sign in sign up
<<
Home , Preload (cardiology), Strain pattern

ECG Workshop The Fundamentals

Darrell E. Jones, DO David Kassop, MD, FACC ACTIVITY DISCLAIMER

The material presented here is being made available by the American Academy of Family Physicians for educational purposes only. Please note that medical information is constantly changing; the information contained in this activity was accurate at the time of publication. This material is not intended to represent the only, nor necessarily best, methods or procedures appropriate for the medical situations discussed. Rather, it is intended to present an approach, view, statement, or opinion of the faculty, which may be helpful to others who face similar situations.

The AAFP disclaims any and all liability for injury or other damages resulting to any individual using this material and for all claims that might arise out of the use of the techniques demonstrated therein by such individuals, whether these claims shall be asserted by a physician or any other person. Physicians may care to check specific details such as drug doses and contraindications, etc., in standard sources prior to clinical application. This material might contain recommendations/guidelines developed by other organizations. Please note that although these guidelines might be included, this does not necessarily imply the endorsement by the AAFP. DISCLOSURE

It is the policy of the AAFP that all individuals in a position to control content disclose any relationships with commercial interests upon nomination/invitation of participation. Disclosure documents are reviewed for potential conflict of interest (COI), and if identified, conflicts are resolved prior to confirmation of participation. Only those participants who had no conflict of interest or who agreed to an identified resolution process prior to their participation were involved in this CME activity.

All individuals in a position to control content for this session have indicated they have no relevant financial relationships to disclose.

The content of my material/presentation in this CME activity will not include discussion of unapproved or investigational uses of products or devices. Darrell E. Jones, DO

Physician, U.S. Army Special Operations Command, Fort Bragg, North Carolina; Assistant Professor, Uniformed Services University of the Health Sciences, Department of Family Medicine, Bethesda, Maryland; Adjunct Faculty, Womack Army Medical Center (WAMC) Family Medicine Residency Program, Fort Bragg, North Carolina

Dr. Jones serves as the chief of primary care for family member and soldier care. He earned his osteopathic medical degree from Nova Southeastern University College of Osteopathic Medicine in Davie, Florida, in 2005, and he completed his family medicine residency at WAMC. He is one of the few physicians to serve at the Military Free-Fall School in Yuma, Arizona, where he gained unique knowledge of high-altitude medicine and free-fall and skydiving injuries. Dr. Jones deployed to Afghanistan twice in three years and spent 13 months supporting Operation Enduring Freedom. He served for two years as the student coordinator and director of medical simulation for the WAMC family medicine program, and he received the Family Medicine Faculty of the Year Award for two consecutive years. For the past 10 years, Dr. Jones has moonlighted in multiple emergency departments, treating 2,500 patients annually. In addition, he has presented at the Uniformed Services Academy of Family Physicians annual conference for the past three years and volunteers as an adjunct member of the faculty for the WAMC Family Medicine Residency Program. David Kassop, MD, FACC

Chief of , Division of Medicine, Womack Army Medical Center, Fort Bragg, North Carolina; Assistant Professor of Medicine, Uniformed Services University of the Health Sciences (USUHS), Bethesda, Maryland

Dr. Kassop is a Medical Corps Officer, Active Duty, in the U.S. Army, with more than 10 years in service. He earned his undergraduate degree from the United States Military Academy (West Point) in 2003, and earned his medical degree from the USUHS in 2007. At Walter Reed National Military Medical Center in Bethesda, Maryland, he completed a fellowship and an internal medicine residency. He is board certified in cardiovascular disease and internal medicine through the American Board of Internal Medicine (ABIM), and specializes in invasive cardiology and advanced cardiovascular imaging. Dr. Kassop is a fellow of the American College of Cardiology and the American College of Physicians. He has co- authored more than 10 peer-reviewed publications and has presented at national and international medical society conferences. Learning Objectives

