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ECG Workshop The Fundamentals

Darrell E. Jones, DO

David Kassop, MD, FACC

ACTIVITY DISCLAIMERThe material presented here is being made available by the American Academy of Family Physicians for

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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

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unapproved or investigational uses of products or devices.

Darrell E. Jones, DOPhysician, 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 Cardiology, 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 cardiovascular

disease 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…

• Rapid diagnosis in ACS

• Structural heart disease (cardiomyopathies, valvular disease, congenital heart disease)

• Pericardial disease

• Evaluation of arrhythmias and conduction disorders

• Channelopathies (LQTS, Brugada, CPVT)

• Drug toxicity, electrolyte disturbances

• Clinical disorders (PE, CNS disorders, dextrocardia)

• Pacemaker function

• 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/ischemia/infarct• Other

Electrophysiology

• Heart has inherent electrical properties• Depolarization of SA node electrical signal cardiac muscle 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

misalud.com

Limb Leads

Rhythm Strip

Precordial Leads

Standards

• Time/ Intervals

• Chart speed 25 mm/sec

• 40 ms/small box 200 ms/large

• 5 large boxes/second

• Voltage

• 10 small = 1 mV = full standard

40 ms (.04 sec)

200 ms

0.1 mV

The P’s and Q’s of ECG

P wave: Atrial depolarization

QRS Complex: Ventricular

Depolarization

T wave: Ventricular Repolarization

EKG Practice

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

• Or, count the # of beats on the rhythm strip and multiply by 6 (10 second strip)

• Rate > 100 is tachycardia• Rate < 60 is bradycardia

100 75

Rhythm

• Fast or Slow?

• Bradycardia – 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 ventricle 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 arrhythmia• Define the underlying rhythm

• Evaluate for ectopy (PVC, PAC)

EKG Practice

AV BlocksFirst 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 2Fixed PR interval with periodic dropping of the QRS complex

Third degree:AV dissociation

(P not matching up with QRS))

EKG Practice

Axis Graph

• 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; left axis deviation, if II also neg

• (-) in I, (+) in AVF; right axis deviation

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 lung disease/PE, dextrocardia, limb lead reversal

EKG Practice

Intervals

• PR interval: 120 - 200 ms (3 - 5 small boxes)

• QRS complex: < 120 ms (< 3 small boxes)• Wide QRS indicates:

• Bundle branch block

• 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

EKG Practice

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-mitraleLAE RAE

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 wavesLAE RAE

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

Ventricular Hypertrophy - SimplifiedParameter LVH RVH

Axis Left Right

Atrial abn LAE RAE

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

V1 IIV1 II

EKG Practice

• 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

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 heart rate?

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 fibrillation

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 cardiomyopathy

AES Question

What type of block is present?

A. Right bundle branch block (RBBB)

B. Left bundle branch block (LBBB)

C.Non-specific interventricular conduction block

(NSIVCB)

D.Incomplete left bundle branch block (iLBBB)

ECG5: 55 y/o male with chronic hypertension

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 atrial enlargement

D.Left axis deviation

ECG Basics

Module 2: Acute Coronary Syndrome

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 Myocardial Infarction (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

ST-elevation myocardial infarction (STEMI)

Non-ST Elevation ACS (NSTE-ACS)

– Non-ST elevation myocardial infarction (NSTEMI)

– Unstable angina (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/InfarctInjury• 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

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

• Anterolateral: V4-6, I, aVL

• Lateral: I, aVL

• Inferior: II, III, aVF

• Inferolateral: II, III, aVF, V5-6

• Posterior: R>S in V1, V2

Left Anterior Descending (LAD) artery

Left Circumflex (LCx) artery

Right Coronary Artery (RCA)

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

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-/myocarditis 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)

Unstable AnginaSubtotal 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 NSTEMIPossible ECG findings

• ST segment depressionSN 25%, SP 95%, LR+ 5.3, LR- 0.79

• Symmetrical T-wave inversionSN 32%, SP 91%, LR+ 3.6, LR- 0.74

• Q-wavesQ 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

• Chart speed 25 mm/sec

• 40 ms/small box 200 ms/large

• 5 large boxes/second

• Voltage

• 10 small = 1 mV = full standard

40 ms (.04 sec)

200 ms

0.1 mV

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 L-PDA

Prox LAD

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 heart failure. Serial cardiac enzymes negative.

Mid to distal LAD Infarct

Distal RCA Infarct

LVG End-diastole LVG End-systole

*Akinetic distal

anterior and inferior walls

**Akinetic, aneurysmal

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

1. ECG

2. Physical Exam & Risk assessment

ACSRiskFactorsandPresentingSignsandSymptoms

Test Sensitivity(%) Specificity(%) LR(+) LR(-)

History

Abnormalpriorstresstest 12 96 3.1 0.92

Peripheralarterydisease 7.5 97 2.7 0.96

PriorCAD 41 79 2.0 0.75

Diabetes 26 82 1.4 0.9

Symptoms

Paininleftarmand/orshoulder 54 65 1.49 0.76

Paininrightarmand/orshoulder 32 86 2.35 0.81

Paininbotharms 32 86 2.35 0.81

Oppressivepain 77 35 1.79 0.70

Sweating 41 85 2.44 0.72

Absenceofchestwalltenderness 92 36 1.47 0.23

Painsimilartopreviousischemia 47 79 2.2 0.67

Changeinpatternovertheprevious24hours 27 86 2.0 0.84

PhysicalExam

Hypotension 3.1 99 3.9 0.98

ECGFindings

STdepression 25 95 5.3 0.79

IschemicECG(anyT-waveinversion,ST-depressionorQwave)

32 91 3.6 0.74

TIMIScore

5-7 6.8

3-4 2.4

2 0.94

0-1 0.31

Note:ThedatalistedabovearefrompatientswhopresentedtotheED.TheprevalenceofACSina

primarycaresettingismuchlowerandthesensitivitiesandspecificitiesarealsomuchlower.

