Left posterior hemiblock (LPH)/

ECG OF THE MONTH Left Postero-inferior Depolarization Delay Keywords Electrocardiography Intraventricular conduction delay, Inferoposterior hemiblock, Left posterior fascicular block, Left posterior hemiblock SR MITTAL Left postero-inferior depolarization delay is less frequent than left antero-superior depolarization delay. It is usually associated with significant disease of conduction tissue. Electrocardiographically, it is characterized by right axis deviation, rs configuration in leads I, avl and qr configuration in leads II, III and avf. Amplitude of QRS complexes is increased in limb leads. Diagnosis needs exclusion of other causes of right axis deviation. It can give wrong impression of inferior ischemia. Left posterior hemiblock (LPH)/ Left posterior fascicular block (LPFB)/ Infero-posterior hemiblock (IPH). those directly involving the fascicles. Chronic diseases may produce (a) Left postero-inferior depolarization delay is a better term because It describes the area of depolarization by the fascicle and helps in better understanding of electrocardiographic findings. Left bundle branch fans into a number of interconnecting fibers with significant inter individual variability. It is difficult to define two independent and separate half of left bundle. Postero-inferior depolarization delay may occur due to diseases other than Figure 1. Diagram showing position of left posterior fascicle in LV inflow tract. AVN- atrio-ventricular node, HB- His bundle, LAF Left anterior fascicle, LPF- left posterior fascicle, MV- Mitral valve, RBB- Right bundle branch. Dr. SR Mittal is Head, Department Cardiology at Mittal Hospital and Research Centre, Ajmer, Rajasthan 214 Cardiology Today VOL. XVIII NO. 5 SEPTEMBER-OCTOBER 2014

progressive delay in conduction rather than block. Only patients with sudden appearance of ECG findings during an acute cardiac illness can be considered to have a fascicular block. Many persons have isolated electrocardiographic findings without the clinical criteria considered necessary for diagnosis of LPH. These patients could be having delayed depolarization of posteroinferior left ventricle for reasons not yet clear. Figure 2. Electrocardiogram showing left posterior fascicular block (a) Classical left posterior hemiblock is less common than left anterior hemiblock because: (Left posterior fascicle is thicker. It has dual arterial supply from circumflex artery and right coronary artery. It is located near the left ventricular inflow tract 1 (Fig. 1) and is, therefore, not involved in diseases of aortic valve. (b) It is unusual in otherwise healthy persons.1 (c) Coronary artery disease is the commonest cause. (i) QRS duration is 100 ms or less. Figure 3. Electrocardiogram showing left posterior fascicular block. Figure 4. Diagram showing frontal plane QRS vector and mean frontal plane QRS axis in left posterior fascicular block. LAF- Left anterior fascicle, LPF- Left posterior fascicle Cardiology Today VOL. XVIII NO. 5 SEPTEMBER-OCTOBER 2014 215

ECG OF THE MONTH Figure 5. Diagram showing genesis of QRS changes in limb leads in left posterior fascicular block. Figure 6. Diagram showing QRS vector in horizontal plane and it s effect on QRS in left posterior fascicular block. (ii) Mean frontal plane QRS axis is between + 900 to +120.0 Usually QRS axis does not deviate beyond + 1200 in uncomplicated LPH. 2 (iii) RS or rs configuration in leads I and avl. 3 (iv) qr configuration in leads II, III, avf. R wave is usually tallest in lead III. 2 (v) QRS voltage is increased in limb leads. 2 (vi) S wave up to V6.3 Absence of other conditions producing right axis deviation Asthenic habitus, chest deformities Right ventricular overload Lateral infarction. Some authorities feel that evidence of left ventricular abnormalities must exist. 3 Some of the patients mentioned above could be having inferoposterior depolarization delay without LPH. Necessity of left ventricular abnormalities is likely to increase specificity at the cost of sensitivity. Initial stages of infero-posterior Figure 7. Diagram showing frontal plane QRS vector and it s effect on QRS in limb leads in (A) Antero-lateral infarction (B) Left posterior fascicular block and (C) Antero-lateral infarction with left posterior fascicular block. 216 Cardiology Today VOL. XVIII NO. 5 SEPTEMBER-OCTOBER 2014

