The heart normally contracts at a regular rhythm and the rate varies according to age and state of physical activity. Irregularity of rhythm or heart-rate too fast or too slow beyond physiological range is called cardiac arrhythmia or dysrhythmia. The muscular contraction of the heart is initiated by electrical impulses spontaneously generated by a specialised group of cells situated in the sino-atrial node (SA node).
Impulses generated at SA node are transmitted through the auricular wall to the bundle of His, which consists of A V node and its branches. The right bundle divides into branches in the wall of right ventricle while the left bundle divides into two fascicles anterior and posterior and then branches in the left ventricular wall. The terminal branches of the bundle of His are called Purkinje fibres. More recent researches show that the intraventricular conduction system is more complex.
The right bundle branch is more or less a continuation of bundle of His, entering right ventricle. The left branch actually divides into three fascicles in most people — anterior, posterior and anteroseptal. There is intricate intercommunication between anterior and posterior divisions. Autonomic-impulse-forming-tissue is present in SA node, coronary sinus. His-Purkinje system and in the A.V. node. This area of SA node and the top of bundle of His is called junctional tissue.
The S.A. node is controlled by both sympathetic and parasympathetic nerves; hence its impulse formation is under nervous influence. But autonomic nervous control of A.V. node is not so well marked. It is also thought that A.V. junction may have two separate pathways of conduction, one being faster route and the other slower (Marriot). This may explain re-entry phenomenon.
If sinus node (SA node) fails to generate impulses, the cells of A.V. node and bundle of His can generate impulses but at a slower rate.
Normally depolarization starts at the SA node and the impulse travels through the auricular walls towards auriculo-ventricular junction. This is the ‘P’ wave of the ECG. As SA node is the master-controller of cardiac rhythm, normal rhythm is known as sinus rhythm.
Each P wave is followed by the PR interval, i.e. the time taken for the impulse before ventricles receive the order to contract and at the end of PR interval ‘QRS’ wave form is depicted denoting electrical activity of the ventricles.
It is sometimes seen that the heart rate is increased during inspiration, while decreased during expiration. This is due to vagal effect and this periodic change of rate and rhythm is called sinus arrhythmia. The normal rate of impulse formation of SA node is 60 to 80 per minute in adults while the A.V. node can beat only at slower rate of about 50 per minute. So the AV node can only originate a beat when SA node is silent. If AV node is silent ventricular conducting cells can beat only at 30 to 40 per minute.
Sinus Tachycardia:
Tachycardia means rapid heart action. Normal heart rate at birth varies from 120 to 140 per minute. As the age advances heart rate goes on diminishing and is between 70 and 80 per minute by the age of 18. In adults, the rate may be as low as 60 per minute especially in atheletes, while in adults, pulse rate more than 90 per minute is abnormal.
Underlying causes of tachycardia are emotional outburst, anxiety, fever, thyrotoxicosis, carditis, heart failure, constrictive pericarditis, large haemorrhage and shock. Sympathomimetic drags or any disorder stimulating sympathetic nervous system will cause sinus tachycardia. Rapid heart rate may be observed in otherwise normal ECG and should be interpreted against clinical background. Whenever a patient complains of palpitation, aetiological basis should be searched for carefully.
Sinus Bradycardia:
Bradycardia or slow heart rate by itself is not abnormal. It is due to increased vagal tone. Healthy adults (especially atheletes) may have a slow heart rate but usually not less than 60 per minute. Slow heart rate may also be due to jaundice, myxoedema, raised intracranial pressure and cardiac depressant drugs, e.g. digitalis, quinidine, verapamil, lidocaine, β-receptor blockers e.g. propranolol, also phenylamine lactate.
If heart rate falls below 60 per minute careful evaluation is indicated especially to exclude heart block. Slow heart rate is either due to sinus bradycardia or heart block.
Re-Entry:
This is a phenomenon which can occur in the heart muscle if conduction of some part is depressed than the remaining portion. Normally, wave of depolarization spreads equally in the muscle wall but if one region becomes transiently less conductive, a normal impulse already travelling the normal part (non-depressed area) of the myocardium can pass in a retrograde manner This may lead to abnormal rhythm, due to passage of the impulse going round and round.
The re-entry phenomenon may cause tachycardias of atrial, AV nodal and ventricular origin. An excellent account of this subject is given in Marriot’s Practical Electrocardiography.
Sinus Arrhythmia:
As we know inspiratory quickening of heart rate and expiratory slowing is called sinus arrhythmia. This is due to changing vagal tone. Sinus arrhythmia can be exaggerated by drugs which increase vagal tone e.g. digitalis. It can be abolished by exercise or atropine. Sinus arrhythmia is often noted in children and adolescents and is otherwise normal. It is related to rhythmic variations associated with impulse formation at the respiratory centre.
Ectopic Rhythms:
Cardiac impulse normally originates in the SA node but when it arises elsewhere in the myocardium, it is called ectopic rhythm. Ectopic focus may be in atrial, junctional or ventricular tissue. Broadly speaking, if the focus is above the ventricles, it is supraventricular and if it is in the ventricle it is ventricular.
Supraventricular arrhythmias are atrial fibrillation, atrial flutter, atrial or nodal tachycardias. Extrasystoles or premature beats may originate from atria, A.V. node or the ventricles. The intricate path of transmission of cardiac impulse from SA node to AV node still remains controversial.
As ectopic beats are premature, the interval between ectopic beat and preceding normal beat (coupling interval) is shorter than the interval between any two normal beats.
This fact is most important in management because treatment to control the ectopic beats may be desirable, while suppression of escape beats and beats due to intermittent BBB may be dangerous. Remember all beats with abnormal configuration are not to be designated as ectopic bests.
