Management of cardiac arrhythmias

Definition of arrhythmia - background on cardiac physiology including conduction in heart - action potential - pathogensis of arrhythmia - causes and risk factors for arrhythmia- diagnosis of arrhythmia - symptoms of tachyarrhythmias and bradyarrhythmias - investigations for arrhythmia - treatment of arrhythmia - pharmacological and other modalities of therapy for arrhythmia - managment of different types of arrhythmias

1. Arrhythmias Management Dr. Sameh Ahmad Muhamad abdelghany Lecturer Of Clinical Pharmacology Mansura Faculty of medicine

2. Arryth mia Introduction      Normal Cardiac Physiology Pathogenesis & causes Diagnosis Treatment CONTENTS

3. INTRODUCTION

4. Introduction Definiton : a – “without” rhuthmos – “ ryhtm ” i.e it means “without rhythm”. Also known as “ cardiac dysrhythmia” Cardiac arrhythmias are a group of conditions in which the heart beats with an irregular or abnormal rhythm. Arrhythmia /dysrhythmia: abnormality in the site of origin of impulse, rate, or conduction

5. Introduction Arrhythmia affects millions of people. Atrial fibrillation and atrial flutter resulted in 112,000 deaths in 2013, up from 29,000 in 1990. Sudden cardiac death is the cause of about half of deaths due to cardiovascular disease or about 15% of all deaths globally. About 80% of sudden cardiac death is the result of ventricular arrhythmias. Arrhythmias may occur at any age but are more common among older people.

6. NORMAL CARDIAC ELECTROPHYSIOLOGY

7. Normal cardiac rhythm Heart rate should be between 60 and 100 per minute. All the cardiac impulses should originate from the SA node of the heart. The impulse should conduct through the normal conduction pathway. The impulse should pass through conducting pathways with normal velocity

8. Normal Electrical Conduction System SA node Inter-nodal pathways AV node Bundle of his Left & Right bundle branches Purkinje fibers

9. Electrical Conduction System EKG Waveforms One complete cardiac cycle = P, Q, R, S, (QRS complex), and T wave P wave : Atrial depolarization (contraction) QRS Complex : Ventricular depolarization, atrial repolarization T wave : Ventricular repolarization (resting phase)

10. Electrical Conduction System EKG Waveforms

11. Electrophysiology - resting potential A transmembrane electrical gradient (potential) is maintained, with the interior of the cell negative with respect to outside the cell Caused by unequal distribution of ions inside vs. outside cell Na+ higher outside than inside cell Ca+ much higher “ “ “ “ K+ higher inside cell than outside Maintenance by ion selective channels, active pumps and exchangers

12. Cardiac action potential Divided into five phases (0,1,2,3,4) Phase 4 : resting phase (resting membrane potential) Phase cardiac cells remain in until stimulated Associated with diastole portion of heart cycle

13. Cardiac action potential Addition of current into cardiac muscle (stimulation) causes Phase 0 :opening of fast Na channels and rapid depolarization Drives Na+ into cell (inward current), changing membrane potential Transient outward current due to movement of Cl- and K+ Phase 1 : initial rapid repolarization Closure of the fast Na+ channels Phase 0 and 1 together correspond to the R and S waves of the ECG

14. Cardiac action potential Phase 2 : plateau phase sustained by the balance between the inward movement of Ca+ and outward movement of K + Has a long duration compared to other nerve and muscle tissue Normally blocks any premature stimulator signals (other muscle tissue can accept additional stimulation and increase contractility in a summation effect) Corresponds to ST segment of the ECG.

15. Cardiac action potential Phase 3 (repolarization) K+ channels remain open Allows K+ to build up outside the cell, causing the cell to repolarize K + channels finally close when membrane potential reaches certain level Corresponds to T wave on the ECG

16. Cardiac action potential

17. Cardiac action potential Differences between nonpacemaker and pacemaker cell action potentials Thera are only 3 phases:0,3,4 Pacemaker cells: Slow, continuous depolarization during rest Continuously moves potential towards threshold for a new action potential (called a phase 4 depolarization )

18. Cardiac action potential Differences between non pacemaker and pacemaker cell action potentials Pacemaker cells: Slow, continuous depolarization during rest Continuously moves potential towards threshold for a new action potential (called a phase 4 depolarization )

