Cardiac Dysrhythmias.


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Cardiac Dysrhythmias for 4th class med students.

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Cardiac Dysrhythmias.

  2. 2. Dysrhythmias: <ul><li>The heart beat is normally initiated by an electrical discharge from the sinoatrial (sinus) node. </li></ul><ul><li>The atria and ventricles then depolarise sequentially as electrical depolarisation passes through specialised conducting tissues ( </li></ul><ul><li>The sinus node acts as a pacemaker and its intrinsic rate is regulated by the autonomic nervous system; vagal activity slows the heart rate, and sympathetic activity accelerates it via cardiac sympathetic nerves and circulating catecholamines . </li></ul><ul><li>If the sinus rate becomes unduly slow, a lower centre may assume the role of pacemaker. This is known as an escape rhythm and may arise in the AV node (nodal rhythm) or the ventricles (idioventricular rhythm). </li></ul><ul><li>A cardiac arrhythmia is a disturbance of the electrical rhythm of the heart. </li></ul><ul><li>Often a manifestation of structural heart disease but may also occur in the context of an otherwise normal heart. </li></ul><ul><li>Symptoms are more likely to occur if the arrhythmia is associated with extremes of heart rate. </li></ul><ul><li>Arrhythmias can cause palpitation, dizziness, syncope, chest discomfort or breathlessness, and can trigger heart failure or even sudden death . </li></ul><ul><li>A heart rate of more than 100/minute is called a tachycardia and a heart rate of less than 60/minute is called a bradycardia . </li></ul>
  3. 3. Mechanisms of tachycardia <ul><li>Are 3 : </li></ul><ul><li>Increased automaticity-the tachycardia is produced by repeated spontaneous depolarisation of an ectopic focus, often in response to catecholamines . </li></ul><ul><li>Re-entry-the tachycardia is initiated by an ectopic beat and sustained by a re-entry circuit . Most tachyarrhythmias are due to re-entry . </li></ul><ul><li>Triggered activity, can cause ventricular arrhythmias in patients with coronary heart disease. This is a form of secondary depolarisation arising from an incompletely repolarised cell membrane . </li></ul><ul><li>Bradycardia may be due to : </li></ul><ul><li>reduced automaticity (e.g. sinus bradycardia) </li></ul><ul><li>blocked or abnormally slow conduction (e.g. atrioventricular block. </li></ul>
  4. 4. Arrhythmia <ul><li>May be: </li></ul><ul><li>‘ Supraventricular' (sinus, atrial or junctional) </li></ul><ul><li>Ventricular. </li></ul><ul><li>Supraventricular rhythms usually produce narrow QRS complexes because the ventricles are depolarised normally through the AV node and bundle of His. </li></ul><ul><li>Ventricular rhythms produce broad bizarre QRS complexes because the ventricles are activated in an abnormal sequence. </li></ul><ul><li>Occasionally a supraventricular rhythm can produce broad or wide QRS complexes due to coexisting bundle branch block or the presence of accessory conducting tissue </li></ul>
  5. 5. SINUS RHYTHMS : SINUS ARRHYTHMIA <ul><li>Phasic alteration of the heart rate during respiration (the sinus rate increases during inspiration and slows during expiration) </li></ul><ul><li>is a consequence of normal parasympathetic nervous system activity and can be pronounced in children. </li></ul><ul><li>Absence of this normal variation in heart rate with breathing or with changes in posture may be a feature of autonomic neuropathy ( </li></ul><ul><li>SINUS BRADYCARDIA A sinus rate of less than 60/min may occur in healthy people at rest and is a common finding in athletes. </li></ul><ul><li>Some pathological causes it . </li></ul><ul><li>Asymptomatic sinus bradycardia requires no treatment. </li></ul><ul><li>Symptomatic sinus bradycardia usually responds to intravenous atropine 0.6-1.2 mg . </li></ul><ul><li>SINUS TACHYCARDIA This is defined as a sinus rate of more than 100/min, and is usually due to an increase in sympathetic activity associated with exercise, emotion, pregnancy or pathology ( </li></ul><ul><li>Young adults can produce a rapid sinus rate, up to 200/min, during intense exercise </li></ul>
  6. 6. Sinus bradycardia <ul><li>Myocardial infarction </li></ul><ul><li>Sinus node disease (sick sinus syndrome) </li></ul><ul><li>Hypothermia </li></ul><ul><li>Hypothyroidism </li></ul><ul><li>Cholestatic jaundice </li></ul><ul><li>Raised intracranial pressure </li></ul><ul><li>Drugs, e.g. β- blocker, digoxin, verapamil </li></ul>
  7. 7. Sinus tachycardia <ul><li>Anxiety </li></ul><ul><li>Fever </li></ul><ul><li>Anaemia </li></ul><ul><li>Heart failure (bronchodilators ) </li></ul><ul><li>Thyrotoxicosis </li></ul><ul><li>Phaeochromocytoma </li></ul><ul><li>Drugs, e.g. β- adrenoceptor agonists </li></ul>
  8. 8. ATRIAL TACHYARRHYTHMIAS ATRIAL ECTOPIC BEATS (EXTRASYSTOLES, PREMATURE BEATS ) <ul><li>These usually cause no symptoms but can give the sensation of a missed beat or an abnormally strong beat. </li></ul><ul><li>In most cases these are of no consequence, although very frequent atrial ectopic beats may herald the onset of atrial fibrillation. </li></ul><ul><li>Treatment is rarely necessary . </li></ul>
  9. 9. ATRIAL TACHYCARDIA <ul><li>Atrial tachycardia may be a manifestation of increased atrial automaticity, sinoatrial disease or digoxin toxicity. </li></ul><ul><li>It produces a narrow complex tachycardia with abnormal P-wave morphology, sometimes associated with atrioventricular block if the atrial rate is rapid. </li></ul><ul><li>It may respond to β- blockers, which reduce automaticity, or class I or III antiarrhythmic drugs ( </li></ul><ul><li>The ventricular response in rapid </li></ul><ul><li>atrial tachycardias may be controlled by AV node-blocking drugs. </li></ul><ul><li>Catheter ablation therapy can be offered to patients with recurrent or drug-resistant atrial tachycardia . </li></ul>
