11/7/2011 DISCLOSURES. Can t miss ECG findings L. Thomas Richards, MD Assistant Professor of emergency medicine OBJECTIVES OBJECTIVES

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1 Topics in Emergency Medicine 2011 Can t miss ECG findings L. Thomas Richards, MD Assistant Professor of emergency medicine DISCLOSURES I am involved in the following healthcare-related commercial pursuits, but they are in no way germane to the current topic of the electrocardiogram and it s use in clinical emergency medicine: 1. I am the President of TessArae, a private molecular diagnostics company providing targeted sequencing in genetic and infectious disease. 2. I served for four years on the Board of Directors of Cowen Group, a publicly-traded healthcare investment bank and hedge fund. OBJECTIVES Examine three common presentations to the ED which compel the EM provider to consider several cardiac etiologies at once: 1. Syncope in a Healthy Adult 2. Ischemic Chest Pain 3. SOB/Hypotension/JVD OBJECTIVES Review the distinguishing features of each ECG Where appropriate, review the pathology which leads to the abnormal findings Consider the implications of the ECG on initial management and interventions Can t Miss ECGs will focus on: 1. Rare ECGs for common etiologies 2. Common ECGs for rare etiologies 1

2 CASES CASE I: Syncope in a Healthy Adult CASE I: Syncope In a Healthy Adult CASE II: Ischemic Chest Pain CASE III: SOB / Hypotension / JVD CASE I: Syncope in a Healthy Adult HPI: 32M, first run in several years, 20 min into run brief episode of CP / palp, followed by syncope All: none Meds: risperdone PMH: bipolar disease FH: father 35, unknown cause SH: occ ETOH / daily tob / no rec drugs ROS: occ palps VS: / %RA Exam: HEENT nl abd NT CTAB MSK nl reg, no MRG neuro / psych nl CASE I: Syncope in a Healthy Adult Diagnostic yield of ECG <5% Even worse in young patients small UCLA study in 2008 showed a 0% yield for age<40, and 10% unrelated, abnormal findings Standard of care still remains 12-lead ECG for all syncope Inexpensive Non-invasive Chance at identifying a life-threatening etiology 2

3 Syncope in a Healthy Adult: ECG for Cardiac Etiologies The obvious (conditioned by looking at older patients?) 1. Bradycardia / Tachycardia / AV block 2. Ischemia 3. LVH The less obvious (to be discussed here) 1. Wolff-Parkinson-White Syndrome 2. Long QT Syndrome 3. Brugada Syndrome 4. Hypertrophic Obstructive Cardiomyopathy Wolff-Parkinson-White Syndrome Wolff-Parkinson-White (WPW) or Pre-Excitation Syndrome -wave <0.12s >0.12s short PR interval delta wave lengthened QRS terminal QRS normal (compared to LBBB, eg) Sinus Rhythm and WPW bypass tract = delta wave depends on tract location (50% left lateral) usually followed by normal ventricular depolarization often transient, even in the same patient 3

4 Transient Delta Wave in WPW WPW and R-sided Bypass Tract wave No wave ECG Variants of WPW R-sided bypass tract short PR + delta wave in II, lat leads tall R-wave in V1 even greater lengthened QRS Reentrant Rhythms and WPW orthodromic variant begins with an atrial premature beat bypass tract refractory? enters at AV node narrow QRS reenters through bypass tract retrograde atrial depolarization negative P-wave 4

5 Reentrant Rhythms and WPW antidromic variant begins with an atrial premature beat AV node refractory? enters through bypass tract wide QRS reenters through AV node retrograde atrial depolarization negative P-wave Atrial Fibrillation and WPW Atrial Fibrillation and WPW wide tachycardia (enters ventricle at bypass tract) irregularly irregular (afib) bypass tract has short refractory period beats approach rate of 300 bpm never use nodal blockers accelerates the rate ventricular arrhythmias tx with procainamide or shock instead Ventricular Tachycardia 5

6 V-Tach vs. Afib with WPW Ventricular Tachycardia regular rates between 150 and 200 bpm Long QT Syndrome Atrial Fibrillation and WPW irregular some rates approach 300 bpm Long QT Syndrome >0.50s Notched T-U wave normal QT interval varies by ventricular rate corrected QT (QTc) = measured QT / RR estimate: nl < half RR QTc >.45s abnormal risk of degeneration to torsades de pointes predict torsades? QTc >.50s T-U waves Long QT Torsades de Pointes 6

