Electrocardiogram (ECG) Interpretation_Module 1 of 2

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Electrocardiogram (ECG) Interpretation

Module 1 of 2

Marc Imhotep Cray, M.D.

Learning Objectives • To recognize normal rhythm of heart  “Normal Sinus Rhythm (NSR)” • To recognize 15 most common rhythm disturbances (3-Lead ECG) • To Interpret an acute myocardial infarction on a 12-Lead ECG, including: anterior, lateral, anterolateral and inferior wall MIs

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Topics Outline • • • • •

ECG Basics How to Analyze a Rhythm Normal Sinus Rhythm Cardiac Dysrhythmias Diagnosing a Myocardial Infarction

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Review of ECG Basics Normal ECG Morphology Features include:  Regular rhythm at 60-100 bpm  Normal P wave morphology and axis (upright in I and II, inverted in aVR)  Narrow QRS complexes (< 100 ms wide)  Each P wave is followed by a QRS complex  The PR interval is constant

Marc Imhotep Cray, M.D.

EKG Paper ECG tracings are recorded on grid paper  Horizontal axis of EKG paper records time, w black marks at top indicating 3 second intervals o Each second is marked by 5 large grid blocks thus each large block equals 0.2 second

 Vertical axis records EKG amplitude (voltage) o Two large blocks equal 1 millivolt (mV) o Each small block equals 0.1 Mv

 Within large blocks are 5 small blocks each representing 0.04 seconds Marc Imhotep Cray, M.D.

ECG Paper cont’d. • Horizontally – One small box - 0.04 s – One large box - 0.20 s • Vertically – One large box - 0.5 mV

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ECG Paper cont’d. 3 sec

3 sec

• Every 3 seconds (15 large boxes) is marked by a vertical line • This Helps When Calculating Heart Rate Note: Strip above and those that follow are not marked but all are 6 seconds long Marc Imhotep Cray, M.D.

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Autorhythmicity • Some heart cells (SA, AV node and Purkinje) show automaticity ability to generate a heart beat – These cells have an intrinsic rhythmicity which generates a pacemaker potential

• Heart does not require nerve or hormonal input to beat – Heart transplant patients nerves are severed but heart beats on

Marc Imhotep Cray, M.D.

Normal Impulse Conduction Sinoatrial node AV node Bundle of His Bundle Branches Purkinje fibers

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Impulse Conduction & the ECG Sinoatrial node AV node Bundle of His Bundle Branches Purkinje fibers

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“PQRST”

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PR Interval Atrial depolarization + delay in AV junction (AV node/Bundle of His) delay allows time for atria to contract before ventricles contract

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Pacemakers of Heart • SA Node - Dominant pacemaker with an intrinsic rate of 60 - 100 beats/ minute • AV Node - Back-up pacemaker with an intrinsic rate of 40 - 60 beats/minute • Ventricular cells - Back-up pacemaker with an intrinsic rate of 20 - 45 bpm

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How to Analyze a Rhythm

Rhythm Analysis

 Step 1:  Step 2:  Step 3:  Step 4:  Step 5:

Marc Imhotep Cray, M.D.

Calculate rate Determine regularity Assess the P waves Determine PR interval Determine QRS duration

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Step 1: Calculate Rate 3 sec

3 sec

Option 1 (6-second x 10 method) • Count # of R waves in a 6 second rhythm strip, then multiply by 10 Interpretation? 9 x 10 = 90 bpm Marc Imhotep Cray, M.D.

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Step 1: Calculate Rate cont’d.

R wave Option 2 (300, 150, 100, 75, 60, 50 method) – Find a R wave that lands on a bold line – Count number of large boxes to next R wave – If second R wave is 1 large box away rate is 300, 2 boxes - 150, 3 boxes - 100, 4 boxes - 75, etc. (cont.) Marc Imhotep Cray, M.D.

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Step 1: Calculate Rate 3 1 1 0 5 0 7 6 5 0 0 0 5 0 0

• Option 2 (cont.) – Memorize the sequence: 300 - 150 - 100 - 75 - 60 - 50 Interpretation? Approx. 1 box less than 100 = 95 bpm

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Step 2: Determine regularity R

R

• Look at R-R distances (using a caliper or markings on a pen or paper) • Regular (are they equidistant apart)? Occasionally irregular? Regularly irregular? Irregularly irregular? Interpretation? Regular

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Step 3: Assess the P waves

• Are there P waves? • Do the P waves all look alike? • Do the P waves occur at a regular rate? • Is there one P wave before each QRS? Interpretation? Normal P waves w 1 P wave for every QRS