AdaptedfromBruyninckxR,AertgeertsB,BuntinxF.Signsandsymptomsindiagnosingacutemyocardial

infarctionandacutecoronarysyndrome:adiagnosticmeta-analysis.BrJGenPract.2008;58(547);e1-

AndFanaroffAC,RymerJA,GoldsteinSA,etal.Doesthepatientwithchestpainhaveacutecoronary

syndrome?Therationalclinicalexaminationreview.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

1. ECG

2. Physical Exam & Risk assessment

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 elevationCardiac Non-cardiac

Cardiogenic or hypovolemic shock Drug toxicity

Peri-/myocarditis, cardiomyopathy (HCM), infiltrative disease (amyloidosis, sarcoidosis)

Pulmonary embolism/pulmonary hypertension

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 cardiac arrest 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

• Atrial fibrillation / Atrial flutter

• Supraventricular tachycardia

• Ventricular arrhythmias

Bradyarrhythmia

Tachyarrhythmia

Case 1: 18 y/o female with a history of Marfans

syndrome presenting with palpitations

Atrial Fibrillation - Classification

• Paroxysmal AF

• Persistent AF

• Long-standing

• Permanent AF

• Valvular

– Rheumatic MS

– Prosthetic valve

– Mitral valve repair

• Nonvalvular

85 y/o male with asymptomatic, permanent atrial fibrillation (well-controlled)

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 usePister 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

ECG courtesy of Ryan Flannigan, MD FAAP FACC

24 y/o male with h/o cardiac surgery presents with palpitations

2:1 atrial flutter (atypical)

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 FlutterChronic 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:

31 y/o female presents to the ED for persistent palpitations

SVT – AVNRT – retrograde p-waves after the QRS

Regular

➢ Sinus tachycardia (ST)

➢ Atrial tachycardia (AT)

➢ AVNR/AVRT

➢ Junctional tachycardia (JT)

➢ Atrial flutter with non-variable

block (AFL)

Supraventricular Tachycardia

Irregular

➢ Multifocal atrial tachycardia (MAT)

➢ Atrial fibrillation (AF)

➢ Atrial flutter with variable block

• Narrow complex tachycardia that arises above the ventricles

• QRS may be wide in aberrant conduction or pre-excitation

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 Node

Bundle of His

Fast pathwaySlow pathway

Atrioventricular Reentrant Tachycardia

(AVRT)

• Reentrant tachycardia

• Electrical pathway

– Atrium

– Atrioventricular node

– Accessory pathway

AVRTAccessory 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

Atrium

AV Node

Bundle of His

Accessory pathway

16-year old female with palpitations

Treatment of SVT

Acute Management1. 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

• Ventricular 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

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)

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

• 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

• Chronotropic incompetency

• End organ hypoperfusion

Causes of Acute/Chronic Bradycardia

• Inferior myocardial ischemia/infarct

• Sinus node dysfunction (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

• Sinus bradycardia 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

14 y/o female with lightheadedness when standing up quickly

20 y/o female s/p cryo-ablation for SVT

14 y/o male with palpitations s/p cryo-ablation

40 y/o male with h/o heart surgery at age 3 y/o

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 yoAthletic hearts 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

• Incomplete RBBB

• Early Repolarization

• T wave inversion V1-V3, <16 yo

• 1st Deg AV Block

• Sinus Bradycardia

• Sinus Arrythmia

• Mobitz Type 1

• LVH or RVH

• ST elevation with TWI in V1-V4 in

Black Athletes

• Ectopic atrial or Junctional Rhythm

Benign Athletic ECG

In Isolation:

• Left Axis Deviation

• Left Atrial Enlargement

• Right Axis Deviation

• Right Atrial Enlargement

• Complete RBBB

*2 or more of these requires

appropriate work up*

• T wave inversion

• ST Segment Deviation

• Pathologic Q Waves

• Complete LBBB

• QRS >140ms duration

• Epsilon wave

• Ventricular Pre-excitation

• Prolonged QT Interval

Abnormal ECG Findings

• Brugada Type 1 pattern

• Profound Bradycardia <30

• PR interval >400 ms

• Mobitz Type II

• 3rd deg AV blocks

• ≥ 2 PVCs

• Atrial Tachyarrhythmias

• Ventricular Arrhythmias

• 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

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

Darrell.e.jones26.mil@mail.mil

David Kassop, MD

david.kassop.mil@mail.mil

ecg workshop the fundamentals - aafp home...ecg workshop the fundamentals darrell e. jones, do david...

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