1. Compare and contrast the findings of ECG tests in different patient cases.

2. Relate the implications of ECG readings to potential cardiac disease.

3. Compare the findings of an ECG to a patient’s clinical presentation.

4. Compare the results of multiple ECG findings from the same patient. ECG Basics

Module 1: Introduction Why is this important? • Patient care • Clinical competence • Expectation as a primary care provider • Credentialing • Accessible diagnostic test that can provide a wealth of information… Why is this important? • Rapid diagnosis in ACS • Structural disease (, valvular disease, congenital heart disease) • Pericardial disease • Evaluation of and conduction disorders • Channelopathies (LQTS, Brugada, CPVT) • Drug toxicity, electrolyte disturbances • Clinical disorders (PE, CNS disorders, dextrocardia) • Pacemaker function Why is this important? • Normal ECG • > 95% likelihood normal LV systolic function • low risk of structural heart abnormalities • Normal vs. Abnormal • Normal variant vs. Pathologic Approach to Reading ECGs Always be Systematic • Utilize a comprehensive algorithm • The order of the algorithm is less important than doing it the same way every time • Look at all the wave features in all the leads • Analyze your rhythm strip(s)! Approach to Reading ECGs • Clinical context is key • Beware of bad data, to include lead placement and artifact • ALWAYS COMPARE TO PRIOR ECGs • When in doubt, describe what you see • Never be afraid to ask for help! Interpretation Algorithm • Rate • Rhythm • Axis • Intervals • Blocks • Hypertrophy/enlargement • Injury//infarct • Other Electrophysiology • Heart has inherent electrical properties • Depolarization of SA node  electrical signal  cells contract • Contraction propagates through the heart  mechanical contraction • Once depolarization completes, the cardiac muscle re-polarizes • Sum of myocyte potentials are measured by surface ECG Demonstration of Electrophysiology The Leads Two groups: • Limb leads • Record cardiac depolarization in relation to a vector between 2 points on the body • Can be further categorized to augmented leads • Precordial leads • Record the depolarization from the heart to the chest wall Limb Leads Precordial Leads

Rhythm Strip

misalud.com Standards • Time/ Intervals Time • Chart speed 25 mm/sec

• 40 ms/small box  Voltage 200 ms/large • 5 large boxes/second 0.1 mV • Voltage • 10 small = 1 mV = full 40 ms (.04 sec) standard 200 ms The P’s and Q’s of ECG

RR ST

PR QT

T wave: Ventricular QRS Complex: Ventricular Depolarization P wave: Atrial depolarization EKG Practice Rate

• Rate: Normal HR is between 60 and 100 bpm • HR = 300/N {300, 150, 100, 75, 60, 50, 43, 37} 300 100 75

150

• Or, count the # of beats on the rhythm strip and multiply by 6 (10 second strip) • Rate > 100 is • Rate < 60 is bradycardia Rhythm

• Fast or Slow? • – look for AV block • Tachycardia – Supraventricular or Ventricular • Wide or narrow? • Clues to where the beats are coming from • Wide may be coming from the or due to aberrant conduction • Narrow means it is coming from above the AV node • Regular or Irregular? • Irregularly irregular v. regularly irregular Rhythm • Sinus Rhythm • P wave before every QRS complex AND… • P wave axis normal (upright in leads I, II, III) • Anything that is not sinus rhythm is an • Define the underlying rhythm • Evaluate for ectopy (PVC, PAC) EKG Practice EKG Practice EKG Practice AV Blocks First degree: PR interval is constant and longer than 200 ms Second degree: Type 1 (Wenkebach) Progressive lengthening of the PR interval before dropping the QRS complex Type 2 Fixed PR interval with periodic dropping of the QRS complex Third degree: AV dissociation (P not matching up with QRS)) EKG Practice EKG Practice EKG Practice Axis Graph Axis • Criteria • Normal -30 to +90 (… to +110 if <40 y/o)

• Determine if net QRS voltage in limb leads is (+) or (-) • If QRS is (+) in I and AVF, then axis normal • (+) in I, (-) in AVF; , if II also neg • (-) in I, (+) in AVF;

Differential Diagnosis • Left axis deviation: • LAFB, LVH, inferior MI, LBBB (in some cases), ostium primum ASD, severe hyperkalemia

• Right axis deviation: • LPFB, RVH, lateral MI, RBBB (in some cases), ostium secundum ASD, chronic disease/PE, dextrocardia, limb lead reversal Interpretation Algorithm • Rate • Rhythm • Axis • Intervals • Blocks • Hypertrophy/enlargement • Injury/ischemia/infarct • Other EKG Practice EKG Practice Intervals

• PR interval: 120 - 200 ms (3 - 5 small boxes) • QRS complex: < 120 ms (< 3 small boxes) • Wide QRS indicates: • • Abnormal depolarization (PVC) • Severe LVH • Ventricular rhythms • QT interval: <.45 sec at normal rate • Pearl: QT should be less that ½ the preceding R to R interval Blocks: LBBB

• QRS > 120 ms • Broad monophasic R wave in I, V5, V6 which is usually notched or slurred • Absence of septal Q waves in lateral leads • Displacement of ST/T in direction opposite the major vector of the QRS Blocks: RBBB

• QRS > 120 ms • rSR’ wave in V1 or V2 • Wide “slurred” S wave in I, V5, V6 LBBB RBBB Interpretation Algorithm • Rate • Rhythm • Axis • Intervals • Blocks • Hypertrophy/enlargement • Injury/ischemia/infarct • Other EKG Practice EKG Practice Interpretation Algorithm • Rate • Rhythm • Axis • Intervals • Blocks • Hypertrophy/enlargement • Injury/ischemia/infarct • Other Enlargement – Left atrial

