There are whole books devoted to the topic of ECG interpretation, and careers are made out of the specific details involved. However, the basics are relatively simple and will help identify the main and important features of an ECG.
One of the most important things to remember when you are looking at an ECG is that it is a two-dimensional representation of what is going on in three dimensions. In other words, you're looking at simple, flat, squiggly lines, which are representing the intensity and direction of electrical activity through a real-life object.
As a result, it's important to know what parts of the heart different leads are pointing to in order to understand the significance of your findings. The direction that each of the leads is pointing in gives you the information about direction. The height of the waves gives you information about intensity. Since I know that, I usually ask myself three main questions, and then check five things in each of the leads. The three questions are:
What is the rate? How quickly is the heart beating - or, more accurately, how quickly is a QRS complex being produced (because this may not always lead to a heart beat).
What is the rhythm? The heart should be beating in a regular rhythm, but what if it isn't? What is it called, and what does it mean?
What is the cardiac axis? I like to think of this as the general direction that the electrical activity of the heart is travelling in. Is it going in the right direction? And if not, why not?
The five things I look at in each lead are the five elements of the ECG complex: the P wave, the PR interval, the QRS complex, the ST segment and the T wave.
Another important feature to consider is the QT interval, as detailed below. So, take your pen and ECG in hand, and work through the questions below...
Working out the rate is quite easy. We are interested in how quickly the ventricles are firing, because they are the part of the heart that actually pump blood around the body. On most ECG machines the 'ventricular rate' is written as a number, but it may be worth checking to see this is right.
If normal ECG paper is being used and the ECG is moving at 25mm/sec, the easiest way to work out the rate is by counting how many 'big squares' you get between R waves. Then divide 300 by this number. For example, if you have 4 big squares between each R wave, then you know the ventricular rate is 75. Another way is to count the number of R waves you get in 30 big squares, and then multiply by ten.
The normal rate of the heart beating is between 60 and 100 beats per minute. This is the normal frequency with which the sinoatrial node sends off its electrical signal to spread through the heart. If the rate is between these two values, it is a good sign - there may be other things wrong, but a normal rate is reassuring.
If the rate is too slow, it suggests that there is something abnormal about the conducting system of the heart. It may be that the sino-atrial node is not working well, or even not at all; if this is the case, something else has to take over, and nothing is quite as quick as the sino-atrial node. Other parts of the system may be damaged, causing the electrical signal to get delayed - e.g. a first, second or third degree heart block. Usually this will be easier to work out from another part of the ECG, but it can slow down the rate, and a slow rate should therefore be a prompt to look out for such abnormalities in the rest of the ECG.
It may be caused by drugs which slow the heart rate (e.g. beta-blockers such as bisoprolol). A heart attack may cause damage to any part of the conducting system and therefore reduce the heart rate, or a collection of fluid around the heart can compress it and slow the rate. When the salts are at the wrong concentration in the blood (e.g. high potassium), this can also be a cause. Rarer causes are raised intracranial pressure (suspected if the blood pressure is rising - the 'Cushing's Reflex'), infections such as typhoid, or problems with the adrenal gland that stop it working properly.
If the rate is too fast, it is also possible that something is wrong with the conducting system. Because all heart cells have the capacity to start a heartbeat, if one of them is damaged, it can misfire - potentially meaning that the heart beats more quickly. If it starts in the atria, the heartbeat is starting above the ventricles - a supraventricular tachycardia. If it starts in the ventricles, this is a ventricular tachycardia.
Again, drugs and salt imbalances can affect the rate at which the heart beats. When salts are not balanced properly, heart cells may be activated in an illogical order, which will ruin the natural way of regulating the direction of electrical flow. If the flow does not carry on in the right direction, loops will be set off which will reactivate sections of the heart too quickly - leading to a faster heart rate. A similar principle leads to a tachycardia when there is dead heart muscle after a heart attack, or when heart muscle is stretched inappropriately, disrupting the way in which the electrical impulse travels through the heart.