19. Cardiac action potential in Pace maker cells

20. Cardiac action potential

21. ARRYTHMIA PATHOGENESIS

22. Arrhythmia pathogenesis Disorder of impulse formation: Automaticity. Triggered Activity. Early after depolarization. Delayed after depolarization. Disorder of impulse conduction: Impulse Block Re - entry phenomena

23. Abnormal automaticity The SA node is the heart’s natural pacemaker Any impulses fired from elsewhere in the heart before or concurrently with SA node firing can lead to premature heartbeats or sustained abnormal heartbeats. Problems associated are sinus tachyarrhythmia sinus bradyarrhythmia Abnormality in site of impulse generation ,ectopic loci Escape rhythms

24. Triggered automaticity This is an abnormal secondary upstroke which occur only after a normal initial or “triggering “ upstroke or action potential. These secondary upstrokes are called after --depolarization's This may be of two types Early after depolarization Delayed after depolarization

25. Triggered automaticity Early After depolarization Delayed After depolarization

26. Abnormal impulse conduction Conduction block may occur due to depression of impulse conduction at AV node & bundle of His, due to vagal influence or ischaemia . Types : 1st degree heart block – slowed conduction 2nd degree block – some supraventricular complex not conducted 3rd degree block – no supraventricular complex are conducted

27. Re-entry phenomena It can be of two types Anatomically defined re-entry E.g Wolf ParkinsonWhite syndrome( wpw ) Functionally defined re-entry Mostly seen in patients with ischemic heart disease

28. Re-entry phenomena(anatomical)

29. Re-entry circuit

30. Two features of arrhythmias Site of origin Atria Atrioventricular node (AV node) Ventricles Affect on heart rate Too slow heart rate (bradycardia) Too fast heart rate(tachycardia)

31. Classification of arrhythmias Abnormal heart pulse formation Sinus arrhythmia Atrial arrhythmia Atrioventricular junctional arrhythmia Ventricular arrhythmia Abnormal heart pulse conduction Sinus-atrial block Intra-atrial block Atrio -ventricular block Intra-ventricular block Abnormal heart pulse formation and conduction

32. CAUSES & RISK FACTORS

33. Causes Coronary artery disease. Electrolyte imbalances in your blood (such as sodium or potassium). Structural changes of the heart Scarring of the heart, often the result of a heart attack Healing process after heart surgery. Hypertension (high blood pressure)

34. Causes Diabetes Drug abuse Excessive coffee consumption Hyperthyroidism (an overactive thyroid gland) Mental stress Smoking Some dietary supplements &some herbal treatments Some medications

35. DIAGNOSIS

36. Symptoms of tachycardia breathlessness (dyspnea) dizziness syncope (fainting, or nearly fainting) fluttering in the chest chest pain lightheadedness sudden weakness

37. Symptoms of bradycardia angina (chest pain) trouble concentrating confusion difficulties when exercising dizziness fatigue (tiredness) lightheadedness palpitations shortness of breath syncope (fainting or nearly fainting) diaphoresis, or sweating

38. Symptoms of arrythmias

39. Investigations blood and urine tests EKG (electrocardiogram) Holtermonitor - a wearable device that records the heart for 1-2 days echocardiogram chest X-ray heart catheterization

40. Investigations

41. TREATMENT OF ARRYTHMIAS

42. Management of arrhythmias Pharmacological therapy. Cardio version. Pacemaker therapy. Surgical therapy Interventional therapy

43. Pharmacologic Rationale & Goals The ultimate goal of antiarrhythmic drug therapy : Restore normal sinus rhythm and conduction Prevent more serious and possibly lethal arrhythmias from occurring. Antiarrhythmic drugs are used to : decrease conduction velocity change the duration of the effective refractory period (ERP) suppress abnormal automaticity

44. Mechanisms of Anti-arrhythmic drugs To suppress automaticity ↓ Rate of phase 0 ↓ Slope of phase 0 ↑ Duration of ERP(effective refractory period) Resting membrane potential more negative Abolishing reentry Slow conduction ↑ ERP

45. Anti arrhythmic drugs Anti-tachycardia agents Anti-bradycardia agents

46. Anti-tachycardia agents Vaugham Williams classification Class I : Natrium channel blocker Class II : ß-receptor blocker Class III : Potassium channel blocker Class IV : Calcium channel blocker Others: Adenosine, Digitalis

