Review

What rhythms are present?

What is this rhythm and simple description of rhythm abnormality?

What is the rhythm?

What is the rhythm?

What is the rhythm?

Bonus: What serious / life threatening abnormality is present?

ECG 101 - Bundle Branch Blocks - Scott E. Ewing DO Lecture #5

Heart Physiology: Sequence of Excitation Figure 17.14a

QRS Axis (Frontal Plane) Hexaxial diagram Lead axis designated by angular position relative to lead I (0°) Mean QRS electrical axis measured with respect to this display

Normal Conduction Conditions required normal intraventricular impulse conduction Left and right ventricles are not in an enlarged state that would prolong the time required for their activation and recovery No myocardial ischemia or infarction to disrupt the spread of the activation and recovery waves Rapid impulse conduction through the right- and left-ventricular Purkinje networks so that the endocardial surfaces are activated almost simultaneously No accessory pathways for conduction from the atria to the ventricles

Left Bundle Branch Block

LBBB

Successive Ventricular Activation Comparison of patterns of QRS morphology in lead V1 when the two ventricles are activated successively rather than simultaneously A ventricular beat Bundle branch block Ventricular tachycardia. Artificially paced ventricular rhythm

LBBB – Definition QRS duration ≥120 ms Broad, notched R waves in lateral precordial leads (V5 and V6) and usually leads I and aVl Small or absent initial R waves in right precordial leads (V1 and V2) followed by deep S waves Absent septal Q waves in left-sided leads Prolonged intrinsicoid deflection (>60 ms) in V5 and V6

LBBB Comparison Normal leads V1 and V6 Typical QRS-T patterns in RBBB and LBBB Note the secondary T wave inversions in leads with an rSR' complex with RBBB and in leads with a wide R wave with LBBB

Normal ECG

Typical LBBB

Interpretation: NSR with LBBB QRS duration 0.16 second Broad, notched R waves in lateral precordial leads Small or absent initial R waves in right precordial leads followed by deep S waves Absent septal Q waves in left-sided leads Prolonged intrinsicoid deflection (>60 ms) in V5 and V6 Secondary T wave changes such that the ST-T wave vector points opposite in direction of the major vector of the QRS

Interpretation: NSR with LBBB Complete LBBB may be associated with a normal, leftward, or rarely rightward axis LBBB may mask or mimic the pattern of underlying myocardial infarction LBBB is important as often a marker of underlying organic heart disease Hypertensive heart disease Severe coronary disease Cardiomyopathy Valvular disease

LBBB Mechanisms Almost completely reorganized pattern of LV activation Initial septal activation right septal surface, absence of normal septal Q waves Excitation wave spreads slowly by conduction from muscle cell to muscle cell LV endocardial activation requires additional 40 – 180 ms QRS complex is prolonged and can be very wide Once LV activation begins, it proceeds in a relatively simple and direct manner around the free wall and then to the base of the heart

LBBB Mechanisms Activation across the LV projects positive forces to left-sided leads and negative ones to right-sided leads Spread through working muscle fibers results in notching and slurring from discontinuous propagation ST-T wave changes are generated by abnormalities in conduction, called secondary T wave abnormalities ST-T wave changes produced by direct abnormalities of the recovery process are called primary T wave abnormalities (often ischemic in origin)

LBBB Clinical Significance Usually patients with underlying heart disease With CAD, correlates with more extensive disease, more severe LV dysfunction, and reduced survival rates Duration of the QRS complex often inversely related to LV EF Abnormal ventricular activation pattern induces hemodynamic perturbations abnormal systolic function with dysfunctional contraction reduced ejection fraction and lower stroke volumes reversed splitting of the second heart sound functional mitral regurgitation

LBBB Clinical Significance Functional abnormalities in phasic coronary blood flow and reduced coronary flow reserve caused by delayed diastolic relaxation result in septal defects on exercise nuclear perfusion scans Obscures or simulates other EKG patterns Diagnosis of LVH is complicated by the increased QRS amplitude and axis shifts intrinsic to LBBB Very high prevalence of LVH with LBBB makes defining criteria with high specificity difficult Diagnosis of infarction may be obscured

