Basics of ECG Interpretation

Royal College of Physicians

Conference Student Track

September 2018

Dr. Stephen Noe, DMS-c, MPAS, PA-C

Objectives

• Explain how depolarization and repolarization of cardiac myocytes produces a predictable waveform patter on an ECG.

• Identify patterns of myocardial ischemia, injury, and infarction on an ECG.

• Explain how myocardial ischemia, injury, and infarction produce predictable waveform patterns on the ECG.

• Explain the pathophysiology and clinical significance of atrioventricular block, bundle branch block, hypertrophy, and QT prolongation.

• Identify atrioventricular block, bundle branch block, hypertrophy, and QT prolongation on an ECG.

• Explain the pathophysiology and clinical significance of chronotropic incompetence, sinus pause, sinus exit block, and sick sinus syndrome.

Cardiac Depolarization and Repolarization

ECG Basics

• ECG complexes appear upright (Positive) if electricity is moving towards the area of the myocardium that ECG complex represents

• ECG complexes appear downright (Negative) if electricity is moving away from the area the myocardium that ECG complex represents

Bipolar Limb Leads (I, II, III)

Unipolar Limb Leads

Chest Leads

Chest Leads

ECG Leads

ECG Waveforms

PR Interval: Start of P wave to QRS

Complex; time from SA node activation

to AV node activation

QT Interval: Start of QRS to end of T

wave

Measurement Intervals

Calculating Rate

Calculating Axis

RCA: supplies the RV and the inferior portion of the LV, the AV node and the conalbranch supplies the SA node

LAD: supplies the anterior portion of the LV, the interventricular septum, and the perforating branches supply the bundle branches

LCx: supplies the lateral wall of the LV, less commonly supplies the SA and/or AV node

Primary (injury – ST segment elevation)

Reciprocal* (ST segment depression)

Anterior (V1-V4) Inferior (II, III, aVF)

Lateral (I, aVL, V5-V6) Inferior (II, III, aVF)

Inferior (II, III, aVF) Lateral (I, aVL, V5-V6)

Posterior Anterior (V1-V4)

First Degree AVB Consistent PR interval length > 200 ms (one large block)

Second Degree

AVB Type I (Wenckebach)

Progressive lengthening of PR interval from cycle to cycle prior to a dropped QRS

Second Degree AVB Type II

Punctual P wave with unpredictable dropped QRS; consistent PR interval length

Third Degree AVB Consistent P-P interval, consistent R-R interval,

no association between P waves and QRS complexes

Consider BBB when QRS > 100 millisecondsV1 V6

LBBB QRS negative

Wide QS wave

QRS positive

Tall R wave with no septal Q wave

RBBB rSR’ qRS (slurred S in Lead I)

Sgarbossa criteria

• Used to diagnose myocardial infarction in patients with LBBB and paced ventricular rhythms

• In LBBB, the QRS is always predominantly negative (deep S wave) and ST-segment elevation occurs in the right precordial leads

• Modified Sgarbossa criteria have improved diagnostic accuracy over original Sgarbossa criteria• > 1 lead with > 1 mm of concordant ST-segment elevation

• > 1 lead of V1-V3 with > 1 mm of concordant ST-segment depression

• > 1 lead anywhere with > 1 mm ST-segment elevation and proportionally excessive discordant ST-segment elevation, as defined by > 25% of the depth of the preceding S wave

modified: excessively discordant ST-segementelevation (> 25% of the depth of the preceding S wave)

Atrial enlargement: P waves in Leads II and V1

Ventricular Hypertrophy

LVH S in V1 or V2 (which ever is taller) + R in V5 or V6 (which ever is taller) > 35 mm

OR

Any precordial lead > 45 mm

R wave in aVL > 11 mm

R wave in I > 12 mm

R wave in aVF > 20 mm

RVH R:S > 1 in V1 and/or V2**voltage criteria cannot be used in the setting of abnormal conduction**

main QRS vector

main QRS vector

Prolonged QTi• QTc > 500 ms (normal QTi < 460 ms)

• Primary causes• Genetic (LQT 1, 2, 3, Romano-Ward syndrome)

• Acquired causes• Medications (antibiotics, antifungals, antipsychotoics, antidepressants) www.qtdrugs.org