  10. 10. ATRIAL FLUTTER <ul><li>Characterised by a large (macro) re-entry circuit within the right atrium, usually encircling the tricuspid annulus. </li></ul><ul><li>The atrial rate is approximately 300/min. </li></ul><ul><li>It is usually associated with 2:1, 3:1, or 4:1 atrioventricular block (with corresponding heart rates of 150, 100, 75). </li></ul><ul><li>Rarely, in young patients, every beat is conducted, producing a heart rate of 300/min and haemodynamic collapse. </li></ul><ul><li>The ECG shows saw-toothed flutter waves ( </li></ul><ul><li>When there is regular 2:1 AV block it may be difficult to identify flutter waves which are buried in the QRS complexes and T-waves. </li></ul><ul><li>Atrial flutter should always be suspected when there is a narrow complex tachycardia of 150/min. </li></ul><ul><li>Carotid sinus massage or intravenous adenosine may help to establish the diagnosis by temporarily increasing the degree of AV block and revealing the flutter waves </li></ul>
  11. 11. Management <ul><li>Digoxin, β- blockers or verapamil can be used to control the ventricular rate ( </li></ul><ul><li>However, in many cases it may be preferable to try and restore sinus rhythm by direct current (DC) cardioversion or drug therapy. </li></ul><ul><li>Amiodarone, propafenone or flecainide may be effective and can also be used to prevent recurrent episodes of atrial flutter. </li></ul><ul><li>Flecainide should always be prescribed with an AV node-blocking drug, e.g. a β- blocker. </li></ul><ul><li>Catheter ablation offers a 90% chance of complete cure and is the treatment of choice for patients with persistent and troublesome symptoms . </li></ul>
  12. 12. ATRIAL FIBRILLATION <ul><li>The most common sustained cardiac arrhythmia, with an overall prevalence of 0.5%. </li></ul><ul><li>The prevalence rises with age, affecting 2-5% of 70-year-olds and 9% of those aged over 80 years. </li></ul><ul><li>Characterised by the presence of multiple, interacting re-entry circuits looping around the atria. </li></ul><ul><li>Episodes are often initiated by salvoes of ectopic beats that can arise from conducting tissue in the pulmonary veins or from diseased atrial tissue. </li></ul><ul><li>AF is more likely to become sustained in atria that are enlarged, or in which conduction is slow (as is the case in many forms of heart disease). </li></ul><ul><li>During episodes of AF, the atria beat rapidly, but in an uncoordinated and ineffective manner. The ventricles are activated irregularly at a rate determined by conduction through the AV node. </li></ul><ul><li>This produces the characteristic 'irregularly irregular' pulse. </li></ul><ul><li>The ECG shows normal but irregular QRS complexes; there are no P waves but the baseline may show irregular fibrillation waves . </li></ul>
  13. 13. ATRIAL FIBRILLATION <ul><li>AF can be classified as paroxysmal (intermittent, self-terminating episodes), persistent (prolonged episodes that can be terminated by electrical or chemical cardioversion) or permanent. </li></ul><ul><li>In patients seen for the first time with AF it can be difficult to identify which form of the arrhythmia is present. </li></ul><ul><li>Unfortunately for many patients, paroxysmal AF will become permanent as the underlying disease process that predisposes to AF progresses . </li></ul>
  14. 14. COMMON CAUSES OF AF <ul><li>Coronary artery disease (including acute myocardial infarction ) </li></ul><ul><li>Valvular heart disease, especially rheumatic mitral valve disease </li></ul><ul><li>Hypertension </li></ul><ul><li>Sinoatrial disease </li></ul><ul><li>Hyperthyroidism </li></ul><ul><li>Alcohol </li></ul><ul><li>Cardiomyopathy </li></ul><ul><li>Congenital heart disease </li></ul><ul><li>Chest infection </li></ul><ul><li>Pulmonary embolism </li></ul><ul><li>Pericardial disease </li></ul><ul><li>Idiopathic (lone AF ) </li></ul>
  15. 15. AF: <ul><li>AF may be the first manifestation of many forms of heart disease particularly those that are associated with enlargement or dilatation of the atria. </li></ul><ul><li>Alcohol, hyperthyroidism and chest disease are also common causes of AF, although multiple aetiological factors often coexist such as the combination of alcohol, hypertension and coronary disease. </li></ul><ul><li>About 50% of all patients with paroxysmal AF and 20% of patients with persistent or permanent AF have otherwise normal hearts: an entity sometimes known as 'lone atrial fibrillation ‘. </li></ul><ul><li>AF can cause palpitation, breathlessness and fatigue. </li></ul><ul><li>In patients with poor ventricular function or valve disease it may precipitate or aggravate cardiac failure because of loss of atrial function and heart rate control. </li></ul><ul><li>A fall in blood pressure may cause lightheadedness, and chest pain may occur with underlying coronary disease. </li></ul><ul><li>AF is often completely asymptomatic, in which case it is usually discovered as the result of a routine examination or ECG . </li></ul>
