[Uncomplicated and complicated myocardial peripheral blocks]. / Bloqueos miocárdicos periféricos no complicados y complicados.

Septal necrosis + peripheral left blocks. Because of an extensive septal necrosis, the manifestation of the initial ventricular activation forces decreases in the precordial leads. With left bifascicular block (LASB + LPSB), the first ventricular activation forces become more evident and the electrical signs of septal necrosis can be concealed. In the presence of a trifascicular block, the manifestation of the first ventricular electromotive forces diminishes again and the electrical signs of septal necrosis become evident once more. Small Q waves are present in leads V1 to V4. Extensive anterior necrosis + left peripheral blocks. This necrosis is manifested by QS complexes from V2 to V6. An associated left bifascicular block reduces the electrical manifestation of dead tissue: QS complexes persist only in V3 and V4. In turn, a coexisting trifascicular block causes the presence of QS complexes from V2 to V5. Posteroinferior necrosis + left peripheral blocks. Electromotive forces of the ventricular activation shift upward, due to a posteroinferior necrosis, and QS or QR complexes are recorded in leads aVF, II and III. An associated left bifascicular block displaces the main electromotive forces downward, posteriorly and to the left, due to a delay of the posteroinferior activation fronts. The ventricular complexes become positive and wider in all leads, reflecting the potential variations of the inferior portions of the left ventricle: aVF, II, III, sometimes V5 and V6. Consequently, the electrical signs of necrosis are reduced or abolished. Right ventricular peripheral blocks do not conceal the electrocardiographic signs of univentricular and biventricular dead myocardium.

Antiarrhythmic and arrhythmogenic action of inosine in experimental ventricular tachyarrhythmias.

OBJECTIVE: To study the possible action of inosine on experimental ventricular tachyarrhythmias. MATERIAL AND METHODS: We used 92 mongrel dogs weighing 13 kg-17 kg, anesthetized with 30 mg/kg sodium pentobarbital applied intravenously. Myocardial lesions were induced by injecting 1 ml-1.5 ml of 70% phenol in the free wall of the left ventricle. In 36 dogs, the ventricular arrhythmia (VT) was induced 30 min later with aconitine crystals inserted into the periphery of the damaged area; in 16, VT was due only to myocardial damage and in the other 13 VT was spontaneously originated. Twenty-nine animals constituted the control group; no inosine was administered to them. The possible effects of inosine were studied in 63 animals. Leads II, aVR or aVL, right and Left unipolar intraventricular leads and that on the wall of the superior vena cava were recorded under control conditions, once the myocardial damage had been induced, during the ventricular tachycardia, and following the injection of inosine. Of the 63 inosine-treated animals; in 34, VT was due to aconitine; in 16, it was produced only by the myocardial damage and, in 13, VT was presented spontaneously. RESULTS: Sinus rhythm was not reestablished in the animals of the control group. Inosine reestablished the sinus rhythm in 26 of 34 dogs (76%) that received phenol and aconitine, in 13 of the 16 (81%) presenting only the myocardial damage, and in 6 of the 13 (46%) with spontaneous ventricular tachycardia. In some experiments, inosine induced supraventricular tachycardias, ventricular-atrial blocks, and ventricular pre-excitation phenomena. CONCLUSIONS: In this experimental series, inosine showed antiarrhythmic and arrhythmogenic effects, similar to those of adenosine from which it derives.

[Left posterolateral extensive myocardial infarct. An electroanatomical comparison]. / Infarto posterolateral izquierdo extenso. Cotejo electro-anatómico.

A complete ECG thoracic circle allows exploring some heart structures not explored by the conventional electrocardiogram. It provides a direct indication on the location of the damaged myocardium. In fact, posterolateral infarctions can be limited to the inferior third of the left ventricle or can cover the entire free left ventricular wall from the base up to the heart apex and can be univentricular or biventricular. On the other side, the unipolar thoracic leads and the high abdominal leads MD, ME, MI show the evolution of the signs of injury, characteristic of the acute stage of infarction, toward necrosis. We present the example of a 61-year-old man, whose ECG shows signs of subepicardial or transmural injury and of necrosis in the low precordial leads V5 and V6, as well as in the high left posterior leads V8 and V9. This fact suggests the presence of an acute extensive myocardial infarction extending from the base to the heart apex. Moreover, the moderate elevation of the RS-T segment from to V9R to V7R indicates the presence of subepicardial injury in the high posterior regions of the right ventricular wall. These electrocardiographic data were confirmed by the radioactive isotope study and, definitively, by the anatomical findings.

