1. RATE
   1. Rate calculation
      1. Six-second method: # R-R intervals x10
2. RHYTHM
3. Check:
   • bottom rhythm strip for regularity
     • i.e. regular, regularly irregular, and irregularly irregular. 
   • P wave before each QRS, QRS after each P
   • PR interval (for AV blocks)
   • QRS (for bundle branch blocks)
   • prolonged QT
4. Recognize “patterns” such as
   • f. atrial fibrillation, PVC’s
   • g. PAC’s, escape beats
   • h. ventricular tachycardia
   • i. paroxysmal atrial tachycardia
   • j. AV blocks
   • k. bundle branch blocks

4. AXIS

Lead I	Lead aVF	differential
Normal axis (0 to +90 degrees)
Positive	Positive
Left axis deviation (-30 to -90)
Positive  Also check lead II. To be true left axis deviation, it should also be down in lead II	Negative	LVH left anterior fasicular block inferior wall MI note: Bifascicular block = RBBB + LAFB
Right axis deviation (+90 to +180)
Negative	Positive	RVH left posterior fascicular block lateral wall MI.
Indeterminate axis (-90 to -180)
Negative	Negative

4. HYPERTROPHY 
   • LVH — left ventricular hypertrophy
     1. S wave in V1 or V2 + R wave in V5 or V6 > 35mm
     2. aVL   R wave > 12mm. 
   • RVH — right ventricular hypertrophy
     1. R wave > S wave in V1 and gets progressively smaller to left V1-V6 (normally, R wave increases from V1-V6). 
   • Atrial hypertrophy (leads II and V1) 
     • Right atrial hypertrophy
       • Peaked P wave in lead II > 2.5 mm in amplitude
       • V1 has increase in the initial positive direction
     • Left atrial hypertrophy
       • Notched wide (> 3mm) P wave in II
       • V1 has increase in the terminal negative direction.

5. INFARCT

Ischemia	Represented by symmetrical T wave inversion (upside down) Look in leads I, II, V2-V6.
Injury	Acute damage — look for elevated ST segments.
Infarct	“Pathologic” Q waves. To be significant, a Q wave must be at least one small square wide or one-third the entire QRS height.

6. Certain leads represent certain areas of the left ventricle:

V1-V2	anteroseptal wall	II, III, aVF	inferior wall
V3-V4	anterior wall	I, aVL	lateral wall
V5-V6	anterolateral wall	V1-V2	posterior wall (reciprocal)

Imposters: ECG Causes of ST segment elevation: ELEVATION

Electrolyte abnormalities
Left bundle branch block
Aneurysm of left ventricle
Ventricular hypertrophy
Arrhythmia disease (Brugada syndrome, ventricular tachycardia)
Takotsubo/Treatment (iatrogenic pericarditis)
Injury (myocardial infarction or cardiac contusion)
Osborne waves (hypothermia or hypocalcemia)
Non-atherosclerotic (vasospasm or Prinzmetal’s angina)

Pericarditis: 

• ECG: Usually diffuse ST elevation, Can be associated with PR depression (elevation in aVR), No reciprocal changes, The morphology of the ST segment

Acute Myocarditis

• Myocarditis can occur alone or in combination with pericarditis
• Can cause similar ST changes to pericarditis
• Focal myocarditis can cause regional ST elevation even with ST depression and can be difficult to distinguish from a STEMI

Early Repolarization

• A usually benign ECG pattern with an incidence of 5 to 13% of people so very common especially in young healthy athletes
• ST elevation (J point elevation) of 1 mm or more in 2 or more contiguous leads (usually inferior or lateral or both)
• ST morphology similar to pericarditis
• No reciprocal changes

PE ECG changes:

• Sinus tachycardia – the most common abnormality; seen in 44% of patients.
• Complete or incomplete RBBB
• Right ventricular strain pattern –  T wave inversions in the right precordial leads (V1-4) ± the inferior leads (II, III, aVF). This pattern is seen in up to 34% of patients and is associated with high pulmonary artery pressures.
• Right axis deviation
• SI QIII TIII  pattern – deep S wave in lead I, Q wave in III, inverted T wave in III. This “classic” finding is neither sensitive nor specific for pulmonary embolism; found in only 20% of patients with PE. 

ACS is rarely associated with tachycardia

Both ACS and PE will present with elevated troponin

Ultrasonography may be useful in differentiating the two

AF ECG Changes 

• Irregularly irregular rhythm.
• No P waves.
• Absence of an isoelectric baseline.
• Variable ventricular rate.
• QRS complexes usually < 120 ms unless pre-existing bundle branch block, accessory pathway, or rate related aberrant conduction.
• Fibrillatory waves may be present and can be either fine (amplitude < 0.5mm) or coarse (amplitude >0.5mm).
• Fibrillatory waves may mimic P waves leading to misdiagnosis.

Atrial Flutter ECG Changes:

• Narrow complex tachycardia
• Regular atrial activity at ~300 bpm
• Flutter waves (“saw-tooth” pattern) best seen in leads II, III, aVF — may be more easily spotted by turning the ECG upside down!
• Flutter waves in V1 may resemble P waves
• Loss of the isoelectric baseline
• Fixed AV blocks
  • Ventricular rate is a fraction of the atrial rate, e.g.
  • 2:1 block = 150 bpm
  • 3:1 block = 100 bpm
  • 4:1 block = 75 bpm
• Variable AV block
  • The ventricular response is irregular and may mimic AF
  • On closer inspection, there may be a pattern of alternating 2:1, 3:1 and 4:1 conduction ratios

 

Important ECG Patterns

Hyperkalaemia	Bradycardia / AV blockHR 30Flattend P wavePeaked T wavesSine wave
HypoKalemia (also Barycardia, HypocalcaemiaHypomagnesaemiaHypothermia)	Prominent U waves(if >1-2mm or 25% of the height of the T wave)
Sodium Channel Blockade  tricyclic antidepressant	Broad complex, QRS > 100ms positive R’ wave in aVR(+ tachycardia)
Digoxin Toxicity	Atrial tachycardia high grade AV block Frequent Ventricular Ectopic Beats(VEB) Rx: Digiband
Digoxin effect	Downsloping ST depression with a characteristic “Salvador Dali sagging” appearanceFlattened, inverted, or biphasic T waves.Shortened QT interval.
Pericardial Effusion	Low voltage  Electrical alternans+Sinus tachy
Pericarditis	Widespread concave ST elevation and PR depression throughout
Raised ICP Due to SAH Intraparenchymal haemorrhage	Cerebral T wavesGiant inverted T waves widespread Long QT DDx – Wellens
Brugada Syndrome	Coved STE in V1-3
Arrhythmogenic Right Ventricular Cardiomyopathy	Epsilon waves Signs of RVH
hypothermia	positive deflection at the J point (negative in aVR and V1)
Long QT
Wellens (critical stenosis of the  LAD)	Biphasic T Waves in V2,V3 (Type A)  Deeply Inverted T Waves in V2,V3 (Type B)
De Winter’s T Waves (anterior STEMI equivalent that presents without obvious ST segment elevation)	ST depression and peaked T waves in the chest leads
Delta Wave	A slurred upstroke to the QRS complex Short PR interval (< 120ms)Broad QRS (> 100ms)
Not a pacemaker! ☺