Being able to read an ECG is a vital skill for all FY1 doctors. Please note that this article is not a replacement for book learning. Interpreting ECGs is difficult, but can be learnt by practice! This article presents a structured way in which to approach an ECG so that you can determine the main findings. I also cover common pathology which you will need to know when you are released on patients for the first time.
An electrocardiogram is a trace of the electrical activity of the heart, taken from different places to allow for a full 3D view of its conduction. The main principles are that if current is travelling in the direction of the lead, there is a positive deflection, if it is travelling away from a lead there is a negative deflection, and if it is travelling perpendicular to a lead then there is a biphasic deflection. If you understand this, and know the conduction pathway of the heart, you are half way there!
The P wave shows atrial contraction/depolarisation, the QRS complex shows ventricular contraction/depolarisation and the T wave shows ventricular repolarisation.
Don’t worry there is more on this below. For a more detailed description of why the ECG is shaped as it is can be found here.
The first thing you need to do when looking at an ECG (or indeed any investigation) is check that it refers to the right patient, and also at what time it was taken (important to link in with history). It can also be helpful to check the calibration (the open box at the start of each line should be 1cm (2 big squares) high. This refers to the deflection created by 1mV). It is then good to follow the same sequence of looking at the:
The best way to measure the rate is to use the rhythm strip (lead II that runs the whole way across the bottom) and count the number of big squares in between the R waves (or S waves), simply because the spikes are easy to see.
Rate = 300 / no. of big squares
Eg. if there are 5 big squares between each r wave, then the rate will be 300/5 = 60 bpm.
It is more complicated to calculate the rate in irregular rhythms, because the rate is constantly changing. Therefore an average can be used for the entire rhythm strip, which is 10s long. Count the number of r waves and multiply by 6. Normal rate is between 60 and 100.
This is usually apparent, but it is much easier to see by taking another sheet of paper, and marking the interval between two r waves, then seeing if it is the same distance between the next two. If rhythm is normal, it is called sinus rhythm. Arrhythmias are covered later.
NB. It is normal for rhythm to alter from inspiration to expiration.
This is the mean direction of the QRS complex conduction. It is calculated using the 6 limb leads, and can quickly and easily be calculated if you remember the diagram below:
Bright blue angles = right axis deviation (RAD) and orange angles = left axis deviation (LAD)
There are two rules for finding the axis of the heart:
1. The axis is perpendicular (at 90 degrees) to the limb lead with the equiphasic QRS complex.
2. The axis points in the direction of the most positive R waves (at an angle perpendicular to the lead in which the QRS is equiphasic).
eg. Lead II has equiphasic QRS complex, lead III has positive QRS complex, lead I has negative QRS complex = axis of 150 degrees (Right axis deviation)
P wave - duration should be 0.08-0.12s and amplitude should be < 2.5mm (0.25mV). If conduction is starting in the sino-atrial node (SAN) then P waves should be negative in aVR and positive in lead II. Conversely, if the SAN is not working such as in sick sinus syndrome, then the AV node takes over the pacing, and the P waves will be reversed (retrograde p waves) such that there will be positive waves in aVR and negative waves in lead II.
P waves are best reviewed in leads II and V1. Enlarged pointy P waves in lead II and biphasic p waves with larger upwards deflection in V1 = P pulmonale - enlarged right atrium.
Enlarged m shaped notched p waves (>0.04s between notches) in lead II and biphasic p waves with larger downward deflection in V1 = P mitrale - enlarged, hypertrophied left atrium.
You also need to check whether each P wave precedes a QRS complex. If it doesn’t, why doesn’t it? If P waves are not present, then patient may be in atrial fibrillation (irregularly irregular rhythm), or atrial flutter (faster rate, saw toothed base-line, can be either regular or irregularly irregular rhythm). If they are present, but do not immediately precede the qrs complex, then the patient may be in heart block.
PR interval - should be 0.12-0.2s. If prolonged, consider heart block, or extra-SAN pacing from either the AVN or ventricles. If shortened, consider Wolf-Parkinson-White or alternative extra-SAN pacemakers.