[On the diagnostic value of indirect electrocadiographic signs of left posterolateral basal infarction]. / Acerca del valor diagnóstico de los hallazgos ECG indirectos de infarto miocárdico posterolateral basal izquierdo.

The left basal posterolateral infarct does not give pathological Q waves nor ventricular QS complexes in the low lateral leads V5 and V6. For that, the increased voltage of R waves in the lead V2 and or transitional leads V3 and V4, constitutes only an indirect sign of the presence of dead myocardium in the left posterolateral basal regions. Naturally, in these cases, a differential diagnosis with left ventricular or biventricular hypertrophy is mandatory. Therefore it is suitable to register left posterior thoracic leads V7-V9 or, preferably, a complete thoracic circle. We present here three examples: two experimental and another clinical, in which the electrocardiographic findings corresponded to anatomical data of a left posterolateral basal infarction. This fact speaks for a no absolute but relative diagnostic value of the indirect electrocardiographic signs of altered ventricular depolarization and repolarization in the left posterolateral basal regions of the left ventricle.

[Electrical manifestations of dead myocardium associated to proximal blocks of intermediate degree]. / Aspectos eléctricos de la asociación de miocardio inactivable y bloqueos tronculares de grado intermedio.

The electrical manifestation of dead myocardium associated to incomplete bundle branch block, i.e., with a limited "jumping wave" phenomenon, are exposed. Our description is based on previous experimental studies and validated by electro-anatomical comparisons. In previous experimental reports, the electrical manifestations of dead myocardium in the presence of varying degrees of associated block have also been described. The main electrocardiographic changes are related to the location and extent of damaged region and to degree of bundle branch block. If a left bundle branch block coexists with dead myocardium, small Q waves are registered in left unipolar leads exploring the damaged area. In these leads, the signs of subepicardial or transmural injury are increased. When a right proximal block coexists, the main changes concern the morphologies registered in the unipolar right epicardial and precordial leads. The electrical changes are due to the spatial orientation of the electromotive forces of ventricular depolarization and repolarization. The electrocardiographic changes described here can be satisfactorily understood in the light of the present knowledge on the ventricular electrical phenomenon.

[Electrocardiographic features of right ventricular hypertrophy in chronic cor pulmonale]. / Aspectos electrocardiográficos de la hipertrofia ventricular derecha en el cor pulmonale crónico.

The electrophysiological criteria for diagnosing right ventricular hypertrophy, characteristic of chronic cor pulmonale, are described. Right ventricular hypertrophy due to a sustained systolic overload can be global or regional. In the first situation, as for example, an idiopathic pulmonary hypertension, the magnitude and manifestation of all the main vectors resulting from the depolarization of this ventricle are increased: Ils (septal), llr (parietal), and Illr (basal). When the right ventricular hypertrophy is of the segmental (regional) type, as for example, that due to a chronic bronchial obstruction, the magnitude and manifestation of only some right vectors are increased. In this condition, only the magnitude of the right basal vector (Illr) is augmented. In the presence of subepicardial or transmural ischemia of the right ventricle, negative T waves of primary type are recorded in right precordial and transitional leads, where the Q-Tc interval is prolonged in the absence of digitalis effect. Two demonstrative examples of the correlations existing between the electrocardiographic and anatomical findings in global and regional hypertrophies, respectively, of the right ventricle are presented.

[On the electrical manifestations of some heart diseases associated with ventricular preexcitation]. / Manifestaciones eléctricas de alteraciones miocárdicas asociadas a preexcitación ventricular.

Electro-Vectorcardiographic curves, corresponding some heart diseases, must be analyzed in the light of the ventricular depolarization sequence, as well as on the heart's position and rotation. A more than 30-msec interval between the end of the initial slurring (delta) and the vertex of the R wave in the left unipolar leads or the main axis of the vectorcardiographic ventricular curves, allows us to infer the coexistence of left ventricular hypertrophy. On the other hand, segmental irregularities or distorsions of the electric curves suggest the presence of a limited myocardial zone unable to be activated. Extensive or multiple deformations of these curves are more suggestive of a diffuse myocardial damage. Sometimes signs of preexcitation, due to a pharmacological action, can also appear.

