HOW TO READ ECG - Lead I: right arm to left arm

Graph paper divided into 1-mm2 gridlike boxes. When the recording - Lead II: right arm to left foot
speed of 25mm/s, the smallest (1mm) horizontal divisions correspond
to 0.04s (40ms), with heavier lines at intervals of 0.20s (200ms). - Lead III: left arm to left foot

Vertically, the ECG graph measures the amplitude of a specific wave  Normal cardiac axis
or deflection (1mV = 10 mm with standard calibration). o Lead II has the most positive deflection compared
to leads I and III
The PR interval measures the time (normally 120–200 ms) between  Right axis deviation
atrial and ventricular depolarization, which includes the physiologic o Lead III has the most positive deflection
delay imposed by stimulation of cells in the AV junction area. o Lead I should be negative
o associated with right ventricular hypertrophy
The QRS interval (normally 100–110 ms or less) reflects the duration
 Left axis deviation
of ventricular depolarization. o Lead I has the most positive deflection
The QT interval subtends both ventricular depolarization and o Leads II and III are negative
(primarily) repolarization times and varies inversely with the heart o associated with heart conduction abnormalities
rate. A rate-related (“corrected”) QT interval, QTc, can be calculated 4. P waves (LEAD II)
as QT/√RR and is normally ≤0.44s. Some references give the QTc
upper normal limits as 0.45s in men and 0.46s in women.  Are P waves present?
o If P waves are absent, is there any atrial activity?
 Sawtooth baseline (flutter waves)
 Chaotic baseline (fibrillation waves)
 Flat line (no atrial activity at all)
 Is each P wave followed by a QRS complex?
 Check duration, direction and shape
o morphology
 upright in leads I, II, and aVF
 inverted in lead aVR
 biphasic in lead V1
o amplitude
 0.05 to 0.25mV (0.5 to 2.5 small boxes)
o duration
 0.06-0.11 seconds (1.5 to 2.75 small
1. Heart Rate boxes)

 can be computed from the inter-beat (RR) interval by: 5. PR Interval

o dividing the number of large (0.20s) time units
between consecutive R waves into 300 - should be between 120-200ms (3-5 small squares)
o or the number of small (0.04s) units into 1500
- prolonged PR interval (>0.2s) suggests the presence of AV delay or
 If the patient’s heart rhythm is irregular,
AV block
o count the number of complexes on the rhythm
strip (typically 10 seconds long) then multiply the  first degree heart block
average number of complexes into a full-minute o FIXED prolonged PR interval of >200ms (5 small
(so multiply by 6) squares)
 second degree heart block (type 1)
2. Heart Rhythm
o also known as Mobitz type 1 AV block or
 can be regular or irregular Wenckebach phenomenon
 irregular rhythms can be o progressive prolongation of PR interval until atrial
o regularly irregular impulse is not conducted and QRS complex is
o irregularly irregular dropped
 if suspicious of AV block, map out the atrial rate and o AV nodal conduction resumes with the next beat
ventricular rhythm separately (i.e. mark P waves and R and the sequence of progressive prolongation
waves) and see if the PR interval changes, if QRS complexes and eventual dropping repeats
are missing or if there is complete dissociation between the  second degree heart block (type 2)
two o also known as Mobitz type 2 AV block
o consistent PR interval duration with
3. Cardiac Axis intermittently dropped QRS complexes due to
failure of conduction
- describes the overall direction of electrical spread within the heart o intermittent dropping typically follows a
repeating cycle of every 3rd (3:1 block) or 4th (4:1
- normally, the axis should spread from 11 o’clock to 5 o’clock
block) P wave
- look at LEADS I, II, III

ATMB (Batch Insignis 2022) Personal Guide

  third degree heart block (complete) o J point segment
o occurs when there is no electrical communication  where the S wave joins the ST segment
between atria and ventricles  benign early repolarization is common
o presence of P waves and QRS complexes have no under the age of 50
association with each other (atria and ventricles  over 50, ischemia is more
function independently) common
o narrow-complex escape rhythms (QRS of <0.12s  raised J point with widespread ST
duration) originate ABOVE bifurcation of bundle elevation in multiple territories makes
of His ischemia less likely
o broad-complex escape rhythms (QRS of >0.12s  T waves are also raised
duration) originate BELOW bifurcation  T waves remains the same
size and ST segment is raised
- shortened PR interval in STEMI
 P wave is originating somewhere closer to the AV node 7. ST segment
o SA node is not in a fixed place
o some atria are smaller than others - between the end of S wave and start of T wave
 faster shortcut
o accessory pathway associated with a delta wave - normally should be an isoelectric line (neither elevated nor
(Wolff Parkinson White Syndrome) depressed)

6. QRS Complex  ST elevation

o significant when >1mm (1 small square) in two or
- pay attention to the following characteristics: more contiguous limb leads or >2mm in two or
more chest leads
 width o most commonly caused by acute full-thickness
o narrow (<0.12s) myocardial infarction
 impulse is conducted down the bundle  ST depression
of His o ≥0.5mm in ≥2 contiguous leads indicate
 atrial ectopic myocardial ischemia
o broad (>0.12s)
 abnormal depolarization sequence 8. T waves
 ventricular ectopic
 bundle branch block - repolarization of the ventricles
 height  Tall T waves
o small o >5mm in limb leads
 <5mm in limb leads or <10mm in chest o >10mm in chest leads
leads o associated with hyperkalemia (tall “tented” T
o tall waves) and hyperacute STEMI
 imply ventricular hypertrophy  Inverted T waves
 morphology o normally inverted in V1 and a normal variant in
o delta wave lead III
 ventricles are being activated earlier o in other leads, it’s a nonspecific sign of:
than normal from a point distant to the  ischemia
AV node  BBB (V4-V6 in LBBB and V1-V3 in RBBB)
o Q wave  pulmonary embolism
 pathological  LVH (in lateral leads)
 >25% of the size of R wave  hypertrophic cardiomyopathy
that follows it or (widespread)
 >2mm in height  general illness
 >40ms in width  Biphasic T waves
 Q waves in V2-V4 with T wave inversion o two peaks
suggestive of previous anterior MI o indicative of ischemia and hypokalemia
o R and S waves  Flattened T waves
 assess R wave progression across the o nonspecific sign that may represent ischemia or
chest leads (small in V1 to large in V6) electrolyte imbalance
 poor progression could be a
sign of previous MI but can
also occur in very large
people
 transition from S>R to R>S should occur
in V3 or V4

ATMB (Batch Insignis 2022) Personal Guide

9. U waves

- not a common finding

- >0.5mm deflection after the T wave best seen in V2 or V3

- become larger the slower the bradycardia

 seen in various electrolyte imbalances, hypothermia and

secondary to antiarrhythmic therapy (digoxin,
procainamide or amiodarone)

ATMB (Batch Insignis 2022) Personal Guide