1. Assistance Prof. Dr .Ghazi F. Haji Cardiologist
Arrhythmias
Assistance Prof. Dr .Ghazi F. Haji
Cardiologist

3. A cardiac arrhythmia
@is a disturbance of the electrical rhythm of the heart
@Arrhythmias are might be occur in :
1- structural heart disease
2-healthy heart.
A heart rate > 90/min is tachycardia
heart rate < 60/min is a bradycardia.

4. Mechanisms of tachycardia • Increased automaticity. • Re-entry
Mechanisms of tachycardia • Increased automaticity.. • Re-entry. (Most tachyarrhythmias are due to re-entry). • Triggered activity.. Mechanisms of Bradycardia may be due to: • Reduced automaticity, e.g. sinus bradycardia. • Blocked or abnormally slow conduction, e.g. AV block

5. Classification of arrhythmia ;
1- Supraventricular (Narrow QRS complex )
(sinus ,atrial .junctional)
2-Ventricular (wide ,bizzar QRS complex)
Sometime :supraventricular with wide QRS complex
1-BBB
2-accessory conduction

6. Noticeable arrhythmia symptoms may include:
A fluttering in your chest A racing heartbeat (tachycardia) A slow heartbeat (bradycardia) Chest pain Shortness of breath Lightheadedness Dizziness Fainting (syncope) or near fainting Polyurea

7. Sinus rhythm :
@Sinus arrhythmia : change in heart rate during respiration (increase in inspiration VS expirat)occur in children,autonomic neuropathy
@Sinus bradycardia :
In -atheletic -sleep
MI.
Sinus node dysfunction(sick sinus syndrom(tachy-brady syndrome)
hypothyroidism,hypothermia,cholestaesis juandic
increase intracranial pressure .
drugs (b-blocker .calcium channel blocker .antiarrhythmic drugs)
Treatment : (if asymptomatic –no treatment .if symptomatic -atropin) pacemaker if not response

8. @Sinus tachycardia: (physiological ,pathological)
The upper limit of normal rate for sinus tachycardia is thought to be 220 bpm minus age.
cause by anxiety ,fever. anemia. thyrotoxosis .phaeochrmocytoma .pregnancy .heart failure ,drugs(sympathomametic ,b-agoinst like ventolin,butadinie )
Treatment :if asymptomatic not need treatment
if ymptomatic :treated depend on types , onset and hemodynamic status

9. Atrial rhythm : #Atrial ectopic beat (extrasystolic ,premature beat)
no symptoms or sensation of a missed beat or an abnormally strong beat.
The ECG –shows a premature but otherwise normal
QRS complex; if visible, the preceding P wave has a
different morphology
Treatment ;avoid .b blocker

10. Atrial tachycardia
@Atrial tachycardia caused by sinoatrial disease or digoxin produces a narrow complex tachycardia with abnormal P- wave : β-blockers class I or III anti-arrhythmic drugs .Catheter ablation.

11. Atrial flutter
due to a large (macro) re-entry circuit, usually within the RA encircling the tricuspid annulus. The atrial rate is approximately 300/min, and is usually associated with 2:1, 3:1 or 4:1 AV block. The ECG shows saw-toothed flutter waves .

12. Management
Treatment : 1-Carotid sinus pressure or intravenous adenosine may help to establish the diagnosis 2-Digoxin, β-blockers or verapamil can be used to control the ventricular rate . 3-direct current (DC) cardioversion or by using intravenous amiodaron 4-Beta-blockers or amiodarone can also be used to prevent recurrent episodes of atrial flutter. 5-Catheter ablation offers a 90% chance of complete cure

13. Atrial fibrillation
@Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, with an overall prevalence of 0.5%,The prevalence rises with to multiple re-entry circuits looping around the irregular’ pulse. The ECG -irregular QRS complexes; there are no P can be classified Paroxysmal –self terminated within 7days Persistent –last more than 7 days Permanent- if not terminated or relapse within 24hof cardio version Lone –absence of structural heart disease ,