Acute myocardial infarction. ST segment elevation and sequential changes help in diagnosis of acute myocardial infarction. Figure 8. Diagram showing frontal plane QRS vector and it s effect on QRS in limb leads in (A) Left posterior fascicular block and (B) Left posterior fascicular block with infarction in antero-superior region of LV. depolarization delay may not qualify the rigid criteria mentioned above and may contribute to wrong impression about incidence and etiology of LPH. Major QRS vector is directed inferiorly, posteriorly and to right frontal plane QRS axis is, therefore, shifted to right (Figure 4). Left ventricular depolarization starts through the unblocked anterosuperior fibers. Initial mean frontal plane QRS vector is, therefore, directed anteriorly, superiorly and to left. This produces initial r wave in leads I, avl and initial q in leads II, III, avf (Figure 5A). Subsequently the impulse spreads to posteroinferior region of LV. Later part of the QRS vector is, therefore, directed inferiorly, posteriorly and to right. This results in terminal S wave in leads I, avl and terminal R wave in leads II, III and avf (Figure 5B). Mean QRS voltages are increased due to lack of opposition from the blocked inferoposterior fascicle. As major QRS vector is towards positive pole of lead III, R is usually tallest in lead III. 2 In horizontal plane, the late QRS vector is directed posteriorly (Figure 8) with the result that S wave persists up to lead V6. Like other intraventricular conduction disorders, repolarization vector is directed opposite to the terminal QRS vector. This results in low to inverted T wave in leads II, III, avf and upright T wave in I and avl. It may give a wrong impression of inferior ischemia. Old antero-lateral myocardial infarction. In uncomplicated antero-lateral myocardial infarction initial QRS vector is directed inferiorly and to right. This produces Q wave in leads I, avl and R wave in leads II, III, avf (Fig 7 A). Terminal vector is directed superiorly and to left producing terminal R in leads I, avl and terminal S in leads II, III, avf (Fig 7 A). T wave is inverted in leads I, avl and upright in II, III, avf. In LPH, the QRS vectors are in opposite direction (Fig 7 B). When anterolateral myocardial infarction is complicated by LPH (Fig 7C), there is superimposition of two vectors. Initial vector is dominantly affected by the infarction whereas terminal vector is dominantly affected by LPH. Initial as well as terminal QRS vectors are therefore, directed away from leads I and avl. This produces QS complex in leads I, avl and R wave in Figure 9. Electrocardiogram showing anterior myocardial infarction with left posterior fascicular block. Cardiology Today VOL. XVIII NO. 5 SEPTEMBER-OCTOBER 2014 217

ECG OF THE MONTH Right bungle branch block (RBBB) LPH in presence of RBBB results in Frontal plane QRS axis more than + 1200. QRS axis should be calculated from amplitude (and not area) of initial 0.04 second Extremely tall R in II, III, avf. This combination is frequently associated with diffuse involvement of atrio-ventricular and intra-ventricular conduction tissue. Figure 10. Electrocardiogram showing (A) Inferior myocardial infarction (B) Effect of development of left posterior fascicular block. leads II, III, avf. 3 Total amplitude of QRS is also reduced. Other causes of RBBB with a QRS axis of more than + 1200 RBBB + right ventricular hypertrophy RBBB + vertical heart RBBB + extensive lateral infarction. However, unlike RBBB + LPH, above Infarction or fibrosis in the area depolarized by left anterior fascicle. In setting of LPH, initial depolarization via antero-superior fascicle produces initial r in leads I, avl and initial q in II, III, avf (Figure 8 A). Infarction or fibrosis in the antero-superior region reduces the magnitude of this vector. Amplitude of r in I, avl and q in II, III, avf is reduced (Figure 8 B, Figure 9). Old inferior MI LPH produces tall R waves in leads II, III and avf. The q wave of old inferior infarction may appear relatively small as compared to accompanying R wave. (Figure 10). However, criteria of wide Q is still applicable. Amplitude of R wave is also recued due to loss of inferior vector (Figure 11). Symmetrical arrowhead inversion of T wave also supports diagnosis of old infarction (Figure 12). Figure 11. Diagram showing frontal plane QRS vector and it s effect on inferior leads in(a) Left posterior fascicular block and (B) Left posterior fascicular block with inferior infarction. 218 Cardiology Today VOL. XVIII NO. 5 SEPTEMBER-OCTOBER 2014