47. Class I – Na+ channel blockers The primary action of these class of drugs is To limit the conductance of Na+ across the cell membrane Reduce the rate of phase 4 depolarization They are further divide into three subclasses Subclass IA Subclass IB Subclass IC

48. Na+ channel blockers(subclass IA) Less use in clinic The anti arrhythmic drugs include quinidine procainamide. are open state Na+ channel blockers . This class of drugs moderately delay the channel recovery. They suppress the AV conduction and prolong refractoriness

49. Na+ channel blockers(subclass IB) block the Na+ channels more in inactivated than in open state , but do not delay channel recovery. have little or no effect at slower heart rates, and more effects at faster heart rates do not change or may decrease the action potential duration. Class IB drugs tend to be more specific for voltage gated Na channels than Ia E.g Lidocaine - Mexiletine Perfect to ventricular tachyarrhythmia

50. Na+ channel blockers(subclass IC) Most prominent action is on open state Na+ channels and have the longest recovery time delay conduction and prolong the P-R interval, broaden the QRS complex have minimal effect on action potential duration E.g Moricizine – Propafenone Can be used in ventricular and/or supra-ventricular tachycardia and extrasystole. This class of drug has high proarrhythmic potential

51. Cardiac Na+ channels

52. Class II – adrenergic agents are conventional beta blockers act by blocking the effects of catecholamines at the β1- adrenergic receptors, thereby decreasing sympathetic activity on the heart. They decrease conduction through the AV node. They prolong PR interval, but no effects on QRS or QT interval E.g. Propranolol - Metoprolol Perfect to hypertension and coronary artery disease patients associated with tachyarrhythmia

53. Class III – K+ channel blockers acts by prolonging repolarization. Not affect the sodium channel, so conduction velocity is not decreased. The prolongation of the action potential duration and refractory period, combined with the maintenance of normal conduction velocity, prevent re-entrant arrhythmias . Class III agents have the potential to prolong the QT interval of the ECG E.g Amiodarone - Bretylium

54. Class IV- calcium channel blockers The primary action of this class of drug is to inhibit Ca2+ mediated slow inward current. They decrease conduction through the AV node, and shorten phase two (the plateau) of the cardiac action potential. As they reduce the contractility of the heart, so may be inappropriate in heart failure. They slow sinus rhythm, prolong PR interval, no effect on QRS complex E.g. Verapamil - Diltiazem used in supraventricular tachycardia

55. Others Adenosine be used in supraventricular tachycardia Digoaxin : Used to control ventricular rate in AF – AFL -PSVT

56. Adenosine Endogenously produced important chemical mediator used in PSVT Mechanism: Activation of Ach sensitive K+ channel causes membrane hyper polarization of SA node and results in depression of SA node slowing of AV conduction and shortening of action potential in atrium indirectly reduces CA++ current in AV node with depression of reentry in PSVT.

57. Anti-bradycardia agents ß- adrenic receptor activator : Isoprenaline Epinephrine M-cholinergic receptor blocker: Atropine Non-specific activator: Aminophylline

58. Proarrhythmic effect of antiarrhythmic agents Class Ia , Ic : Prolong QT interval, will cause VT or VF in coronary artery disease and heart failure patients Class III : Like Ia , Ic class agents Class II, IV : Bradycardia

59. New developments Agents Similar to Amiodarone Dronedarone, budiodarone , celivarone Others Ranolazine, vernaklant , ivabradine Nutritional alternatives Berberine, coenzymeQ10, taurine

60. Non-drug therapy Cardioversion : For tachycardia especially hemodynamic unstable patient Radiofrequency catheter ablation (RFCA): For those tachycardia patients (SVT, VT, AF, AFL) Artificial cardiac pacing: For bradycardia, heart failure and malignant ventricular arrhythmia patients.