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Step 4: Determine PR interval

• Normal: 0.12 - 0.20 secondsďƒ (3 - 5 sm boxes) Interpretation? 0.12 seconds

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Step 5: QRS duration

• Normal: 0.04 - 0.12 seconds. (1 - 3 sm boxes) Interpretation? 0.08 seconds

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NSR Summary

• Rate 90-95 bpm • Regularity regular • P waves normal • PR interval 0.12 s • QRS duration 0.08 s Interpretation? Normal Sinus Rhythm

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Normal Sinus Rhythm

Basic Rhythm Analysis • Rate – too fast or too slow? • Rhythm – regular or irregular? • Is there a normal looking QRS? Is it wide or narrow? • Are P waves present? • What is relationship of P waves to QRS complex?

Marc Imhotep Cray, M.D.

NSR Parameters

• Rate 60 - 100 bpm • Regularity regular • P waves normal • PR interval 0.12 - 0.20 s • QRS duration 0.04 - 0.12 s Any deviation from above is • Sinus tachycardia • Sinus bradycardia or • A dysrhythmia Marc Imhotep Cray, M.D.

Normal Sinus Rhythm 12 lead ECG in sinus rhythm

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Arrhythmia Formation Arrhythmias can arise from problems in: • Sinus node • Atrial cells • AV junction • Ventricular cells

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SA Node Problems SA Node can: • fire too slow • fire too fast

Sinus Bradycardia Sinus Tachycardia*

*Sinus Tachycardia may be an appropriate response to stress.

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Atrial Cell Problems Atrial cells can: • fire occasionally from a focus Premature Atrial Contractions (PACs)

• fire continuously due to a looping reentrant circuit Atrial Flutter

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Atrial Cell Problems Atrial cells can also: • fire continuously from multiple foci Atrial Fibrillation or • fire continuously due to multiple micro re-entrant “wavelets” Atrial Fibrillation

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Key Scientific Point  Multiple micro re-entrant “wavelets” refers to wandering small areas of activation which generate fine chaotic impulses

Atrial tissue

 Colliding wavelets can, in turn, generate new foci of activation

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AV Junctional Problems AV junction can: • fire continuously due to a looping re-entrant circuit Paroxysmal Supraventricular Tachycardia (PSVT)

• block impulses coming from SA Node AV Junctional Blocks

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Ventricular Cell Problems Ventricular cells can: • fire occasionally from 1 or more foci Premature Ventricular Contractions (PVCs) • fire continuously from multiple foci Ventricular Fibrillation (VF) • fire continuously due to a looping re-entrant circuit  Ventricular Tachycardia (VT)

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Analyzing a Rhythm Table Component Characteristics Rate bpm is commonly ventricular rate. If atrial and ventricular rates differ, as in a 3rd-degree block, measure both rates. Normal: 60–100 bpm. Slow (bradycardia): <60 bpm. Fast (tachycardia): >100 bpm Regularity Measure R-R intervals and P-P intervals. Regular: Intervals consistent. Regularly irregular: Repeating pattern. Irregular: No pattern P Waves If present: Same in size, shape, position? Does each QRS have a P wave? Normal: Upright (positive) and uniform PR Interval Constant: Intervals are same. Variable: Intervals differ. Normal: 0.12–0.20 sec and constant QRS Interval Normal: 0.06–0.10 sec. Wide: >0.10 sec. None: Absent QT Interval Beginning of R wave to end of T wave Varies with HR. Normal: Less than half the R-R interval Dropped Occur in AV blocks. Occur in sinus arrest. beats Marc Imhotep Cray, M.D.

Cardiac Dysrhythmias

Dysrhythmias • • • • •

Sinus Rhythms Premature Beats Supraventricular Arrhythmias Ventricular Arrhythmias AV Junctional Blocks

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Sinus Rhythms • • • •

Sinus Bradycardia Sinus Tachycardia Sinus Arrest Normal Sinus Rhythm

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Rhythm #1

• Rate? • Regularity? • P waves?

30 bpm

• PR interval?

0.12 s 0.10 s

• QRS duration?

regular normal

Interpretation? Sinus Bradycardia Marc Imhotep Cray, M.D.

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Sinus Bradycardia

• Deviation from NSR - Rate < 60 bpm

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Sinus Bradycardia cont’d.

• Etiology: SA node is depolarizing slower than normal, impulse is conducted normally (i.e. normal PR and QRS interval)

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Rhythm #2

• Rate? • Regularity? • P waves?

130 bpm

• PR interval?

0.16 s

• QRS duration?

0.08 s

regular normal

Interpretation? Sinus Tachycardia Marc Imhotep Cray, M.D.