Q wave - Q waves can occur in healthy hearts, but Q waves are generally considered pathological if they are >0.04s in duration, and/or >1/4 of the following R wave in amplitude.
Pathological Q waves are a sign of transmural myocardial death, and are therefore not seen in early MI. Once they occur however, they often persist indefinitely (unless primary coronary intervention is carried out immediately). It is vital that you compare an ECG taken in an acute setting with a previous ECG to establish whether this is a new Q wave or a remnant from a previous infarct.
QRS complex - QRS duration should be <0.12s. If prolonged, there is a conduction abnormality such as in bundle branch block, or premature ventricular ectopic beats.
R wave progression - R waves should increase in size through the chest leads, with biphasic RS wave in V3/V4.
T wave - T wave duration is not as important as T wave shape and size.
Tall T waves may be present in hyperkalaemia (typically ‘tented’ in shape), acute phase myocardial ischaemia and LBBB.
Inverted T waves may be present in many conditions including ischaemia, pericarditis and pulmonary embolism.
QT interval - In rough terms, the QT interval should not be longer than half the R-R interval. Prolonged QT can predispose to possibly life threatening ventricular tachyarrhythmias.
Many drugs, eg haloperidol, amiodorone, sotalol, prolong the QT interval.
Hypercalcaemia shortens the QT interval (also predisposes to ventricular tachyarrhythmias).
Right ventricular hypertrophy
Causes: long standing pulmonary hypertension from severe pulmonary disease; congenital heart disease eg pulmonary stenosis, atrialseptal defect, tetralogy of Fallot and Eisenmenger’s syndrome; mitral stenosis (RVH and left atrial enlargement).
NB T wave inversion in V1 to V3 may also occur due to RV overload such as acute pulmonary embolism.
Left ventricular hypertrophy
LVH is important to recognise, as it can occur in serious clinical conditions such as hypertension, aortic stenosis, aortic regurgitation, mitral regurgitation and dilated cardiomyopathy.
NB LVH with RAD suggests biventricular hypertrophy. Although for a true diagnosis of any of these enlargements, an echocardiogram is required.
Septum polarised from left to right. Left bundle still intact, so left ventricle contracts before right. Right ventricle contracts after left.
V1 - rSR’ with wide R’ wave. May be a notched R wave rather than the classic rSR’
V6 - qRS with wide S wave. May also have inverted T waves in precordial leads (V1-3)
Complete RBBB occurs is QRS is >0.12 sec in duration, and incomplete if 0.1-0.12 sec.
RBBB can occur in any condition affecting the right side if the heart, and can be permanent or temporary. It can also occur in people with no heart disease (with normal QRS duration)
Septum depolarizes from right to left. The right bundle intact so right ventricle contracts first. The left ventricle contracts after the right.
QRS complex is always -ve in V1 all +ve in V6. There is loss of the septal R wave in V1, and a wide W shape.
There are no q waves in V6 and a wide M shaped wave.
Leads with tall R waves can have inverted T waves.
LBBB is only present in patients with heart disease. It may be the fist sign of advanced coronary artery disease, valvular heart disease, hypertensive heart disease and cardiomyopathy.
If you are struggling with interpreting bundle branch block don't worry, it is hard to get your head around. A good tip is to think about which ventricle is being depolarised last, and therefore in which lead will it be positive in. Eg in LBBB the LV will depolarise after the RV, therefore in the more left sided (V6) leads, there will be a positive deflection late in the QRS complex.
Ischaemia occurs when heart muscle is not perfused by blood. If not reversed quickly, this results in myocardial death and scarring. The ECG can be used to detect myocardial ischaemia, and to locate the likely location of the infarct.
Blood supply to the heart:
It is important to keep these in mind when interpreting an ECG. Different leads focus on different aspects of the heart, and ischaemic changes in these leads indicate the location of the affected area:
There are 3 phases of infarction:
NB ST elevation in all leads is seen in pericarditis
ST elevation is relevant if >1mm in limb leads and >2mm in chest leads.