[On the ventricular arrhythmias in Chagasic chronic cardiomyopathy]. / En torno a las arritmias ventriculares en la miocardiopatía chagásica crónica.

Some authors have shown a high prevalence of electric circuits localized in the epicardium in Chagasic cardiomyopathy. Other authors have found in these patients, during electric mapping, mid-diastolic potentials and earlier myocardial activation in epicardial regions than in the endocardium. In a previous study, we found electrocardiographic signs of subepicardial ischemia in 66% of seropositive Chagasic patients against 16% of seronegative Chagasic ones. In the case presented here, a Chagasic dilated cardiomyopathy, we found electrocardiographic signs of subepicardial injury in the left free ventricular wall, related with histological findings of lymphocytic inflammation in these regions. In contrast, the endocardium was completely free from inflammation foci.

[An ECG-anatomical comparison in a case of Williams' syndrome]. / Cotejo electro-anatómico en un caso de síndrome de Williams.

A case of Williams' syndrome in a 22 years old man, is described. Clinical data, as well as those of laboratory and of imageneology study, are reported. An electro-anatomical comparison permitted to verify the value of electrocardiographic signs of enlargement of the four heart chambers, due to a mixed overload. It permitted also to establish the value of the signs of the interatrial block, probably due to myocardial atrial fibrosis, and those suggesting hyperkalemia. The electrocardiogram always is very useful because it furnishes certain functional aspects permitting to allow structural inferences, in following subjects with congenital or acquired heart diseases.

Risk factors, echocardiographic patterns, and outcomes in patients with acute ventricular septal rupture during myocardial infarction.

Ventricular septal rupture (VSR), which can complicate an acute myocardial infarction (MI), carries a high mortality rate. Because precordial and transesophageal echocardiography can identify the type of rupture and assess right ventricular (RV) function at the patient's bedside, we examined the prognostic significance of echocardiographic patterns in postinfarct VSR by postulating that complex rupture and RV involvement carry a worse prognosis. Seventeen patients (10 men; mean age 66 years) who had confirmed postinfarct VSR underwent precordial and transesophageal echocardiography followed by coronary angiography. Serial 12-lead and right precordial leads were also available. Type of septal rupture was classified as simple or complex based on autopsy-proved echocardiographic criteria. Three patients had inferior wall MI and 14 had anterior wall MI. ST-segment elevation persisted >72 hours in all 3 patients who had inferior wall MI and in 12 who had anterior wall MI. Segmental wall motion abnormalities helped in detecting the left ventricular entry site, and use of unconventional views superimposed with color flow Doppler provided the RV exit site. RV function was better appreciated with transesophageal echocardiography. Two patients who had inferior wall MI and 7 who had anterior wall MI had complex ruptures. All 3 patients who had inferior wall MI and 7 who had anterior wall MI had electrocardiographic and echocardiographic evidence of RV involvement. Mortality rate was higher in patients who had complex rupture (78% vs 38%, p <0.001) and in those who had RV extension (71% vs 29%, p <0.001). In conclusion, persistent ST elevation is a common finding in patients who have postinfarct VSR. Complex VSR and RV involvement are significant determinants of clinical outcome.

[Early and late effects of adenosine in experimental ventricular tachycardia]. / Efectos tempranos y tardíos de la adenosina en taquicardias ventriculares experimentales.

INTRODUCTION AND OBJECTIVE: To study the action of adenosine in experimental ventricular tachycardia. MATERIAL AND METHOD: We studied 173 mongrel dogs weighing 13-17 kg anesthetized with 30 mg/kg sodium pentobarbital given intravenously. Myocardial lesions were provoked with the injection of 1-1.5 mL phenol in the free wall of the left ventricle. Ventricular arrhythmia was induced 30 min later with aconitine crystals inserted into the periphery of the damaged area. The potential early and delayed antiarrhythmic action of adenosine was systematically investigated in 85 animals. Leads DII, aVR and aVL, unipolar right and left intraventricular leads, and one unipolar lead on the wall of the superior vena cava were used to record control tracings and tracings in the presence of myocardial damage during ventricular tachycardia and after injection of the drug. RESULTS: Sinus rhythm did not reappear in 72 control animals that did not receive adenosine. In the 63 animals with aconitine-induced ventricular tachycardia associated to myocardial damage, the optimal response to 6 mg adenosine-early and fleeting sinus rhythm-was seen in 45% of the dogs; delayed sinus rhythm was seen in 5%. In 67% of the 18 animals with ventricular tachycardia due only to myocardial damage, early and late sinus rhythm appeared with doses of 6 and 12 mg, and late sinus rhythm was seen with a dose of 12 mg. CONCLUSIONS: The antiarrhythmic action of adenosine was seen not only in ventricular tachycardia due to aconitine (triggered activity), but also in tachycardia induced by the myocardial damage (microreentries).