  16. 16. AF IN OLD AGE <ul><li>Prevalence : rises with age, reaching >10% in those > 80 years. </li></ul><ul><li>Symptoms : sometimes asymptomatic but often accompanied by diastolic heart failure . </li></ul><ul><li>Hyperthyroidism : AF may be the dominant feature of otherwise silent or occult hyperthyroidism . </li></ul><ul><li>Cardioversion : followed by high rates (∼70% at one year) of recurrent AF . </li></ul><ul><li>Stroke : AF is an important cause of cerebral embolism. It is found in 15% of all stroke patients and 2-8% of those with TIAs . </li></ul><ul><li>Anticoagulation : although the risk of thromboembolism rises, the hazards of anticoagulation also rise with age because of increased comorbidity, particularly cognitive impairment and falls . </li></ul><ul><li>Target INR : if anticoagulation is recommended, in those over 75 years, care should be taken to maintain an INR below 3.0 because of the increased risk of intracranial haemorrhage . </li></ul><ul><li>Aspirin : a safer alternative if anticoagulation cannot be recommended, but its benefits in reducing the risk of stroke are less significant and consistent than with warfarin </li></ul>
  17. 17. AF Risks: <ul><li>AF is associated with a twofold increase in mortality and significant morbidity which are largely attributable to the effects of the underlying heart disease and the risk of cerebral embolism. </li></ul><ul><li>Careful assessment, risk stratification and therapy can improve the outlook considerably . </li></ul>
  18. 18. Management <ul><li>A full history, physical examination, 12-lead ECG, echocardiogram and thyroid function tests. </li></ul><ul><li>Additional investigations such as exercise testing may be needed to determine the nature and extent of any underlying heart disease. </li></ul><ul><li>Biochemical evidence of hyperthyroidism is found in a small minority of patients with otherwise unexplained AF . </li></ul><ul><li>When AF complicates an acute illness (e.g. chest infection, pulmonary embolism), effective treatment of the primary disorder will usually restore sinus rhythm. </li></ul><ul><li>The main objectives are to restore sinus rhythm as soon as possible, prevent recurrent episodes of AF, optimise the heart rate during periods of AF, minimise the risk of thromboembolism and treat any underlying disease . </li></ul><ul><li>Paroxysmal atrial fibrillation Occasional attacks that are well tolerated do not necessarily require treatment, but β- blockers are the drug of choice if symptoms are troublesome. </li></ul><ul><li>Beta-blockers are particularly useful for treating patients with AF associated with ischaemic heart disease, hypertension and cardiac failure.&may prevent AF in those who are prone to episodes during exertion or at times of stress. </li></ul><ul><li>Class Ic drugs ) such as propafenone or flecainide are also effective at preventing episodes but should be avoided in patients with coronary disease or left ventricular dysfunction. </li></ul><ul><li>60% of patients treated . </li></ul>
  19. 19. Management <ul><li>Amiodarone is the most effective agent for preventing AF but its side-effects restrict its use to patients in whom other measures fail. </li></ul><ul><li>Digoxin and verapamil are not effective drugs for preventing paroxysms of AF, although they serve to limit the heart rate when AF occurs by blocking the AV node. </li></ul><ul><li>Radiofrequency ablation has emerged as a promising treatment for paroxysmal AF in patients who do not have structural heart disease . </li></ul><ul><li>It is usually directed at the ostia of the pulmonary veins from which triggering ectopic beats may emanate. </li></ul><ul><li>Ablation prevents AF in up to 70% of patients with prior drug-resistant episodes, although anti-arrhythmic drugs often need to be continued afterwards to maintain sinus rhythm. </li></ul><ul><li>An alternative strategy, suitable for patients with structural heart disease, is 'overdrive' atrial pacing, which helps to maintain sinus rhythm in patients with bradycardia-related AF (which is often a manifestation of sinoatrial disease) and which may suppress the ectopic triggers for AF. </li></ul>
  20. 20. Persistent & permanent : Management <ul><li>There are two options for treating persistent AF : </li></ul><ul><li>Attempting to restore and maintain sinus rhythm: rhythm control </li></ul><ul><li>Accepting that AF will be permanent and using treatments to control the ventricular rate and to prevent embolic complications: rate control . </li></ul><ul><li>Rhythm control: An attempt to restore sinus rhythm is particularly appropriate if the arrhythmia has precipitated troublesome symptoms and there is a modifiable or treatable underlying cause. </li></ul><ul><li>Electrical cardioversion :is initially successful in three-quarters of patients but relapse is frequent (25-50% at 1 month and 70-90% at 1 year). </li></ul><ul><li>Attempts to restore and maintain sinus rhythm are most successful if AF has been present for < 3 months, the patient is young, and there is no important structural heart disease . </li></ul><ul><li>Immediate DC cardioversion, after the administration of intravenous heparin, is appropriate if AF has been present for less than 48 hours. </li></ul><ul><li>An attempt to restore sinus rhythm by infusing intravenous flecainide (2 mg/kg over 30 minutes, maximum dose 150 mg) is a safe and attractive alternative to electrical cardioversion if there is no underlying structural heart disease. </li></ul><ul><li>In other situations, DC cardioversion should be deferred until the patient has been established on warfarin, with an international normalised ratio (INR) of between 2.0 and 3.0, for a minimum of 3 weeks, and any underlying problems, such as hyperthyroidism, have been dealt with. </li></ul>
  21. 21. Persistent & permanent : Management <ul><li>Anticoagulation should be maintained for at least 1 month and ideally for 6 months following successful cardioversion; if relapse occurs, a second (or third) cardioversion may be appropriate. </li></ul><ul><li>Concomitant anti-arrhythmic therapy with drugs such as amiodarone or β- blockers may reduce the risk of recurrence . </li></ul>