Another important cause of tachycardias is a congenital problem, such as Wolff-Parkinson-White syndrome, where the natural barrier between the atria and the ventricles is disrupted by a channel that allows the electrical impulse through. This disruption to the normal direction of electrical flow can also lead to the production of loops that lead to a faster heart rate.
Working out the rhythm is also quite simple, but you have to be careful. Ultimately the question you are asking is whether or not the QRS complexes are regular. The temptation will always be to just 'eyeball' the ECG and have a guess. You can often see if the rhythm is irregular, but you have to make sure - don't just assume you can work it out 'from a distance'.
The first step is to get an idea of the rhythm by putting a piece of paper over the ECG and mark off every R wave. Then move the piece of paper along the ECG and see if they still line up. If they line up, this means that the distance between each R wave stays the same - in other words, it is a regular rhythm.
If it's not regular, you need to work out if it's regularly irregular, or irregularly irregular. In other words, you want to know if it's following a pattern or not. Even if the distance between R waves changes, is it changing in some kind of logical pattern, or it is just a random sequence? An irregularly irregular heart beat (a random pattern) is usually caused by atrial fibrillation. A regularly irregular heart beat (a regular pattern of changing distances) can be a normal effect of breathing (sinus arrhythmia), or may be a sign of heart block. To work out which, you need a second step.
The second thing you want to do is ask whether or not every QRS complex is associated with a P-wave. If there are QRS complexes without a P-wave before them, then this suggests the ventricles are firing without any control from the sino-atrial node. Rogue ventricles are a dangerous thing, so it's important to recognise this.
One very important rhythm is atrial fibrillation (AF), which gives an irregularly irregular rhythm - that is, a completely random pattern of QRS complexes. What is more, you often can't see any P waves at all. If you can see P waves, they tend to appear as an irregular, fine, bubbling baseline. This appears this way because there is no organised, co-ordinated activity in the atria - they are 'fibillating'. The atrioventricular (AV) node has a rate control on it, so it will only allow some of these impulses through. This leads to an irregular beat.
If there are P waves and QRS complexes but the P wave does not come before the QRS complex in a normal way, this means there is some kind of block between the signal in the atria and the impulse through the ventricles. It is called heart block. It often suggests some kind of damage to the normal conducting system, perhaps because of a heart attack in the past. Heart block can be first degree, second degree or third degree.
In first degree heart block, the PR interval is prolonged; this means it's taking longer for the impulse to get from the atria to the ventricles. In second degree heart block some of the impulses from the atria get through, and others don't. In third degree heart block, there is no relationship between P waves and QRS complexes; they may even happen at the same time, with P waves appearing over QRS complexes. In third degree (or 'complete') heart block, there is a big risk that the ventricles stop beating altogether, and so it is important to sort this out.
The cardiac axis is the main direction of electrical flow. As described in the article on the ECG, the squiggly line which makes up the ECG is squiggly because the direction of electrical flow through the heart changes through the heart beat. However, the flow is predominantly in one main direction - usually from top right to bottom left, or from the sino-atrial node towards the apex (pointy end) of the heart.
The cardiac axis is a way of describing this main direction - and, more usefully, whether or not there is any change or deviation from the norm. If the axis is deviated to the left, it is left axis deviation. If it's deviated to the right, it is right axis deviation.
Understanding how to calculate it requires an understanding of the ECG itself; if the cardiac axis faces the same direction as the leads, the QRS complex in that lead will be mainly positive. If the cardiac axis faces away from the lead, it will be mainly negative. If it is at right angles (or perpendicular) to the lead, it will be neutral.
I remember it simply in terms of the directions the leads face. Remember, aVL looks to the left, aVR looks to the right, and aVF looks to the foot, with Leads I to III looking around in an arc around the apex. So if the cardiac axis moves around to the left, it's going to get more positive in I and aVL, and more negative in III. If it's moving around to the right, it'll get more positive in III, and more negative in I and aVL. Let's work through the examples.