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Sinus Tachycardia

• Deviation from NSR - Rate > 100 bpm

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Sinus Tachycardia cont’d.

• Etiology: SA node is depolarizing faster than normal, impulse is conducted normally • Remember: sinus tachycardia is a response to physical or psychological stress, not a primary arrhythmia.

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Sinus Arrest • Etiology: SA node fails to depolarize and no compensatory mechanisms take over • Sinus arrest is usually a transient pause in sinus node activity

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Premature Beats • Premature Atrial Contractions (PACs)

• Premature Ventricular Contractions (PVCs)

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Rhythm #3

• Rate? • Regularity? • P waves?

70 bpm

• PR interval?

0.14 s (except 2/7) 0.08 s

• QRS duration?

occasionally irreg. 2/7 different contour

Interpretation? NSR w PAC Marc Imhotep Cray, M.D.

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Premature Atrial Contractions (PACs)

• Deviation from NSR – These ectopic beats originate in atria (but not in SA node) therefore, contour of P wave, PR interval, and timing are different than a normally generated pulse from SA node

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PAC cont’d.

• Etiology: Excitation of an atrial cell forms an impulse that is then conducted normally through AV node and ventricles

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Key Scientific Point • When an impulse originates anywhere in atria (SA node, atrial cells, AV node, Bundle of His) and then is conducted normally through ventriclesďƒ QRS will be narrow (0.04 - 0.12 s)

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Rhythm #4

• Rate? • Regularity? • P waves?

60 bpm

• PR interval?

0.14 s 0.08 s (7th wide)

• QRS duration?

occasionally irreg. none for 7th QRS

Interpretation? Sinus Rhythm with 1 PVC Marc Imhotep Cray, M.D.

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Premature ventricular contractions (PVCs)

• Deviation from NSR – Ectopic beats originate in ventricles resulting in wide and bizarre QRS complexes – When there are more than 1 premature beats and they look alike, called “uniform” – When they look different, called “multiform” Marc Imhotep Cray, M.D.

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PVCs cont’d.

• Etiology: One or more ventricular cells are depolarizing and impulses are abnormally conducting through ventricles

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Key Scientific Point • When an impulse originates in a ventricle, conduction through ventricles will be inefficient and QRS will be wide and bizarre

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Ventricular Conduction

Normal

Abnormal

Signal moves rapidly through ventricles

Signal moves slowly through ventricles

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Supraventricular dysrhythmias • Atrial Fibrillation • Atrial Flutter • Paroxysmal Supraventricular Tachycardia (PSVT)

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Rhythm #5

• Rate? • Regularity? • P waves?

100 bpm

• PR interval?

none 0.06 s

• QRS duration?

irregularly irregular none

Interpretation? Atrial Fibrillation Marc Imhotep Cray, M.D.

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Atrial Fibrillation cont’d.

• Deviation from NSR – No organized atrial depolarization so no normal P waves (impulses are not originating from SA node) – Atrial activity is chaotic (resulting in an irregularly irregular rate) – Common, affects 2-4%, up to 5-10% if > 80 years old

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Atrial Fibrillation cont’d.

• Etiology: due to multiple re-entrant wavelets conducted betw R & L atria and impulses are formed in a totally unpredictable fashion • AV node allows some of impulses to pass through at variable intervals (so rhythm is irregularly irregular)

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Rhythm #6

• Rate? • Regularity? • P waves?

70 bpm

• PR interval?

none 0.06 s

• QRS duration?

regular flutter waves

Interpretation? Atrial Flutter Marc Imhotep Cray, M.D.

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Atrial Flutter

• Deviation from NSR – No P waves Instead flutter waves (note “sawtooth” pattern) are formed at a rate of 250 - 350 bpm – Only some impulses conduct through AV node (usually every other impulse)

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Atrial Flutter cont’d.

• Etiology: Reentrant pathway in right atrium with every 2nd, 3rd or 4th impulse generating a QRS (others are blocked in AV node as node repolarizes)

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Rhythm #7

• • • • •

Rate? Regularity? P waves? PR interval? QRS duration?

Interpretation? Marc Imhotep Cray, M.D.

74 148 bpm Regular  regular Normal  none 0.16 s  none 0.08 s Paroxysmal Supraventricular Tachycardia (PSVT)

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Paroxysmal Supraventricular Tachycardia (PSVT)

• Deviation from NSR – heart rate suddenly speeds up, often triggered by a PAC (not seen here) and P waves are lost

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AV Nodal Blocks • 1st Degree AV Block • 2nd Degree AV Block, Type I • 2nd Degree AV Block, Type II • 3rd Degree AV Block

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Rhythm # 8

• Rate? • Regularity? • P waves?