The origin of ectopic beats is not always easy to determine and not only long strips of ECG recording is required but also it may be necessary to record simultaneous records of two leads.
Atrial Extrasystole (Ectopics):
The focus of extrasystoles (ES) or premature beats may be in the auricular wall or AV node An ectopic beat is a premature beat and as a result the next regular sinus impulse is delayed The ectopic beat is felt earlier at the wrist (or may not be felt at all if the ventricular contraction is weak) and the next beat is delayed.
ECG will show deformed or inverted P but QRS is normal in shape and direction but the PQRST complex occurs early and there is a pause till next normal beat, which is not fully compensatory. The distance between the two normal sinus beats is actually less than two cycles.
In auricular or nodal ES, QRS complex may not be normal, looking if there is bundle branch block.
If the atrial ectopic beat occurs too early it may get blocked either at AV node or in bundle branch (still remaining refractory) leading to prolonged PR interval and atrial ectopic beat This may appear in ECG as partial or complete BBB (functional partial or complete RBB) As the resulting QRS complexes are broad, this can be mistaken for ventricular ectopic beat.
Atrial ectopics can occur in healthy young people and are then benign but they may occur in all Kinds of heart disease as well as during anaesthesia or after cardiac surgery.
Treatment depends on the cause.
Nodal Extrasystole (AV Junctional Beats):
The impulse may originate from the AV node or bundle of His. This is called nodal extrasystole. The impulse spreads upwards in the atria (retrograde) and downwards (antegrade) in the ventricles The QRS complex is normal and is supraventricular type.
The timing of P wave is uncertain, its configuration is abnormal. It may precede or may merge, with, or follow, QRS complex. Discharge of sinus node again does not allow full compensatory pause. Cardiac muscles being inherently irritable subnormal cardiac impulses are created due to undue excitation.
Ventricular Premature Beats or Extrasystole (VPB):
(Ventricular ectopic beats)
VPB may arise from either of the two ventricles, the QRS complex is wide and T-wave is in opposite direction of major component of QRS complex. The subsequent normal impulse reaches ventricular muscle in its refractory pause and does not result in a contraction.
So there is compensatory pause after the ventricular extrasystole. The total duration between the previous and the subsequent normal beat is equal to two beats. Extrasystoles may be unifocal or multifocal the unifocal beats are similar in appearance while multifocal beats are different m contour and coupling intervals.
If ventricular extrasystole occurs earlier in diastole, the next normal impulse may produce a contraction which is interpolated between two normal beats. Extrasystoles may produce coupling of beats, known as pulsus bigeminus.
When ventricular ectopics occur too early in the cardiac cycle, it may almost come nearest to T-wave and this is called ‘R on T’ ventricular ectopics. In these situations sudden ventricular tachycardia or ventricular fibrillation may be precipitated, hence requires close watch and treatment.
Similarly late ventricular ectopics may occur immediately following normal wave and therefore the normal impulse depicting the normal P wave will not be able to initiate a normal QRS. The ectopic ventricular beat may also have a slurred up-stroke, hence may be mistaken for a delta wave of .Wolff-Parkinson-White syndrome.
Parasystole:
In this type the ectopic, ventricular focus discharges in between two normal beats without disturbing the normal sinus rhythm. Occasionally ventricles may be simultaneously activated by both ectopic and normal impulses, and then the resulting beat is a fusion beat.
U-wave in ECG represents supranormal recovery phase. Subthreshold stimuli can activate /ventricles during this phase. Any stimulus can form parallel pacemaker competing for control. This phenomenon is known as parasystole. Sinus impulse and parasystolic impulse may overlap to produce a fusion beat. Though prognosis is not bad, parasystole may mask underlying ventricular tachycardia. Parasystolic rhythm, more often than not, is unresponsive to anti-arrhythmic therapy.
Aetiology of Extrasystoles:
Though it may occur in healthy individuals, these may be associated with myocardial disease. Tea, coffee and tobacco in excess may be responsible. In elderly people these should be more seriously considered especially when they are frequent. They arise from many sites i.e. when they are multifocal; they are pathognomonic of myocardial disease, and/or digitalis toxicity. In patients of I.H.D. occurrence of frequent E.S. often heralds an impending infarction, though some cardiologists do not agree to this view.
Clinical Features:
Ectopic beats are sometimes forceful and the patient complains of palpitations and becomes apprehensive. Increased volume of post-extrasystolic normal beat may be felt as a thrust. Sometimes anxious patient becomes panicky. Flutterring sensation occurs due to irregularity. Patient may also have a sinking feeling.
Treatment:
Infrequent extrasystoles require no therapy especially in the young. The background is important. If there is no adverse history and clinical findings are normal, reassuring the patient usually suffices. Aggravating factors like excessive tea, coffee, alcohol, tobacco should be banned. However, when they are associated with some cardiac pathology or digitalis intoxication, they will need proper treatment.
Injudicious use of drugs may be more harmful. Most drugs often used indiscriminately have some side-effects. In young people without heart disease, remove possible exciting factors and keep watch.
When there is a background myocardial disease, close watch is more important. Ventricular E.S., coupled beats, multifocal E.S and unusual premature beats (so called R on T-wave) are more serious. In olden day’s quinidine used to be given to suppress these EB’s but suppression serves no useful purpose. Now we have newer drugs but none of them are free from side-effects.
Beta-adrenergic agents may be used carefully orally but are contraindicated in heart failure, bronchial asthma, diabetes mellitus and peripheral vascular disorders.
Disopyramide orally in dosage of 100 to 150 mg 3 to 4 times daily may be useful. The side-effects are anticholinergic in type e.g. dry mouth, urinary retention (in elderly) and dangerous in presence of glaucoma.