Take for example, a normal cardiac axis. This is where the main direction of the electrical flow is between -30 degrees and +90 degrees, relative to Lead I. This is a pretty broad range, and most of the time the direction should fall between these angles.
This means that the electrical flow is travelling in the same direction as Leads I and II, and usually in the same direction as lead III. All three of these leads are normally positive.
Because the normal cardiac axis includes up to -30 degrees, lead III can have a negative QRS complex. This means a positive QRS in lead I and II and a negative QRS in lead III is still consistent with a normal cardiac axis. However, generally speaking you should see all three of these leads with a QRS in the same upwards direction.
Now let's think about left axis deviation. This is where the main direction of the electrical flow has shifted around to the left, so that it is less than -30 degrees relative to Lead I.
This means that the electrical flow is travelling in the same direction as Lead I, but in the opposite direction to leads II and III. This will lead to a positive QRS in Lead I, but a negative QRS in leads II and III.
If it's deviated to left, it may be that the left ventricle has got larger - so there's more electrical flow on the left, and the main direction of electrical flow is further to the left. Additionally, if part of the left bundle of the electrical system has failed, the electrical wave starts on the right and then has to travel to the left to make up for the part of the system which has failed. This may also lead to a left axis deviation.
Next, right axis deviation. As expected, this is where the direction of flow has shifted around to the right, so that it is more than 90 degrees relative to Lead I.
Since the electrical flow is in the same direction as II and III now, you'll see a positive QRS in these leads. The electrical flow is predominantly away from I, so this will be a predominantly negative QRS.
Right axis deviation may be normal in those who are tall, or who have dextrocardia (where the heart is on the opposite side of the chest to normal; although in this case there would be a large number of other abnormalities confusing the ECG). Deviation to the right can also suggest an enlargement of the right ventricle, or a right bundle branch block, for the same reason that a left-sided equivalent leads to left axis deviation.
In very rare cases, you may see a negative QRS in leads I and II, and a positive one in lead III. This means the axis has shifted completely in the wrong direction, so that it is between -90 degrees and +180 degrees relative to Lead I. This is called extreme (right) axis deviation. The most likely explanation is that there was an error in the placement or connection of the leads.
The P wave is the part of the ECG that gives an indication of the action in the atria. It is a small bump on the baseline that shows when the atria are contracting, and should look like a little bowler hat.
A large P wave can be suggestive of a number of things depending on the way it is enlarged. If it is tall, it may suggest a low potassium level, or a large right atrium. If the left atrium is enlarged, the electrical flow needs to divert for longer through the left atrium as well as the right, leading to a wide or 'bifid' (double) P wave.
A small P wave may be suggestive of a high potassium level in the blood.
As mentioned elsewhere, if the atria are not contracting properly but are instead fibrillating, the P wave will be replaced by a dithering slightly wobbly baseline or no P waves at all. The inaction of the atria is displayed rather well in the absence of a P wave. Occasionally you may find atria which are fluttering, rather than fibrillating; this appears as a 'saw tooth' pattern, almost always at a rate of 300 per minute.
The PR interval is the delay between the depolarisation of the atria and the depolarisation of the ventricles. This gap is created at the atrioventricular (AV) node, because the AV node has a cap on it to prevent electrical signals getting through too quickly. It is an important delay, because it prevents the heart from beating too quickly, and ensures regulated activity.
The PR interval is therefore calculated from the beginning of the P wave until the beginning of the QRS complex. Although we talk about the AV node causing a delay, we're talking in terms of extremely short periods of time - the delay should be less than 200ms or 5 small squares.
If there is damage in the heart, particularly around the AV node, it may cause this delay to get longer. The AV node is stopped from conducting electricity so well, and so the time that it takes to get through this section is increased; the gap between the P wave and the QRS complex is longer, and the PR interval is seen as being greater. This is first degree heart block.