7 Classic Torsades de Pointes Polymorphic V-tach or TdP Rotation of QRS axis about the baseline Long QT Syndrome: Etiologies Congenital (rare: 7 genes identified) More commonly acquired: Drug-Induced Antiarrhythmics (procainamide, sotalol, amiodarone) Antibiotics (macrolides, fluoroquinilones) Psychotropics (antipsychotics, TCAs, SSRIs) Methadone GI (cisapride, droperidol) Metabolic Electrolytes (hypokalemia, hypomagnesemia, hypocalcemia) Anorexia, starvation Hypothyroid Hypothermia Long QT Recommendations Avoid QT-prolonging drugs: ECG abnormalities (QT already long, dynamic T- waves, bradycardia) Electrolyte abnormalities (hypo K+, Mg++, Ca++) Impaired hepatic/renal function Concurrent QT prolonging drug use Other CYP450++ drugs (cimetidine, grapefruit juice) Structural heart disease (LVH, CHF) ECG pre-tx and during therapy Treat torsades de pointes with IV magnesium 7

8 Brugada Syndrome Brugada Pattern, V1-V3 Type 1 Type 2 V2 > V3 or V1 ST elevation descends in upward convexity to inverted T-wave ( ski slope ) pseudo RBBB pattern mimics rabbit ears Type 1 most common Types 2 and 3 show saddle back ST pattern often intermittent Brugada Syndrome Identified in 1992 by the Brugada brothers series of SCD patients Asian predominance Phillipines: bangungut ( to rise and moan in sleep ) Thailand: lai tai ( death during sleep ) Inherited defect in Na+ channel, male>female Acquired by Na+ channel blockade TCA s, anti-psychotics, cocaine Sudden death from Vfib likely heterogeneity of Na+ channels in RV Brugada Syndrome Dx and Tx Risk of SCD higher in resting BS patterns (rather than induced or transient) BS pattern at rest and Hx of: Vfib/Vtach Syncope FH sudden death or Brugada pattern Nocturnal Sx EP induced VT AICD is the only effective Tx 8

9 HOCM Molecular cause of structural heart disease Multi-factorial risk for sudden death Disorganized myocytes (sarcomere mutation) can cause ventricular arrhythmias Septal hypertrophy obstructs the aortic outflow tract LVH reduces diastolic filling HOCM Hypertrophic Obstructive Cardiomyopathy (HOCM) tall R-wave in V1 (large septal forces) deep, narrow lateral Q-waves (large initial septal depolarization) septal +/- apical hypertrophy whorled pattern 9

10 Hypertrophic Obstructive Cardiomyopathy (HOCM) HOCM with Apical Hypertrophy ST segment repolarization abnormalities LVH with deep, inverted precordial and inferior T-waves deep,septal Q-waves, pseudo infarct pattern HOCM Dx and Tx HPI: exertional syncope, CP Exam: valsalva induced AS murmur ECG: LVH, Q-waves, deep inverted T-waves Echocardiogram is the gold standard Avoid: Diuretics, nitrates, vasodilators, digoxin Competitive sports (limit to low intensity ) Therapy Β-blockers, verapamil, disopramide Refractory myectomy, ETOH ablation AICD for Hx of Vfib/tach or end-stage CHF Syncope in the Healthy Adult: Read Every ECG for The less obvious 1. Delta waves / short PR of WPW 2. QTc > 0.45s ( half RR ) 3. V2 for ski slope of Brugada 4. Signs of HOCM (LVH, deep TWI, lat Qs) 10

11 Syncope in the Healthy Adult: Critical Therapeutic Pearls Afib w/ WPW: wide, irreg and fast 1. No nodal blockade! 2. Procainamide or shock Long QT: Torsades de Pointes 1. IV magnesium Brugada: AICD HOCM 1. β-blockade 2. Restrict intensive exercise CASES CASE I: Syncope In a Healthy Adult CASE II: Ischemic Chest Pain CASE III: SOB / Hypotension / JVD CASE II: Ischemic Chest Pain HPI: 65F, 30m substernal CP/pressure rad to L arm/ jaw, associated with nausea and diaphoresis All: none Meds: ASA, lisinopril, atenolol, simvistatin PMH: HTN, CAD, prev MI, demand pacer (sick sinus) FH: HTN, DM, CAD SH: no ETOH / daily tob / no rec drugs ROS: recent worsening DOE VS: /90 20 Exam: 98%RA diaphoretic, in pain abd NT HEENT nl MSK nl CTAB, pacer scar neuro / psych nl reg, no MRG CASE II: Ischemic Chest Pain Easy to make decision with obvious STEMI on ECG when machine reads: ***Acute MI*** What about two challenges: 1. Reading STEMI in conduction delays 2. No STEMI, but other signs of critical LAD disease 11