If there is no infarct, transient ischaemia is shown by ST segment depression
Heart block occurs when there is a disruption to conduction from the atria to the ventricles.
First-degree heart block: PR interval is prolonged (>0.2s) by the same amount each beat (uniformly) due to conduction being delayed by the AVN.
Second-degree heart block: AV conduction fails intermittently, 2 different types occur.
Wenckebach is commonly caused by beta blockers, calcium channel blockers and digoxin, as well as inferior MI. It rarely progresses to third degree block.
Mobitz type II however often progresses to complete (third-degree) heart block, and is therefore an indication for a permanent pacemaker.
Third degree (complete) heart block:
There are 5 supraventricular arrythmias you need to know about:
1. Atrial Premature Beats (APB) - An ectopic beat that arises from an area of the ventricle which is not the SAN. It occurs before it should do, but with a complete set of waves (although the P wave may be incorporated into the preceding T wave) and a tight QRS. There is often a slight pause after the APB as the SAN resets.
NB. Sometimes the APB causes aberrant ventricular depolarisation with a resultant wide QRS which can take on RBBB or LBBB morphology.
2. Paroxysmal Supraventricular Tachycardias - A run of 3 or more APBs together.
3. Junctional Escape Rhythms - A junctional beat can be spotted by looking for retrograde (inverted) p waves which can be either just before, just after, or incorporated into the QRS complex. These are beats which are started from the AVN as a result of SAN failure. The SAN will usually take over pacing for the next beat, if it does not, then the heart is in junctional escape rhythm.
The AVN usually conducts at 30-50 bpm.
4. Atrial Flutter - NOT TO BE CONFUSED WITH ATRIAL FIBRILLATION. These are two different conditions, with different pathology and treatment. Atrial flutter is caused by an abnormality within the atrial conduction pathway. An area, usually in the atrial septum, slows down the conduction pathway in one part, whilst the rest of the atria contract. The abnormal area then depolarises after the rest of the atria, creating another wave of contraction. This causes a reentry tachycardia, with the atria contracting 250-350 times a minute. Not all of these beats are conducted to the ventricles, causing saw-toothed F waves.
Atrial flutter can be cured by ablating the responsible area as a day-case procedure (Tony Blair underwent this procedure as PM).
5. Atrial Fibrillation - Rather than orchestrated contraction, the cells of the atria depolarise at random, causing fibrillation, and an irregularly irregular beat with absent P waves.
There are even fewer ventricular arrythmias you need to know about, but they can be life-threatening, so should be taken seriously.
1. Ventricular Premature Beats (VPB) - Like APBs they occur before they are expected, but the QRS complex is wide because of conduction originating from within the ventricles. The T wave also points in an opposite direction to the QRS complex.
If there are multiple VPBs, it is important to comment on the morphology (beats originating from the LV often have a RBBB appearance and vice versa), and whether all are the same or different (uniform or multiform).
2. Ventricular Tachycardia - When 3 or more VPBs are together, this becomes VT. If the episode lasts for >30s then it is sustained VT, and can be associated with syncope and progression to VF arrest.
Analyse VT in a similar way to VPBs, are they all the same shape (monomorphic or polymorphic)? Monomorphic VT rarely occurs in people without structural heart disease, such as previous MI, cardiomyopathy, or severe valvular disease. If it is polymorphic, consider whether the QRS is cyclically changing from a predominantly negative deflection to a predominately positive deflection through consecutive beats. This may be representative of torsades de pointes ("twisting of the points"), a condition characterised by prolonged QT interval and distinctive polymorphic VT. This is an important diagnosis as it is often precipitated by drugs or electrolyte disturbances, which must be altered to correct the arrythmia.
3. Ventricular Fibrillation - Uncoordinated fibrillation of the ventricles, lead to a complete lack of cardiac output and death. Seen as irregular low voltage squiggles on the ECG or pulseless electrical activity. Requires immediate defibrillation by unsynchronized DC shock.
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