ECG Workshop The Fundamentals - AAFP Home...ECG Workshop The Fundamentals Darrell E. Jones, DO David...
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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
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
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It is the policy of the AAFP that all individuals in a position to control content disclose any
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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, 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…
Why is this important?
• 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
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/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)
Time
Vo
ltag
e
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
PR QT
RRST
EKG Practice
Rate
• 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
300
150
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
EKG Practice
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
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; 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
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:
• 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
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-mitraleLAE 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 wavesLAE 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
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
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 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
1 MI)
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
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
• 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
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-/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)
Time
Vo
ltag
e
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
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
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-
e8.
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
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 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
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
• Paroxysmal AF
• Persistent AF
• Long-standing
AF
• Permanent AF
• Valvular
– Rheumatic MS
– Prosthetic valve
– Mitral valve repair
• 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 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:
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
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
(AFL)
• 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
Left and right bundle branches
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
QRS
Atrium
AV Node
Bundle of His
Left and right bundle branches
Accessory pathway
16-year old female with palpitations
ECG courtesy of Ryan Flannigan, MD FAAP FACC
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
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]
ECG courtesy of Ryan Flannigan, MD FAAP FACC
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)
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
• 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
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 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
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
David Kassop, MD