12 Acute CP and LBBB Is the LBBB new? Recently Proposed ECG Criteria for STEMI ST elevation 1. V2 and V3 >2.5mm (men <40), >2.0mm (men >40) and >1.5mm (women) 2. All other leads >1mm (men/women) in any two contiguous leads 3. Posterior and R-sided leads 1. >0.5mm in V7-V9 2. >0.5mm in V3R, V4R New LBBB (!) LBBB: Using Sgarbossa Criteria Sgarbossa Criteria in LBBB Concordant STE: >1mm in any lead 2. ST depression: >1mm in V1-V3 3. Discordant STE: >5mm in any lead 12

13 Satisfies Sgarbossa Criteria in LBBB Sgarbossa Criteria in LBBB Concordant STE ST depression V2 Insensitive (<20%) but highly specific (98-100%) for acute MI Discordant elevation, especially in V1-V3, may occur in non-ischemic LBBB, especially with large Q-waves (not as specific a finding) May be read in paced rhythms just as in LBBB Other findings have been described, particularly T-wave inversion in the same direction as the QRS complex (concordant TWI) Subtle Signs of Acute MI in LBBB Concordant TW Inversion in LBBB Subtle concordant STE Abnormal concordant T-waves V2-V6 Abnormal concordant T-waves Normal discordant T- waves 13

14 V Pacing and Sgarbossa Criteria RBBB and STEMI ST depression V2, V3 RBBB terminal, slurred S in I, V6 Anteroseptal ST elevations Abnormal concordant T-waves RBBB and STEMI The Widowmaker : LAD Lesions and the ECG RBBB should not obscure STEMI STE can be read in both limb leads and precordial leads Q-wave replaces typical R-wave in V1-V3 Pathologic Q replaces R from RSR 14

15 Wellens Syndrome Wellens Syndrome Biphasic T-wave inversions in V2 Also called LAD-T waves Deep, precordial T-wave inversions Biphasic TW in leads V2- V4 Can occur in the absence of CP Often predict a critical or proximal LAD lesion Biphasic T-waves in V2-V4 Deep TWI: Differential Diagnosis Hyperacute T s Early LAD Occlusion Q-wave and non-q-wave MI Myocarditis / late pericarditis LVH HOCM LBBB Pulmonary embolism ICH ( cerebral T-waves ) Normal variant (juvenile T-wave patterns) Inferolateral reciprocal ST depression ST elevation in avr Hyperacute precordial T-waves 15

16 Proximal LAD Triad 1. STE in AVR 3. ST depression in V5 2. RBBB Ischemic Chest Pain: ECG Pearls STEMI and conduction delay 1. Sgarbossa criteria apply to LBBB and pacing 2. TW concordance=ischemia 3. RBBB does not obscure STEMI LAD lesion findings on ECG 1. Wellens syndrome and biphasic Qs 2. Precordial deep TWI 3. Hyperacute T s in early STEMI 4. STE AVR + RBBB + lateral ST depression CASES CASE I: Syncope In a Healthy Adult CASE II: Ischemic Chest Pain CASE III: SOB / Hypotension / JVD CASE III: SOB / Hypotension / JVD HPI: 75F, rapid onset SOB and L>R anterior CP, assoc with nausea, diaphoresis, pre-syncope All: none Meds: ASA, diltiazem, chemo, prednisone, inhalers PMH: HTN, breast Ca, COPD FH: HTN, DM, CAD SH: occ ETOH / 50 pack-year ROS: recent bilateral leg swelling VS: /50 24 Exam: 91%RA diaphoretic, resp dist abd NT HEENT: +JVD MSK: B 2+ pit edema dist BS B neuro / psych nl reg, tach, no MRG 16