• Terminal deflection of P wave in lead V1 is one small box deep • Broad or notched P wave in lead II • P-mitrale LAE RAE V1

II Enlargement – Right atrial

• Initial deflection of P wave in lead V1 is 1.5 boxes tall • Peaked P wave in lead II (> 2.5 boxes tall) • “Gothic” P waves LAE RAE V1

II Hypertrophy - LVH • Romhilt-Estes Criteria: LVH= 5 points • Voltage (3 pts) • R or S in limb >20 • S in V1/V2 >30 • R in V6 >30 • ST-T changes [strain pattern] (3 pts or 1 pt if digitalis) • LAE (3 pts) • LAD (2 pts) • QRS > 90 ms (1 pt) • Intrinsicoid deflection (V5-6) > 50 ms (1 pt) • Cornell Criteria, Sokolow-Lyon Hypertrophy - RVH • RAD > +110 • Tall R wave in V1 (R>S) • R in V1 > 7 mm, S < 2 mm • rSR’ in V1, R’ > 10 mm • ST-T changes [strain pattern] (V1-V3) • RAE, widened QRS - Simplified Parameter LVH RVH Axis Left Right

Atrial abn LAE RAE V1 II V1 II V1/V2 Big S (>30mm) Big R V5/V6 Big R (>30mm) Big S Strain (repol abn) I, aVL, V5, V6 II, III, V1, V2, V3 EKG Practice EKG Practice EKG Practice Other • Voltage • Amplitude of the entire QRS complex (R+S) <10 mm in ALL precordial leads AND < 5 mm in ALL limb leads • Alterations in QRS amplitude (electrical alternans) • T-wave analysis: Tall “peaked”, deeply inverted • U-waves: Amplitude < 25% of the height of the T- wave Interpretation Algorithm • Rate • Rhythm • Axis • Intervals • Blocks • Hypertrophy/enlargement • Injury/ischemia/infarct • Other EKG Practice EKG Practice EKG Practice Conclusion • ECG is an important diagnostic tool that provides a “window” into the structure and function of the heart • Approach ECG analysis systematically • Formulate a differential diagnosis for any abnormalities • Clinical context • Beware of bad data! • Do not be afraid to ask for help ECG1: 25 y/o athlete AES Question What is the ? A. 43 bpm B. 60 bpm C.48 bpm D.75 bpm ECG2: 78 y/o female with h/o TIA AES Question What is the rhythm? A. Sinus rhythm B. Atrial C.Ectopic atrial rhythm D.Supraventricular tachycardia (SVT) ECG3: 82 y/o male with CAD AES Question What is the axis? A. Left axis deviation (LAD) B. Right axis deviation (RAD) C.Right superior axis D.Normal axis ECG4: 44 y/o female with non- ischemic dilated AES Question

What type of block is present? A. Right bundle branch block (RBBB) B. (LBBB) C.Non-specific interventricular conduction block (NSIVCB) D.Incomplete left bundle branch block (iLBBB) ECG5: 55 y/o male with chronic AES Question • Based on this ECG, the diagnosis of LVH includes all of the following except… A. Voltage B. Secondary ST/T abnormalities (strain pattern) C.Left D.Left axis deviation ECG Basics

Module 2: Chest pain

• 20-40% of general population will have chest pain during their lifetime • 1.5% of the population will see a Primary Care Physician for chest pain each year • 5% of emergency room visits and up to 40% of admissions are for chest pain

• Chest pain is often the presenting symptom of MI BUT… • Most patients with chest pain DO NOT have MI Chest Pain Evaluation 1. ECG 2. Physical Exam & Risk categorization 3. Cardiac troponins 4. Additional confirmatory testing Acute (MI) Evidence of myocardial necrosis in a clinical setting • Rise or fall of cardiac biomarker

PLUS at least one of the following • Symptoms of ischemia • New significant ST-T changes or new left bundle branch block • Development of pathological Q-waves • New loss of viable myocardium or new regional wall motion abnormality on imaging • Intracoronary thrombus on angiography or autopsy Acute Coronary Syndrome (ACS) Sudden plaque rupture with resulting obstructive thrombosis of a coronary artery leading to decreased myocardial blood flow with ensuing myocyte necrosis (Type 1 MI)

ST-elevation myocardial infarction (STEMI) Non-ST Elevation ACS (NSTE-ACS) – Non-ST elevation myocardial infarction (NSTEMI) – Unstable (UA) ACS • STEMI Symptoms characteristic of myocardial ischemia with persistent ST elevation or new left bundle branch block on ECG

• NSTEMI Symptoms suggestive of myocardial ischemia with elevated cardiac troponin levels but no ST elevation

