Demetrio Sodi-Pallares

The activation of the interventricular septum

Abstract The process of septal activation in the dogs heart was studied by means of unipolar leads, distant bipolar leads, and bipolar leads using contiguous electrodes. The electrodes used in this study permitted the registration of the electrical phenomenon in any part of the septal surfaces and even in the interior of the septal muscle. The exact location of the site at which the lead was taken was determined precisely by post-mortem studies of the animal. The following findings were demonstrated: 1. 1. The mean process of septal activation is developed from below upward. 2. 2. Extrasystoles produced in the epicardial surface of the apex of the ventricles cause a process of activation of the septum which proceeds from below upward, similar to normal activation. Extrasystoles provoked in the base of the ventricles produce a septal activation which proceeds from above downward, contrary to the normal process of septal activation. 3. 3. The first region to be activated in the right surface of the septum is that portion in contact with the anterior papillary muscle. Those portions activated later are the part of the septum corresponding to the apex, the middle portions between the apex and the base septum, and, still later, those regions near the insertion of the atrioventricular valves and the pulmonary valves. These data are in accord with the distribution of the right branch of the bundle of His, since this branch descends enveloped in a sheath of connective tissue, and its first ramifications appear at the level of the base of the anterior papillary muscle. The remainder of the ramifications invade the septum from below upward. 4. 4. The differences found between the times of arrival of the wave of activation to the first and last portions of the right surface of the septum fluctuate between 0.02 and 0.03 second. 5. 5. In the left surface of the septum, the differences pointed out in 4 are much less and generally do not exceed 0.01 second. In the majority of the experiments, the first regions to be activated on the left side were those between the apex and the base. This is, in general, in accord with the appearance of the first ramifications of the left branch, which begins to subdivide at levels higher than the right branch. 6. 6. The greater part of the muscular tissue which makes up the septum behaves electrically as the left ventricle. For instance, when right bundle branch block is produced, the time of arrival of the wave of excitations is not altered, whereas with the production of left bundle branch block, there is a considerable retardation of the arrival of the wave of excitation. The muscular tissue, which behaves electrically as the left ventricle, approaches very closely the right surface of the septum, and there are even parts of the right surface that behave as left ventricle. The wave of activation reaches these portions rapidly (about 0.01 second). This makes it impossible to accept the concept that in bundle branch block the wave of excitation crosses the septum slowly (it was supposed in 0.04 to 0.05 second). All the evidence indicates that the retardation of the wave of excitation in bundle branch block takes place in the septum, but in a very small region, probably 1 to 2 mm., and very near the right surface. 7. 7. In one case limited portions of the left septal surface were found which behaved electrically as the right ventricle. That is to say, there was no retardation of the arrival of the wave of excitation when left bundle branch block was provoked but a marked retardation when right bundle branch block was produced. 8. 8. Anatomical cuts of the interventricular septum indicate that the distribution of the muscular fibers of the two ventricles is not incompatible with the findings related in paragraphs 6 and 7. 9. 9. In two experiments we were able to show the existence of a small zone in the superior portion of the septum and in its muscular substance, whose activation was not delayed with either right or left bundle branch block. This zone corresponds approximately to the site where Mahaim has described the accessory paraspecific bundle. Nevertheless, in this respect, our experiments are few, and for the present we do not feel that we should draw any definite conclusions.

Electrocardiogram in chronic cor pulmonale

Abstract After the study of the electrocardiograms of fifty cases of chronic cor pulmonale, we consider that the principal diagnostic signs (see Fig. 11) are: (1) high and peaked P waves with prominent auricular T waves in Leads II, III, and V F ; (2) negative P waves in V L ; (3) right deviation and a decreased value of  QRS ; (4) a small ventricular gradient (frequently deviated); (5) signs of clockwise rotation of the heart (S 1 -Q 3 ) and backward position of its apex (S 1 ,S 2 , and S 3 ; S 1 and S 2 with right deviation of  QRS ); (6) diphasic (of the − + type) or negative T waves in Leads III, II, and V F ; (7) small R waves in the precordial leads; (8) deep S waves in the left precordial leads; (9) diphasic (of the + − type) or negative P waves in the right precordial leads; and (10) negative T waves in the right precordial leads. In the differential diagnosis, we emphasize that: 1. (1) The delay of the intrinsic deflection in the right precordial leads is frequently attended (36 per cent) by a complication which gives rise to further strain on the right ventricle. 2. (2) The absence or diminished amplitude of the S wave in the left precordial leads is frequently attended (75 per cent) by a complication of the “ cor aortale ” type (Fig. 12). 3. (3) A QS complex, usually in the right precordial leads, a W-shaped complex, or a deep Q wave in these leads is a frequent finding (36 per cent) in chronic cor pulmonale, without clinical signs suggestive of a myocardial infarct or a dead zone.