mentioned conditions are not associated with tall R in II, III, avf. QRS duration of more than 0.10 sec (Figure 13 ) It suggests additional intra-ventricular conduction delay. Figure 12. Electrocardiogram showing left posterior fascicular block with inferior infarction (symmetrical T wave inversion in leads II, III, avf). Posterior chest leads(v7 to V9) and right sided chest leads (V3R to V6R) also show infarction pattern. Changes in T wave Deep symmetrical T wave inversions are abnormal. T wave polarity in the direction of terminal part of QRS (Figure 14) are abnormal. If there is terminal S in II, III, avf, an upright T wave may be normal (Figure 15). Causes of right axis deviation other than LPH. (a) Right ventricular hypertrophy (Figure 16) P-pulmonale and prominent r in V1 help differentiation. Figure 13. Electrocardiogram showing left posterior fascicular block with broad QRS. There is ST segment elevation in leads II, III, avf, V7 to V9 and V4R to V6R. Figure 14. Electrocardiogram showing left posterior fascicular block with positive T wave in leads II, III, avf. Figure 15. Electrocardiogram showing left posterior fascicular block with terminal S wave in leads II, III avf and positive T wave in these leads Cardiology Today VOL. XVIII NO. 5 SEPTEMBER-OCTOBER 2014 219

ECG OF THE MONTH Figure 17. Electrocardiogram from a patient of emphysema mimicking left posterior fascicular block. QRS shows low voltage. There is no increase in size of R in II, III, avf. LPH also produces persistent S wave in V5 V6 and this finding alone should not be taken as a sign of RVH. (b) Vertical heart (Figure 17) Eg. - slender body - emphysema- QRS voltage is low as opposed to LPH. (c) Chest deformities. (d) Extensive lateral infarction. Abnormal Q waves, ST segment elevation, and symmetrical T wave inversion in leads I, avl and leads V5, V6 help identification (Figure 18). QRS Figure 16. Electrocardiogram showing right ventricular hypertrophy mimicking left posterior fascicular block. Figure 18. Electrocardiogram from a patient of lateral infarction mimicking left posterior fascicular block QRS in limb leads shows low voltage. ST segment is elevated in leads I and avl. Figure 19. A- Showing major QRS vector in left lateral accessory path. B - Electrocardiogram from a patient of left lateral accessory path. 220 Cardiology Today VOL. XVIII NO. 5 SEPTEMBER-OCTOBER 2014

voltage in limb leads is reduced rather than increased. (e) Pre-excitation from left lateral accessory path (Figure 19). Short P-R interval and presence of delta wave help diagnosis. Lead V1 shows prominent R. (f) Some cases of hyperkalemia. (g) Technical dextrocardia. Inverted P and T wave in lead I and upright P and T wave in lead avr help suspicion. QRS amplitude in limb leads is normal as opposed to LPH. Most important feature of LPH is not the degree of right axis deviation but the increase in size of R in leads II, III and avf.2 1. Mirvis DM, Gold berger AL. Electrocardiography. In Bonow RO, Mann DL, Zipes DP, Libby P(eds). Braunwald s Heart Disease. Elsevier, Missouri ; 2012:126 65. 2. Schamroth C. The hemiblocks (fascicular block). In Schamroth C(ed). An introduction to electrocardiography. Blackwell Science, France; 1982:105 15. 3. deluna AB, Goldwasser D, Fiol M, Bayes- Genis A. Surface electrocardiography. In Fuster V, Walsh RA, Harrington RA(eds). Hurst s The Heart. Mc Graw Hill, New York; 2011:307 70. Cardiology Today VOL. XVIII NO. 5 SEPTEMBER-OCTOBER 2014 221