• UA Symptoms suggestive of myocardial ischemia without elevated cardiac troponins

O’Gara PT, Kushner FG, Ascheim DD, et al. American College of Emergency Physicians; Society for Cardiovascular Angiography and Interventions. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;61(4):e78-e140. Injury/Ischemia/Infarct Injury • New ST elevation • Convex upward = “frowning” or “tombstoning” • Localized to an anatomic region • T often inverted before ST returns to baseline

Ischemia • New ST depressions (horizontal, downsloping) (>0.5mm) in 2 contiguous leads and/or • New T inversions (> 1mm) in 2 contiguous leads • Does NOT localize to an anatomic region Infarct • Pathologic Q-waves (new vs. old) in 2 contiguous leads STEMI Total occlusion of coronary artery

ST elevation in 2 or more contiguous leads

• V2 and V3 – > 2 mm in men >40 y/o or > 2.5 mm in men <40 y/o – > 1.5 mm in women

• V1, V4-6, I, II, III, aVL, and aVF – > 1 mm • Reciprocal ST changes Localization of MI with ST Elevation

• Anteroseptal: V1-3 • Anterior: V2-V4 Left Anterior Descending (LAD) artery • Anterolateral: V4-6, I, aVL • Lateral: I, aVL Left Circumflex (LCx) artery • Inferior: II, III, aVF • Inferolateral: II, III, aVF, V5-6 Right Coronary Artery (RCA) • Posterior: R>S in V1, V2 Normal Variants include:

1. Ramus Intermedius Artery [anterolateral wall]

2. Left-PDA with AVn (15%)

3. SAn from proximal LCx (40%)

4. Long, wrap-around LAD covering the inferior wall Left Main – STEMI Equivalent • LM disease – ST elevation in aVR > ST elevation in V1 – Diffuse, reciprocal changes represent extensive subendocardial ischemia • ST elevation >1 mm in aVR is associated with increased mortality in STEMI

ECG 1

Where is the lesion?

Where is the lesion? Inferior STEMI – There’s more to do! 1. Evaluate for AV blocks 2. Evaluate for posterior injury/infarct – Posterior ECG (V7 - V9) along the left scapula – Subtle finding! 3. Evaluate for RV injury/infarct – Right-sided ECG (V1R – V6R) – Volume sensitive, preload dependent! • Where is the lesion? • What is the abnormal rhythm?

Differential Diagnosis of ST-elevation MI

• Early repolarization • Peri-/ or cardiomyopathy (HCM, Takotsubo) • Ventricular aneurysm • Pulmonary embolism • Severe neurologic injury • Coronary spasm • Repolarization abnormalities • Ventricular hypertrophy, BBB, pacing, Brugada, hyperkalemia, hypothermia • Lead transposition or malposition Non-ST Elevated MI (NSTEMI) Subtotal occlusion of coronary artery -Acute plaque rupture (Type1) -Myocardial supply/demand mismatch (Type2)

Accounts for approximately 70% of ACS Patients typically have more co-morbidities (HTN, HLD, DM2)

+ cardiac biomarkers (Trop) NSTEMI - cardiac biomarkers (Trop) UA

ECG findings are consistent with myocardial ischemia, though not required ECG NSTEMI Possible ECG findings • ST segment depression SN 25%, SP 95%, LR+ 5.3, LR- 0.79 • Symmetrical T-wave inversion SN 32%, SP 91%, LR+ 3.6, LR- 0.74 • Q-waves

Q wave in V2-3 >0.02 sec, QS complex V2 and V3, or Q wave >0.03 sec and > 0.1 mV deep in 2 contiguous leads SN 32%, SP 91%, LR+ 3.6, LR- 0.74 Standards • Time/ Intervals Time • Chart speed 25 mm/sec

• 40 ms/small box  Voltage 200 ms/large • 5 large boxes/second 0.1 mV • Voltage • 10 small = 1 mV = full 40 ms (.04 sec) standard 200 ms Baseline ECG 56 y/o male with HTN, HLD, and DM2 with acute substernal chest pain. Negative serial cardiac enzymes.