[On Q-wave and non-Q wave myocardial infarcts]. / Infartos miocárdicos con onda Q y sin onda Q.

Much has been said, and is still being said, on Q-wave and non-Q wave myocardial infarcts, trying to relate this electrocardiographic behavior with the culprit coronary arteries and the location of the damaged myocardium. However, it seems logic to bear in mind that the presence or absence of abnormal Q waves depends on the relation established between the zone of damaged myocardium and the width of the electrical endocardium. It must be recalled that the presence of normal Q waves is possible in leads that seem to move away from the first vector of ventricular activation. Besides, the electrical endocardium, i.e., the territory of distribution of Purkinje's network, is situated mainly in the lower half of the ventricles and is virtually absent in basal regions. This endocardium constitutes a histological-functional entity, since the Purkinje fibers, which receive at the same time the activation impulses, are depolarized simultaneously without producing differences in potential. Therefore, these fibers cannot supply an electrical contribution either in normal condition or in the presence of limited damage. Nevertheless, when the damaged zone reaches beyond the exterior limits of this endocardium, for example, in regions where it is small, the exploring electrode can register abnormal Q waves, due to the activation fronts that are moving away, followed by R waves originated in contiguous bands of non-damaged myocardium. We present two characteristic examples of the electrocardiographic manifestations of a transmural left ventricle infarct (QS complexes) and of a subendocardial infarct, reaching beyond the borders of the electrical endocardium (QR complexes). In both of these cases, the electrocardiographic data agree with the anatomical findings.

[On metabolic therapeutics G-I-K in surgery of cardiac patients]. / Utilidad de la terapéutica metabólica G-I-K en cirugía de cardiacos.

The basic principles of the metabolic therapeutics with glucose-insulin-potassium solutions, already proposed by Dr. Demetrio Sodi Pallares, are exposed. Chronologic succession of this treatment during the preoperative, transoperative and postoperative phases of heart surgery, as well as some personal observations of one of the authors, are described. The glucose-insulin-potassium solution is a powerful system, providing very useful energy to protect the injured myocardium during cardiovascular surgery. Many publications support this assertion. The most recent ones indicate a reduction of low output syndromes due to interventions on coronary arteries, as well as a significant diminution of circulating fatty acids after primary angioplasty. The mentioned solution, in higher concentrations than the initial one, could become routine therapeutics in medicine and surgery centers, in general.

[ECG in ventricular hypertrophy]. / El electrocardiograma en las hipertrofias ventriculares.

The electrophysiological criteria for the diagnosis of ventricular hypertrophies, in the light of the sequence of ventricular depolarization and repolarization, are described. Hypertrophy of the right ventricle due to sustained systolic overloading can be global or segmental. In the first case, the magnitude and manifestation of the main vectors resulting from depolarization of this ventricle, i.e., IIs, IIr and IIIr, are increased. In the second case, the magnitude and manifestation of only some vectors resulting from its depolarization are increased; for example, vector IIr (right parietal) in the most frequent type of Fallot's tetralogy and vector IIIr (right basal) in chronic corpulmonale of obstructive origin. Left ventricular hypertrophy, which is generally of global type (aortic stenosis, systemic arterial hypertension), induces an increase in magnitude and manifestation of all the main vectors resulting from depolarization of this ventricle: I (first septal), II (left parietal) and III (left basal). But the left ventricular hypertrophy can also be of segmental type; for example, in idiopathic hypertrophic cardiomyopathy, in which the manifestation of an anteroseptal vector usually predominates. Biventricular hypertrophies produce different electrocardiographic patterns, depending on the preponderance of right or left electromotive ventricular forces. An example of electrocardiographic findings in biventricular hypertrophy is presented. It corresponds to an 18 year-old woman with a large patent ductus arteriosus compressing the left inferior laryngeal nerve, which produced a cardio-vocal syndrome. The patient had pulmonary and systemic hypertension and arterial hyposaturation. The surgical treatment of the patent ductus arteriosus normalized the pulmonary pressure as well as the arterial saturation.

