A simple view of the electrocardiogram (ECG)
This Post should be taken together with the Post entitled:
"The epidemic of coronary heart disease – the peak in 1967–70”.
This Post should be taken together with the Post entitled:
"The epidemic of coronary heart disease – the peak in 1967–70”.
We have all heard of the ECG, and today everyone will have seen
There is no necessity to go into details and I will indicate only the basic features. The reason for doing this is that many of my Posts have been on the subject of coronary heart disease (CHD), the major clinical consequence of which is myocardial infarction (MI), loosely called a heart attack. The ECG is a major defining feature of the MI. A Post on this subject will appear shortly and so I have written this Post on the ECG in anticipation. To include clinical MI details and details of the ECG in a single Post would be cumbersome.
The normal ECG
The standard ECG has 12 simultaneous recordings taken from nine leads, each looking at the heart from a different direction and therefore able to detect abnormalities in different parts of the heart. I will not go into any detail, about these 12 recordings.
The normal ECG shows three components:
- the “P” wave results from contraction (electrical depolarisation) of the atriums (atria);
- the “QRS” complex results from contraction (electrical depolarisation) of the ventricles;
- the “T wave” results from recovery (electrical repolarisation) of the ventricles.
The QRS complex has three components, Q,R and S.
- Q is an initial downward (negative) deflection of the recording. This does not occur in the normal ECG, except certain leads that need not concern us. It appearance usually indicates serious damage.
- R is an upward (positive) deflection. it is usually the initial part of what is effectively an RS complex. It can however follow an initial Q wave.
- S is a downward (negative) deflection that follows an R wave. It is not always present.
It might be asked as to why the nomenclature of the waves is in the form of the letters “P….T”. The answer lies in the history of the electrical recording of the heart.
There is no necessity to go into the structure of the heart in detail, just a reminder of the circulation sequence of right atrium, right ventricle, pulmonary artery and circulation through the lungs, then left atrium, left ventricle and aorta leading into systemic circulation.
The relaxation phase of the ventricles (diastole) sucks blood into the right and left sides of the heart, and then the early contraction of the atriums (the P wave) completes the filling of the ventricles with a final “push”. The contraction of the ventricles follows (systole) with ejection of blood into the pulmonary and systemic circulations.
The heart has a natural pacemaker to control its rate to to stimulate an orderly contraction. It is called the sino-atrial (SA) node and it is situated in the right atrium, at the point of entry of the major veins, the superior and inferior vena cava.
|Electrical conducting tissue of the heart
|Spread of electrical impulse within the heart
The electrical impulse that stimulates contraction of the heart muscle starts in the upper part of the right atrium and spreads across both atriums. It is picked by a secondary pacemaker, the atrioventricular (AV) node, which is situated it the junction of the atriums and the ventricles. This passes the signal though two bundles of conductive tissue, one in the wall of each ventricle. These stimulate an orderly contraction of the ventricles.
How the heart works
During the 1780s Luigi Galvani (1737–1798) at the University of Bologna, followed by Alessandro Volta (1745–1827) discovered that muscles contract (twitch) in response to electrical stimulation, the “frog legs experiments”. The interaction between electricity and muscles was far from clear, but during the following century it gradually became more clear.
In the 1880s it was realised that the heart muscle, like skeletal muscle, worked by electro-chemical processes. Chemical reactions created an electric potential (like in a battery) and sudden release of that electric potential (depolarisation) enabled immediate muscle activity, that is contraction as that is what muscle do. Following this muscle action the chemical process would re-charge the electric potential within the cells of the heart muscle, the process of repolarisation).
We can see this in the ECG: the first thing that happens is the P wave. This is a recording of the electrical depolarisation of the atriums (preferred international English, otherwise atria). The muscle bulk of the atriums is low and so the P wave is of very small amplitude. There is no visible wave produced by the repolaristion of the atriums as it coincides with the QRS complex that represents the depolarisation of the ventricles.
The QRS complex is followed after a brief delay (technically the Q-T interval) by the T wave, representing the repolarisation of the ventricles. There is then a rest until the next heart beat, the next P wave.
The depolarisation of the ventricles leads their immediate contraction and thus the blood within the ventricles is ejected into circulation, from the right ventricle into the pulmonary artery and thus through the lungs, and from the left ventricle into the aorta. The muscle of the left ventricle is of much greater thickness than the right (the blood must be propelled a much greater distance and against a much greater pressure) and its depolarisation makes the dominant contribution to the QRS complex.
The history of the ECG
The slow advances during the 19th century of the understanding of the physiology, the functioning, of the heart led to some practical albeit rudimentary developments. The British physiologist Augustus Waller (1856–1922) was a lecturer at St Mary’s Hospital, London. In 1870 he invented a device for recording the electric activity of the heart. He used “A,B,C….” to identify the recorded phases of the heart beat. He used a capillary tube filled with mercury to identify the electrical impulse of the heart, a change in height of the mercury column allowing a pattern to be observed.