Deep, symmetrical T-wave inversions in the precordial leads Wellens’ Sign Prox-LAD 86 y/o male with h/o HTN and HLD admitted for NSTEMI Osial D1

Prox LAD

Prox L-PDA Non-dominant RCA Infarct: Pathologic Q waves • An initial negative deflection of a QRS complex • Pathologic: • 1 box wide and 1 box deep, or • 1/3 the amplitude of the QRS complex • May represent a recent or remote myocardial infarction • Imaging evidence of regional myocardial non- viability (thinned, fails to contract) Inferior-lateral MI (remote) with persistent anterior ST-elevation associated with LV aneurysm 68 y/o female with h/o HTN, HLD, and DM2 admitted for new- onset . Serial cardiac enzymes negative. Distal RCA Infarct

Mid to distal LAD Infarct LVG End- LVG End-

*Akinetic distal anterior and inferior walls

**Akinetic, aneurysmal apex

Consistent * with prior myocardial * ** infarction Conditions may cause difficulty interpreting ST segment • Ventricular hypertrophy • Paced rhythm • Bundle branch block • Prior MI with Q-waves and/or persistent ST elevation Chest Pain Evaluation 1. ECG 2. Physical Exam & Risk assessment 3. Cardiac troponins 4. Additional confirmatory testing ACS Risk Factors and Presenting Signs and Symptoms

Test Sensitivity(%) Specificity(%) LR (+) LR (-) History Abnormal prior stress test 12 96 3.1 0.92 Peripheral artery disease 7.5 97 2.7 0.96 Prior CAD 41 79 2.0 0.75 Diabetes 26 82 1.4 0.9

Symptoms Pain in left arm and/or shoulder 54 65 1.49 0.76 Pain in right arm and/or shoulder 32 86 2.35 0.81 Pain in both arms 32 86 2.35 0.81 Oppressive pain 77 35 1.79 0.70 Sweating 41 85 2.44 0.72 Absence of chest wall tenderness 92 36 1.47 0.23 Pain similar to previous ischemia 47 79 2.2 0.67 Change in pattern over the previous 24 hours 27 86 2.0 0.84

Physical Exam Hypotension 3.1 99 3.9 0.98

ECG Findings ST depression 25 95 5.3 0.79 Ischemic ECG ( any T-wave inversion, ST- 32 91 3.6 0.74 depression or Q wave)

TIMI Score 5-7 6.8 3-4 2.4 2 0.94 0-1 0.31 Note: The data listed above are from patients who presented to the ED. The prevalence of ACS in a primary care setting is much lower and the sensitivities and specificities are also much lower.

Adapted from Bruyninckx R, Aertgeerts B, Buntinx F. Signs and symptoms in diagnosing acute myocardial infarction and acute coronary syndrome: a diagnostic meta-analysis. Br J Gen Pract. 2008; 58(547);e1- e8.

And Fanaroff AC, Rymer JA, Goldstein SA, et al. Does the patient with chest pain have acute coronary syndrome? The rational clinical examination review. JAMA. 2015; 314(18): 1955-1965.

Symptoms

• Diaphoresis LR 2.44 • Pain radiating to both arms LR 2.35 • Pain similar to previous event LR 2.2 • Change in pain in last 24 hours LR 2.2

• Presence of chest wall tenderness LR 0.23

• Cannot rule out MI based on symptoms Chest Pain Evaluation

1. ECG 2. Physical Exam & Risk assessment 3. Cardiac troponins 4. Additional confirmatory testing Cardiac troponin • Cardiac troponins T and I – Highly specific to myocardial cells – T and I are clinically equivalent • Sensitivity 79-83% • Specificity 93-95% • Measured at presentation and 3-6 hours after onset of symptoms • Diagnosis of myocardial necrosis – > 99% of upper reference level – Increase or decrease of at least 20% Non-ischemic causes of Troponin elevation

Cardiac Non-cardiac

Cardiogenic or Drug toxicity

Peri-/myocarditis, cardiomyopathy (HCM), infiltrative disease Pulmonary embolism/ (amyloidosis, sarcoidosis) Vasculitis End-stage renal disease/renal failure

Hypertensive crisis Sepsis and critically ill patients

Cardiac contusion Severe acute neurologic injury (stroke, subarachnoid hemorrhage) Surgery, ablation, or defibrillation shocks Rhabdomyolysis

Cardiotoxic agents (anthracyclines, herceptin) Strenuous exercise (marathon) Bonus Round… • In both cases, where is the lesion? Case 1: 45 y/o male with acute onset crushing chest pain

Case 2: 27 y/o male with sudden in the field. Initial ECG after stabilized. AES Question Which of these conditions notoriously make interpreting ST segments difficult?

A. LBBB and Paced Rhythm B. Paced Rhythm and Afib C. Ventricular Rhythm and Afib D. RBBB and WPW E. LBBB and 2nd Deg AV Block AES Question What separates UA from NSTEMI?

