T angle to widen, the prognosis for complete recovery was excellent. Prolongation of the P-R interval tended to persist, whereas primary T-wave changes subsided. An intraventricular block (Group C) involved the superior branch of the left main bundle branch to the left ventricle in 8 children; and of these, 4 died, but only one as a result of myocarditis. One child with only incomplete right bundle branch block recovered. Of 14 children with a major conduction block (Group D), 11 died. Six of these children had complete bundle branch block: there were 3 fatalities. Complete A-V block was the most ominous ECG sign, in that it was consistently followed by death in 8 children. However, in one of these children the block regressed and death resulted from polyneuritis and respiratory failure. Out of the total 229 cases, 15 deaths occurred in that group of 47 patients in whom there was evidence of myocardial involvement; 10 deaths were due to this involvement and peripheral vasodilatation. One child died early from obstructive, laryngeal diphtheria, and 4 succumbed to the late effects of progressive polyneuritis complicated by pulmonary hypoventilation and infection. Autopsy was carried out on 8 children, for whom correlations of ECG, clinical, and pathologic data were presented. Early death in 3 children (Cases 40, 44, and 47) was associated with complete A-V block and histologic evidence of extensive myocardial disease, and in one child (Case 35), with right bundle branch block and a hemorrhagic myocardium. The child who died early from laryngeal obstruction (Case 31) had parietal block by ECG and interstitial edema of the myocardium. Death due to peripheral neural and respiratory causes late in the course of illness of 3 children (Cases 33, 38, and 46) was associated with regression of ECG changes and much less severe histologic evidence of myocarditis.

Abnormalities in the electrocardiogram induced by emotional strain: Possible mechanism and implications

Psychic trauma and emotional strain may produce abnormalities in the electrocardiogram in some predisposed subjects. The common abnormalities are RS-T segment depression and isoelectric, diphasic or negative T waves in various leads. In more severe cases the QRS complex may also be involved. Its voltage may increase, it may undergo directional changes, become slurred, notched and widened or assume the appearance of complete bundle branch block. The electrocardiographic changes are unstable, unpredictable and variable in their appearance, and are more apt to occur in the presence of coronary disease. The changes appear to be caused by stimulation of the sympathetic and parasympathetic centers of the brain by conscious or subconscious disturbances. The impulses are thence transmitted to the nerve endings in the heart affecting the conduction system, the myocardium and the coronary vessels. The resulting spasm of the latter may produce myocardial ischemia and even necrosis. Another possible mechanism is the release into the blood stream of endocrine products, especially the catecholamines induced by sympathetic nerve stimulation, and these may affect the heart. The observations may help in the differential diagnosis of an organically normal and a diseased heart and more particularly in explaining the electrocardiographic manifestations occurring in coronary disease, especially when there is no clinical evidence of acute structural myocardial damage.

QRS alterations produced by auricular and ventricular paroxysmal tachycardia in the presence of bundle branch block patterns: An experimental study in dogs

Experimental auricular and ventricular tachycardias have been produced at various sites of the heart in the presence of bundle branch block. The following conclusions can be made: 1. 1. Supraventricular tachycardias do not alter complete bundle branch block patterns significantly. They may, however, increase incomplete types of bundle branch block. 2. 2. Ventricular tachycardias from the ventricle below the intact branch produce bundle branch block patterns from the opposite side. 3. 3. The QRS morphology of ventricular tachycardias from the ventricle below the affected bundle branch depends upon the time of the cardiac cycle in which the stimuli occur. Between the T wave and the beginning of P, complete bundle branch block patterns are produced. Stimuli which fall into the P-R interval fuse with the activation wave coming from the auricle through the unaffected branch and result in narrowed or relatively normal QRS complexes. Fusion beats can be seen which exhibit the typical morphology of the WPW syndrome if the ventricular stimulus is discharged immediately after the P wave.