14. @structural remodelling occurs with atrial fibrosis and dilatation that further predispose to AF is often completely can cause palpitation, breathlessness and fatigue. In patients with poor ventricular function or valve disease it may precipitate or aggravate cardiac failure fall in BP may cause lightheadedness, and chest pain may occur with underlying coronary is associated with significant morbidity and a twofold increase in mortality

15. Common causes of atrial fibrillation
• Coronary artery disease (including acute MI) • Valvular heart disease, especially rheumatic mitral valve disease • Hypertension • Sinoatrial disease • Hyperthyroidism • Alcohol • Cardiomyopathy • Congenital heart disease • Chest infection • Pulmonary embolism • Pericardial disease • Idiopathic (lone AF)

16. Management
Assessment of patients with newly diagnosed AF includes a full history, physical examination, 12-lead ECG, echocardiogram,thyroid function tests. ect The goal of treatment: 1-restore sinus rhythm 2-prevent recurrent episodes of AF, 3-, minimize the risk of thromboembolism

17. Paroxysmal atrial fibrillation
1-not necessarily require treatment. 2-Beta-blockers are normally used Beta-blockers reduce the ectopic firing that normally initiates AF. 3-Class Ic drugs such as propafenone or flecainide, are also effective at preventing episodes but should not be given to patients with coronary disease or left ventricular dysfunction .4-Amiodarone is the most effective agent for preventing AF but its side-effects restrict its use to patients and verapamil are not effective drugs for preventing paroxysms of AF, If no response or because of side effects of drugs –can do 5-Cardiac ablation -Ablation prevents AF in approximately 70% of patients. Complication s are *small risk of embolic *stroke or cardiac tamponade.

18. Persistent and permanent atrial fibrillation
There are two options for treating persistent AF: $= rhythm control: attempting to restore and maintain sinus rhythm $=rate control: accepting that AF will be permanent and $=prevent embolic complications.

19. Rhythm control. An attempt to restore sinus rhythm
Attempts to restore and maintain sinus rhythm are most successful 1- if AF has been present for < 3 months 2-the patient is young 3- no important structural heart disease.

20. 1-Immediate DC cardioversion after the administration of intravenous heparin is appropriate if AF has been present for < 48 hours. 2-Chemical cardioversion is performed with drugs, such as amiodarone, dronedarone, procainamide, dofetilide, ibutilide, propafeno ne, or flecainide.(Vernakalant, an investigational drug) In other situations, >48h AF--DC cardioversion deferred until the patient has been established on warfarin, with an international normalised ratio (INR) > 2.0 for a minimum of 4 weeks,. 3-Anticoagulation should be maintained for at least 3 months following successful cardioversion Concomitant therapy with amiodaroneor β-blockers may reduce the risk of recurrence. 4-Catheter ablation( radiofrequency ablation The Maze procedure) but it is a less effective treatment for persistent AF than for paroxysmal AF.

21. Rate control. If sinus rhythm cannot be restored, treatment
should be directed at maintaining an appropriate heart β-blockers or rate-limiting calciu m antagonists such as verapamil or ablation+a permanent pacemaker must be implanted beforehand. This is known as the ‘pace and ablate’ strategy.

22. Prevention of thromboembolism
Loss of atrial contraction and left atrial dilatation cause stasis of blood in the LA and may lead to thrombus formation in the left atrial appendage. This predisposes patients to stroke and other forms of systemic (target INR 2.0–3.0) reduces the risk of stroke by about reduces the risk of stroke by only one-fifth is valuable in risk stratification.

