The following is a basic primer in interpretation of the ECG (EKG). It is intended solely for teaching purposes, and should not be relied upon in clinical decision making.

ECGs can be very confusing, and there are dozens of different methods of interpretation. It's perhaps best if everyone works out their own individual approach, but here's just one approach you can build upon:

2. Go through the ECG systematically;
3. Correlate ECG and clinical findings,
and if necessary, go back and do a

Of the above steps, the fourth seems counter-intuitive and unnecessary. In fact, it's the most important. As in all medicine, complacence is dangerous. Avoid it!

2.What is therate?
3.Is this sinus rhythm? If not, what is going on?
4.What is the mean frontal plane QRS axis (You may wish at

5.Are the P waves normal (Good places to look are II and V1)
6.What is the PR interval?
7.Are the QRS complexes normal? Specifically, are there:

osignificant Q waves?
ovoltage criteria for LV hypertrophy?
opredominant R waves in V1?
owidened QRS complexes?

Before we move through the systematic approach outlined above, we will outline a few basics. More advanced readers may wish toskip these basics, and move on to the systematic part of the tutorial.

When cell membranes in the heart depolarise, voltages change and currents flow. Because a human can be regarded as a bag of salt water (with baad attitude), in other words, a volume conductor, changes in potential are transmitted throughout the body, and can be measured. When the heart depolarises, it's convenient (and fairly accurate) to represent the electrical activity as adipole --- a vector between two point charges. Remember that a vector has both a size (magnitude), and adirection. By looking at how the potential varies around the volume conductor, one can get an idea of the direction of the vector. This applies to all intra-cardiac events, so we can talk about a vector (or axis) for P waves, the QRS complex, T waves, and so on.

In the above picture, the schematic ECG lead on the right `sees' the (red) vector moving towards it, shown as a positive deflection in the ECG trace; the lead at 90 degrees to this sees nothing!

We assume some knowledge of heart anatomy. Note that the normal heart has, electrically speaking, only two chambers, an atrial and a ventricular `chamber'. Propagation of electrical activity spreads freely within atria and ventricles, but communicationbetween these two chambers is limited to the AV node. Everyone knows that the P wave corresponds to atrial depolarisation, the QRS complex to ventricular depolarisation, and the T wave to repolarisation of the ventricle.

In order to be able to record myocardial activity, the electrocardiograph needs to be able to detect tiny changes in potential on the body surface. We are talking about signals that are often around 1mV, and may be smaller. In addition, we need some reference point to which we relate the potential changes.

Bipolar leads: the reference point is on one limb, the
`sensing' electrode (if you wish) is on another limb. The
leads are termed I, II, and III.

Unipolar leads: The reference point is several leads joined together, and the sensing lead is on one limb. These leads are conventionallyaugmented, in that the reference lead on the limb being sensed is disconnected from the other two.