  22. 22. Persistent & permanent : Management <ul><li>Rate control : </li></ul><ul><li>If sinus rhythm cannot be restored, treatment should be directed towards maintaining an appropriate heart rate. </li></ul><ul><li>Digoxin, β- blockers or rate-limiting calcium antagonists such as verapamil or diltiazem will reduce the ventricular rate by increasing the degree of AV block. </li></ul><ul><li>This alone may produce a striking improvement in overall cardiac function, particularly in patients with mitral stenosis. </li></ul><ul><li>Beta-blockers and rate-limiting calcium antagonists are often more effective than digoxin at controlling the heart rate during exercise and may have additional benefits in patients with hypertension and/or structural heart disease. </li></ul><ul><li>Combination therapy (e.g. digoxin + atenolol ) is often advisable . </li></ul>
  23. 23. Management <ul><li>In exceptional cases, poorly controlled and symptomatic AF can be treated by deliberately inducing complete heart block with transvenous catheter radiofrequency ablation; a permanent pacemaker must be implanted beforehand . </li></ul>
  24. 24. Management <ul><li>Prevention of thromboembolism: </li></ul><ul><li>Loss of atrial contraction and left atrial dilatation cause stasis of blood in the left atrium, and may lead to thrombus formation in the left atrial appendage. </li></ul><ul><li>This predisposes patients to stroke and other forms of systemic embolism. </li></ul><ul><li>The annual risk of these events in patients with persistent AF is ∼5% but it is influenced by many factors and may range from less than 1% to 12% </li></ul><ul><li>Several large randomised trials have shown that treatment with adjusted-dose warfarin (target INR 2.0-3.0) reduces the risk of stroke by about two-thirds, at the cost of an annual risk of bleeding of approximately 1-1.5%, whereas treatment with aspirin reduces the risk of stroke by only one-fifth </li></ul><ul><li>Warfarin is thus indicated for patients with AF who have specific risk factors for stroke. For patients with intermittent AF, the risk of stroke is proportionate to the frequency and duration of AF episodes. Patients with frequent, prolonged (> 24-hour) episodes of AF should be considered for warfarin anticoagulation . </li></ul>
  25. 25. RFs FOR THROMBOEMBOLISM IN AF <ul><li>Previous ischaemic stroke or transient ischaemic attack </li></ul><ul><li>Mitral valve disease </li></ul><ul><li>Age over 65 </li></ul><ul><li>Hypertension </li></ul><ul><li>Diabetes mellitus </li></ul><ul><li>Heart failure </li></ul><ul><li>Echocardiographic features of: left ventricular dysfunction, left atrial enlargement or mitral annular calcification </li></ul>
  26. 26. EFFECT OF RISK STATUS & TREATMENT ON THE ANNUAL RISK OF STROKE IN NON-RHEUMATIC AF Warfarin Aspirin Untreated Risk group Very high 5% 10% 12% Previous stroke or transient ischaemic attack High 2.5% 5% 6.5% Age > 65 and one other risk factor Moderate Age > 65, no other risk factors 1.5% 3% 4% Age < 65, other risk factors Low 0.5% 1% 1.2% Age < 65 and no other risk factors
  27. 27. Anticogulation in AF: <ul><li>Anticoagulation with warfarin reduces the risk of ischaemic stroke in non-rheumatic atrial fibrillation by about 62% (absolute risk reduction 2.7% for primary prevention and 8.4% for secondary prevention), while aspirin reduces the risk by only 22% (absolute risk reduction 1.5% for primary prevention and 2.5% for secondary prevention </li></ul>
  28. 28. AF Embolism risk: <ul><li>A careful assessment of the risk of embolism will help to define the possible benefits of antithrombotic therapy which must be balanced against the potential hazards of treatment. </li></ul><ul><li>Echo is a valuable aid in risk stratification. </li></ul><ul><li>Warfarin is indicated in patients at high or very high risk of stroke, unless anticoagulation poses unacceptable risks. </li></ul><ul><li>Comorbid conditions that may be complicated by bleeding, such as peptic ulcer, uncontrolled hypertension, alcohol misuse, poor drug compliance and potential drug interactions, are all relative contraindications to warfarin. </li></ul><ul><li>Patients at moderate risk of stroke may be treated with warfarin or aspirin after discussing the balance of risk and benefit with the individual. </li></ul><ul><li>Young patients (under 65 years) with no evidence of structural heart disease have a very low risk of stroke; they do not require warfarin but may benefit from aspirin treatment . </li></ul>
  29. 29. SUPRAVENTRICULAR' TACHYCARDIAS <ul><li>(SVT) is commonly used to describe a range of regular tachycardias that have a similar appearance on an ECG. </li></ul><ul><li>These tachycardias are usually associated with a narrow QRS complex and are characterised by a re-entry circuit or automatic focus involving the atria. </li></ul><ul><li>The term SVT is misleading, as in many cases the ventricles also form part of the re-entry circuit, e.g. in patients with atrioventricular re-entrant tachycardia . </li></ul>
  30. 30. NODAL RE-ENTRY TACHYCARDIA (AVNRT <ul><li>This is due to re-entry in the right atrium and AV node and produces a regular tachycardia with a rate of 140-220/min. </li></ul><ul><li>It tends to occur in hearts that are otherwise normal, and episodes may last from a few seconds to many hours. </li></ul><ul><li>The patient is usually aware of a fast heart beat and may feel faint or breathless. </li></ul><ul><li>Polyuria, mainly due to the release of atrial natriuretic peptide, is sometimes a feature, and cardiac pain or heart failure may occur if there is coexisting structural heart disease. </li></ul><ul><li>The ECG usually shows a tachycardia with normal QRS complexes but occasionally there may be rate-dependent bundle branch block </li></ul>
