This guide demonstrates how to read an ECG in a systematic and effective manner. If you want to put your ECG interpretation knowledge to the test, check out ourECG quiz on the new Geeky Medics quiz platform.
Confirm the name and date of birth of the patient matches the details on the ECG.
Check the date and time the ECG was performed.
Step 1 – Heart Rate
What’s a normal adult heart rate?
Normal – 60-100 bpm
Tachycardia > 100 bpm
Bradycardia < 60 bpm
Regular Heart Rhythm
If a patient has a regularheartrhythm their heart rate can be calculated using the following method:
Count the number of large squares present within one R-R interval
Divide 300 by this number to calculate the heart rate
4 large squares in an R-R interval
300/4 = 75 beats per minute
Irregular Heart Rhythm
If a patient’s heart rhythm is irregular the first method of heart rate calculation doesn’t work (as the R-R interval differs significantly throughout the ECG). As a result, you need to apply a different method such as:
Count the number of complexes on the rhythm strip (each rhythm strip is typically 10 seconds long)
Multiply the number of complexes by 6 (giving you the average number of complexes in 1 minute)
10 complexes on a rhythm strip
10 x 6 = 60 beats per minute
Step 2 – Heart rhythm
A patient’s heart rhythm can be regular or irregular.
Irregular rhythms can be either:
Regularlyirregular (i.e. a recurrent pattern of irregularity)
Mark out several consecutive R-R intervals on a piece of paper, then move them along the rhythm strip to check if the subsequent intervals are similar.
If you are suspicious that there is some atrioventricularblock (AV block), map out the atrialrate and the ventricularrhythm separately (i.e. mark the P waves and R waves). As you move along the rhythm strip, you can then see if the PR interval changes, if QRScomplexes are missing or if there is completedissociation between the two.
Step 3 – Cardiac axis
Cardiac axis describes the overall direction of electrical spread within the heart.
In a healthy individual, the axis should spread from 11 o’clock to 5 o’clock.
To determine the cardiac axis you need to look at leads I, II and III.
Second-degree heart block (Mobitz type 1 AV block or Wenckeback phenomenon)
Second-degree AV block (type 1) is also known as Mobitz type 1 AV block or Wenckebach phenomenon.
Typical ECG findings in Mobitz type 1 AV block include progressive prolongation of the PR interval until eventually the atrial impulse is not conducted and the QRS complex is dropped.
AV nodal conduction resumes with the next beat and the sequence of progressive PR interval prolongation and the eventual dropping of a QRS complex repeats itself.
Second-degree heart block (Mobitz type 2 AV block)
Second-degree AV block (type 2) is also known as Mobitz type 2 AV block.
Typical ECG findings in Mobitz type 2 AV block include a consistent PR interval duration with intermittently dropped QRS complexes due to a failure of conduction.
The intermittent dropping of the QRS complexes typically follows a repeating cycle of every 3rd (3:1 block) or 4th (4:1 block)P wave.
Third-degree heart block (complete heart block)
Third-degree (complete) AV block occurs when there is no electrical communicationbetween the atria and ventricles due to a complete failure of conduction.
Typical ECG findings include the presence of P waves and QRS complexes that have no association with each other, due to the atria and ventricles functioning independently.
Cardiac function is maintained by a junctional or ventricularpacemaker.
Narrow-complex escape rhythms (QRS complexes of <0.12 seconds duration) originate above the bifurcation of the bundle of His.
Broad-complex escape rhythms (QRS complexes >0.12 seconds duration) originate from below the bifurcation of the bundle of His.
Tips for remembering types of heart block
To help remember these degrees of AV block, it is useful to remember the anatomical location of the block in the conducting system:
First-degree AV block:
Occurs between the SA node and the AV node (i.e. within the atrium)
Second-degree AV block:
Mobitz I AV block (Wenckebach) – occurs IN the AV node (this is the only piece of conductive tissue in the heart which exhibits the ability to conduct at different speeds)
Mobitz II AV block – occurs AFTER the AV node in the bundle of His or Purkinje fibres
Third-degree AV block:
Occurs anywhere from the AV node down causing complete blockage of conduction
Shortened PR Interval
If the PR interval is shortened, this can mean one of two things:
Simply, the P-wave is originating from somewhere closer to the AV node so the conduction takes less time (the SA node is not in a fixed place and some people’s atria are smaller than others).
The atrial impulse is getting to the ventricle by a fastershortcut instead of conducting slowly across the atrial wall. This is an accessorypathway and can be associated with a deltawave (see below which demonstrates an ECG of a patient with Wolff Parkinson White syndrome).
