Focal Block Research Articles

Effects of graded focal cold block in rostral areas of the medulla.

Unilateral focal cold blocks (20 degrees C) in structures located ventrolaterally in rostral medulla consistently caused apnoea or deep depression of inspiratory motor output. The inhibitory effect could be correlated with the cooling temperature. Apnoeic response occurred either with complete absence of any inspiratory activity or combined with low level tonic inspiratory motor activity ('tonic apnoea'). The appearance of apnoea was CO2-independent, whereas the tonic component of the latter increased with increasing levels of PCO2. The results suggest that the structures in the deep, ventro-lateral aspect of rostral medulla, from which apnoea can be induced, correspond partly to the nucleus paragigantocellularis lateralis (nPGL) and the nucleus preolivaris. These structures appear to be relevant for the drive inputs necessary for respiratory rhythmogenesis. Unilateral focal cooling in the rostral medulla, including the 'Bötzinger Complex', caused increments in respiratory rate both in vagotomized and non-vagotomized animals. The increase in respiratory rate in response to cooling in the region of the 'Bötzinger Complex' was combined with either an enhancement or some depression of respiratory motor output. This area in the rostral part of the ventral respiratory group (VRG) seems not to be crucial for respiratory rhythmogenesis, but to play a role in determining both the intensity and timing of the respiratory activity. All effects of unilateral cold block were bilaterally symmetrical.

Transient Focal Septal Block

A 65-year-old woman with an acute myocardial infarction, as judged by serial enzyme changes, developed transitory Q waves in leads V2 to V4 and leads 2, 3, and aVF during an attack of pain in the chest. These Q waves were not present 12 hours later. It is suggested that these changes represent a focal block in the septal fibers of the left bundle-branch system. This defect could underlie the transient right precordial Q waves seen in myocardial infarction or ischemia, as well as the fixed Q waves of many patients without septal infarction at autopsy.

Rate-Dependent Variation in the Duration of the QRS Complex with Left Anterior Fascicular Block

The case of a 67-year-old man with combined ischemic and valvular heart disease is presented. Electrocardiographic abnormalities included left anterior fascicular block with a variable duration of the QRS complex. The width of the QRS complex was dependent on the length of the cycle, being broader with short than with long preceding R-R intervals. This is interpreted as a tachycardia-dependent focal block coexisting with a fixed delay in fascicular conduction.

Right focal blocks.

Right focal blocks.

Left Anterior Hemiblock Concealing Diaphragmatic Infarction and Simulating Anteroseptal Infarction

Pathologic Q waves on the surface electrocardiogram often reflect transmural myocardial infarction. 1 Gunnar RM Pietras RJ Blackaller J et al. Correlation of vectorcardiographic criteria for myocardial infarction with autopsy findings. Circulation. 1967; 35: 158-171 Crossref PubMed Scopus (68) Google Scholar , 2 Horan LG Flowers NC Johnson JC Significance of the diagnostic Q wave of myocardial infarction. Circulation. 1971; 43: 428-436 Crossref PubMed Scopus (195) Google Scholar Intraventricular conduction defects may sometimes be responsible for pathologic Q waves, erroneously suggesting infarction. 3 Rosenbaum MB Elizari MV Lazzari JO The Hemiblocks. Tampa Tracings, Oldsmar, Florida1970 Google Scholar , 4 Gambetta M Childers RW Rate dependent right precordial Q waves: “Septal focal block.”. Am J Cardiol. 1973; 32: 196-201 Abstract Full Text PDF PubMed Scopus (40) Google Scholar In addition, evidence of myocardial infarction may be concealed by the development of intraventricular conduction defects. 3 Rosenbaum MB Elizari MV Lazzari JO The Hemiblocks. Tampa Tracings, Oldsmar, Florida1970 Google Scholar This report describes a patient with acute diaphragmatic infarction in whom development of transient left anterior hemiblock (with possible septal fascicular block) concealed a diaphragmatic infarction and simulated anteroseptal infarction.

Electrophysiological and mechanical investigations on the dual action of prostaglandin E1 in the pregnant rat myometrium in vitro.

Effects of prostaglindin E1 (PGE1) on the myometrial activity of the pregnant rat were investigated by recording the contractile response and intracellular electrical activity. PGE1 (10-9--10-6 g/ml) caused a depression of the contractile activity in the fresh preparations of either longitudinal or circular muscle strip (within 2-5 hr after exposure to the artificial saline media). However neither membrane potential nor action potential was significantly affected by the treatment with the agents. By contrast, in the aged preparations (bathed in the saline media longer than 2-5 hr), an increase in the contractile response dose-dependently was caused. The generation of action potential was facilitated without depolarization of the membrane. The inhibitory response induced by PGE1 in the fresh preparation was converted to an excitatory response when treated with bretylium. The discussion covers the inhibitory effect of PGE1 which is mediated through intrauterine adrenergic system, and is perhaps due to the focal hyperpolarization block of the conduction of excitation. The excitatory effect is very likely caused by a direct action on myometrial cell membrane.