60 bpm

• PR interval?

0.36 s 0.08 s

• QRS duration?

regular normal

Interpretation? 1st Degree AV Block Marc Imhotep Cray, M.D.

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1st Degree AV Block

• Deviation from NSR – PR Interval > 0.20 s

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1st Degree AV Block cont’d.

• Etiology: Prolonged conduction delay in AV node or Bundle of His

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Rhythm # 9

• Rate? • Regularity? • P waves?

50 bpm

• PR interval?

lengthens 0.08 s

• QRS duration?

regularly irregular nml, but 4th no QRS

Interpretation? 2nd Degree AV Block, Type I Marc Imhotep Cray, M.D.

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2nd Degree AV Block, Type I Mobitz type I (Wenckebach) • Deviation from NSR – PR interval progressively lengthens, then impulse is completely blocked (P wave not followed by QRS)

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2nd Degree AV Block, Type I cont’d.

• Etiology: Each successive atrial impulse encounters a longer and longer delay in AV node until one impulse (usually 3rd or 4th) fails to make it through AV node

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Rhythm # 10

• Rate? • Regularity? • P waves?

40 bpm

• PR interval?

0.14 s 0.08 s

• QRS duration?

regular nml, 2 of 3 no QRS

Interpretation? 2nd Degree AV Block, Type II Marc Imhotep Cray, M.D.

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2nd Degree AV Block, Type II Mobitz type II • Deviation from NSR – Occasional P waves are completely blocked (P wave not followed by QRS) – Progressive lengthening of PR interval until a QRS is dropped – Consistent ratio of conducted to dropped QRS complexes NB: Requires a pacemaker Marc Imhotep Cray, M.D.

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Rhythm #11

• Rate? • Regularity? • P waves?

40 bpm

• PR interval?

none wide (> 0.12 s)

• QRS duration?

regular no relation to QRS

Interpretation? 3rd Degree AV Block Marc Imhotep Cray, M.D.

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3rd Degree AV Block

• Deviation from NSR – P waves are completely blocked in AV junction QRS complexes originate independently from below junction – Complete dissociation between atrial and ventricular rates NB: Requires a pacemaker

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3rd Degree AV Block cont’d.

• Etiology: There is complete block of conduction in AV junction atria and ventricles form impulses independently of each other • Without impulses from atria, ventricles own intrinsic pacemaker kicks in at around 30 - 45 bpm

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Remember • When an impulse originates in a ventricle, conduction through ventricles will be inefficient and QRS will be wide and bizarre

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#12 Ventricular Tachycardia • • • • •

Ventricular cells fire continuously due to a looping re-entrant circuit Rate usually regular, 100 - 250 bpm P wave: may be absent, inverted or retrograde QRS: complexes bizarre, > .12 Rhythm: usually regular

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#13 Ventricular Fibrillation • • • • •

Rhythm: irregular-coarse or fine, wave form varies in size & shape Fires continuously from multiple foci No organized electrical activity No cardiac output Causes: MI, ischemia, untreated VT, underlying CAD, acid base imbalance, electrolyte imbalance, hypothermia etc.

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#14 Asystole • Ventricular standstill, no electrical activity, no cardiac output – no pulse! • Cardiac arrest, may follow VF or PEA (Pulseless electrical activity) • Remember! No defibrillation with Asystole • Rate: absent due to absence of ventricular activity Occasional P wave may be identified

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#15 Idioventricular Rhythm • • • • • • •

Escape rhythm (safety mechanism) to prevent vent. standstill HIS/purkinje system takes over as heart’s pacemaker Treatment: pacing Rhythm: regular Rate: 20-40 bpm P wave: absent QRS: > .12 seconds (wide and bizarre)

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Diagnosing a Myocardial Infarction

Diagnosing a myocardial infarction To Dx a MI you need to go beyond looking at a rhythm strip and obtain a 12-Lead ECG

Rhythm Strip Marc Imhotep Cray, M.D.

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The 12-Lead ECG • 12-Lead ECG sees heart from 12 different views helps you see what is happening in different portions of heart – rhythm strip is only 1 of these 12 views 12 lead ECG in sinus rhythm

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Which coronary artery?  Site of infarct can be determined by correlating ECG findings w knowledge of coronary circulation o However, nml coronary vasculature varies widely from individual to individual so only possible to make generalizations

 Idea is you should be able to look at a 12 lead ECG pattern of ischemia or infarction and predict coronary lesion location that will show at cardiac catheterization

Marc Imhotep Cray, M.D.

