Cardiac arrhythmias. Classification. Extrasystoly. Paroxismal tachycardia. Heart blocks. Atrial fibrillation. Ethiology. Pathogenesis. Clinical pattern of an attack. ECG signs. Cardiac rrhythm disorders dangerous for patient’s life. Principles of treatment and prophylaxis
Arrhythmias
Any deviations from the normal rhythm of the heart are called arrhythmias. These imply alterations in the heart rate, in succession or force of heart contractions, and also changes in the sequence of excitation and contraction of the atria and ventricles. Most arrhythmias are connected with functional changes or anatomical affections of the heart’s conduction system.
Under normal conditions, the sino-atrial node has the highest automaticity . therefore it is the pacemaker of the cardiac rhythm. Impulses are generated in the sino-atrial node at regular intervals (from 60 to 70 beats per min). The impulses are transmitted from sinus node (Wenckebach, Bachman, Thorel bundles) to the atrioventricular node at 0.8-1 m/s. This rate sharply decreases in the region of the atrioventricular node and the atrial systole therefore ends earlier than the excitation spreads over onto the miocardium of the ventricles to cause their contraction. Impulses are trasmitted from the aitrioventricular node through the His bundle at a higher rate (1—1.5 m/s), while the rate of its propagation in Purkinje’s fibres is as high as 3-4 m/s. Excitation is the triggering mechanism for the heart contraction. During the heart contraction, and immediately after systole, its discharges and is absolutely refractory; then its excitability gradually restores.
Automaticity is characteristic of the entire conduction system of the heart, but iormal conditions it is inhibited by the high activity of the sino-atrial node, which is the automaticity centre of the first order. If the sino-atrial node is affected, or the transmission of excitation is impared, the atrioventricular node becomes the pacemaker of the second-order i.e. automaticity centre. Impulses are generated here at a rate of 40 to 50 per the His bundle is affected, the impulses causing contraction of the heart may be genn the Purkinje fibres (automaticity centre of the third order), but the rate of the cardiac then slows down to 20-30 beats per min.
The normal cardiac rhythm may change (1) in affected automaticity of the sino-atrial node, when the rate or sequence of impulses is altered; (2) in development of a focus of increased activity in the myocardium, which generates impulses to initiate heart contractions apart from their generation in the sino-atrial node (ectopic arrhythmia); (3) in disordered conduction of the impulses from the atria to the ventricles or inside the venitricules themselves. Abnormal rhythm can also be due to impaired contractility of the myocardium. Arrhythmia can sometimes depend on changes in such functions of the heart such as automaticity, excitability, conduct i contractility.
Arrhythmias associated with altered automaticity of the sino-atrial node (sinus arrhythmia). When automaticity of the sino-atrial node is upset, the rate of impulse generation may either accelerate (sinus tachycardia) or slow down (sinus bradycardia), or the sequence of impulses may be changed with their generation at irregular intervals (sinus arrhythnia).
Sinus tachycardia is directly connected with effects of biologically active substances which increase excitability of the sino-atrial node. This phenomenon may also depend on the change in the tone of the vegitative nervous system. It develops with intensified effect of the sympathetic nervous system. The rate of cardiac contractions in sinus tachycardia varies from 90 to 120 and sometimes to 150—160 per min. Sinus tachvcardia develops during meals, physical exertion and emotional stress, elevated body temperature, the heart rate increases by 8—10 per each degree over
The clinical signs of sinus tachycardia is heart palpitation. The T-P interval on ECG shortens and the P wave may superimpose on the T wave.
Always consider pain as a possible cause of tachycardia.
There’s a long list, however:
• Any cause of adrenergic stimulation (including pain);
• thyrotoxicosis;
• hypovolaemia;
• vagolytic drugs (e.g. atropine)
• anaemia, pregnancy;
• vasodilator drugs, including many hypotensive agents;
• FEVER
• myocarditis
If the rate is almost exactly 150, always make sure that you are not mistaking atrial flutter with a 2:1 block for sinus tachycardia. A common error.