23. CHA2DS2-VASc Hypertension> 140/90 H 2 Age>75y A2 Diabetes D
Congestive heart failure C
Hypertension>
140/90 H 2
Age>75y A2
Diabetes D
Prior Stroke or TIA or thromboembolism S2
Vascular diseasesVascular disease (e.g. peripheral artery disease, myocardial V
Age 65-74y A
Sex category (female ) Sc

24. consideration
Anticoagulant
Risk
Score
Aspirine dialy
None or aspirin
low
Aspirine dialy or riase to INR2-3
Aspirine ,warfarin or other
moderate 1
Riase INR 2-3
Warfarin or other anticoagulant
dabigatran, rivaroxabanand apixaban
Moderate to high
2 or more

25. Quiz 1-describe the ECG 2- What are the treatment

26. Supraventricular’ tachycardias
(SVT) is a narrow QRS complex : Atrioventricular nodal re-entrant tachycardia (AVNRT)(120- is due to re-entry in a circuit involving the AV node and its two right atrial input pathways: a ‘fast’ pathway and ‘slow’ pathway tends to occur in hearts that are otherwise normal and episodes may last from a few seconds to many hours. 1-a fast heart beat and may feel faint or breathless. 2-Polyuria, The ECG usually shows a tachycardia with normal QRS complexes

27. Supraventricular tachycardia

28. Management
Treatment is not always carotid sinus pressure or other Measures that increase vagal tone (e.g. Valsalva adenosine or alternative drugs include β-blockers or severe haemodynamic compromise, the tachycardia should be terminated by DC episodes are frequent or disabling, prophylactic oral therapy with a β-blocker or verapamil may be ablation offers a high chance ofcomplete cure and is usually preferable to long-term drug treatment.

29. Wolff–Parkinson–White syndrome and atrioventricular re-entrant tachycardia(AVRT)
@In these conditions, an abnormal band of conductingTissue connects the atria and ventricles. is known as an accessory pathway.
50%-concealed accessory pathway -\ does not alter the appearance of the ECG in sinus rhythm.
50%--conduction takes place partly through the AV node and partly through the accessory pathway-short PR interval and a ‘slurring’ of the QRS complex, called a delta wave known as Wolff Parkinson–White syndrome.
The ECG appearance of this tachycardia may be indistinguishable from that of AVNRT .

30. @. It should be treated as an emergency, usually with DC cardioversion
It should be treated as an emergency, usually with DC atrial fibrillation occurs, it may produce a dangerously rapid ventricular rate because the accessory pathway lacks the rate-limiting properties of the AV node anti-arrhythmic drugs, such as flecainide, propafenone or amiodarone , can also be used. Catheter ablation is first-line treatment in symptomatic patients and is nearly always and verapamil shorten the refractory period of the accessory pathway and should be avoided.

31. Ventricular tachy arrhythmias
@Ventricular ectopic beats(extrasystoles, premature beats) ventricular ectopic beats are premature, broad and bizarre The complexes may be unifocal or multifocal . ‘Couplet’ and ‘triplet’ beats produce a low stroke volume because left ventricular contraction occurs before filling is pulse is therefore irregular, with weak or missed beats Patients are usually asymptomatic but may complain of an irregular heart beat, missed beats or abnormally strong beats.

32. Ventricular ectopic beats in otherwise healthy subjects increases with age. disappear with is not necessary unless the patient is highly symptomatic, in which case β-blockers can be such as an echocardiogram (looking for structural heart disease) and an exercise stress test (to detect underlying ischaemic heart disease).

33. Ventricular ectopic

34. Ventricular ectopic beats associated with heart disease
@acute MI . Persistent, frequent (> 10/hour) ventricular ectopic beats in patients who have survived the acute phase of MI indicate a poor long-term outcome. Other than β-blockers, anti-arrhythmic drugs do not improve and may even worsen prognosis. .. Treatment should be directed at the underlying condition.

35. Ventricular tachycardia (VT)
@The common causes of VT include acute MI, ischaemic heart disease particularly when it is associated with a ventricular aneurysm or poor left ventricular is caused by abnormal automaticity or triggered or by re-entry may complain of palpitation or symptoms of low cardiac output, such as dizziness, dyspnoea or syncope. The ECG shows tachycardia with broad, abnormal QRS complexes with a rate > 120/min . VT may be difficult to distinguish from SVT with bundle branch block or pre-excitation(WPW syndrome).