• Electrolyte abnormalities (hypokalemia)

• Risk for VT, VF, and R on T phenomenon (PVC falls at peak of T wave, may precipitate VT, VF)

• Brugada syndrome• Association of characteristic ECG pattern w/ risk of ventricular tachyarrhythmias

Disorders of the SA node

• Sick sinus syndrome: • resting bradycardia, prolonged pauses, and chronotropic incompetence; may also have tachy-

brady syndrome (sinus or junctional bradycardia interrupted by paroxysms of tachycardia, usually SVT; termination of the tachycardia is often followed by a slow recovery of sinus rhythm))

• Chronotropic incompetence: • inability of the sinus node to effectively increase the sinus rate and allow for physiologic demand

that is present with activity; associated with fatigue and exercise intolerance

• Sinus pause:• failure of impulse formation; sinus node fails to pace for at least one cycle before (sinus arrest –

pause of > 3 seconds without atrial activity) resuming normal function; all P waves have the same morphology, P-P interval including the pause is unrelated to the underlying P-P interval; this is a form of sick sinus syndrome; may cause syncope

• Sinus exit block:• dysfunction of conduction of the action potential generated in the SA node to the surrounding

myocardium; classified like AV block (1st, 2nd type I, 2nd type II, 2:1, 3rd); the P-P interval of the pause is a multiple of the underlying P-P interval

Expect next PQRST here5 large boxes =

1 sec5 large boxes

= 1 sec5 large boxes

= 1 sec5 large boxes

= 1 sec

sinus arrest (> 3 seconds)

800 ms 2600 ms

Pause is > 3 P-P intervals and less than 4 P-P intervals;

therefore not sinus exit block

Ref

eren

ces

• Ganong’s Review of Medical Physiology, 25th edition (Barrett, et. al)• Chapter 29: Origin of the Heartbeat & the Electrical Activity of the Heart

• Pathophysiology of Disease, 7th edition (Hammer, et. al)• Chapter 10: Cardiovascular Disorders: Heart Disease

• Physiology, 4th edition (Costanzo)• Chapter 1: Cellular Physiology

• Chapter 4: Cardiovascular Physiology

• Cardiovascular Physiology, 8th edition (Mohrman, et. al)• Chapter 2: Characteristics of Cardiac Muscle Cells

• Hurst’s: The Heart, 14th edition (Fuster, et. al)• Chapter 4: Functional Anatomy of the Heart

• Chapter 78: Electrophysiologic Anatomy

• Chapter 79: Mechanisms of Cardiac Arrhythmias and Conduction Disturbances

• Chapter 80: Genetics of Channelopathies and Clinical Implications

• Chapter 82: Invasive Diagnostic Electrophysiology

• Chapter 83: Atrial Fibrillation, Atrial Flutter, and Atrial Tachycardia

• Chapter 84: Supraventricular Tachycardia: Atrial Tachycardia, Atrioventricular Nodal Reentry, and Wolf-Parkinson-White Syndrome

• Chapter 85: Ventricular Arrhythmias

• Chapter 86: Bradyarrhythmias

• Chapter 87: Antiarrhythmic Drugs

• Current Medical Diagnosis & Treatment: Cardiology, 5th edition (Crawford, et. al)• Chapter 11: Supraventricular Tachycardias

• Chapter 12: Atrial Fibrillation

• Chapter 13: Ventricular Tachycardia

• Chapter 14: Conduction Disorders and Cardiac Pacing

• EKGs for the Nurse Practitioner and Physician Assistant, 2nd edition (Knechtel)

• Harrison’s Principles of Internal Medicine, 19th edition (Kasper, et.al)• Chapter 52: Palpitations

• Chapter 268: Electrocardiography

• Chapter 269e: Atlas of Electrocardiography

• Chapter 273e: Principles of Electrophysiology

• Chapter 274: The Bradyarrhythmias: Disorders of the Sinoatrial Node

• Chapter 275: The Bradyarrhythmias: Disorders of the Atrioventricular Node

• Chapter 276: Supraventricular Tachyarrhythmias

• Chapter 277: Ventricular Arrhythmias

• Chapter 278e: Atlas of Cardiac Arrhythmias