The good thing about first degree heart block is that it is predictable - every P wave is still followed by a QRS complex. The problem comes when the heart block gets worse. Sometimes the damage is less consistent; so the AV node may let half the impulses or a third of the impulses through. Other times, it may be that the PR interval gets longer and longer until eventually no QRS complex follows (and then it starts back at the beginning again); this is called "Wenkebach phenomenon", or Mobitz Type 1 second degree heart block.
If the PR interval is impossible to determine because there is no relationship between P waves and QRS complexes, you have third degree heart block.
The QRS complex is the part of the ECG tracing which shows the electrical activity in the ventricles. The letters come from the series of waves which make it up, each one having a strict definition. The Q wave is the first downward reflection to follow the P wave before the R wave. If there is no downward deflection before the R wave, then there is no Q wave. It is quite normal not to have Q waves. The R wave is the first upward deflection after the P wave, and the S wave is the first downward deflection after the R wave.
If the electricity travels through the ventricles down the normal route - through the specialised cells designed to provide the best conducting system possible - then it will travel through the heart quickly; in other words, the QRS complex will be short. A normal QRS complex is less than 120ms or 3 small squares.
Any lengthening of the QRS complex is important, because it means that the electricity is taking longer to get through the ventricles - in other words, there's something wrong with the normal conducting system. It may be that the impulse for the electrical signal isn't even coming from the sino-atrial node or the AV node; if it comes from something completely outside the normal conducting system, then it won't travel down the normal paths, and the QRS complex will be prolonged. It may also be a completely abnormal shape.
Sometimes an R' wave may be noticed, caused by an upward deflection after the S wave, giving an "M" shape or RSR' pattern; this is caused by a bundle branch block, where one of the bundles coming out of the Bundle of His is broken, leading to the electricity supply having to come from the other half. A bundle branch block is important, especially if it is left-sided, (i.e. the "M" shape happening in the lead V6) because it may be a sign that someone has just had or is having a heart attack.
Q waves should be very small. They can be a little bit bigger in lead III and aVR because these leads are basically pointing at the opposite side of the heart to the normal direction of electrical flow. You may also get 'septal Q waves', caused by depolarisation of the septum, in I, aVL, V5 and V6. However, if they last longer than 40ms (i.e. one small square) in any of the leads except for III and aVR, they are abnormal. They should also be very shallow - less than 25% of the height of the R wave, and less than 1/3 of the height of the total QRS complex.
Big Q waves in the wrong place are called pathological Q waves. They happen when a particular part of the heart has died (infarcted). If the heart cells are completely dead, there is no electrical activity in them, and so they act like a window; instead of seeing the electrical activity in the wall of the heart, the ECG leads will pick up the electrical activity on the opposite side of the heart, traveling in the opposite direction - like a window looking through the heart.
Q waves are a late sign of a heart attack (or 'myocardial infarction'). By this point, the heart tissue has already completely died, and the heart attack itself happened several hours ago. It's better to catch it early - and for that, you're better of looking at the ST segment and T wave.
The ST segment describes the delay between the end of the ventricular depolarisation (the QRS complex) and the beginning of ventricular repolarisation (the T wave). In other words, this is the gap between the electricity moving through the ventricles, and the ventricles returning to a position where they can be activated again. This is a refractory period, where the ventricles won't get set off by further electrical stimulation; it makes sure that the ventricles don't beat too quickly.
So it's pretty boring, right? No. This is a really important part of the ECG. If nothing else, the ECG has been able to provide an incredibly useful way of demonstrating that someone is having a heart attack, and it's all to do with this ST segment. In a normal situation, this ST segment is isoelectric. This means it's level at zero, not positive, not negative.
It can be low or depressed. The major cause may be ischaemia (that is, insufficient blood supply to the heart cells), or even infarction (i.e. the blood supply is so insufficient that the heart cells have died). A low potassium, a large ventricle and excess digoxin can also cause ST depression.