  31. 31. Management <ul><li>Treatment is not always necessary. </li></ul><ul><li>An attack may be terminated by carotid sinus pressure or other measures that increase vagal tone (e.g. Valsalva manoeuvre). </li></ul><ul><li>Intravenous adenosine or verapamil will restore sinus rhythm in most cases. </li></ul><ul><li>Suitable alternative drugs include β- blockers, flecainide and digoxin. </li></ul><ul><li>In an emergency when there is severe haemodynamic compromise, the tachycardia should be terminated by DC cardioversion . </li></ul><ul><li>If attacks are frequent or otherwise disabling, prophylactic oral therapy with a β- blocker, verapamil, disopyramide or digoxin may be indicated. </li></ul><ul><li>Catheter ablation offers a very high chance of complete cure and is usually preferable to long-term drug treatment . </li></ul>
  32. 32. Management <ul><li>In these conditions there is an abnormal band of conducting tissue which connects the atria and ventricles. It resembles Purkinje tissue in its physiology, in that it conducts very rapidly, and is known as an accessory pathway. </li></ul><ul><li>In around half of cases this pathway only conducts in the retrograde direction (from ventricles to atria) and thus does not alter the appearance of the ECG in sinus rhythm, known as a concealed accessory pathway. </li></ul><ul><li>In the remainder of cases, conduction takes place partly through the AV node and partly through the rapidly conducting accessory pathway during sinus rhythm. </li></ul><ul><li>Premature activation of ventricular tissue via the pathway produces a short PR interval and a 'slurring' of the QRS complex, called a delta wave known as a manifest accessory pathway. </li></ul><ul><li>As the AV node and bypass tract have different conduction speeds and refractory periods, a re-entry circuit can develop, causing tachycardia, when this is associated with symptoms, the condition is known as Wolff-Parkinson-White syndrome. </li></ul>
  33. 33. Management <ul><li>The ECG appearance of this tachycardia may be indistinguishable from that of AVNRT. </li></ul><ul><li>Carotid sinus pressure or intravenous adenosine can terminate the tachycardia. </li></ul><ul><li>If atrial fibrillation occurs, it may produce a dangerously rapid ventricular rate because the accessory pathway lacks the rate-limiting properties of the AV node known as pre-excited atrial fibrillation and may cause collapse, syncope and even death. </li></ul><ul><li>It should be treated as an emergency, usually with DC cardioversion. </li></ul><ul><li>Prophylactic anti-arrhythmic drug therapy is only indicated in symptomatic patients and is aimed at slowing the conduction rate and prolonging the refractory period of the bypass tract, using agents such as flecainide, propafenone or amiodarone </li></ul><ul><li>Digoxin and verapamil shorten the refractory period of the accessory pathway and should be avoided. </li></ul><ul><li>Catheter of the accessory pathway is the treatment of choice for symptomatic patients. </li></ul>
  34. 34. VENTRICULAR TACHYARRHYTHMIAS <ul><li>VENTRICULAR ECTOPIC BEATS (EXTRASYSTOLES, PREMATURE BEATS) </li></ul><ul><li>The QRS complexes of ventricular ectopic beats are of abnormal morphology because the bundle branches are activated one after the other, rather than simultaneously. </li></ul><ul><li>The ECG shows premature broad, bizarre QRS complexes which may be unifocal (identical beats arising from a single ectopic focus) or multifocal (varying morphology with multiple foci -' Couplet' and 'triplet' are terms used to describe two or three successive ectopic beats, whereas a run of alternate sinus and ectopic beats is known as ventricular 'bigeminy'. </li></ul><ul><li>Ectopic beats produce a low stroke volume because left ventricular contraction occurs before filling is complete&pulse is therefore irregular, with weak or missed beats . </li></ul>
  35. 35. VENTRICULAR TACHYARRHYTHMIAS <ul><li>VENTRICULAR ECTOPIC BEATS (EXTRASYSTOLES, PREMATURE BEATS) </li></ul><ul><li>Patients are usually asymptomatic but may complain of an irregular heart beat, missed beats or abnormally strong beats (due to the increased output of the post-ectopic sinus beat). The significance of ventricular ectopic beats (VEBs) depends on the presence or absence of underlying heart disease . Ventricular ectopic beats in otherwise healthy subjects VEBs are frequently found in healthy people, and their prevalence increases with age. Ectopic beats in patients with otherwise normal hearts are more prominent at rest, and disappear with exercise. Treatment is not necessary unless the patient is highly symptomatic, in which case β- blockers can be used . VEBs are sometimes a manifestation of otherwise subclinical heart disease, particularly coronary artery disease . </li></ul>
  36. 36. Ventricular ectopic beats associated with heart disease <ul><li>Frequent VEBs often occur during acute myocardial infarction but need no treatment. </li></ul><ul><li>Persistent frequent (> 10 per hour) ventricular ectopic beats in patients who have survived the acute phase of myocardial infarction indicate a poor long-term outcome. </li></ul><ul><li>Other than β- blockers, anti-arrhythmic drugs do not improve and may even worsen prognosis . </li></ul><ul><li>VEBs are common in patients with heart failure, when they are associated with an adverse prognosis, but again the outlook is no better if they are suppressed with anti-arrhythmic drugs. </li></ul><ul><li>Effective treatment of the heart failure may suppress the ectopic beats . </li></ul><ul><li>VEBs are also a feature of digoxin toxicity, are sometimes found in mitral valve prolapse, and may occur as 'escape beats' in the presence of an underlying bradycardia. </li></ul><ul><li>Treatment should always be directed at the underlying condition . </li></ul>
