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- Technical details: Name, patient number, date of ECG, rate of ECG reading (25mm/sec) and voltage (1mV = 1cm, should be 2cm)
- Rate and rhythm:
Determine rate by dividing 300 by number of squares between QRS complexes.
<60 = bradycardia > 100 = tachycardia
Is the rhythm regular or irregular: Use the card method, marking 3 successive points and comparing on rhythm strip
Are QRS complexes preceded by a p wave? If yes, then there is sinus rhythm.
An irregularly irregular pattern without P waves indicates AF. NB P waves are inverted in AVR
- Axis: As a general rule, if leads I & II are +ve, then axis is normal
- P waves: Dissociation between QRS complex indicates complete heart block. Look for bifid appearance in left atrial enlargement (P mitrale) and large concave appearance in right atrial enlargement (P pulmonale)
- PR interval: Time between start of P wave and QRS complex, normally 0.12-0.20 (3-5 squares). Constant prolongation seen in 1st degree block. Short PR interval can be due to rapid conduction down accessory pathway
- QRS complex: Normally 0.12secs long. Wide QRS complex seen in ventricular conduction defects (BBB). Tall complexes seen in RFH or LVH (Large R wave in C1 if RVH and Large R wave in C6 if LVH, with S waves in opposite leads). Transition point is normally at V3/V4
- QT interval: From start of QRS to end of T wave, normally 0.40secs and prolonged in low K and Ca. Reduced in high K and Ca
- ST segment: Elevation in infarction and depression in ischaemia
- T wave: Tall in high K, and flat in low K: Normally inverted in V1-V2 as well as leads III and VR. Abnormal in V4-6 and leads I and II
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Common pathology
- AF: Common causes include: Hypertension, IHD, thyrotoxicosis, valvular disease
- Heart block:
1st degree: Fixed prolongation of PR interval
Mobitz Type 1/ Wenckebach: Progressive PR prolongation, then missed P wave
Mobitz type 2: Occasional non-conducted beats (P waves normal)
2:1/ 3:1: Normal P wave rate, but 2 or 3 P waves per QRS complex
Complete block: No relation between P waves and QRS complex
RBBB seen as a characteristic RSR pattern on V1 and an M pattern in V6
LBBB seen in an acute ST elevation MI, is seen as an M pattern in V6
- Myocardial Infarct:
ECG can be normal
Raised ST segments
T wave inversion in leads I, II and V4-V6
Appearance of pathological Q waves: defined as >1 small square, and if present in more than 1 lead
Can eventually be followed within days by pericarditis, seen as a saddle shaped appearance of the ST elevation element
Anterior infarct affects leads: V3 and V4, maybe V2-V5
Inferior infarct seen in leads: AVF, leads II and III
Lateral infarct seen in leads: V5, V6, V1 and AVL
Posterior infarct seen as dominant R waves in lead V1
- PE:
Can present as normal ECG with sinus tachycardia
P pulmonale
RAD
RVH signs, i.e. Peaked R waves in V1 and deep S waves in V6
Classical S1, Q3, T3 pattern: S waves in lead I, Q waves in lead III and inverted T waves in lead III
RBBB
- Hypertrophy:
V1 covers RV territory; with V6 covering LV. RVH shows R waves in V1 and S waves in V6, with LVH showing R waves in V6 and S waves in V1. Hypertrophy is in the region where there is a dominant R wave.
- Metabolic abnormalities:
Digoxin toxicity presents as a downward sloping ST segment, or the characteristic reverse tick sign
Hyperkalaemia may show as wide QRS complexes
- Supraventrcular rhythms:
Narrow QRS complexes
Normal T waves
Wide complex in WPW as accessory pathway has a slower conduction or in BBB
NB Atrial tachycardia has rate of 150-200bpm, atrial flutter 300bpm and AF 300-600bpm. Always look at the rate. If the rate is normal (60-100), consider a 2:1 or 3:1 block
Atrial flutter is a regular sawtooth pattern on the ECG, with varying degrees of block (2:1, 3:1 or 4:1). Determine block by dividing the P wave time by the QRS (i.e. 300/150 indicates flutter with a 2:1 block). Can be confirmed by CSM, which will prevent conduction through the AV node and thus reduce number of QRS complexes
- Ventricular Rhythms:
Wide complex > 0.12secs
Abnormal T waves
Author:
Mr Adnan Darr MBCHB, BSc, MSc, MRCS
| Speciality:
Cardiology
| Date Added:
02/10/2011
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