Electrocardiographic diagnosis of myocardial infarction in the presence of bundle branch block (right and left), ventricular premature beats and wolff-parkinson-white syndrome

Summary The diagnostic difficulties in the recognition of myocardial infarction in the presence of bundle branch block and the Wolff-Parkinson-White syndrome are discussed. However, through a “deductive” approach in the analysis of the electrocardiogram, such difficulties may be eliminated to a great extent. The knowledge of the sequence of cardiac activation in normal and abnormal circumstances as in bundle branch block, “pre-excitation syndrome”, and extrasystolia, is fundamental. To sum up, the “deductive” approach to clinical electrocardiography not only facilitates the general diagnosis but also indicates the limitations in arriving at a precise diagnosis of infarction.

The mechanism of complete and incomplete bundle branch block

Abstract The propagation of the wave of activation in the interventricular septal mass of the dogs heart was studied under control conditions and with different degrees of bundle branch block. Unipolar leads, differential leads with contiguous electrodes, and distant bipolar leads were recorded at different levels of the septum. The following are the main findings: 1. 1. Under control conditions the process of activation in the interventricular septum develops from left to right and below upward. The velocity of propagation in most of the septal mass, which is formed mainly by the left ventricular muscle, is very rapid, approximately 1,000 to 1,200 mm. per second; this suggests that the ramifications of the Purkinje penetrate deeply into the interventricular septum muscle. 2. 2. Varying degrees of right bundle branch block do not modify the sense nor the sequence of the process of activation in the left ventricular mass so that the same velocity exists in the left ventricle as was found in control experiments. 3. 3. Minor degrees of left bundle branch block cause a delay in the time of arrival of the wave of activation to all the left ventricular septal mass, but fail to modify the sense or the velocity of propagation within the same mass. When the degree of the block is of great magnitude, the sense of the activation is inverted in the whole left septal mass. This process is therefore carried out from right to left. Under these conditions, when the impulse propagates in a direction counterwise to the normal, the velocity of propagation within the left septal mass diminishes and in cases of complete block falls around 360 mm. per second. 4. 4. In right as well in left bundle branch block there is a delay (approximately 0.03 to 0.04 second) which occurs in a relatively small portion of the septum (1.5 mm. to 2 mm). very near the right septal surface. This delay occurs precisely when the impulse passes from the regions activated by the normally functioning branch to regions which were previously activated by the blocked branch. It is probable that the delay represents a latency in the propagation of the impulse in this zone. This suggests that the right and the left systems are functionally independent and thus eliminates the possible existence of communications between both branches. We believe that this is the first experimental evidence of the site where the delay takes place in bundle branch blocks. 5. 5. The duration and importance of the septal phenomenon in the determination of ventricular curves is pointed out in normal conditions as well as in defects of intraventricular conduction. 6. 6. The principal implications which have a bearing on clinical electrocardiography are discussed.

The activation of the free left ventricular wall in the dog's heart; in normal conditions and in left bundle branch block.

Abstract In this study a critical attempt was made to review some of the more recent experimental studies on ventricular activation. A study of the activation of the normal free ventricular wall using the cathode-ray tube confirmed our previous observations. The spread of activation in the subendocardial muscle mass and at least one-half of the thickness of the adjacent free ventricular wall, reaches values of 2,000 or more mm. per sec. In these regions QS complexes are recorded as described by Prinzmetal and collaborators. An attempt to explain this morphology is presented. In left bundle branch block the sequence, sense, and speed of activation in the free left ventricular wall are unchanged as compared to the normal control. The alterations in morphology are mainly due to changes in direction of activation and delay of conduction in the interventricular septum.

VENTRICULAR PREMATURE BEATS IN THE DIAGNOSIS OF MYOCARDIAL INFARCTION.

The importance of ventricular premature beats (VPB) in the clinical diagnosis of myocardial infarctions has been pointed out by several authors. Dressler (1943) reported a case in which the electrocardiographic signs of infarction were present in such beats (deep and slurred Q waves in lead III) and absent in the sinus beats. Simonson et al. (1945), Bellet (1953), Scherf and Schott (1953), Katz et al. (1958), Silverman and Salomon (1959), and Anttonen et al. (1959) recognized that myocardial infarctions can be diagnosed from VPB and, at times, even earlier from these cycles than from the sinus beats. The similarity of ventricular activation in VPB and in right bundle-branch block (RBBB) and left bundle-branch block (LBBB) has long been accepted. Consequently, VPB with unipolar patterns of LBBB are right VPB, and VPB with patterns of RBBB are left VPB. The same considerations apply also for supraventricular premature beats (SVPB) with aberrant conduction, since the aberration is due to some degree of either RBBB or LBBB (Bisteni et al., 1960). Thus, right VPB and SVPB with aberration similar to that in LBBB are analysed in the same manner as sinus beats with LBBB. In fact, in these three situations the process of ventricular activation follows a similar sequence: the right ventricle is activated before the left. This type of reasoning applies also for left VPB, RBBB, and SVPB with RBBB: in these three instances the left ventricle is activated before the right. A better knowledge of the ventricular activation process in normal conditions and in bundlebranch block has served for a new approach to the diagnosis and localization of myocardial infarctions. Sodi-Pallares et al. (1957, 1960) have shown that tracings with electrical signs of infarction are better understood when analysed in the light of recent studies concerning the ventricular activation process (Sodi-Pallares et al., 1955; Medrano et al., 1956, 1957, and 1958). It has been demonstrated also that septal infarctions may be more easily recognized in the presence of bundle-branch blocks (Sodi-Pallares, 1956), in contrast with the view generally held. On the basis of these considerations the significance of experimental and clinical VPB in the diagnosis of myocardial infarction is studied in this paper.