Rate-dependent right precordial Q waves: “Septal focal block”

Rate-dependent pathologic Q waves in leads V 1 to V 3 were seen in two patients with myocardial infarction. Months later this conduction defect could be recalled with atrial premature beats, or as a continuing rate-dependent phenomenon. It is suggested that these cases represent a focal block in the septal fibers of the left bundle branch system and that this defect could underlie the transient right precordial Q waves seen in myocardial infarction or ischemia, as well as the fixed Q waves of many patients without septal infarction at autopsy.

Specialized tissues and preferential conduction in the atria of the heart

Many of the widely prevalent concepts in clinical electrocardiography are based on the premise that the spread of electrical activity in the atria is radial, not following special pathways. This review questions that premise on the grounds of recent electrophysiologic, biochemical and anatomic studies that are more logically interpreted as evidence for specialized or preferential conduction in the atria. Certain familiar and widely used diagnoses based on P wave configuration (P mitrale, P pulmonale, coronary sinus rhythm and left atrial rhythm) are discussed with clinical electrocardiographic examples. We conclude that the most tenable current interpretation is that atrial conduction is normally specialized and preferential for particular anatomic pathways, and that a variety of focal blocks of this conduction (either functionally or structurally produced) may thus distort the atrial electrical vector. If further observations in the future support this interpretation, some of the classic concepts in clinical electrocardiography will require drastic revision.

Ventricular Aneurysms in Acute Experimental Chagas' Myocardiopathy

Of 27 puppies infected with Schizotrypanum cruzi two showed electrocardiographic changes in the ST-T segment and in the T wave compatible with parietal myocardial aneurysms. When the thorax was opened, examination confirmed the presence of aneurysms in the free walls of the heart. In one of the cases, histologic examination of the aneurysm showed myocardial fiber changes. Myocytoiysis was the principal change. In it the main electrocardiographic changes were interpreted as subepicardial injury and ischemia. In the second case, the dominant histologic change consisted of dense and extensive myocardial inflammatory infiltrations, which enlarged the interstitial spaces. There were low voltage of QRS, focal block and disturbances in the ventricular repolarization electrocardiographically. Aneurysmal dilatation in acute experimental Chagas' myocarditis appears to be caused by fiber lesions, edema and interstitial inflammatory infiltrations. Intracavitary ventricular pressure will produce a convexity of the myocardial wall during systole, which is reduced during diastole.

Vectorcardiographic study of the QRS loop in patients with left anterior focal block

The authors have studied the vectorcardiograms of 40 patients, 45 years of age or over, whose electrocardiograms showed a QRS duration shorter than 120 msec., a leftward shift of the mean QRS axis and ventricular complexes with a tall R wave in Leads I and aV L, and an rS morphology in Leads II, III, and aV F. Most patients had atherosclerosis, hypertension, or ischemic heart disease. The following vectorcardiographic characteristics were disclosed: (1) The frontal plane loop was open-faced and turned counterclockwise in all cases; (2) the initial vectors were nearly always directed anteriorly and inferiorly; (3) the early vectors travelled horizontally to the left and, to a variable extent, posteriorly; (4) the midtemporal vectors were located in the left, posterior, and superior octant. These vectorcardiographic features were sometimes observed to be transitory or intermittent or to precede the development of a complete left bundle branch block. Their association with a complete right bundle branch block is known to be a common forerunner of complete atrioventricular block. From comparison with experimental data reported in the literature, the characters of the loops observed in these cases are assumed to be related to a delayed activation of the anterolateral wall of the left ventricle and to correspond to left anterior focal block.

The vectorcardiogram in right bundle branch block coexisting with left ventricular focal block

The vectorcardiograms of 4 cases in which left ventricular focal block coexisted with right bundle branch block were presented. In 3 cases there were initial conduction disturbances presumably due to abnormal propagation within an infarcted area (intra-infarction block). The vectorcardiographic characteristics of intrainfarction and peri-infarction block as well as their distinction from bundle branch block were emphasized. One case showed changes suggestive of intra-infarction block, but no evidence of infarction was found at necropsy. Instead there was diffuse myocardial fibrosis. The initial conduction delay was thus attributed to a nonspecific type of focal block. It is concluded that the various types of focal block with initial vectorial abnormalities can be adequately diagnosed in the presence of right bundle branch block.

