Practical Electrocardiography –Bundle Branch Block Scott Ewing, D.O. Cardiology Fellow October 5, 2006
Syllabus • Introduction • Axis Determination • Atrial Arrhythmias, Bradycardias, and AV Conduction Block • Junctional and Broad Complex Tachycardias • Myocardial Ischemia and Acute Myocardial Infarction • Conditions Affecting the Left Side of the Heart • Conditions Affecting the Right Side of the Heart • Conditions Not Primarily Affecting the Heart • Exercise Tolerance Testing
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
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 also important since it is often a marker of underlying organic heart disease (hypertensive heart disease, severe coronary disease, cardiomyopathy or 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 • RV is activated and recovers earlier than the LV, recovery vectors are directed toward the right and away from the left • 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
LBBB Clinical Significance • Usually patients with underlying heart disease • Significantly reduced long-term survival reflecting severity of underlying cardiac 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 ECG 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 left bundle branch block 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 • Hence, atrial flutter with 2:1 conduction and LBBB.
Interpretation: SR with 2:1 AV Block and LBBB • Left atrial abnormality (LAA) also noted • 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: NSR With LBBB • Sinus rhythm at 72 bpm with LBBB with QRS duration 0.16 second, normal AV conduction (PR.0.17 second) and a QT interval at the upper limits of normal (0.42 second) • History of hypertension and idiopathic cardiomyopathy with an LV EF 35% • Ruled out for a myocardial infarction • Serum potassium was normal • 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
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
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
Causes RBBB • Rheumatic heart disease • Cor pulmonale / RVH • Myocarditis or cardiomyopathy • Ischemic heart disease • Degenerative disease of the conduction system • Pulmonary embolus • 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 • Because LV activation remains relatively intact, the early portions of the QRS complex are normal
RBBB Mechanisms • 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 • The late and unopposed emergence of RV forces produces increased anterior and rightward voltage • 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 ECG 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 • The AV Wenckebach sequences are "atypical" in that the RR intervals do not progressively shorten • 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 V1 and lead III • Rate of about 280/min, with a ventricular response at about 70/min • Classic RBBB pattern is also 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 (only in those leads with a terminal R'). Upright T waves in such leads might indicate ischemia, etc. 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: Bundle branch block, especially RBBB does not render the ECG uninterpretable!!
Interpretation: NSR With Prior MI and RBBB • ECG shows sinus rhythm 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
Acute Ischemia and LBBB • Many different electrocardiographic criteria have been proposed for identifying acute infarction with LBBB (none sufficiently sensitive) • Features indicating possible acute ischemia • ST↑ in leads with positive QRS complex “inappropriate concordance” • ST↓ in leads V1, V2, or V3 which have predominantly negative QRS complexes “inappropriate concordance” • Extreme ST↑ (>5 mm) in leads V1 and V2 • If doubt persists, serial electrocardiograms may show evolving changes.
Interpretation: Inferior AMI with LBBB • Sinus bradycardia and LBBB with primary ST-T wave changes • LBBB morphology with primary biphasic and inverted T waves in leads 2, 3 and aVF • Uncomplicated bundle branch blocks should have "secondary" T wave changes • Inverted T waves suggest that a "primary" or ischemic process is evolving in the inferior distribution • Pt had a myocardial infarction with a CK of 700 and 21% MB fraction • Ischemic ECG changes can sometimes be read despite the presence of a bundle branch block
Interpretation: Anterior AMI with LBBB • Evidence of prior and possibly evolving MI superimposed on LBBB • Prior MI is indicated by Q waves as part of a qR in I and V6 • Notching of the ascending limb of the S wave in the mid-left chest leads consistent with prior MI (Cabrera's sign) • Biphasic T waves in the mid-left chest leads raise consideration of evolving ischemia/MI • Statement that "LBBB precludes diagnosing MI" is not correct • Yet, LBBB often does mask changes of prior or acute MI
Bundle Branch Block Review • QRS duration ≥120 ms • LBBB • 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: NSR 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 • Note: there is some baseline artifact here that at times simulates a pacemaker stimulus--however the patient did not have an electronic pacemaker and the P waves and wide QRS are due to native conduction entirely