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ECG 101: Bundle Branch Blocks - Rhythm Abnormality and Clinical Significance

Learn about bundle branch blocks, including their rhythms, abnormalities, and clinical significance. This lecture covers the basics of ECG conduction and the specific characteristics of left bundle branch block (LBBB). Understand the mechanisms, interpretation, and clinical implications of LBBB.

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ECG 101: Bundle Branch Blocks - Rhythm Abnormality and Clinical Significance

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  1. Review

  2. What rhythms are present?

  3. What is this rhythm and simple description of rhythm abnormality?

  4. What is the rhythm?

  5. What is the rhythm?

  6. What is the rhythm?

  7. Bonus: What serious / life threatening abnormality is present?

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

  9. Heart Physiology: Sequence of Excitation Figure 17.14a

  10. 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

  11. 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

  12. Left Bundle Branch Block

  13. LBBB

  14. 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

  15. 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

  16. 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

  17. Normal ECG

  18. Typical LBBB

  19. 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

  20. 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

  21. 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

  22. 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)

  23. 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

  24. 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

  25. 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

  26. 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

  27. 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

  28. 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

  29. Right Bundle Branch Block

  30. RBBB

  31. 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)

  32. 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

  33. Normal ECG

  34. Typical RBBB

  35. 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

  36. 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

  37. 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

  38. 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

  39. 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

  40. 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

  41. 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

  42. 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!!

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