Experimental focal block in the sheep and the dog. An electrocardiographic and histological study.

Experimental focal block in the sheep and the dog. An electrocardiographic and histological study.

Parietal focal block; an experimental and electrocardiographic study

A method of producing focal ventricular block is described. The sequence of the electrocardiographic variations is ascribed to changes in the velocity and direction of the excitatory process in the ventricular wall. The epicardial electrocardiograms resemble those considered indicative of ventricular hypertrophy or of "incomplete" or of "complete" bundle branch block. When the focal block is pronounced a positive deflection appears in the cavitary tracing. The ventricular blocks can be subdivided into "conduction blocks" and "fiber blocks," the former produced by the delay of the stimulus in the specialized conduction system and the latter produced by the delay of the excitatory process in the ordinary heart muscle.

Focal blocks of the right intraventricular conduction: morphology, pathogenesis and clinical significance

Focal blocks of the right intraventricular conduction: morphology, pathogenesis and clinical significance

Spatial vectorcardiography: Right bundle branch block. VIII

The vectorcardiographic patterns and characteristics of right bundle branch block may be summarized as follows: 1. 1. “Classical” right bundle branch block is associated with a QRS SÊ loop inscribed in the right, lower, anterior octant. The progress of the wave of accession is slow, and the time markers are closely spaced throughout the QRS SÊ loop. There is a positive ST vector directed upward, posterior, and to the left. The T SÊ loop is discordant. It points upward, backward, and to the left. Instances of this type of right bundle branch block are rare. 2. 2. Atypical right bundle branch block is characterized by alteration chiefly of the terminal portion of the QRS SÊ loop. This terminal portion is increased in duration, slow and irregular in contour, and invariably directed to the right and anteriorly, to a greater or lesser extent. This terminal portion of the QRS SÊ loop produces the slow, widened S wave of Lead I and the R′ or late R wave of Lead V 1. This terminal abnormality may coexist with any normal or pathological variety of the QRS SÊ loop. The study of a case of transient, atypical complete right bundle branch block revealed that the major portion of the QRS SÊ loop is also affected by the presence of the abnormal conduction, though only to a minor extent. However, the fact that some change is produced in the initial portion of the QRS SÊ loop indicates that the lack of contribution of right ventricular electromotor force to the entire QRS cycle is detectable although of small quantity. This might be considered as evidence that this type of block is true bundle branch block and not merely a “focal block” of the Purkinje system or a local abnormality of muscular conduction in the crista terminalis. It was further observed that the long axis of the T SÊ loop shifted to the left and posteriorly by more than 100 degrees. The significance of the T SÊ loop shift was shown clearly in the patients with marked left ventricular hypertrophy or myocardial damage. The electrocardiographic diagnosis of both of these conditions depends greatly upon evidence of an altered gradient producing inverted T waves in Leads I and V 5 or V 6. That the T-wave change due to right bundle branch block alone would obscure such a diagnostic criterion was suspected from the alteration seen in the patient with transient block and was confirmed in the patients with left ventricular hypertrophy and myocardial damage associated with right bundle branch block. In all of them, T waves were upright in Leads I and V 5 and V 6. The diagnosis of myocardial damage, myocardial infarction, and left ventricular hypertrophy, however, could be made from the configuration of the QRS SÊ loop alone.

The different types of intraventricular block

1. 1. The magnitude and location of delays in appearance of the intrinsic deflection in multiple precordial leads have been used to differentiate various types of intraventricular block. 2. 2. In complete bundle branch block the intrinsic deflection of the involved ventricle arrives 0.05 second or more later than in the case of normal invasion. This delay occurs in all the leads from one side of the precordium. In incomplete bundle branch block the same facts are observed, but the delay is less than 0.05 second. 3. 3. In other types of intraventricular block the delay of the intrinsic deflection occurs only over a small area of the precordium, and the conclusion is drawn that the activation of only a part of the ventricle is delayed. Such types of intraventricular block may be called focal block. They are of major degree when the duration of QRS in the limb leads is 0.12 second or more and of minor degree if QRS is of lesser duration. 4. 4. In general, intraventricular block of the S type corresponds to focal right block, whereas the uncommon type corresponds to right bundle branch block. 5. 5. In general, the common type of intraventricular block corresponds to left bundle branch block when the summit of R 1 shows a plateau and corresponds to focal left block when the summit of R 1 is peaked, with a broad notch on the descending limb of the R wave.

The electrical effects of injury at various myocardial locations

The electrical effects of injury at various myocardial locations