Two main coronary arteries are right coronary artery and left anterior descending coronary artery  SA and AV nodes are supplied by branches of RCA •

Infarct may cause nodal dysfunction (bradycardia or heart block)

 Right-dominant circulation (85%) = PDA arises from RCA  Left-dominant circulation (8%) = PDA arises from LCX  Codominant circulation (7%) = PDA arises from both LCX and RCA  Coronary artery occlusion most commonly in LAD  Coronary blood flow peaks in early diastole

Tao Le T and Bhushan V, Cardiovascular, In: First Aid for the USMLE Step 1 2017. New York, NY: McGraw-Hill ,2017; 271.

Correlating ECG findings w knowledge of coronary circulation

Taylor GJ. 150 practice ECGs: Interpretation and Review, 3rd ed. Malden, Mass: Blackwell Publishing, 2006.

Correlating ECG findings w knowledge of coronary circulation

The 12-Leads 12-leads include: –3 Limb leads (I, II, III) –3 Augmented leads (aVR, aVL, aVF) –6 Precordial leads (V1- V6) Marc Imhotep Cray, M.D.

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Views of the Heart Some leads get a good view of: Lateral portion of heart

Anterior portion of heart

Inferior portion of heart Marc Imhotep Cray, M.D.

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Where do you see ST-T wave changes for following areas of ischemia or infarction?

Diagram showing the contiguous leads in same color

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ST Elevation • One way to diagnose an acute MI is to look for elevation of ST segment

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ST Elevation cont’d. • Elevation of ST segment (greater than 1 small box) in 2 leads is consistent w a myocardial infarction

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Anterior View of Heart • Anterior portion of heart is best viewed using leads V1- V4

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Anterior Myocardial Infarction • If you see changes in leads V1 - V4 that are consistent w a MIďƒ you can conclude that it is an anterior wall myocardial infarction

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Putting it all Together Do you think this person is having a MI If so, where?

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Interpretation Yes, this person in previous slide is having an acute anterior wall myocardial infarction

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Other MI Locations Now that you know where to look for an anterior wall MI let’s look at how you would determine if MI involves lateral wall or inferior wall of heart

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Other MI Locations  Remember 12-leads of ECG look at different portions of heart – limb and augmented leads “see” electrical activity moving inferiorly (II, III and aVF), to left (I, aVL) and to right (aVR) – Whereas, precordial leads “see” electrical activity in posterior to anterior direction

Limb Leads

Marc Imhotep Cray, M.D.

Augmented Leads

Precordial Leads

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Other MI Locations • Now, using these 3 diagrams let’s figure where to look for a lateral wall and inferior wall MI Limb Leads

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Augmented Leads

Precordial Leads

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Anterior MI • Remember anterior portion of the heart is best viewed using leads V1- V4 Limb Leads

Marc Imhotep Cray, M.D.

Augmented Leads

Precordial Leads

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Lateral MI • So what leads do you think lateral portion of heart is best viewed? Leads I, aVL, and V5- V6

Limb Leads

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Augmented Leads

Precordial Leads

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Inferior MI Now how about inferior portion of heart? Leads II, III and aVF

Limb Leads

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Augmented Leads

Precordial Leads

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Putting it all Together Now, where do you think this person is having a MI?

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Inferior Wall MI This is an inferior MI. Note ST elevation in leads II, III and aVF

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Putting it all Together How about now?

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Anterolateral MI This person’s MI involves both the anterior wall (V2-V4) and lateral wall (V5-V6, I, and aVL)!

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Next Module: Reading 12-Lead ECGs  Best way to read 12-lead ECGs is to develop a step-bystep approach (just as we did for analyzing a rhythm strip)  In next Module we present a 6-step and 9-step approaches: 1. Calculate Rate 2. Determine Rhythm 3. Determine QRS axis 4. Calculate Intervals 5. Assess for Hypertrophy 6. Look for evidence of Infarction Marc Imhotep Cray, M.D.

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THE END

See next slide for links to tools and resources for further study.

Companion study tools Video Playlist: ECG Interpretation Strong Medicine ECG Video Edu. , Dr. Eric Strong Reading: Olivieri , B et al. Ch. 28 ECG (Pgs. 820-28). In: USMLE Step 1 Secrets 3rd. Ed. (Eds. Brown TA and Shah SJ) Saunders, 2013. ECG eBook: Shade B. Pocket ECGs: A Quick Information Guide. New York, NY: McGraw-Hill, 2008. (A good one for beginners.) Marc Imhotep Cray, M.D.

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