Understanding ECGs: Minding your Ps and Qs

In the second article in our series Dominic Cox and Hamish Dougall discuss what you need to learn and what you need to understand

In this series of articles on electrocardiograms (ECGs) we hope to convey the basic concepts of reading and using this simple clinical tool. We re-emphasise that a grasp of only a few rudimentary concepts will allow all of us, not just the cardiologists, to understand the majority of clinically important ECGs. In the first article we explained how the heart works as an engine and outlined the power supply (coronary arteries), control (electrical supply), and how that in an ECG, the electrical supply is recorded as it moves across the heart by a series of detectors placed strategically around the body.

An ECG is a two dimensional recording of a three dimensional process. A cardiac electrical impulse does not travel in a single direction down a straight line with an arrow on the end. It in fact spreads out in all directions across the heart. The ECG leads allow us to look at this depolarisation wave from different views--that is, in the vertical and horizontal planes. When the wave is heading towards a specific lead we will get the largest positive deflection in that lead. When it is heading directly away from it we will get the opposite: the largest negative response. Leads looking at right angles to the wave front will see smaller biphasic responses as the wave passes them. In this article we will go through the different parts that make up the ECG recording (see figure 1) in turn. We appreciate that the material in this, and the previous, article may seem a little dry. It is, however, worth trying to grasp the basic concepts without getting bogged down too much in the numbers or fancy syndrome names. Once you understand the basics you can always look these up when you need that information. It would certainly be worth having our first two articles to hand as you read the subsequent articles in this series, which will be much more clinically, and case study oriented.

The P-wave
This is a recording of atrial depolarisation. Most of the time this starts in the sinoatrial (SA) node and the predominant direction of the impulse across the atria is inferiorly and from right to left. This generates a positive deflection in the leads that look at the heart from below. (See figure 2.) As five of the six chest leads are mostly on the left side of the body and in approximately the same vertical plane there will generally not be much difference in the P-wave in these leads with small positive deflections seen in each. Lead V1 looks across the atria and sees the atrial depolarisation pass across its view. Thus the P-wave typically has a biphasic waveform in this particular lead. As we have said before, the chest leads are not good at looking at vertical movement. As one of the predominant movements of this depolarisation is downwards (inferiorly), then the chest leads do not detect this well, apart from lead V1 with its different view on the heart.

Occasionally, if there is damage to the SA node, the initiation of the electrical activity can arise from other parts of the atria. If this is lower down in the atria the impulse has to move in the opposite direction to normal. In these circumstances P-wave deflections are in the opposite direction. (See figure 3.) We point this out, not because it is common or particularly important, but because it is a simple example of seeing what the different leads record in changing circumstances.

The P-wave can be thought to have two components. The first half of the P-wave is made mainly by the right atrium. The second half comes from the left atrium. The best two leads to examine the P-wave are leads II and V1 as they look at the atria in opposite directions. These two leads are typically used as rhythm strips as they emphasis the P-wave. (Lead II looks along the axis of the atria, and V1 looks across the atria.) Disease processes that cause strain on the right atrium cause a typical enlargement of the first half of the P-wave. This gives a taller, peaked P-wave. Lung disease could lead to right atrial strain and thus this tall P-wave is known as P pulmonale. Enlargement of the left atrium causes exaggeration of second part of the P-wave. This leads to the typical bifid "m" shape in lead II, and larger negative deflection in second part of the P-wave in lead V1. This is called P mitrale. (See figure 4.)

The PR interval

The PR interval starts from the beginning of the P-wave (SA node depolarisation), and includes the whole P-wave--that is, the whole of atrial depolarisation. There is then a flat segment as depolarisation reaches the AV node and there is an electrical interlude. The AV node delays conduction of the electrical impulse long enough so that the ventricles are filled by atrial contraction before they themselves contract. The PR interval ends as ventricular depolarisation begins (the start of the QRS complex). Thus disease of the sinus node, atrial tissues, or AV node could affect the formation and passage of electricity prior to ventricular contraction, and can thus be seen as affecting the PR interval.