61. Cardioversion

62. Radiofrequency catheter ablation

63. Artificial cardiac pacing

64. Management of different types of arrythmia

65. Premature beats Premature beats are the most common type of arrhythmia. Premature beats that occur in the atria are called premature atrial contractions, or PACs and those that occur in the ventricles are called premature ventricular contractions PACs are common and may occur as the result of stimulants such as coffee, tea, alcohol, cigarettes, or medications. Treatment is rarely necessary

66. Premature beats

67. Sinus tachycardia Sinus tachycardia is a heart rhythm originating from the SA node with an elevated rate of impulses, defined as a rate greater than 100 beats/min in an average adult. Sinus tachycardia is usually a response to normal physiological situations, such as exercise and an increased sympathetic tone with increased catecholamine release—stress, fright, flight,anger Treatment not required for physiologic sinus tachycardia. Underlying causes are treated if present.

68. Sinus tachycardia

69. Paroxysmal supraventricular tachycardia Here the heart rate ranges from 160 – 250 beats per min There are 2 common types Atrio ventricular reciprocating tachycardia AV nodal reentrant tachycardia

70. AV nodal Re-entrant Tachycardia AVNRT develops because of the presence of two electro physiologically distinct pathways for conduction in the complex the AV node. The fast pathway in the more superior part of the node has a longer refractory period, whereas the pathway lower in the AV node region conducts more slowly but has a shorter refractory period. As a result of the inhomogeneities of conduction and refractoriness, a reentrant circuit can develop in response to premature stimulation.

71. AV Nodal Reciprocating Tachycardia Patients with AVRT have been born with an extra, abnormal electrical connection in the heart. In AVRT, the extra connection, which is often called an accessory pathway, joins one of the atria with one of the ventricles In some patients with AVRT, the accessory pathway is capable of conducting electrical impulses in both directions while in other patients the accessory pathway can only conduct electrical impulses in one direction or the other

72. AV Nodal Reciprocating Tachycardia This difference turns out to be important. In most patients with AVRT, the impulses can only go across the accessory pathway from the ventricle to the atrium. Patients in whom the impulses can travel across the accessory pathway in the other direction - from the atrium to the ventricle - are said to have Wolff-Parkinson-White (WPW) syndrome

73. Management of PSVT Acute Management If the patient is hemodynamically stable, vagal maneuvers e.g carotid massage , can be successfully employed. If not successful, the administration of IV adenosine frequently does so. Intravenous beta blockade or calcium channel therapy should be considered as second-line treatment. Patients with hemodynamic instability require emergency cardioversion .

74. Management of PSVT Long-term management It includes ablation of the accessory pathway. Also, verapamil, diltiazem & β-blockers are effective in 60- 80% of patients.

75. Wolf Parkinson White Syndrome An abnormal band of atrial tissue connects the atria and the ventricles and can electrically bypass the normal conducting pathways A reentry circuit develops causing paroxysms of tachycardia. Drug treatment : flecainide, amiodarone or disopyramide Digoxin and verapamil are contraindicated Transvenous catheter radiofrequency ablation is the treatment of choice

76. Wolf Parkinson White Syndrome

77. Atrial Flutter HR ranges between 200-350/min Here the electrical signals come from the atria at a fast but even rate, often causing the ventricles to contract faster and increase the heart rate. When the signals from the atria are coming at a faster rate than the ventricles can respond to, the ECG pattern develops a signature "sawtooth" pattern, showing two or more flutter waves between each QRS complex

78. Atrial Flutter

79. Atrial Flutter Treatment For acute paroxysm : Cardioversion Recurrent paroxysms may be prevented by class Ic and class III agents The treatment of choice for patients with recurrent atrial flutter is radiofrequency catheter ablation

80. Atrial fibrillations Atrial fibrillation is the most common sustained arrhythmia. It is marked by disorganized, rapid, and irregular atrial activation. The ventricular response to the rapid atrial activation is also irregular Typically the pulse rate will vary between 120 and 160 beats per minute The ECG shows normal but irregular QRS complexes, fine oscillations of the baseline (so-called fibrillation or f waves) and no P waves

81. Atrial fibrillations

82. Atrial fibrillations When atrial fibrillation is due to an acute precipitating event the provoking cause should be treated. Acute management of AF Cardioversion rates delivered synchronously with the QRS complex typically are >90%. Pharmacologic therapy to terminate AF is less reliable. Oral and/or IV administration of amiodarone or procainamide has only modest success. Patients are anticoagulated ( warfarin) for 4 weeks before cardioversion