  37. 37. FEATURES IN FAVOUR OF VT IN THE DIFFERENTIAL DIAGNOSIS OF BROAD-COMPLEX TACHYCARDIA <ul><li>A history of myocardial infarction </li></ul><ul><li>AV dissociation (pathognomonic ) </li></ul><ul><li>Capture/fusion beats (pathognomonic) </li></ul><ul><li>Extreme left axis deviation </li></ul><ul><li>Very broad QRS complexes (> 140 ms) </li></ul><ul><li>No response to carotid sinus massage or i.v. adenosine </li></ul>
  38. 38. VT <ul><li>VT most often occurs in patients with coronary heart disease or cardiomyopathies. </li></ul><ul><li>In these settings it is serious because it may cause haemodynamic compromise or degenerate into ventricular fibrillation . </li></ul><ul><li>It is caused by abnormal automaticity or triggered activity in ischaemic tissue, or by re-entry within diseased ventricular tissue. </li></ul><ul><li>Patients may complain of palpitation or the symptoms of low cardiac output, such as dizziness, dyspnoea or syncope. </li></ul><ul><li>The ECG shows tachycardia with broad, abnormal QRS complexes with a rate above 120/min </li></ul>
  39. 39. VT <ul><li>VT may be difficult to distinguish from supraventricular tachycardia with bundle branch block or pre-excitation (Wolff-Parkinson-White syndrome). </li></ul><ul><li>Intracardiac or oesophageal ECG may help to establish the diagnosis. </li></ul><ul><li>When there is doubt it is safer to manage the problem as VT, which is by far the most common cause of a broad-complex tachycardia . </li></ul><ul><li>The common causes of ventricular tachycardia include acute myocardial infarction, cardiomyopathy and chronic ischaemic heart disease, particularly when it is associated with a ventricular aneurysm or poor left ventricular function . </li></ul><ul><li>Patients recovering from myocardial infarction sometimes have periods of idioventricular rhythm ('slow' VT) at a rate only slightly above the preceding sinus rate and less than 120/min,often reflect reperfusion of the infarct territory and may be a good sign,are usually self-limiting, asymptomatic& do not require treatment. </li></ul><ul><li>. </li></ul>
  40. 40. VT <ul><li>Other forms of ventricular tachycardia, if they last for more than a few beats, will require treatment, often as an emergency . </li></ul><ul><li>VT occasionally occurs in patients with otherwise healthy hearts ('normal heart VT'), usually because of abnormal automaticity in the right ventricular outflow tract or one of the fascicles of the left bundle branch. </li></ul><ul><li>In these cases the prognosis is good and catheter ablation can be curative </li></ul><ul><li>. Management Prompt action to restore sinus rhythm is required and in most cases should be followed by prophylactic therapy. </li></ul><ul><li>DC cardioversion is the treatment of choice if systolic BP is less than 90 mmHg. </li></ul><ul><li>If the arrhythmia is well tolerated, intravenous amiodarone may be given as a bolus followed by an intravenous infusion . </li></ul><ul><li>Intravenous lidocaine can be used but it can depress left ventricular function, causing hypotension or acute heart failure. </li></ul>
  41. 41. VT <ul><li>Hypokalaemia, hypomagnesaemia, acidosis and hypoxaemia can aggravate the situation and must be corrected . </li></ul><ul><li>Beta-blockers may be effective at suppressing VT. </li></ul><ul><li>Amiodarone can be added if additional control is needed. </li></ul><ul><li>Class I anti-arrhythmic drugs can be used acutely but are dangerous in the long term in patients with ischaemic heart disease. </li></ul><ul><li>In patients considered at high risk of arrhythmic death (e.g. those with poor left ventricular function, or in whom VT is associated with haemodynamic compromise), the use of an implantable cardiac defibrillator is recommended. </li></ul><ul><li>Rarely, surgery or catheter ablation can be used to interrupt the arrhythmia focus or CIRCUIT. </li></ul>
  42. 42. TORSADES DE POINTES (TWISTING POINTS ) <ul><li>This form of polymorphic ventricular tachycardia is a complication of prolonged ventricular repolarisation (prolonged QT interval). </li></ul><ul><li>The ECG shows rapid irregular complexes that oscillate from an upright to an inverted position and seem to twist around the baseline as the mean QRS axis . </li></ul><ul><li>The arrhythmia is usually non-sustained and repetitive but may degenerate into ventricular fibrillation. </li></ul><ul><li>During periods of sinus rhythm the ECG will usually show a prolonged QT interval . </li></ul><ul><li>The arrhythmia is more common in women and is often triggered by a combination of aetiological factors (e.g. multiple medications and hypokalaemia). </li></ul><ul><li>The congenital long QT syndromes are a family of genetic disorders that are characterised by mutations in genes that code for cardiac sodium or potassium channels . </li></ul><ul><li>. </li></ul>
  43. 43. TORSADES DE POINTES (TWISTING POINTS ) <ul><li>Treatment should be directed at the underlying cause. </li></ul><ul><li>Intravenous magnesium (8 mmol over 15 minutes, then 72 mmol over 24 hours) should be given in all cases. </li></ul><ul><li>Atrial pacing will usually suppress the arrhythmia through rate-dependent shortening of the QT interval. </li></ul><ul><li>Intravenous isoprenaline is a reasonable alternative to pacing but should be avoided in patients with the congenital long QT syndrome </li></ul>