In 1902, the Dutch physiologist Willem Einthoven constructed a different type of machine, a string galvanometer, which was very cumbersome and required five men to operate it. When it came to a side-by-side assessment of the two machines, the wave-forms on Einthoven’s ECG were given the symbols “P,Q,R,S,T”. Despite being of no practical value in respect of patient care (remember that Einthoven was a physiologist and not a clinical cardiologist) it proved to be a superior method of recording heart activity and its nomenclature has persisted. It was about 15 years later that the ECG came into clinical use, and the machines have become much smaller over years.
|Einthoven's ECG machine, 1902
The use of the ECG
Early concerns were of the functioning of the heart, and they were purely academic studies. Coronary heart disease (CHD) and myocardial infarction (MI) were almost completely unknown at the time of Waller and Einthoven.
Earlier, before his fame and knighthood, Sir James Mackenzie (1853–1925), the father of English cardiology, was working in Burnley, Lancashire, and at its hospital (where I worked). He invented a mechanical “polygraph”, a device that recorded the rhythm of the heart.
|Sir James Mackenzie
The subsequent electrical recordings were superior but it was only the rhythm of the heart that was of clinical importance.
Abnormalities of heart rhythm
The most well-recognised abnormality of rhythm is atrial fibrillation AF). The characteristic of this is a complete irregularity of the pulse, which might become very fast. If this is the case then the pulse will also be low in volume. The output from the heart (cardiac output) is low because the filling phase of the heart (diastole) is too short to allow the ventricles to fill adequately with blood. Also the final push of filling, atrial contraction, is absent.
Atrial fibrillation is a failure of the atriums to contract properly because they are “fibrillating”, that is very rapid unco-ordinated contraction of individual muscle fibres (cells). There are no P waves. The spread of the electrical impulse from the SA node into the atriums is impaired. The response of the ventricles via the AV node is haphazard, and so the ECG shows an irregularity of the QRS complexes.
|ECG: atrial fibrillation
It was for the treatment of atrial fibrillation that Digitalis was introduced by the Birmingham-based botanist and physician William Withering (1741–1799). This treatment was an extract of the plant Digitalis purpurea (common foxglove) and was based on a folk medicine for the treatment of “dropsy”, this being oedema or swelling of the legs due to heart failure, atrial fibrillation often being associated.
Also common are ventricular ectopic beats, that all people might experience as a “missed beat”. They are only very rarely of importance. A ventricular ectopic beat occurs spontaneously, not triggered by or following an atrial beat. The ECG will show a QRS complex, out of sequence with the others and not preceded by a P wave. The QRS complex is likely to be a different appearance depending on the part of the ventricle from which it originated.
|ECG: 2 ventricular ectopic beats
The atrial beats and ventricular beats can become disconnected, and this is called “heart block”. The P waves will be present and also the QRS complexes, but the sequence of them is random. The AV node is not picking up or transmitting the stimulus from the atriums. The ventricles will develop their own rhythm, but the rate becomes very slow. This causes problems such as blackouts, and an implanted artificial pacemaker is necessary to speed up the heart.
|ECG: complete heart block, dissociation of P waves and QRS complexes
Finally for our purposes there is ventricular fibrillation (VF). The ventricles just fibrillate like jelly wobbling. There is no actual contraction of the heart and this is what happens in a “cardiac arrest”.
|ECG: ventricular fibrillation
The ECG in CHD and MI
It was only in the 1920s that the ECG was used in the diagnosis of MI as it was only in that decade that the disease appeared.
The ECG recorded from an individual tells us of events that have happened in the past - ten seconds ago or ten years ago. There is no prediction of the future.
Similarly there is no feature of CHD as such. CHD is a disease (atherosclerosis) that takes place in the arteries on the surface of the heart. The ECG tells us about damage to the heart muscle and the conducting tissue within the muscle.
Only when something is happening either now or in the past does the ECG become abnormal. Someone can have a normal ECG today but develop an MI tomorrow. We cannot predict future health from an ECG. There is no reassurance value from a “routine” ECG performed at a time of good health.
The detection of MI is the main use of the ECG, after identification of rhythm disturbances. It is quite simple and there are two specific changes.
A Q wave might appear, and this indicates major damage to the heart muscle. It is a permanent abnormality and remains as a historical marker of an MI in the past. When a Q wave is seen it cannot be concluded that an MI has just occurred. This would only be the case if it was not present on a previous ECG, or after other tests have been performed. A Q wave resulting from MI is often followed in the long term by an inverted T wave.
|ECG: Q wave followed by inverted T wave
ST segment elevation after an MI is a temporary abnormality at the time of the event. If the ECG is delayed after the development of chest pain, the ST elevation might be missed, having resolved rapidly.
|ECG: ST segment elevation, also small Q waves
When the Q wave is associated with ST segment elevation the diagnosis of an acute MI is clear. This is a "STEMI", ST Elevation MI.
|ECG: small Q wave with high ST segment elevation
The ECG in angina
Angina used to be a disabling but not fatal result of CHD. It is recurrent chest pain occurring on exercise, due to a narrowing of a coronary artery. The ECG at rest is normal, but on exercise ST segment elevation might occur (the exercise ECG). There can rarely be transient elevation of the ST segment at the time of a severe attack of angina.
I hope that this brief review of the ECG is informative but not incomprehensible.