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 conal
branch 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 Reciprocal*
(injury – ST segment elevation) (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 Progressive lengthening of PR interval from cycle
AVB Type I to cycle prior to a dropped QRS
(Wenckebach)
Second Degree Punctual P wave with unpredictable dropped
AVB Type II 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 milliseconds
V1 V6
LBBB QRS negative QRS positive
Wide QS wave 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-segement
elevation (> 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 here
5 large boxes = 5 large boxes 5 large boxes 5 large boxes
1 sec = 1 sec = 1 sec = 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
 • 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
References

• 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