  44. 44. CAUSES OF LONG QT INTERVAL AND TORSADES DE POINTES <ul><li>Bradycardia(Bradycardia compounds other factors that cause torsades de pointes) </li></ul><ul><li>Electrolyte disturbance </li></ul><ul><li>Hypokalaemia </li></ul><ul><li>Hypomagnesaemia </li></ul><ul><li>Hypocalcaemia </li></ul><ul><li>Drugs </li></ul><ul><li>Disopyramide (and other class la anti-arrhythmic drugs , </li></ul><ul><li>Sotalol, amiodarone (and other class III anti-arrhythmic drugs ) Amitriptyline (and other tricyclic antidepressants </li></ul><ul><li>Chlorpromazine (and other phenothiazines </li></ul><ul><li>Erythromycin (and other macrolides) … and many more </li></ul><ul><li>Congenital syndromes </li></ul><ul><li>Romano-Ward syndrome (autosomal dominant ) </li></ul><ul><li>Jervell and Lange-Nielson syndrome (autosomal recessive, associated with congenital deafness ) </li></ul>
  45. 45. TORSADES DE POINTES (TWISTING POINTS ) <ul><li>Long-term therapy may not be necessary if the underlying cause can be removed. </li></ul><ul><li>Beta-blockers or left stellate ganglion block may be of value in patients with a congenital long QT syndrome. </li></ul><ul><li>An implantable cardiac defibrillator is often advisable . </li></ul><ul><li>The Brugada syndrome is a related genetic disorder that may present with polymorphic ventricular tachycardia or sudden death; it is characterised by a defect in sodium channel function, and an abnormal ECG (right bundle branch block and ST elevation in V1 and V2 , but not usually prolongation of the QT interval . </li></ul>
  46. 46. SINOATRIAL DISEASE (SICK SINUS SYNDROME ) <ul><li>Sinoatrial disease can occur at any age, but is most common in the elderly. </li></ul><ul><li>The underlying pathology is not understood but may involve fibrosis, degenerative changes and/or ischaemia of the sinoatrial (sinus) node. </li></ul><ul><li>The condition is characterised by a variety of arrhythmias and may present with palpitation, dizzy spells or syncope, due to intermittent tachycardia, bradycardia, or pauses with no atrial or ventricular activity (sinoatrial block or sinus arrest ) </li></ul><ul><li>A permanent pacemaker may benefit patients with troublesome symptoms due to spontaneous bradycardias, or those with symptomatic bradycardias induced by drugs required to prevent tachyarrhythmias. </li></ul><ul><li>Atrial pacing may help to prevent episodes of atrial fibrillation. Permanent pacing does not improve prognosis and is not indicated in patients who are asymptomatic </li></ul>
  47. 47. COMMON FEATURES OF SINOATRIAL DISEASE <ul><li>Sinus bradycardia </li></ul><ul><li>Sinoatrial block (sinus arrest ) </li></ul><ul><li>Paroxysmal supraventricular tachycardia </li></ul><ul><li>Paroxysmal atrial fibrillation </li></ul><ul><li>Atrioventricular block </li></ul>
  48. 48. ATRIOVENTRICULAR (AV) BLOCK <ul><li>Atrioventricular conduction is influenced by autonomic activity. </li></ul><ul><li>AV block can therefore be intermittent and may only be evident when the conducting tissue is stressed by a rapid atrial rate. </li></ul><ul><li>Accordingly, atrial tachyarrhythmias are often associated with AV block </li></ul><ul><li>First-degree AV block :In this condition AV conduction is delayed so the PR interval is prolonged (> 0.20 seconds </li></ul><ul><li>It rarely causes symptoms . </li></ul>
  49. 49. ATRIOVENTRICULAR (AV) BLOCK <ul><li>Second-degree AV block: </li></ul><ul><li>In this condition dropped beats occur because some impulses from the atria fail to conduct to the ventricles. </li></ul><ul><li>In Mobitz type I second-degree AV block, there is progressive lengthening of successive PR intervals culminating in a dropped beat. </li></ul><ul><li>The cycle then repeats itself. This is known as Wenckebach's phenomenon and is usually due to impaired conduction in the AV node itself. </li></ul><ul><li>The phenomenon may be physiological and is sometimes observed at rest or during sleep in athletic young adults with high vagal tone. . </li></ul>
  50. 50. ATRIOVENTRICULAR (AV) BLOCK <ul><li>Mobitz type II second-degree AV block </li></ul><ul><li>PR interval of the conducted impulses remains constant but some P waves are not conducted. </li></ul><ul><li>This is usually caused by disease of the His-Purkinje system and carries a risk of asystole. </li></ul><ul><li>In 2:1 AV block alternate P waves are conducted so it is impossible to distinguish between Mobitz type I and type II block. </li></ul><ul><li>Third-degree (complete) AV block When AV conduction fails completely, the atria and ventricles beat independently (AV dissociation, Ventricular activity is maintained by an escape rhythm arising in the AV node or bundle of His (narrow QRS complexes) or the distal Purkinje tissues (broad QRS complexes). </li></ul><ul><li>Distal escape rhythms tend to be slower and less reliable. </li></ul>
  51. 51. ATRIOVENTRICULAR (AV) BLOCK <ul><li>Complete heart block: </li></ul><ul><li>Produces a slow (25-50/min), regular pulse that, except in the case of congenital complete heart block, does not vary with exercise. </li></ul><ul><li>There is usually a compensatory increase in stroke volume with a large volume pulse and systolic flow murmurs. </li></ul><ul><li>Cannon waves may be visible in the neck and the intensity of the first heart sound varies due to the loss of AV synchrony. </li></ul>
  52. 52. AV Block: <ul><li>AETIOLOGY OF COMPLETE HEART BLOCK </li></ul><ul><li>Congenital </li></ul><ul><li>Acquired </li></ul><ul><li>Idiopathic fibrosis </li></ul><ul><li>Myocardial infarction/ischaemia </li></ul><ul><li>Inflammation </li></ul><ul><ul><li>Acute (e.g. aortic root abscess in infective endocarditis) </li></ul></ul><ul><ul><li>Chronic (e.g. sarcoidosis; Chagas disease) </li></ul></ul><ul><li>Trauma (e.g. cardiac surgery) </li></ul><ul><li>Drugs (e.g. digoxin, β-blocker) </li></ul>