[Septal and parietal dead myocardium with peripheral monofascicular blocks]. / "Necrosis" septales y parietales con bloqueos periféricos monofasciculares.

We describe the electrical manifestations of dead left septal, left and right parietal myocardium and those of biventricular location, reviewing the electrocardiographic signs of the isolated left and right peripheral blocks. We also describe the electrical manifestations of dead myocardium accompanied by a left anterior subdivision block (LASB) and a left posterior subdivision block (LPSB). These ventricular conduction disorders can reduce or conceal the electrical manifestation of the dead zone. We present a case in which a transient LASB conceals the electrical manifestation of dead anteroseptal myocardium. The association of diaphragmatic dead myocardium with LPSB reduces the electrocardiographic manifestation of dead tissue. We show the electrocardiographic findings obtained in a case of a biventricular anterior infarct with a right anterior subdivision block (RASB), as well as an ECG corresponding to the association of a dead myocardial zone with a right posterior subdivision block (RPSB). These ventricular conduction disorders do not generally conceal the electrocardiographic signs of dead myocardial tissue. The possible association of myocardial damage due to an infarct or a myocardiopathy with ventricular proximal and peripheral blocks must be kept in mind. Besides, it is important to consider that proximal blocks do not modify substantially the signs of dead myocardial tissue, whereas peripheral blocks can reduce or conceal these signs.

[Non-complicated and complicated polyfascicular blocks]. / En torno a los bloqueos polifasciculares no complicados y complicados.

Septal necrosis + Peripheral blocks. Because of an extensive septal necrosis, the manifestation of the initial ventricular activation forces decreases in the precordial leads. With left bifascicular block, first ventricular activation forces become evident, and the electrical signs of a sepatal necrosis are concealed. In the presence of a trifascicular block, the manifestation of the first ventricular electromotive forces diminishes again and the electrical signs of septal necrosis become evident once more. Small Q waves are present in leads V1 to V4. Extensive anterior necrosis + Peripheral blocks. Such a necrosis is manifested by QS complexes from V2 to V6. An associated left bifascicular block reduces the electrical manifestation of dead tissue: QS complexes persist only in V3 and V4. A trifascicular block determines the presence of QS complexes from V2 to V5. Posteroinferior necrosis + Peripheral blocks. Electromotive forces of the ventricular activation shift upward, due to a posteroinferior necrosis. QS or QR complexes are recorded in leads a VF, II, and III. A left bifascicular block displaces the main electromotive forces downward, posteriorly and to the left, due to a delay of the posteroinferior activation. QRS complexes become positive and wider in all leads, the reflect the potential variations of the inferior portions of the left ventricle: aVF, II, and III, sometimes V5 and V6. The electrical signs of necrosis are reduced or abolished. With a trifascicular block, wide and slurred QS complexes appear in aVF, II, III, and sometimes in V5 and V6 too.

[On the clinical value of electrocardiogram]. / En torno al valor clínico del electrocardiograma.

Emphasis is given to the clinical value of the electrocardiogram, a simple, quick and unexpensive method for heart exploration. It provides functional information and reliably reflects the metabolic and electrolytic characteristics of myocardial fibers. Such an information cannot generally be obtained by other more sophisticated and expensive methods. The localization and extension of myocardial infarction, the positional and structural changes observed during the evolution of chronic cor pulmonale of obstructive origin, some characteristics of atrial and ventricular arrhythmias, the site of preexcitation in WPW syndrome and troubles due to a dysfunction of the ionic channels because of metabolic or genic alterations, are particularly examined. 1. A good correlation exists between the anatomical site and electrocardiographic indication of the infarcted area. 2. In the obstructive chronic cor pulmonale, positional and structural changes of the heart are observed. The first ones correspond to a vertical heart, due to a descent of the diaphragm and an increase of lung volume. The structural changes are due to an enlargement of the right heart: dilatation and hypertrophy. 3. Ventricular arrhythmias habitually present the "jumping wave" phenomenon between both septal masses and the consecutive aberrance of the ventricular complexes. 4. In the WPW syndrome, the thoracic circle permits to infer the site of preexcitation by the orientation of the first fronts of anomalous ventricular activation. 5. Modifications in the Q-Tc interval reflect the variations of ionic intracellular concentrations in a more reliable way than the changes of plasmatic concentrations. The aforementioned evidences the great usefulness of the electrocardiogram in the clinical setting.