A. Flipped T-waves in 2 contiguous leads B. ST Elevation in 2 contiguous leads C. Elevated Troponins D. Pathologic Qwaves E. LBBB AES Question Pathologic Q waves are defined as 1 box wide and 1 box deep or Q waves that are:

A. Present in 3 contiguous leads B. 1/3 the amplitude of the QRS C. Accompany flipped T waves D. Present only with chest pain and then resolve Questions? ECG Basics

Module 3: Arrhythmias Arrhythmias and Dysrhythmias Tachyarrhythmia • / • Supraventricular tachycardia • Ventricular arrhythmias

Bradyarrhythmia Interpretation Algorithm • Rate • Rhythm • Axis • Intervals • Blocks • Hypertrophy/enlargement • Injury/ischemia/infarct • Other Tachyarrhythmia Case 1: 18 y/o female with a history of Marfans syndrome presenting with palpitations Atrial Fibrillation - Classification • Valvular • Paroxysmal AF – Rheumatic MS – Prosthetic • Persistent AF valve • Long-standing – AF repair • Permanent AF • Nonvalvular 85 y/o male with asymptomatic, permanent atrial fibrillation (well-controlled) EKG Practice EKG Practice Rate Control • Beta blockers – esmolol – propranolol – metoprolol • Nondihydropyridine calcium channel blockers – diltiazem – verapamil • Digoxin • Amiodarone Rhythm Control • Cardioversion (electrical vs. pharmacologic) • Antiarrhythmic drug therapy • Catheter ablation (radiofrequency, pulmonary vein insolation – PVI) Cardioversion – HD Stable For episodes < 48 hrs & low risk of stroke ➢ Cardiovert

For episodes > 48 hrs (or unknown) or high risk of stroke ➢ Empiric oral anticoagulation x ≥ 3 wks or TEE to r/o LAA thrombus, ➢ Then cardiovert

Oral anticoagulation x ≥ 4 wks after cardioversion Cardioversion • Electrical (synchronized) • Pharmacological – Flecainide/propafenone (IC) [pill-in-pocket] – Ibutilide (III) – IV only – Dofetilide (III) – Oral only – Amiodarone (III) – Toxicity, IV/po Oral Anticoagulation Valvular AFib VKA (warfarin) Nonvalvular AFib VKA or Novel agent

Novel agents: • Apixaban (Xa), Rivaroxaban (Xa), Dabagatran (DT), Edoxaban (Xa) CHA2DS2-VASc • Congestive heart failure • Hypertension • Age > 75 (2 points) • Diabetes mellitus • Prior stroke or TIA or thromboembolism (2 points) • Vascular disease • Age 65-74 years • Sex category (female sex)

January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J AM Coll Cardiol 2014; 64: e1-76. HAS-BLED Score • Hypertension (Uncontrolled > 160 mm Hg) • Abnormal liver/renal function • Stroke • Bleeding history • Labile INR (<60% time in therapeutic range) • Elderly (Age >65) • Drug/alcohol use Pister R, et al. A novel user-friendly score (HAS-BLED) to assess 1-year risk of major bleeding in patients with atrial fibrillation. Chest. 2010; 138: 1093-1100. Case 2: 76 y/o male with palpitations 24 y/o male with h/o cardiac surgery presents with palpitations

2:1 atrial flutter (atypical) ECG courtesy of Ryan Flannigan, MD FAAP FACC Atrial Flutter • Reentrant atrial arrhythmia • Regular atrial rate, variable block • Constant p-wave morphology • Similar risk factors for atrial fibrillation • Atrial flutter and atrial fibrillation can coexist Atrial Flutter Chronic Management -- Anticoagulation same as AFib

1. Rate control • Beta blockers, diltiazem, verapamil (Class 1)

2. Rhythm control • Catheter RF ablation (Class 1) • Amiodarone, dofetiliide or sotalol (Class 2a) • Flecainide or propafenone (Class 2b) Case 3 A five-week old infant presents for her well baby exam. A fast heart rate is noted on physical examination. An ECG shows the following: ECG courtesy of Ryan Flannigan, MD FAAP FACC 31 y/o female presents to the ED for persistent palpitations

SVT – AVNRT – retrograde p-waves after the QRS Supraventricular Tachycardia • Narrow complex tachycardia that arises above the ventricles • QRS may be wide in aberrant conduction or pre-excitation

Regular Irregular ➢ (ST) ➢ Multifocal (MAT) ➢ Atrial tachycardia (AT) ➢ Atrial fibrillation (AF) ➢ AVNR/AVRT ➢ Atrial flutter with variable block ➢ (JT) (AFL) ➢ Atrial flutter with non-variable block (AFL) SA Node

AV Node

Bundle of His

Left and right bundle branches Supraventricular Tachycardia Atrioventricular nodal reentrant tachycardia (AVNRT) • Involves two distinct pathways – Fast and slow • Most common SVT SA Node

AV Slow pathway Node Fast pathway

Bundle of His

Left and right bundle branches Atrioventricular Reentrant Tachycardia (AVRT)

• Reentrant tachycardia • Electrical pathway – Atrium – Atrioventricular node – Accessory pathway AVRT Accessory pathway