Interpretation: Afib with LBBB Coarse atrial fibrillatory waves (lead V1) may be mistaken for atrial flutter waves With atrial fibrillation the atrial activity varies continuously and usually the ventricular response is completely variable QRS complex here shows a typical LBBB morphology with secondary ST-T abnormalities

Interpretation: Atrial Flutter with 2:1 Conduction and LBBB Wide-complex tachycardia Classic LBBB pattern If you look carefully, atrial activity in the limb leads, with negative polarity in lead II, at rate of 320 bpm Thus, atrial flutter with 2:1 conduction and LBBB

Interpretation: SR with 2:1 AV Block and LBBB Patient had a history of prior silent inferior MI, hypertension, and mitral regurgitation (the latter two factors accounting for the prominent LAA) Underwent dual chamber pacemaker implantation for his 2:1 second-degree AV block with marked bradycardia Location of the AV block was likely infranodal, given the presence of the LBBB and normal PR interval in the conducted beats

Interpretation: SR With LBBB Sinus rhythm at 72 bpm with LBBB with QRS duration 0.16 second, normal AV conduction, QT interval at the upper limits of normal (0.42 s) History of hypertension and idiopathic cardiomyopathy with an LV EF 35% Acute MI cannot be ruled out by ECG alone in this context, the findings of tall right precordial T waves and J point elevations of this magnitude are consistent entirely with LBBB

Right Bundle Branch Block

RBBB

RBBB – Definition QRS duration ≥120 ms Broad, notched R waves (rsr', rsR', or rSR' patterns) in right precordial leads (V1 and V2) Wide and deep S waves in left precordial leads (V5 and V6)

RBBB Comparison Normal leads V1 and V6 Typical QRS-T patterns in RBBB and LBBB Note the secondary T wave inversions in leads with an rSR' complex with RBBB and in leads with a wide R wave with LBBB

Normal ECG

Typical RBBB

Interpretation: NSR with RBBB Sinus with RBBB QRS duration > 0.12 second rSR’ complex with a wide terminal R wave in V1 qRS complex with a wide S wave in V6 Secondary T wave changes Usually associated with an underlying pathology causing RVH COPD Pulmonary hypertension Atrial septal defect Pulmonic stenosis Also, age related degenerative changes Finally, LAD occlusion in AMI since LAD typically supplies the proximal right bundle

RBBB Causes Age related degenerative disease of the conduction system COPD Pulmonary hypertension Cor pulmonale / RVH Pulmonic stenosis Pulmonary embolus Rheumatic heart disease Myocarditis or cardiomyopathy Ischemic heart disease (LAD typically supplies the proximal right bundle) Congenital heart disease such as ASD

RBBB Mechanisms Activation of the right side of the septum is initiated after slow transseptal spread of activation from the left septal surface RV free wall then excited slowly, with variable participation of the specialized conduction system Result is delayed and slowed activation of the RV with much or all of the RV undergoing activation after depolarization of the LV has been completed

RBBB Mechanisms Because LV activation remains relatively intact, the early portions of the QRS complex are normal Delayed activation of the RV causes prolongation of the QRS duration and a reduction in the cancellation of RV activation forces by the more powerful LV activation forces Discordant ST-T wave patterns are generated by the same mechanisms as for LBBB; with RBBB, recovery forces are directed toward the earlier-activated LV and away from the RV

RBBB Clinical Significance RBBB is common and often no evidence of structural heart disease With new onset RBBB higher rate of CAD, CHF, mortality With CAD, RBBB suggests advanced disease RBBB interferes with other EKG diagnoses (lesser extent than LBBB) RVH more difficult to make with RBBB because of the accentuated positive potentials in V1 Usual criteria for LVH can be applied but have lower sensitivities Combination of LAA or LAD with RBBB suggests underlying LVH