Step 6 – QRS complex
When assessing a QRS complex, you need to pay attention to the following characteristics:
Width can be described as NARROW (< 0.12 seconds) or BROAD (> 0.12 seconds)
A narrow QRS complex occurs when the impulse is conducted down the bundle of His and the Purkinje fibre to the ventricles. This results in well organised synchronised ventricular depolarisation.
A broad QRS complex occurs if there is an abnormal depolarisation sequence – for example, a ventricular ectopic where the impulse spreads slowly across the myocardium from the focus in the ventricle. In contrast, an atrial ectopic would result in a narrow QRS complex because it would conduct down the normal conduction system of the heart. Similarly, a bundle branch block results in a broad QRS complex because the impulse gets to one ventricle rapidly down the intrinsic conduction system then has to spread slowly across the myocardium to the other ventricle.
Describe this as SMALL or TALL:
Small complexes are defined as < 5mm in the limb leads or < 10 mm in the chest leads.
Tall complexes imply ventricular hypertrophy (although can be due to body habitus e.g. tall slim people). There are numerous algorithms for measuring LVH, such as the Sokolow-Lyon index or the Cornell index.
To assess morphology, you need to assess the individual waves of the QRS complex.
The mythical ‘delta wave’ is a sign that the ventricles are being activated earlier than normal from a point distant to the AV node. The early activation then spreads slowly across the myocardium causing the slurred upstroke of the QRS complex.
Note – the presence of a delta wave does NOT diagnose Wolff-Parkinson-White syndrome. This requires evidence of tachyarrhythmias AND a delta wave.
Isolated Q waves can be normal.
A pathological Q wave is > 25% the size of the R wave that follows it or > 2mm in height and > 40ms in width.
A single Q wave is not a cause for concern – look for Q waves in an entire territory (e.g. anterior/inferior) for evidence of previous myocardial infarction.
R and S waves
Look for R wave progression across the chest leads (from small in V1 to large in V6).
The transition from S > R wave to R > S wave should occur in V3 or V4.
Poor progression (i.e. S > R through to leads V5 and V6) can be a sign of previous MI but can also occur in very large people due to poor lead position.
J point segment
The J point is where the S wave joins the ST segment
This point can be elevated resulting in the ST segment that follows it also being raised (this is known as “High take-off”)
High take-off (or benign early repolarisation to give its full title) is a normal variant that causes a lot of angst and confusion as it LOOKS like ST elevation
Key points for assessing the J point segment:
Benign early repolarisation occurs mostly under the age of 50 (over the age of 50, ischaemia is more common and should be suspected first)
Typically, the J point is raised with widespread ST elevation in multiple territories making ischaemia less likely
The T waves are also raised (in contrast to a STEMI where the T wave remains the same size and the ST segment is raised)
The ECG changes do not change! During a STEMI, the changes will evolve – in benign early repolarisation, they will remain the same.
Step 7 – ST segment
The ST segment is the part of the ECG between the end of the S wave and the start of the T wave.
In a healthy individual, it should be an isoelectric line (neither elevated or depressed).
Abnormalities of the ST segment should be investigated to rule out pathology.
ST-elevation is significant when it is greater than 1 mm (1 small square) in 2 or more contiguous limb leads or >2mm in 2 or more chest leads.
It is most commonly caused by acute full-thickness myocardial infarction.
ST depression ≥ 0.5 mm in ≥ 2 contiguous leads indicates myocardial ischaemia.
Step 8 – T waves
T waves represent repolarisation of the ventricles.
Tall T waves
T waves are considered tall if they are:
> 5mm in the limb leads AND
> 10mm in the chestleads (the same criteria as ‘small’ QRS complexes)
Tall T waves can be associated with:
Hyperkalaemia (“Tall tented T waves”)
Inverted T waves
T waves are normally inverted in V1 and inversion in lead III is a normal variant.
Inverted T waves in other leads are a nonspecific sign of a wide variety of conditions:
Bundle branch blocks (V4 – 6 in LBBB and V1 – V3 in RBBB)
Left ventricular hypertrophy (in the lateral leads)
Hypertrophic cardiomyopathy (widespread)
Around 50% of patients admitted to ITU have some evidence of T wave inversion during their stay.
Observe the distribution of the T wave inversion (e.g. anterior/lateral/posterior leads).
You must take this ECG finding and apply it in the context of your patient.
Biphasic T waves
Biphasic T waves have two peaks and can be indicative of ischaemia and hypokalaemia.
Flattened T waves
Flattened T waves are a non-specific sign, that may represent ischaemia or electrolyte imbalance.
U waves are not a common finding.
The U wave is a > 0.5mm deflection after the T wave best seen in V2 or V3.
These become larger the slower the bradycardia – classically U waves are seen in various electrolyte imbalances, hypothermia and secondary to antiarrhythmic therapy (such as digoxin, procainamide or amiodarone).