• Extranodal AV pathway that connects the atrium to the ventricle • Manifest pathway – Conducts anterograde causing pre-excitation • Concealed pathway – Conducts only retrograde • Pre-excitation – Manifest pathway leading to short PR interval and slurring of QRS Atrium

AV Node Accessory pathway

Bundle of His

Left and right bundle branches 16-year old female with palpitations

ECG courtesy of Ryan Flannigan, MD FAAP FACC Treatment of SVT Acute Management 1. Vagal maneuver or adenosine (Class 1) 2. Hemodynamically stable or unstable? • Hemodynamically unstable – Synchronized cardioversion • Hemodynamically stable – IV beta blocker, diltiazem, verapamil – Synchronized cardioversion Treatment of SVT Ongoing Management • EP study and radiofrequency ablation • Medical therapy – Beta blockers, diltiazem or verapamil (if no pre-excitation) (Class 1) – Flecainide or propafenone (Class 2a) – Amiodarone, dofetilide, or sotalol (Class 2b) – Digoxin (if no pre-excitation) (Class 2b) Wide Complex Tachycardia Wide Complex Tachycardia • (VT) • Supraventricular rhythm with aberrant conduction – Fixed BBB or rate-dependent BBB (RBBB) – Conduction via an accessory pathway – Atrially triggered ventricular pacing Ventricular Arrhythmias • PVC (unifocal, multifocal) • Monomorphic VT • Polymorphic VT – Torsades de Points (TdP) – “twisting of the points” [PMVT + ↑QTc] 16 y/o male with a history of syncope

ECG courtesy of Ryan Flannigan, MD FAAP FACC 11m old male with an abnormal Holter Monitor 11 y/o female with syncope and FHx of seizures (1/2) 11 y/o female with syncope and FHx of seizures (2/2)

TdP 17 y/o female h/o HLHS s/p Fontant s/p cardiac arrest at the dentist’s office (1/2) 17y/o female h/o HLHS s/p Fontant s/p cardiac arrest at the dentist’s office (2/2) Bradyarrhythmias Bradyarrhythmias • Heart rate < 60 bpm • Normal variants – increase in vagal tone – Sleep – Athletes • Symptomatic vs. asymptomatic CO = HR X SV

MAP = (CO x SVR) + CVP Presentation • Pre-/syncope • incompetency • End organ hypoperfusion Causes of Acute/Chronic Bradycardia • Inferior myocardial ischemia/infarct • (sick sinus syndrome) • Atrioventricular node dysfunction • Reflex syncope • Toxins • Systemic disease/infiltrative cardiomyopathy • Electrolytes disturbances • Medications (BB, CCB, Amio, Li, Dig, TCA) • Metabolic (hypoxia, sepsis, myxedema, hypothermia, ↓glc) • ↑ICP, OSA Sinus Node Dysfunction

• Conduction disease involving the sinus node • Most common in elderly • or “tachy-brady” syndrome • Indications for pacemaker placement – Symptomatic bradycardia – Chronotropic incompetence – Symptomatic bradycardia from required drug therapy Atrioventricular Node Dysfunction • Abnormal conduction involving the AV node  AVB – First degree – Second degree, Type 1 (Wenkebach) – Second degree, Type 2 – Third degree / CHB / AV dissociation SA Node

AV Node

Bundle of His

Left and right bundle branches 14 y/o female with lightheadedness when standing up quickly

ECG courtesy of Ryan Flannigan, MD FAAP FACC 20 y/o female s/p cryo-ablation for SVT

ECG courtesy of Ryan Flannigan, MD FAAP FACC 14 y/o male with palpitations s/p cryo-ablation

ECG courtesy of Ryan Flannigan, MD FAAP FACC 40 y/o male with h/o heart surgery at age 3 y/o

ECG courtesy of Ryan Flannigan, MD FAAP FACC ECG courtesy of Ryan Flannigan, MD FAAP FACC Treatment • Treat for reversible causes • Atropine • Isoproterenol • Transcutaneous pacing • Transvenous pacing • Permanent pacemaker AES Question

45 yo M without heart disease presents with regular HR at 180 bpm, chest pain, shortness of breath, occurred all of a sudden, never occurred before, on EKG you see regular narrow complex tachycardia, what is the most likely rhythm?

A. Atrial Flutter B. SVT C. Ventricular Tachycardia D. Atrial Fibrillation E. Sinus Tachycardia AES Question

The CHA2DS2-VASc score is used to estimate risk and determine if patient requires what kind of treatment?