83. Ventricular tachycardia This is a potentially life-threatening arrhythmia because it may lead to ventricular fibrillation, asystole, and sudden death. A condition in which an electrical signal is sent from the ventricles at a very fast but often regular rate. If the fast rhythm self-terminates within 30 seconds, it is considered a non-sustained ventricular tachycardia . If the rhythm lasts more than 30 seconds, it is known as a sustained ventricular tachycardia

84. Ventricular tachycardia

85. Ventricular tachycardia Treatment In hemodynamically compromised : emergency asynchronous defibrillation is done If hemodynamically stable: intravenous therapy with class I drugs or amiodarone . VT in patients with structural heart disease is now almost always treated with the implantation of an ICD to manage anticipated VT recurrence

86. Ventricular fibrillation A condition in which many electrical signals are sent from the ventricles at a very fast and erratic rate. As a result, the ventricles are unable to fill with blood and pump. This rhythm is life-threatening because there is no pulse and complete loss of consciousness. It requires prompt defibrillation to restore the normal rhythm and function of the heart.

87. Ventricular fibrillation

88. Ventricular fibrillation Basic and advanced cardiac life support is needed Implantable cardioverter-defibrillators (ICDs) are first-line therapy in the management of these patients

89. Torsades pointes This is a type of short duration tachycardia that reverts to sinus rhythm spontaneously. It may be Congenital or due to Electrolyte disorders and certain Drugs It may present with syncopal attacks and occasionally ventricular fibrillation. QRS complexes are irregular and rapid that twist around the baseline. In between the spells of tachycardia the ECG show prolonged QT interval

90. Torsades pointes

91. Torsades pointes Treatment: correction of any electrolyte disturbances stopping of causative drug atrial or ventricular pacing Magnesium sulphate for acquired long QT interval IV isoprenaline in acquired cases B blockers in congenital types Patients who remain symptomatic despite conventional therapy and those with a strong family history of sudden death usually need ICD therapy

92. Sinus Bradycardia Physiological variant due to strong vagal tone or atheletic training. Rate as low as 50 at rest and 40 during sleep. Common causes: Hypothermia, hypothyroidism, Drug therapy with betablockers, digitalis and other antiarrhythmic drugs. Acute ischemia and infarction of the sinus node (as a complication of acute myocardial infarction).

93. Sinus Bradycardia

94. Sick sinus syndrome Sick sinus syndrome is a group of arrhythmias caused by a malfunction of the sinus node A condition in which the sinus node sends out electrical signals either too slowly or too fast. There may be alternation between too-fast and too-slow rates. This condition may cause symptoms if the rate becomes too slow or too fast for the body to tolerate.

95. Sick sinus syndrome Artificial pacemakers have been used in the treatment of sick sinus syndrome. Bradyarrhythmias are well controlled with pacemakers, while tachyarrhythmias respond well to medical therapy. However, because both bradyarrhythmias and tachyarrhythmias may be present, drugs to control tachyarrhythmia may exacerbate bradyarrhythmia. Therefore, a pacemaker is implanted before drug therapy is begun for the tachyarrhythmia

96. Atrio ventricular block First degree heart block PR interval is lengthened beyond 0.20 seconds. In first-degree AV block, the impulse conducting from atria to ventricles through the AV node is delayed and travels slower than normal Seldom of clinical significance, and unlikely to progress

97. Atrio ventricular block

98. Atrio ventricular block Second degree A-V Block A- Mobitz type I (Wenckebach phenomenon): Gradually increasing P-R intervals culminating in an omission. When isolated, usually physiological and due to increased vagal tone and abolished by exercise and atropine.

99. Atrio ventricular block Second degree A-V Block B- Mobitz type II: The P wave is sporadically not conducted. Occurs when a dropped QRS complex is not preceded by progressive PR interval prolongation. Pacing is usually indicated in Mobitz II block , whereas patients with Wenckebach AV block are usually monitored

100. Atrio ventricular block

101. Atrio ventricular block Third degree A-V Block Common in elderly age groups due to idiopathic bundle branch fibrosis. Other causes include coronary heart disease, calcification from aortic valve, sarcoidosis or it may be congenital. ECG shows bradycardia, P wave continues which is unrelated to regular slow idioventricular rhythm. Treatment is permanent pacing .

102. Atrio ventricular block

103. thanks For Watching