Some views on the significance of qR and QR type complexes in right precordial leads in the absence of myocardial infarction

Abstract 1. 1. It is considered that qR and QR complexes in right precordial leads in the absence of myocardial infarction are a good indication of right atrial dilatation. 2. 2. This statement was proved in cardiac cases wherein the right cavities were affected. It was furthermore proved by angiocardiography and necropsy studies that the right atrium was enlarged. 3. 3. The similarity of differences of potential recorded at the atrial surface and within the cavity are pointed out by means of the intra-atrial leads in man and in the dog, by atrial epicardial leads in the dog, and by esophageal and bronchial leads in man. 4. 4. Since the same potentials were found over the epicardial surface of the right atrium and within its cavity, qR and QR complexes were registered both at these sites and over the right precordial leads. It was believed the potential was registered very close to the surface of the right atrium. This implies that this atrium was enlarged, in order to approach points C1 and C2 or that a rotation of the heart took place in such a way as to approximate the right atrial wall to the chest wall. 5. 5. These complexes (qR and QR) have been found experimentally in high portions of the interventricular septum which have a delayed activation. When they are registered over the right precordial leads it is probable that the exploring electrode is oriented to these aspects of the septum through the dilated right atrium.

Clinical electrocardiographic and vectorcardiographic diagnosis of the left anterior subdivision block isolated or associated with RBBB

Abstract Experimental findings previously observed in dogs demonstrated that block of the posterior subdivision of the left bundle branch of His (LPSB) delays the activation of the posterior portion of the free left ventricular wall and of the posterior portion of the interventricular septum, and gives rise to characteristic ECG and VCG changes. These observations permit the recognition of LPSB in clinical tracings. In this paper a study of 17 clinical ECG and VCG records is presented. The main ECG characteristics of LPSB are: qR or QR complexes in Leads III and aV F , with slurring and/or a notch in the downstroke of the R; sometimes a slurring in the initial portion is also observed. Also there is a delayed onset of the intrinsicoid deflection of the R wave in aV F (45 msec.). In vertical hearts the above features are also observed in Leads V 5 and V 6 . ÂQRS is generally situated in the fourth quadrant (between +90 degrees and 0 degrees), although it may be deviated to the right. Frequently the S I -Q III pattern is present. The most important VCG data are: clockwise rotation of the VCG frontal plane ( F ), counterclockwise rotation of the VCG horizontal plane ( H ), and slurrings of the initial and terminal portions of the curve in the three planes. LPSB can diminish or mask the ECG and VCG signs of a posteroinferior myocardial infarction. Based on experimental observations, it was concluded that in a postero-inferior infarction, the presence of terminal and slurred R waves with a delayed intrinsicoid deflection in Leads III and aV F , even with QRS complexes of less than 0.12 second, is due predominantly to an associated LPSB rather than to peri-infarction block. LPSB may diminish the manifestations of right bundle branch block in aV R . Nevertheless the rsR complexes persist in Lead V 1 , while the signs of LPSB are recognizable in Leads III, aV F , and V 6 .

A new approach for the recognition of ventricular premature beats

Abstract Experimental work is presented to prove that many extrasystoles, classically diagnosed as ventricular premature beats, are not. Most of them correspond to atrial or nodal extrasystoles with some degree of aberrancy. On the other hand, there are ventricular premature beats with normal QRS duration and supraventricular beats with QRS duration greater than 0.12 second. The differentiation of ventricular and supraventricular premature beats must be established by considering the morphology of the extrasystolic complex as well as the time in the cardiac cycle when the premature beat is recorded. Definitions of ventricular extrasystoles from several recent textbooks are reviewed. A new definition is proposed based on experimental work performed in the dogs heart.

The electrograms of the conductive tissue in the normal dog's heart

Abstract Simultaneous recording of electrograms of the A-V node, bundle of His, right and left branches and the Purkinje tissue was successfully achieved and is herein presented. The speed of the activation wave in some segments of this specific tissue is calculated. A few considerations for future research are also made.