Scott Ewing, D.O. Cardiology Fellow Lecture #4 Practical Electrocardiography - Ischemia, Infarction, and Bundle Branch Blocks Scott Ewing, D.O. Cardiology Fellow Lecture #4

Review Heart Physiology Depolarization ECG Frontal Plane Rate Rhythm QRS Axis

Heart Physiology: Sequence of Excitation Figure 17.14a

Depolarization

Einthoven’s Electrocardiograph

Rate

Rhythm Atrial Junctional Ventricular Pacemaker Last but not least

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

8-Step Method ECG Interpretation Rate Rhythm QRS Axis P wave PR interval QRS complex QT interval ST segment and T wave

Rate

Rhythm Atrial Junctional Ventricular Pacemaker Last but not least

Acute Ischemia and Infarction

Current-of-Injury Patterns With Acute Ischemia / Infarction Resultant ST vector is directed toward the inner layer of the affected ventricle and the ventricular cavity. Overlying leads therefore record ST depression ST vector is directed outward with overlying leads recording ST elevation

Acute Ischemia / NQWMI / NSTEMI Evolving ST-T changes over time without the formation of pathologic Q waves Evolving ST-T changes may include any of the following patterns: Convex downward ST segment depression T wave flattening or inversion Biphasic T wave changes Combinations of above changes

Ischemic T Wave Changes

Ischemic T Wave Inversion

Ischemic Biphasic T Wave Changes

Acute Ischemia - T Wave Changes

Ischemic ST Changes

Acute Ischemia – ST Depression

Acute Ischemia – ST Depression

Acute Ischemia – ST Depression

60-year-old Male

Anterior Ischemia NSR with ventricular ectopy LAD consistent with LAFB T wave inversions in V2-V5 with subtle upward bowing of the ST segments Symmetric T wave inversions, especially with upward bowing of the ST segments is highly suggestive of LAD ischemia LHC showed significant LAD (and OM) disease

Elderly Male

Severe Multivessel Ischemia NSR with profound ST segment depression, consistent with severe subendocardial ischemia and probable NQWMI Profound ST depressions of this type usually indicate severe multivessel disease and sometimes LM disease Patient experienced severe CP and was transferred in cardiogenic shock En route, developed refractory PEA, ventricular fibrillation, and died

84-year-old Female

NQWMI NSR with leftward QRS axis (-7°) LVH may be associated with ST-T abnormalities (i.e. "strain pattern"), like those in lead aVL Prominent horizontal or downsloping ST depressions in other leads (I, II, aVF, V5, V6) strongly suggestive of ischemia superimposed on LVH Patient had positive cardiac enzymes and underwent LHC showing LM and 3V CAD, followed by CABG

Current-of-Injury Patterns With Acute Ischemia / Infarction Resultant ST vector is directed toward the inner layer of the affected ventricle and the ventricular cavity. Overlying leads therefore record ST depression ST vector is directed outward with overlying leads recording ST elevation

AMI /STEMI / Q Wave MI Most acute MI's are located in the LV With proximal RCA occlusion, up to 50% may also have RV infarction as well More leads with MI changes (Q waves and ST elevation), the larger the infarct size and the worse the prognosis LAD and it's branches usually supply the anterior and anterolateral walls of the LV and the anterior two-thirds of the septum LCX and its branches usually supply the posterolateral wall of the LV RCA supplies the RV, the inferior (diaphragmatic) and true posterior walls of the LV, and the posterior third of the septum RCA also gives off the AV nodal coronary artery in 85-90% of individuals; in the remaining 10-15%, this artery is a branch of the LCX

Evolution of ECG Changes Normal ECG prior to MI Hyperacute T wave changes - increased T wave amplitude and width; may also see ST elevation Marked ST elevation with hyperacute T wave changes (transmural injury) Pathologic Q waves, less ST elevation, terminal T wave inversion (necrosis) Pathologic Q waves are usually defined as duration >0.04 s or >25% of R-wave amplitude Pathologic Q waves, T wave inversion (necrosis and fibrosis) Pathologic Q waves, upright T waves (fibrosis)

Evolution of ECG Changes

Evolution of ECG Changes

Infarct - ST Elevation

Inferior Infarct – ST Elevation

Posterior Infarct – ST Elevation!!!

Old Infarct - Anterior Q Waves

Old Infarct - Inferior Q Waves

Persistent ST Changes

Persistent T Wave Changes

34 Year Old Male With Chest Pain

34-year-old male with chest pain

Acute Anterior MI Acute anterior wall Q wave myocardial infarction Reciprocal inferior ST depressions Hyperacute T waves Distribution of changes is consistent with a proximal LAD occlusion Confirmed at LHC and treated with PTCA and stenting

68-year-old female with chest pain

Acute Anterior MI Note Q waves and loss of R waves V1 - V4 ST elevation in V2 - V6 LAFB is also present, but does not account for the loss of R wave progression LHC revealed 3-vessel disease with a 90% mid-LAD "culprit" lesion

53-year-old female with chest pain

Acute Lateral MI ST elevations in I and aVL Reciprocal ST depressions inferiorly consistent with acute lateral MI Remember: ST elevations like this are never reciprocal but indicate the primary region of ischemia (diagonal or circumflex lesion) Confirmed left circumflex occlusion at LHC

36-year-old male with chest pain

Acute Pericarditis Always consider myocardial infarction first when you see ST elevations But don't forget the differential diagnosis of ST elevations Ischemic heart disease Pericarditis Left bundle branch block (LBBB) Normal ("early repolarization") variant Two features here point to pericarditis First, diffuseness of the ST elevations (I, II, III, aVF, V3-V6) Second, PR depression in II, aVF, V4-V6 and PR elevation seen in aVR (attributed to subepicardial atrial injury)

49-year-old male with chest pain

Acute Pericarditis Diffuse ST segment elevations (I, II, aVF, V2-V6) Subtle PR segment deviations (elevated in aVR and depressed in the inferolateral leads) ST elevations are due to a ventricular current of injury from the pericardial inflammation PR changes are due to an associated atrial current of injury Note that the PR and ST segment vectors point in opposite directions, i.e., PR up and ST down in aVR and PR down and ST up in inferolateral leads

Middle aged female with chest pain

Acute Myocardial Infarction Marked inferior and lateral ST segment elevation ST segment depression in anterior leads V1-V4 ST elevations (“current of injury” pattern) indicate transmural ischemia of the infero-lateral wall ST depression most consistent with reciprocal change from the ST elevation generated by the acute posterior and lateral ischemia Remember, acute pericarditis causes diffuse ST segment elevation (e.g., leads I, II, III, aVL, aVF, and the precordial leads) Reciprocal ST depressions of the type seen here (V1-V4), are never a feature of pericarditis alone

52-year-old male with chest pain

ST Elevation Myocardial Infarction Slight inferior ST elevation with T wave inversion Minimal reciprocal ST depression in aVL Relatively low limb lead voltage makes these findings more subtle

Left Bundle Branch Block

LBBB

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 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 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

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 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: NSR 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

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

Causes RBBB 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) Age related degenerative disease of the conduction system 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 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 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 (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 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

Acute Ischemia and LBBB

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

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

Review

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

Interpretation: SR with 2:1 block and RBBB Slow AV nodal conduction (note long PR of conducted beats) 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 (may have neural basis)

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: NSR With PAC’s and LBBB Frequent PACs which appear in a bigeminal pattern, accounting for the “group beating” pattern, simulating sinus rhythm with AV Wenckebach with 3:2 conduction However, the 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)