Sinus bradycardia is connected with slowed excitation of the sino-atrial node, which in turn depends mostly on the increased influence of the asympathetic nervous system on the heart (or decreased influence of the sympathetic nervous system). Automaticity of the sino-atrial node increases in sclerotic affections of the myocardium and in the cold. The heart rate in sinus bradycardia decreases to 50—40 (in rare cases to 30) per min. Bradycardia may occur in well-trained athletes. It is not permanent and the heart rhythm is accelerated during exercise as distinct from pathological bradycardia in atrioventricular block when bradycardia persists during and after exercise. If automaticity of the sino-atrial node sharply decreases (sick-sinus syndrome), the second- or third-order centres may function as the pacemaker, i.e. ectopic arrhythmias develop.
Sinus bradycardia may accur in increased intracranial pressure (tumour or oedema of the brain, meningitis, cerebral haemorrhage), in myxoedema, typhoid fever, jaundice, starvation, lead and nicotine poisoning, and due to effect of quinine and digitalis preparations. It may develop by reflex during stimulation of baroreceptors of the carotid sinus and the aortic arch in essential hypertension, and can be provoked by pressure on the eye-ball (Dagnini-Aschner reflex), or by irritation of receptors of the peritoneum and the internal organs.
Mild bradycardia is not attended by any subjective disorders, nor does it produce any effect on the circulation. Marked bradycardia (under 40 beats per min) may cause nausea and loss of consciousness due to cerebral anaemia. Objective examination reveals slow pulse. The ECG in sinus bradycardia reveals the unchanged atrial or ventricular complexes; the T-P interval only increases to show protraction of electrical diastole of the heart; the P-Q interval sometimes increases insignificantly (to 0.20-0.21 s).
Apart from fit, but otherwise normal individuals, there’s a long list of situations where sinus bradycardia occurs, including:
• hypothermia;
• increased vagal tone (due to vagal stimulation or e.g. drugs);
• hypothyroidism;
• beta blockade;
• marked intracranial hypertension;
• obstructive jaundice, and even in uraemia;
• structural SA node disease, or ischaemia.
Sinus arrhythmia. Sinus arrhythmia and heart rate variability
There is normally a slight degree of chaotic variation in heart rate, called sinus arrhythmia. Sinus arrhythmia is generally a good thing, and loss of this chaotic variation is of ominous prognostic significance. Post myocardial infarction, a metronome-like regularity of the heartbeat is associated with an increased likelihood of sudden death, and just before the onset of ventricular tachycardia (or fibrillation), variability is lost! Absence of any sinus arrhythmia suggests an autonomic neuropathy.
Sinus arrhythmia characterized by irregular generation of impulses due to variations in the tone of the vagus. It would commonly be associated with respiratory phases {respiratory arrhythmia): the cardiac rhythm accelerates during inspiration and slows down during expiration. Sinus arrhythmia is observed in children and adolescents (juvenile arrhythmia), in patients convalescing from infectious diseases, and in certain diseases of the central nervous system. It can be a sign of pathology in rare cases when arrhythmia is not connected with respiration or when it develops in the aged during normal respiration.
Clinically sinus arrhythmia is not attended by any subjective disorders. The cardiac rhythm and pulse rate only change with respiratory phases, and the intervals between the heart complexes (R-R intervals) vary in length on the ECG.
Ectopic arrhythmias. Additional (heterotopic or ectopic) foci of excitation can arise at any site of the conduction system (in the atria, ventricles, atrioventricular region). They can cause premature contraction of the heart before termination of the normal diastolic pause. This premature contraction is called extrasystole, and the disorder of the cardiac rhythm is called extrasystolic arrhythmia. If the activity of the ectopic focus is very high, it can become a temporary pacemaker, and all impulses governing the heart will during this time be emitted from this focus. The cardiac rhythm is then markedly accelerated. The condition is known as paroxysmal tachycardia.-Ectopic arrhythmias are often due to increased excitability of the myocardium. The phenomenon known as re-entry can be another mechanism of ectopic arrhythmia.