QRS-wave
After traversing the AV node, the impulse reaches the Bundle of His and thus its right and left bundle branches which rapidly conduct it to the ventricular myocardium through the Purkinje fibres. (See figure 5.) The QRS complex represents ventricular contraction. Were the ventricles to be the same size as the atria and without a specialised path of conduction then the QRS complex would look similar to a P-wave. However because their size and relative bulk is much greater, and life is just not that simple, a specialised conduction system is required to ensure the ventricular muscle all contracts in a synchronous, rapid, and efficient manner. It is in fact quite remarkable that the whole of activation of the ventricle is so rapid, being as quick as the much smaller atria. This rapid activation of such a bulk of muscle creates a large spiked complex. A typical QRS complex is shown in figure 1. Remember, as with the P-wave the complex looks different depending on where it is being recorded from. (See figure 6.)

QRS complexes are not always so narrow. We will look at this again in future articles when we discuss right and left bundle branch blocks, pacemaker complexes, and broad complex tachycardias. This may sound ominous at the moment but from the work covered in these first two articles you will be able to work out yourself very simply what you would expect to see in an ECG tracing in these different situations.

There is a fair amount of muscle in the interventricular septum. This is, of course, the first bit of the ventricle to be depolarised. Activation actually starts at the left side of the interventricular septum and crosses to the right. (See figure 7.) The wave of depolarisation then spreads down the septum to the apex of the heart. It returns along the outer ventricular walls towards the AV groove. From the arrow you can see that the initial movement is from left to right across the septum.

We have already said that speed and mass of the left ventricular activation predominates the major deflection seen in the QRS complex. The mean QRS "axis" describes the average direction of the various electrical forces that develop during ventricular activation, and is of course impelled by left ventricular energy. This axis is described in the standard vertical plane. Similar to the direction shown for the P-wave in figure 2, figure 8 illustrates that the normal average direction of the QRS lies between aVL (-30⁰) and aVF (+120⁰). Thus lead II will have a large positive QRS. Lead aVR will see the wave going directly away from it--a maximal negative deflection. aVL is perpendicular to this wave front and thus has a smaller biphasic QRS.

Lastly, Q-waves in the wrong place can be a sign of previous myocardial damage--for example, after a myocardial infarction. However, as we have seen you would normally expect to see an initial negative deflection in certain leads. Where this deflection is greater than that outlined above, the Q-waves are defined as pathological--meaning suggestive of a disease process.

T-waves
This wave represents repolarisation of the ventricles. The returning to normal of the ventricle after depolarisation. (Note: the wave that would represent atrial repolarisation occurs during the QRS complex and is therefore not seen.) It is normally positive in I, II, V4-6 (see figure 9). The T- wave and the ST segment are the most sensitive areas of the ECG in terms of looking at disease processes affecting the ventricle. Unfortunately, the changes are not always specific to a single disease. But there are certain patterns which we can recognise. There is no strict criteria for the size of the T-wave. Generally the tallest precordial T-waves are found in V3 or V4 and the smallest in V1 and V2. As a general rule the T-wave should not be less than one eighth and not more than two thirds of the height of the preceding R- wave in each of the leads V3-6. It is peaked in hyperkalaemia (high potassium) and flattened in hypokalaemia (low potassium).

The ST segment
The ST segment lies between the QRS and the T-wave. The normal ST segments do not deviate above or below the isoelectric line (see figure 1) by more than 1 mm. Again we will return to this in future articles as this is one of the disease sensitive areas of the ECG.

QT interval
This is measured from the start of the QRS to the end of the T-wave. The length of this varies with rate. Prolongation of this parameter can be an inherited condition --for example, Romano-Ward and Jervell-Lange-Nielsen syndromes--or acquired--for example, secondary to drugs, toxins, and electrolyte disturbances. These conditions are rare but their significance is that they predispose such patients to potentially serious ventricular arrhythmias. We should emphasise that these conditions are rare and a description is included in this article only for completeness.

The information we have discussed in this article is a mixture of some things you just have to remember such as the names of the waves on the ECG, and some things you have to understand, such as the way in which electricity moves in the heart and creates either an upward or downward deflection on the ECG. A little time spent understanding these concepts is the key to understanding the whole ECG. The ECG in the disease state does become a matter of pattern recognition. Grasping the fundamentals in these first two articles is the code to comprehending all ECGs. This now completes our jaunt through the basics of the ECG. In subsequent articles we look at ECGs in clinical settings.

Dominic Cox, specialist registrar in cardiology, Newcastle upon Tyne

Hamish Dougall, general practitioner and research fellow in general practice, University of Dundee


studentBMJ 2001;09:357-398 October ISSN 0966-6494