The exact cause of this at the cellular level is debated, but it may actually be that the whole line is shifted upwards because of an elevated resting membrane potential. Ischaemia may inhibit normal potassium channels from opening, which initially leads to a slight rise in the resting membrane potential. The ST segment isn't affected as much by this because the depolarisation of ischaemic heart cells is delayed. Because the baseline 'TQ' segment is raised more than the ST segment, the ST segment looks as though it is depressed. This also explains why a fall in the extracellular potassium concentration may have a similar effect.
The ST segment can also be elevated. This is highly suggestive of infarction - the death of heart cells, especially if it is limited to only certain leads that are pointing at a specific part of the heart. Leads looking at the opposite side of the heart may show what is called a reciprocal change - ST depression. However, if the lining of the heart is inflamed (pericarditis) this can also lead to ST elevation, and will tend to be seen in all of the ECG leads. Furthermore, a swelling of the left ventricle known as a ventricular aneurysm can also lead to a rise in the ST segment.
Again, the reasoning behind ST elevation is not always clear. When heart cells die they leak potassium, which will lead to a fall in the resting membrane potential; as with ST depression, the TQ segment drops further than the ST segment, giving the impression of a rise.
Also, increased leakiness to potassium means that the membranes rapidly repolarise, making them positive relative to the normal healthy heart cells. Extracellular current will flow out of the dead, infarcted area towards the normal area - and, more importantly, towards the leads overlying the dead cells, making the ST segment look more positive.
The T wave is the part of the ECG which shows the repolarisation of the ventricles - that is, it's the part where the ventricles come back into a position where they are no longer refractory - where they can start to accept another electrical impulse. It's the part of the ECG where the ventricles 'return to base', ready to receive their next instructions. It is read as a single bump following the QRS complex.
An inverted T wave is a T wave which is upside down, and which suggests that there's not enough blood getting to that part of the heart (i.e. ischaemia). T waves can be inverted in normal people, and are particularly commonly seen inverted in V1, and occasionally in V2 (especially in the very young). You may also see it inverted in III, aVL or aVF. The T wave should normally be negative in aVR; a positive T wave in aVR is strictly speaking an inverted T wave.
A flattened T wave can also suggest ischaemia, or imply a low potassium level.
A tall, 'tented' T-wave suggests that the potassium level is high, although a large T wave with a wide base and a steeper down-slope may be found with ST elevation in a heart attack and is known as a hyperacute T wave.
The QT interval is everything which happens after the start of the Q wave before the end of the T wave. It is the period of time in the ECG that something is happening in the ventricles - and it's important, because it gives an indication of how long it's going to be before the next ventricular depolarisation (and consequently, before the next heartbeat) can occur.
The QT interval changes depending on how quickly the heart is beating - the quicker it is beating, the less time the ventricles have got before they need to be in action again. Consequently, there is no 'normal value' for the QT interval. However, the QT interval can be corrected or adjusted to consider the rate at which the heart is beating, and then compared against the 'normal'. A corrected QT interval (QTc) should be up to 440 millisec.
The QT interval can be corrected using a number of formulas. Traditionally Bazett's formula is used, although it over-corrects for high heart rates and under-corrects for low heart rates. For the sake of simplicity and tradition it continues to be used. The QTc is calculated as the QT interval (in milliseconds), divided by the square root of the RR interval (in seconds). The RR interval is the time between each R wave (i.e. between each heart beat), and can be worked out by dividing 60 by the heart rate.
L. S. Fridericia and a team under A. Sagie have each produced lesser-used alternatives for correcting the QT interval, which are beyond the scope of this article.
A prolonged QT can be from birth - 'long QT syndrome'. It can also be the result of drugs, including antipsychotics like haloperidol, or many drugs and alcohol when taken in overdose. Some antiarrhythmic drugs work deliberately to lengthen the QT interval. Hypothyroidism and a low level of calcium in the blood can also cause the QT interval to lengthen.
A short QT can also be from birth - 'short QT syndrome' - or because of high levels of calcium in the blood. A short QT is less common than a long QT, and arguably less concerning, but short QT syndrome is associated with sudden cardiac death - so not to be ignored!