Extrasystolic arrhythmia. Extrasystole usually develops during normal contractions of the heart governed by the sino-atrial node (nomotopic contractions). Ectopic foci of excitation can arise at any site of the conduction system. Usually excitations arise in the ventricles, less frequently in the atria, the atrioventricular node, and in the sino-atrial node (sinus extrasystole). A nomotopic contraction of the heart that follows extrasystole occurs in a longer (thaormal) lapse of time. This can be explained as follows. During the atrial extrasystole, excitation from the ectopic focus is transmitted to the sino-atrial node to “discharge” it, as it were. The next impulse arises in the sino-atrial node only in a lapse of time that is required to “discharge” the node and to form a new impulse.
Atrial extrasystole. These arise from ectopic atrial foci. Commonly, the ectopic beat always arises at about the same time after the sinus beat!
The ectopic beat usually discharges the SA node, so subsequent beats of SA origin are not in synchrony with the previous sinus rhythm.
If the extrasystole occurs early on, it may find the His-Purkinje system not quite ready to receive an impulse, and a degree of block may be seen. This is termed `aberration’.
In ventricular extrasystole, the time between the extrasystolic contraction and subsequent nomotopic contraction is even longer. The impulse from the heterotopic focus, located in the ventricles, propagates only over the ventricular myocardium; it would not be usually propagated to the atria via Aschoff-Tawara node. The impulse occurs iormal time in the sino-atrial node but it is not transmitted to the ventricles because they are refractory after the extrasystolic excitation. The next impulse from the sino-atrial node will only excite and contract the atria and the ventricles. A long “compensatory” pause therefore follows the ventricular extrasystole which lasts till the next nomotopic contraction.
Extrasystolic arrhythmia is quite common. It may occur in practically healthy individuals as a result of overexcitation of certain sites of the conduction system due to the action of the extracardiac nervous system in heavy smokers and in persons abusing strong tea or coffee; it can occur by reflex in diseases of the abdominal organs. Extrasystole often attends various cardiovascular pathological conditions due to inflammatory or dystrophic affections of the myocardium or its deficient blood supply; or it may be due to hormonal disorders (thyrotoxicosis, menopause), various intoxications, disorders of electrolyte metabolism, etc.
Patients with extrasystole can feel their heart missing a beat (escape beat) and a subsequent strong stroke. Auscultation of the heart reveals its premature contraction with a specific loud first sound (due to a small diastolic filling of the ventricles). Extrasystole can be easily revealed by feeling the pulse: a premature weaker pulse wave and a subsequent long pause are characteristic. If extrasystole follows immediately a regular contraction, the left ventricle may be filled with blood very poorly and the pressure inside it may be so small that the aortic valve would not open during the extrasystolic contraction and the blood will not be ejected into the aorta. The pulse wave on the radial artery will not be then detectable (missing pulse). The ECG of all extrasystoles are characterized by: (1) premature appearance of the cardiac complex; (2) elongated pause between the extrasystolic and subsequent normal contraction. According to the origin, extrasystoles are classified as atrial and atrioventricular (which are given a commoame of supraventricular), and also ventricular (left- and right-ventricular) extrasystoles.
Excitation of the atria only changes in atrial extrasystole because the impulse is generated not in the sino-atrial node, and the ventricles are excited by the usual way. The ECG of atrial extrasystole is characterized by the following signs: (1) premature appearance of the cardiac complex; (2) preservation of the atrial P wave which may be slightly, disfigured and superimposed on the preceding T wave; this depends on abnormal atrial excitation from a heterotopic focus; (3) normal shape the ventricular complex; (4) slight elongation of the diastolic pause interval following the extrasystolic contraction.