17 Acute SOB / Hypotension / JVD Subtle Inferior Ischemia: avl In the absence of LV failure, the life-threatening DDx is narrow: 1. Tension PTX 2. Inferior MI 3. Pulmonary embolism 4. Constrictive pericarditis 5. Pericardial tamponade Our patient had bilateral breath sounds and a normal CXR ST depression or TWI in avl ST depression in V2/V3 Posterior/Lateral MI Posterior MI: Precordial Leads Tall R-wave in V1 Tall R-wave or posterior Q-wave? Q s in V6, I and avl Anterior ST depression or posterior ST elevation? 17

18 Posterior MI: Posterior Leads V7-V9 Tall R-wave in V1 Posterior Q-waves and ST elevation Tall R-wave in V1: DDx Inferior STEMI: STE III>II Rarely a normal variant (1-3%) Posterior MI RBBB RV hypertrophy Wolff-Parkinson-White HOCM Muscular dystrophy Dextrocardia RV infarct more likely get R-sided leads 18

19 ST Elevation V4R-V6R: RV Infarct V4R: the most sensitive lead for RV infarct and RCA occlusion Total RCA Occlusion: Inferior-Posterior-Lateral STE Posterior Inferior Lateral Inferior STEMI: AV Nodal Ischemia 1. ST elevation, III>II 2. Reciprocal anterior ST depressions 3. Wenckebach: Gradual PR prolongation dropped beat Inferior Ischemia? 1. avl T-wave or ST changes early inf MI 2. tall R-wave in V1 posterior leads 3. ST elevation III>II right-sided leads 4. brady arrythmias AV nodal ischemia 19

20 Acute Pulmonary Embolism Saddle Embolism on CT S1 T3 Deep, precordial T-wave inversions Q3 Acute PE: Potential ECG Findings Sinus tachycardia Signs of new R-sided strain 1. S1Q3T3 2. Poor R-wave progression 3. R axis 4. RBBB Deep T-wave inversions, greatest in right and middle pre-cordial leads Acute Pericarditis STE II>III Diffuse ST segment elevation 20

21 Acute Pericarditis PR ST PR ST TP Elevation/depression compared to TP segment Diffuse ST elevation, concave up STE II>III Diffuse PR depression avr acts oppositely ST depression, concave down PR elevation, knuckle sign ECG Features Pericarditis STEMI ST morphology concave up domed STE distribution diffuse anatomical Concurrent STE / TWI - + Reciprocal s avr only common PR abnormalities + - Q-waves - + hyperacute T-waves - + long QT - + Pericardial Effusion: Common Causes Pericardial Tamponade Infection Malignancy Radiation Autoimmune Uremia Idiopathic Trauma Instrumentation Post-MI Postpericardotomy Aortic dissection 21

22 ECG in Pericardial Tamponade Pericardial Tamponade Low volts (effusion) Electrical alternans: alternating amplitudes of QRS segment as heart swings in pericardial sack Concomitant ECG findings of pericarditis, myocarditis or ischemia SOB / Hypotension / JVD: Critical Therapeutic Pearls R/o tension PTX No Sx LV failure likely R-sided lesion 1. pre-load dependent fluid resuscitation 2. avoid pre-load lowering agents (eg nitrates) 3. lower RV afterload (O2, avoid PPV) RV or Posterior STEMI 1. ASA, re-perfusion strategy (lytics vs cath) 2. dobutamine or pacing if indicated PE:? Lytics Tamponade: pericardiocentesis SOB / Hypotension / JVD: ECG Pearls Inferior ischemia 1. avl T-wave or ST changes early inf MI 2. tall R-wave in V1 posterior leads 3. ST elevation III>II right-sided leads 4. brady arrythmias AV nodal ischemia PE: S1Q3T3, RBBB, R-axis, deep TWI Pericarditis: diffuse ST elevation, II>III, PR depression Tamponade: low volts, electrical alternans 22

23 In Summary 1. Routinely review the ECG in young healthy syncope for life threatening etiologies most will be normal, but someday you will save a life 2. Recognize the high risk features in an ECG that seems like it should say STEMI but doesn t you are better than the machine 3. Know how to narrow the differential in critical R heart lesions using ECG your next critical care step depends on it Topics in Emergency Medicine 2011 Can t miss ECG findings L. Thomas Richards, MD Assistant Professor of emergency medicine 23