Interpretation: SR with 2° Type I AV Block and RBBB Sinus rhythm with 1° AV block and 2° Type I AV block A 5:4 Wenckebach sequence is present in the middle of the recording Complete RBBB LAA also noted along with non-specific repolarization abnormalities

Interpretation: Atrial Flutter with 4:1 Conduction and RBBB Flutter waves are well-seen in leads V1 and III Rate of about 280 bpm, with a ventricular response at about 70 bpm Classic RBBB pattern present Patient had rheumatic mitral valve disease, moderate pulmonary hypertension, and tricuspid regurgitation

Interpretation: Anteroseptal MI with RBBB Anterior precordial leads reveal a qR pattern marked ST elevation, and upright T waves Three points are worth making with regard to a RBBB Secondary T wave inversions are typically seen in the right precordial leads (leads with a terminal R'). Upright T waves in such leads might indicate ischemia. T wave inversions in leads with no terminal R' might also be ischemic ST elevations are not normally seen in RBBB Right precordial Q waves may be seen in RBBB without an infarct (especially in the setting of acute right ventricular overload), but if the Q waves extend past V2 or if they are slurred or wide, they suggest pathology Bottom Line: RBBB does not render the ECG uninterpretable!!

Interpretation: SR With Prior MI and RBBB SR with PAC’s RBBB causing widely but physiologically split S2 on physical exam Pathologic Q wave V1-V3 due to prior anteroseptal MI caused by left anterior descending occlusion

Fascicular Blocks

Conduction System LAF and LPF indicate the left anterior and left posterior fascicles, respectively (1), (2), and (3) indicate the locations at which intraventricular conduction abnormalities can produce alterations of the QRS complex and T wave

Conduction Anatomy LV opened to reveal the LBB and its fascicles Anterior and posterior fascicles of the LBB are also designated superior and inferior, respectively, because these terms indicate their true anatomic positions

Conduction Anatomy LV viewed from apex upward towards base Interventricular septum (S), LV free wall (FW), anterior (A) and inferior (I) regions of the LV Typical appearances of the QRS complexes in leads I and aVF are presented for normal, LAFB, and LPFB LV activation

Left Anterior Fascicular Block Left axis deviation (usually  -60 degrees) Small Q in leads I and aVL, small R in II, III, aVF Usually normal, sometimes slightly prolonged QRS duration Late intrinsicoid deflection in aVL (> 0.045 s) Increased QRS voltage in limb leads

LAFB Mechanisms Initial activation of LV free wall via LPF Activates inferior and rightward, thus Q wave leads I and aVL Spreads superior and leftward, prominent R wave lead I and prominent S wave lead aVF Left axis deviation to at least -45 degrees QRS duration normal or prolonged 0.01-0.04 s

Left Anterior Fascicular Block 53-year-old woman with no medical problems (A) 75-year-old man with a long history of poorly treated hypertension (B) Arrows indicate the deep S waves in leads II, III, and aVF that reflect extreme left axis deviation

Left Posterior Fascicular Block Right axis deviation (usually  120 degrees) Small R in leads I and aVL, small Q in II, III, aVF Usually normal, sometimes slightly prolonged QRS duration Late intrinsicoid deflection in aVF (> 0.045 s) Increased QRS voltage in limb leads No evidence of right ventricular hypertrophy

LAPB Mechanisms Initial activation of LV free wall via LAF Activates superior and leftward, thus Q wave leads II, III, aVF Spreads inferior and rightward, prominent R wave lead aVF and prominent S wave lead I Right axis deviation to at least +90 degrees QRS duration normal or prolonged 0.01-0.04 s

Left Posterior Fascicular Block Healthy 77-year-old woman Arrows indicate the deep S waves in leads I and aVL typical of both LPFB and RVH