In atrioventricular (nodal) extrasystole the Aschoff-Tawara node impulse is transmitted to the atria retrogradely, from boil to top. The ventricles are excited iodal extrasystole in the usual way. The following signs are characteristic of the ECG iodal extrasystolr (1) premature appearance of the cardiac complex; (2) changes in the P wave which becomes negative to show the retrograde atrial excitation (in some cases the P wave is absent on the ECG); (3) the position of the P wave is differ respect to the ventricular complex changes, which depends on the ranning of the excitation wave onto the atria and the ventricles. If excitation of the atria is followed by excitation of the ventricles, the negative P wave is recorded before the ORS complex; if the ventricles are excited first the negative P wave follows the QRS complex. If the atria and ventricle are excited synchronously, the P wave is not recorded separately but superimposes the QRS complex to alter its configuration. In other cases, the configuration of the ventricular complex in
Ventricular extrasystole. excitation order changes sharply in ventricular extrasystole. The ventricular impulse is not usually transmitted retrogradelly through the Aschoff-Tawara node and the atria are not therefore excited. As the focus of excitation is located in one ventricle, the ventricles are not excited synchronously (as iormal cases), .but each after another, i.e. that ventncle is excited first where the ectopic is located The time of excitation of the ventricles is therefore longer and ORS complex is wider. The ECG is characterized by the following: (1) premature appearance of the ventricular complex (2) absence of P wave; (3) deformation of the QRS complex; (4) since the sequence of relaxation in the ventricles is not synchronous the shape and the height of the T wave changes as well. As a rule, it is enlarged and its direction is opposite to that of the maximum wave of the complex (the T wave is negative if R wave is high and
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positive if S wave is deep). (5) The ventricular extrasystole is followed by a complete compensatiry pause (except in interpolated extrasystoles): the ventricles are excited by the sinus impulse that follows the extrasystole but the ventricle are in refractory at this moment.
Configuration of the ventricular complex in various ECG leads depends on the location of ectopic focus. . Left-ventricular extrasystole is characterized by a high R wave in the third standard lead and the deep S wave in the first lead. In right-ventricular extrasystole there will be opposite changes.
Chest leads are very important for the topic diagnosis of ventricular extratrasystole. Left-ventricular extrasystoles are characterized by the presence of the extrasystolic complex with a high R wave in the right leads and a broad or deep S wave in the left chest leads. In right-ventricular extrasystole, on the contrary, the deep S wave is recorded in the right leads, and a high R wave in the left chest leads. If excitability of myocardium is high, several (rather than one) ectopic foci may exist, extrasystoles are generated in various heart chambers and having different figuration then appear on the ECG {polytopic extrasystole).
Wherever an ectopic focus may arise, its impulses may alternate in the certain order with the normal impulses of the sino-atrial node, phenomenon is known as allorhythmia. Extrasystole may alternate each sinus impulse (bigeminy), or it may follow two normal pulses (trigeminy), or three normal impulses (quadrigeminy). If the heterotopic focus is even more active, a normal contraction may be followed by several extrasystoles at a run (group extrasystole) which sometimes precedes an attack of paroxysmal tachycardia.
Because ventricular extrasystoles arise within an ectopic focus within the ventricular muscle, the QRS complex is wide, bizarre, and unrelated to a preceding P wave. There is usually a constant relationship (timing) between the preceding sinus beat and a subsequent ventricular beat, because the preceding beat influences the ectopic focus.
The ventricular beat is not usually conducted back into the atria. What happens to the atrial beat that occurred, or was about to occur when the VE happened? Usually, this is blocked, but the subsequent atrial beat will occur on time, and be conducted normally.