  53. 53. AV Block: <ul><li>Stokes-Adams attacks: </li></ul><ul><li>Episodes of ventricular asystole may complicate complete heart block or Mobitz type II second-degree AV block&in patients with sinoatrial disease. </li></ul><ul><li>This may cause recurrent syncope or 'Stokes-Adams' attacks. </li></ul><ul><li>A typical episode is characterised by a sudden loss of consciousness, which frequently occurs without warning and may result in a fall. </li></ul><ul><li>Convulsions (due to cerebral ischaemia) can occur if there is prolonged asystole. </li></ul><ul><li>There is pallor and a death-like appearance during the attack, but when the heart starts beating again there is a characteristic flush. </li></ul><ul><li>In contrast to epilepsy, recovery is rapid. </li></ul><ul><li>The carotid sinus syndrome and the vasovagal syndrome may cause similar symptoms. </li></ul>
  54. 54. AV Block: <ul><li>Management AV block complicating AMI: </li></ul><ul><li>Acute inferior myocardial infarction is often complicated by transient AV block because the right coronary artery supplies the AV junction. </li></ul><ul><li>There is usually a reliable escape rhythm, and if the patient remains well, no treatment is required. </li></ul><ul><li>Symptomatic second-degree or complete heart block may respond to atropine (0.6 mg i.v., repeated as necessary) or if this fails, a temporary pacemaker. </li></ul><ul><li>In most cases the AV block will resolve within 7-10 days. </li></ul><ul><li>Second-degree or complete heart block complicating acute anterior myocardial infarction is usually a sign of extensive ventricular damage involving both bundle branches and carries a poor prognosis. </li></ul>
  55. 55. AV Block: <ul><li>Management AV block complicating AMI: </li></ul><ul><li>Asystole may ensue and a temporary pacemaker should be inserted as soon as possible. </li></ul><ul><li>If the patient presents with asystole, i.v. atropine (3 mg) or i.v. isoprenaline (2 mg in 500 ml 5% dextrose, infused at 10-60 ml/hour) may help to maintain the circulation until a temporary pacing electrode can be inserted. </li></ul><ul><li>Transcutaneous pacing can provide effective temporary support. </li></ul><ul><li>Chronic AV block Patients with symptomatic bradyarrhythmias associated with AV block should receive a permanent pacemaker </li></ul><ul><li>Asymptomatic first-degree or Mobitz type I second-degree AV block (Wenckebach's phenomenon) does not require treatment but may be an indication of serious underlying heart disease. </li></ul><ul><li>A permanent pacemaker is usually indicated in patients with asymptomatic Mobitz type II second-degree or complete heart block because there is evidence that pacing can improve their prognosis,exception may be young asymptomatics with congenital complete heart block who have a mean daytime heart rate of more than 50 per minute. </li></ul>
  56. 56. BUNDLE BRANCH BLOCK AND HEMIBLOCK <ul><li>Interruption of the right or left branch of the bundle of His delays activation of the appropriate ventricle, broadens the QRS complex (0.12 seconds or more) and produces the characteristic alterations in QRS morphology . </li></ul>
  57. 57. COMMON CAUSES OF BUNDLE BRANCH BLOCK <ul><li>Right bundle branch block </li></ul><ul><li>Normal variant </li></ul><ul><li>Right ventricular hypertrophy or strain, e.g. pulmonary embolism </li></ul><ul><li>Congenital heart disease, e.g. atrial septal defect </li></ul><ul><li>Coronary artery disease </li></ul><ul><li>Left bundle branch block </li></ul><ul><li>Coronary artery disease </li></ul><ul><li>Hypertension </li></ul><ul><li>Aortic valve disease </li></ul><ul><li>Cardiomyopathy </li></ul>
  58. 58. RBBB: <ul><li>Can be a common normal variant but left bundle branch block (LBBB) usually signifies important underlying heart disease. </li></ul><ul><li>Both forms of bundle branch block may be due to conducting tissue disease but are also features of other types of heart disease </li></ul><ul><li>The left branch of the bundle of His divides into an anterior and a posterior fascicle. </li></ul><ul><li>Damage to the conducting tissue at this point (hemiblock) does not broaden the QRS complex, but alters the mean direction of ventricular depolarisation (mean QRS axis), causing left axis deviation in left anterior hemiblock and right axis deviation in left posterior hemiblock ( </li></ul><ul><li>The combination of right bundle branch and left anterior or posterior hemiblock is known as bifascicular block . </li></ul>
  59. 59. CLASSIFICATION OF ANTI-ARRHYTHMIC DRUGS ACCORDING TO THEIR EFFECT ON THE INTRACELLULAR ACTION POTENTIAL <ul><li>Class I - membrane-stabilising agents (sodium channel blockers ) </li></ul><ul><li>A. Block Na + channel and prolong action potential </li></ul><ul><ul><li>Quinidine, disopyramide </li></ul></ul><ul><li>B. ) Block Na + channel and shorten action potential </li></ul><ul><ul><li>Lidocaine, mexiletine </li></ul></ul><ul><li>C. ) Block Na + channel with no effect on action potential </li></ul><ul><ul><li>Flecanide, propafenone </li></ul></ul>
  61. 61. IMPLANTABLE CARDIAC DEFIBRILLATORS (ICDS <ul><li>KEY INDICATIONS FOR ICD THERAPY </li></ul><ul><li>Primary prevention </li></ul><ul><li>After myocardial infarction, if LV ejection fraction < 30% </li></ul><ul><li>Mild to moderate symptomatic heart failure, on optimal drug therapy, with LV ejection fraction < 35% </li></ul><ul><li>Secondary prevention </li></ul><ul><li>Survivors of VF or VT cardiac arrest not due to transient or reversible cause </li></ul><ul><li>VT with haemodynamic compromise or significant LV impairment (LV ejection fraction < 35% </li></ul>
  64. 64. CARDIAC RESYNCHRONISATION THERAPY (CRT) <ul><li>' CRT improves symptoms and quality of life, and reduces mortality in patients with moderate to severe symptomatic heart failure who are in sinus rhythm, with left bundle branch block and LV ejection fraction ≤35% .' </li></ul>