Bifascicular Block RBBB with a LAFB or LPFB

Review

Bundle Branch Block QRS duration ≥120 ms LBBB RBBB Broad, notched R waves in leads V5 and V6 and usually leads I and aVl Small or absent initial r waves in leads V1 and V2 followed by deep S waves Absent septal q waves in left-sided leads Prolonged intrinsicoid deflection (>60 ms) in V5 and V6 RBBB Broad, notched R waves (rsr', rsR', or rSR' patterns) in leads V1 and V2 Wide and deep S waves in leads V5 and V6

Bundle Branch Block Review Normal leads V1 and V6 Typical QRS-T patterns in RBBB and LBBB Note the secondary T wave inversions in leads with an rSR' complex with RBBB and in leads with a wide R wave with LBBB

Interpretation: SR With LBBB Patient had hypertrophic obstructive cardiomyopathy with chronic LBBB Note evidence of LAA Most patients with LBBB have LVH Presence of LAA with LBBB is also strongly suggestive of underlying LVH

Interpretation: SR with 2:1 block and RBBB Slow AV nodal conduction and infra-nodal block of His-Purkinje disease RBBB, also LAA and LVH Dual-chamber pacemaker was implanted Marked T-wave inversions in the anterolateral leads with QT prolongation, which was not due to MI or CAD Prominent T-wave inversions like these have been reported after episodes of profound bradycardia and syncope

PSVT with RBBB Classic RBBB morphology (rsR' in V1) making VT unlikely No definite atrial activity is seen (P waves or flutter waves) Regular rate 150 bpm excludes afib Flutter waves? No. Rhythm most consistent with PSVT Most likely AVNRT

Interpretation: SR With PAC’s and LBBB Frequent PACs which appear in a bigeminal pattern, accounting for the “group beating” pattern, simulating SR with AV Wenckebach with 3:2 conduction Second P wave in each couplet is premature and has a different morphology, since it comes from an ectopic atrial site Biphasic P waves with prominent negative component in V1 indicative of LAA Subtle but important supportive finding is the distinct notching of the ascending part of the S wave in lead V5 with the LBBB This finding in leads V3-V5 with LBBB is referred to a Cabrera’s sign and is a marker of myocardial scarring due to myocardial infarction or other causes Biventricular heart failure was present with severe LV dysfunction with a LV EF 20-25% and both MR and TR (due to chemotherapy-induced cardiomyopathy)

Interpretation: SR with LAFB Pure LAFB causes marked LAD (-45 degrees to -90 degrees) Typically with rS complexes in II, III, and aVF, and qR complexes in I and aVL QRS duration of <120 ms RS or Rs complexes may be seen in the left chest leads with left anterior fascicular block

Interpretation: SR with RBBB and LAFB Complete RBBB with LAFB RBBB causes the classic RSR' morphology in V1 LAFB causes the left axis deviation Note: the subtle variation in P wave morphology here is due to baseline artifact and not to wandering atrial pacemaker

Interpretation: SR with RBBB and RAD probably due to LPFB 76 year old man with idiopathic CM and a wide QRS, no clinical/echocardiographic evidence of RVH, no clinically significant CAD by cardiac catheterization Borderline sinus bradycardia (59 bpm), prolonged PR interval (250 ms) and RBBB with marked RAD Upright P wave in lead I precludes left arm/right arm lead reversal Three major causes of RBBB with RAD in adults Right ventricular overload/hypertrophy syndromes, acute or chronic Lateral MI with RBBB RBBB with LPFB, a diagnosis of exclusion, requiring ruling out RV overload or lateral MI, in particular as causes of the RAD Non-diagnostic Q waves in the infero-lateral leads here without clinical evidence of prior MI This patient was referred for EP study because of findings of RBBB with alternating right and left axis deviation on other ECGs, consistent with severe His-Purkinje (infranodal) conduction disease Finding confirmed at EPS which revealed a markedly prolonged HV interval (91 ms, increasing to 110 ms after procainamide infusion) with only a minimally prolonged AH interval (123 ms) at a baseline sinus cycle length of 993 ms (about 60 bpm) Pt underwent dual chamber PPM implantation because of the high risk of progression to complete heart block