Rarely, the ventricular beat may be conducted retrogradely and capture the atrium (resulting in a P wave after the QRS, with an abnormal morphology as conduction through the atrium is retrograde). The atrial pacemaker is now reset! In the following rather complex tracing, we have a ventricular rhythm (a bit faster than one might expect, perhaps an accelerated idioventricular rhythm) with retrograde P waves, and something else — some of the P waves are followed by a normal looking `echo’ beat as the impulse is conducted down back in Because the intrinsic rate of an ectopic focus often tends to be slow-ish, extrasystoles will tend to arise more commonly with slower rates. In addition, if the rate is varying, extrasystoles will tend to `squeeze in’ during long RR intervals. Some have called this the “rule of bigeminy“.
Couplet
Two VE’s are termed a couplet.
Fusion beat
Occasionally, a VE occurs just after a sinus beat has started to propagate into the His-Purkinje system. This results in a `fusion beat’, which combines the morphology of a normal sinus beat and that of the extrasystole.
Paroxysmal tachycardia. This is a sudden acceleration of the cardiac rhythm (to 180—240 beats per min). At attack of paroxysmal tachycardia exist from several seconds to a few days and terminate just as unexpectivelly as it begins. During an attack, all impulses arise from a monotopic focus because its high activity inhibits the activity of the sino-atrial node. Paroxysmal tachycardia (like extrasystole) may occur in increased nervous excitability, in the absence of pronounced affections of the heart muscle, but it arises more likely in the presence of heart disease (e.g. myocardial infarction, heart defects or cardiosclecrosis).
•During an attack of paroxysmal tachycardia, the patient feels strong palpitaition, discomfort in the chest, and weakness. The skin turns pale, when attack persists, cyanosis develops. Paroxysmal tachycardia is followed by swelling and pulsation of the neck veins, because during accelerated pulse (to 180-200 per min) the atria begin contracting before ventricular systole ends to increase venous pressure. Auscultation of the heart during the attack of paroxysmal tachycardia reveals decreased diastolic pause, the heart rhythm becomes pendulum. The first sound increases due to insufficient ventricular filling. The pulse is rhythmic, very fast, and small. Arterial pressure may fall. If an attack persists (especially if it develops in a heart disease) symptoms of cardiac insufficiency develop.
Like in extrasystole, the heterotopic focus in paroxysmal tachycardia i be located in the atria, the atrioventricular node, and the ventricles. It pos\sible to locate the focus only by electrocardiography: a series of ex-stoles follow on an ECG at regular intervals and at a very fast rate. In supraventricular PT the P wave cannot be seen because of accelerated
Supraventricular tachyarrhythmias (SVT)
Irregular SVT
By far the commonest cause of irregular SVT is atrial fibrillation, where the atrial rate is in the region of 450 to 600/min, and the atria really do not contract rhythmically at all. The atrium “fibrillates”, writhing like a bag of worms. The conventional view of the pathogenesis of AF is that there are multiple re-entrant `wavelets’ moving through the atrial muscle, but recent evidence suggests that much AF actually arises from ectopic activity in the muscular cuff surrounding the pulmonary veins where they enter the left atrium. AF is thought to beget further AF through “electrical remodelling” — electrophysiological changes that are induced in atrial myocytes due to fast rates and the consequent calcium loading.
Regular SVT
Atrial flutter is common. The atrial rate is commonly 300/min, and there is usually a 2:1 block, resulting in a ventricular response rate of 150/min. Other ratios are possible, and sometimes the ratio varies. This rhythm is often unstable, and the heart may flip in and out of sinus rhythm, or there may be runs of atrial fibrillation.
Distinguishing causes of SVT
A few pointers are in order. The important thing to look for is the P wave.
Ventricular tachycardia
Three or more ventricular extrasystoles are a bad sign, and are termed ventricular tachycardia (VT). There is usually severe underlying myocardial disease. Sustained VT (more than about 30 beats) often degenerates into ventricular fibrillation, resulting in death.