[Electrical features of hypertrophied left heart]. / Aspectos eléctricos de la hipertrofia del corazón izquierdo.

Chronological and spatial characteristics of the main resultant vectors of the left atrial and ventricular depolarization in normal conditions and in presence of hypertrophy, due to a sustained overload, are described. The coexistence of interatrial, intraatrial, and intraventricular conduction disorders can modify the orientation of these vectors. The main electrocardiographic sign of left atrial hypertrophy is a P wave duration > 0.10 sec in adults. In case of left ventricle hypertrophy, the time of onset of the intrinsicoid deflection (TOID) is prolonged in the near left unipolar leads, and the S wave voltage is increased in opposite regions, i.e. in the right precordial or transitional leads. It is necessary to bear in mind other useful electrocardiographic signs. Hence, absence of the right basal vector (IIId) manifestation in a clockwise rotating heart is probably due to an increase in the basal electromotive forces of the left ventricle (vector IIIi) due to hypertrophy or ipsilateral ventricular conduction disorders. For a correct evaluation of these signs, it is mandatory to perform a rational analysis of the traings, not just a stereotyped electrical exploration. Besides it is very important to determine the Q-Tc interval in the left unipolar leads to establish whether, in these leads, the inverted T wave is of secondary type (normal Q-Tc) or of primary type (prolonged Q-Tc) due to a coexisting subepicardial or transmural ischemia. From these considerations, the usefulness of the thoracic circle and high abdominal unipolar leads is inferred.

An experimental contribution to the concept of "jumping wave" phenomenon in the interventricular septum.

OBJECTIVE: The purpose of this study was to evaluate the existence of a histologically bipartite interventricular septum and the electrical independence of both septal masses, as well as to understand the changes of septal activation fronts in the presence of bundle branch blocks. METHODOLOGY: We examined the histological characteristics of both septal masses in 12 canine hearts. Furthermore, in another 11 anesthetized dog hearts, we analyzed morphological and chronological data of intraseptal records with normal activation and in the presence of proximal blocks. RESULTS: A histological discontinuity between the two septal masses in canine hearts seems to exist. Analysis of intraseptal and intracavitary electrical records confirmed slow transmission of the activation fronts from one septal mass to the other when proximal blocks were present. Morphological and chronological changes of the intracavitary complexes agree with the "jumping wave" phenomenon theory. CONCLUSIONS: These results support the validity of this approach to the activation of both septal masses and explain the chronological and morphological changes of the intracavitary records in the presence of ventricular blocks. In addition, this approach is a useful tool to detect the possible coexistence of dead septal tissue.

[Ventricular conduction disorder in presence of dead myocardium]. / Trastornos de conducción ventricular y miocardio inactivable.

In the presence of an advanced degree left bundle branch block (LBBB) with an extensive "Jumping wave" phenomenon, the septal activation abnormally spreading originates septal electromotive forces of greater duration and consequently more important than normal ones. The coexistence of an inactive anteroseptal myocardium with an advanced degree block causes the phenomenon of "Jumping wave" begins in postero-septal regions. Therefore the external left electrodes see the first ventricular activation fronts moving away and register Q waves. The presence of transmural inactive myocardium in the free left ventricular wall permits the corresponding external electrodes to record the morphology of the ipsilateral intraventricular complex: S. An intermediate degree LBBB produces a limited right to left "Jumping wave" phenomenon. When it is associated to septal inactive myocardium, the electrical manifestations of left block are reduced, but those of myocardial necrosis persist: loss of the manifestation of first right septal vector and presence of Q waves in left leads. Because of an advanced degree right bundle branch block (RBBB) with an extensive "Jumping wave" phenomenon, electromotive septal forces of greater duration and consequently more important than normal ones, are originated also. The coexistence of inactive antero-septal myocardium with an advanced degree RBBB causes the phenomenon of "Jumping wave" begins in inferior postero-septal regions. Therefore, the transitional leads see the first fronts of the said phenomenon moving away and register Q waves. The presence of inactive transmural right parietal myocardium permits the corresponding external electrodes to record the morphology of the ipsilateral polyphasic intraventricular complex. An intermediate degree RBBB, associated to antero-septal necrosis, is characterized by the reduction of the electrocardiographic signs of the said block and the presence of Q waves in the right precordial and transitional leads.