A. Rate Control B. Rhythm Control C. Cholesterol D. Cardioversion E. Anticoagulation Questions? Module 4

Physicals Well Physical Cardiology • Now we know how to diagnose, when do we worry • Referral is the question? What can you clear? • Who should we screen? Screening ECGs • USPSTF recommends against screening low risk individuals • ACC/AHA admits little evidence for screening low risk individuals • ACP recommends against screening ECGs for low risk asymptomatic patients Why is the ECG not a good screening for CAD? • 30-50 % of individuals with normal coronary arteriogram have ECG abnormalities • 30% of individuals with CHD on angiogram have normal ECG • However, patients with abnormal findings have 5-10 fold increase in risk of CAD Asymptomatic 25-74 yoa Some Patients Are Special • Competitive Athletes prior to participation • High risk occupations • Persons with occupations involving public safety (Firefighters, Police Officers, Military, Pilots, Drivers) • Most of us have completed physicals which require us to order and interpret an EKG Athlete ECG Screening • What makes Athletes different? • SCD is the #1 cause of CV mortality • Majority of SCD can be identified on resting ECG • 2015 Expert consensus created the Seattle Criteria to evaluate asymptomatic 12-35 yo Athletic with ECG Seattle Criteria • International Consensus, continues to make further changes • 2-4% False Positive Rate • 98-100% Sensitivity for SCD • Recent study showed 68% sensitivity and 70% specificity among Ped Cardiologist • Reduces false positive by 40% compared to 2010 guidelines Who is an Athlete • Individual who regularly engages in exercise or training for sport • Intense athletic training at least 4-8 hours per week • Symptoms or Family hx of SCD would cause modification of guidelines Benign Athletic ECG

• Incomplete RBBB In Isolation: • Early Repolarization • Left Axis Deviation • inversion V1-V3, <16 yo • 1st Deg AV Block • Left Atrial Enlargement • Sinus Bradycardia • Right Axis Deviation • Sinus Arrythmia • • Mobitz Type 1 • Complete RBBB • LVH or RVH • ST elevation with TWI in V1-V4 in Black Athletes *2 or more of these requires • Ectopic atrial or appropriate work up* Abnormal ECG Findings

• T wave inversion • Brugada Type 1 pattern • ST Segment Deviation • Profound Bradycardia <30 • Pathologic Q Waves • PR interval >400 ms • Complete LBBB • Mobitz Type II • QRS >140ms duration • 3rd deg AV blocks • Epsilon wave • ≥ 2 PVCs • Ventricular Pre-excitation • Atrial Tachyarrhythmias • Prolonged QT Interval • Ventricular Arrhythmias RBBB • Incomplete RBBB (QRS <120 but with RBBB pattern) suggests mild delay RV conduction is due to RV remodeling • RBBB is defined as >140 ms, ~2% of the young adult male population • One small study revealed zero pathologic isolated RBBB after Echo • RBBB is still considered a borderline finding and must be in isolation to be considered normal AV Blocks • 1st deg AV block – normal unless extreme PR interval >400 ms, 7% athletes • Mobitz Type I – normal in well trained athletes – should return to 1:1 ratio with exercise • Mobitz Type II – Abnormal in all situations RVH/LVH

• LVH and RVH criteria are common – Cardiac mass – Athletic cardiac remodeling • RV increase in size due to regular training • 64% of trained athletes meet LVH criteria, but ECG findings correlate poorly with Echo findings • LVH in isolation <2% of HCM patients • Commonly a/w TWI in inferior and lateral leads, Q waves, or ST segment depression • 0/627 athletes with RVH on ECG demonstrated RV thickness on Echo Early Repolarization • J point elevation >0.1mV, a/w slurring or notching, Inf and Lat leads • 45% Caucasian athletes and 60-90% Black athletes • Black Athletes also exhibit TWI at V1-V4, particularly after early repol • No a/w SCD in athletes Bradycardia/Sinus Arrhythmia • <60 for adults, but athletic hearts <30 in absence of symptoms • Resolves with physical activity • Arrhythmia a/w breathing more common in athletes • Ectopic atrial rhythm in 8% of athletes Juvenile Pattern • TWI in V1-V3 in athletes <16 yoa (ie not reached physical maturity) • 10-15% of adolescent ages 12-14 years of age LAD/RAD and RAE/LAE

• Considered a borderline finding by Seattle criteria • Atrial enlargement accounted for 42% of ECG findings • Higher prevalence in athletes >20 hours/week of intense exercise/training • 0/579 RAE and RAD revealed significant structural abnormalities • Exclusion of AE and AD brought false positive rate from 13% to 7.5%, but decreased sensitivity from 91% to 89.5% • Again in isolation, no further w/u required AES Question Which one of these single findings are concerning and should be worked up during a sports physical? A. RBBB B. Sinus Bradycardia <50 C. Prolonged QT Interval D. Mobitz Type I (Wenkebach) E. RVH AES Question Early Repolarization is not associated with Sudden Cardiac Death

A. True B. False Questions????? Darrell Edward Jones, DO [email protected]

David Kassop, MD [email protected]