Arrhythmias due to disordered myocardial conduction. Transmission of the impulse may be blocked at any part of the heart’s conduction system. The following types of heart blocks are distinguished: (1) sinoatrial block, in which beats are sometimes missing in the sino-atrial node and the impulse is not transmitted to the atria; (2) intra-atrial block, in which transmission of excitation through the atrial myocardium is impaired; (3) atrioventricular block, in which conduction of impulses from the atria to the ventricles is impaired; (4) intraventricular block, in which conduction of impulses through the His bundle and its branches is impaired.
Block may develop in inflammatory, dystrophic, and sclerotic affections of the myocardium (e.g. rheumatic and diphtheritic myocarditis, cardiosclerosis). The conduction system may be affected by granulous cicatrices, toxins, etc. Conduction is often impaired in disordered coronary circulation, especially in myocardial infarction (the interventricular septum is involved). Block may be persistent and intermittent. Persistent block usually connected with anatomic changes in the conduction system whereas intermittent block depends largely on the functional condition in the atrioventricular node and the His bundle and is often connected with increased influence of the parasympathetic nervous system; atropine sulphate is an effective means that restores conduction.
Sino-atrial block is characterized by periodic missing of the heart beat and pulse beat. -r, in the presence of a regular sinus rhythm (neither P wave nor the QRST complexes are recorded); the length of diastole doubles.
SA node block. Intra-atrial block can only be detected electrocardiographically because clinical signs are absent. since the time of atrial excitation increases, the length of the P waves is increased too.
This is a diagnosis of deduction, as no electrical activity is seen. An impulse that was expected to arise in the SA node is delayed in its exit from the node, or blocked completely. A second degree SA block can be `diagnosed’ if the heart rate suddenly doubles in response to, say, administration of atropine. If the SA node is blocked, a subsidiary pacemaker will (we hope) take over, in the atrium, AV node, or ventricle.
Intraatrial block is characterised by prolongation of P wave:
AV nodal blocks
There are three “degrees” of AV nodal block:
1. First degree block:
simply slowed conduction. This is manifest by a prolonged PR interval;
Conduction intermittently fails completely. This may be in a constant ratio (more ominous, Type II second degree block), or progressive (The Wenckebach phenomenon, characterised by progressively increasing PR interval culminating in a dropped beat — this The QRS complex
2. Second degree block:
– Mobitz Type I second degree heart block;
– Mobitz Type II second degree heart block;
– Mobitz Type III second degree heart block;
. Atrioventricular block is most important clinically. It is classified into three degrees by gravity. The first degree can only be revealed electrocar-diographically by the increased P-Q interval (to 0.3-0.4 s and more). This block cannot be detected clinically, except that splitting of the first sound may sometimes be detected by auscultation (splitting of the atrial component).
The second-degree atrioventricular block is characterized by dualism of its signs.
Mobitz I. Conduction of the Aschoff-Tawara node and His bundle is impaired: each impulse transmitted from the atria to the ventricles increases and the P-Q interval on the ECG becomes longer with each successive beat. A moment arrives at which one impulse does not reach the ventricles and they do not contract, hence the missing QRS complex on an ECG. During a long diastole, which now follows, the conduction power of the atrioventricular system is restored, and next impulses will again be transmitted, but their gradual slowing down will be noted again; the length of the P-Q interval will again increase in each successive complex. Period which follows the P wave is called the Samoilov– Wenckebach period.
Mobitz II. This type of block is characterized by periodically missing ventricular contractions, and hence missing beats, which correspond to the Samoilov-Wenckebach period.
Mobitz III type of the second-degree atrioventricular block can be characterised by a worse conduction. The P-Q interval remains constant, but only i second, third, or (less frequently) fourth impulse is transmitted to the’ tricles. The number of P waves on the ECG is therefore larger than ventricular complexes. This is known as incomplete heart block with a 2:1, 3:1, etc. ratio. Considerable deceleration of the ventricular rhythm and slow pulse are characteristic, especially in 2:1 block. If each third or fourth beat is missing, the pulse is irregular and resembles trigeminy or quadrigeminy with early extrasystoles and pulse deficit. The heart rhythm slows down significantly, the patient may complain of giddiness, everything going black before his eyes, and transient loss of consciousness due to anaemia of the brain.
The third-degree atrioventricular block is called complete heart block. Atrial impulses do not reach the ventricles and the sino-atrial node becomes the only pacemaker for the ventricles. The ventricles contract by their own automaticity in the centres of the second or third order. The number of their contractions in complete he block is about 30-40 per min, and ventricular rhythm slows down with lower position of the pacemaker in the conduction system.
The ECG in complete heart block is characterized by the following signs: (1) atrial P waves and ventricular complexes are recorded dependently of each other, and part of the P waves may superimpose on ventricular complex and become invisible on the ECG; (2) the number of ventricular complexes is usually much smaller than the number of atrial waves; the pacemaker arises from the Aschoff-Tawara node or His bundle. The heart rate in persistent complete heart block may be sufficiently decreased (40 50 beats/rnin) but the patient may be unaware of the disease for a time. Examination of such patients reveals slow, rhythmic, and full pulse. Tie heart sounds are dulled but a loud first sound (“pistol-shot” according to Strazhesko) may be heard periodically. It occurs due to simultaneous contractions of the atriums and ventricles. If the ventricular nun slows down significantly (to 20 beats/min and less), or when incomplete heart block converts into a complete one patients condition significantly worthens. When the impulses from the atria are not conducted to the ventricles, Their automaticity has not yet developed, attacks (the Morgagni-Stokes syndrome) may occur due to disordered blood supply in the central nervous system. During an attack the patient loses consciousness, falls, general epileptiform convulsions develop, the respiration becomes deep, the skin is pallid, the pulse is very slow or even impalpable.
Bundle branch blocks
Involves the left and/or right bundle branches, which transmit the heart signal to the ventricles.Left bundle branch block (LBBB) is further classified as complete or partial (anterior fascicular block or posterior fascicular block). Right bundle branch block (RBBB) is also classified as complete or partial. Other types of bundle branch block include bifascicular block and trifascicular block.
A broadened QRS complex suggests a bundle branch block, although there are other causes:
RBBB
Diagnostic criteria for right bundle branch block are somewhat empiric, but useful. Here they are:
1. Tall R’ in V1;
2. QRS duration 0.12s or greater (some would say, >= 0.14);
In addition, there is usually a prominent S in the lateral leads (I, V5, V6).
RBBB is sometimes seen iormal people, or may reflect congenital heart disease (e.g. atrial septal defect), ischaemic heart disease, cardiomyopathy, or even acute right heart strain.
Diagnose this as follows:
1. No RBBB can be present;
2. QRS duration is 0.12s or more;
3. There must be evidence of abnormal septal depolarization. The tiny q waves normally seen in the left-sided leads are absent. (And likewise for the normal tiny r in V1).
In addition, the VAT is prolonged, and tall, notched R waves are seen in the lateral leads (RR’ waves). There is usually a notched QS complex in V1 and V2.
Left anterior hemiblock (LAHB) is interruption of the thin anterosuperior division of the left bundle. Suspect it if there is left axis deviation (past -45o) without another cause (such as inferior myocardial infarction, or some types of congenital heart disease or accessory pathways).
Other features of LAHB include an initial QRS vector which is down and to the right, a long VAT, and several other minor changes.
LAHB may indicate underlying heart disease, but is much more worrying when associated with other abnormalities (such as PR interval prolongation or RBBB).
The diagnosis of left posterior hemiblock is mentioned only to be avoided!
Bundle-branch block can only be detected electrocardiographically. On ECG deformed QRS complexes will be recorded cccording to the location of block. Besides QRS complex is wide due to prolongation of the period of inner deviation, ST segment is displaced opposite to the direction of the maximum wave of the QRS complex. If the right branch of the bundle is affected, the shape of the ventricular complexes resembles that of left-ventricular extrasystoles and vice versum. It has no subjective signs.