36. Wide QRS
Narrow QRS

37. @idioventricular rhythm (‘slow’ VT) at a rate only slightly above the preceding sinus rate and below 120/ min. These episodes often reflect reperfusion of the infarct territory and may be a good sign. They are usually self-limiting and asymptomatic, and do not require heart VT’), usually because of abnormal automaticity in the right ventricular outflow tract or one of the fascicles of the left bundle branch. The prognosis is good and catheter ablation can be curative

38. Management
@Synchronised DC cardioversion is the treatment of choice if systolic BP is < 90 amiodarone may be given as a bolus followed by a continuous lidocaine can be used but may depress left ventricular function, causing hypotension or acute Hypokalaemia, hypomagnesaemia, acidosis and hypoxaemia should be Class Ic anti-arrhythmic drugs should not be used for prevention of VT in patients with ischaemic heart disease In patients at high risk of arrhythmic death (e.g. those with poor left ventricular function, or where VT is associated with haemodynamic compromise), the use of an implantable cardiac defibrillator is recommended .

39. Features in favour of ventricular tachycardia in the differential diagnosis of broad-complex tachycardia
@History of MI • AV dissociation (pathognomonic) • Capture/fusion beats (pathognomonic,) • Extreme left axis deviation • Very broad QRS complexes (> 140 ms) • No response to carotid sinus massage or i.v. adenosine

40. Torsades de pointes (ventricular tachycardia) Polymorphic VT
@The ECG shows rapid irregular complexes that oscillate from an upright to an inverted position and seem t twist around the baseline as the mean QRS axis into ventricular periods of sinus rhythm, the ECG will usually show a prolongeQT interval (> 0.42 s at a rate of 60/min). arrhythmia is more common in women and is often triggered by a combination of aetiological factors (e.g. QT-prolonging medications and hypokalaemia).

41. Causes of long QT interval and torsades de pointes
Bradycardia Electrolyte disturbance • Hypokalaemia • Hypomagnesaemia • Hypocalcaemia Drugs • Disopyramide (and other class Ia anti-arrhythmic drugs, p. 573) • Sotalol, amiodarone (and other class III anti-arrhythmic drugs) • Amitriptyline (and other tricyclic antidepressants) • Chlorpromazine (and other phenothiazines) • Erythromycin (and other macrolides) Congenital syndromes • LQT1: gene affected KCNQI: K+ channel, 30–35% • LQT2: gene affected HERG: K+ channel, 25–30% • LQT3: gene affected SCNSA: Na+ channel, 5–10% • LQT4–12: rar

42. @Thecongenital long QT syndromes are a family of genetic disorder
@Thecongenital long QT syndromes are a family of genetic should be directed at the underlying cause. Intravenous magnesium should be given in all isoprenaline is a reasonable alternative to pacing. Beta-blockers are effective at preventing syncope in patients with congenital long

43. Sinoatrial disease (sick sinus syndrome)
@occur at any age but is most common in older underlying pathology involve fibrosis, degenerative changes or ischaemia of the SA(sinus) present with palpitation, dizzy spells or syncope, due to intermitten tachycardia, bradycardia, or pauses with no atrial or ventricular activity (SA block or sinus permanent pacemaker.

44. Common features of sinoatrial disease
Sinus bradycardia • SA block (sinus arrest) • Paroxysmal atrial tachycardia • Paroxysmal atrial fibrillation • AV block

45. Atrioventricular and bundle branch block
First-degree AV block In this condition, AV conduction is delayed so the PR interval is prolonged (> 0.20 s;). It rarely causes symptoms.

47. Second-degree AV block
Second-degree AV block. In Mobitz type I second-degree AV block :there is progressive lengthening of successive PR intervals culminating in a dropped beat.. This is known as Wenckebach’s phenomenon and is usually due to impaired conduction in the AV node itself.. In Mobitz type II second-degree AV block -the PR interval of the conducted impulses remains constant but some P waves are not conducted. This is usually caused by disease of the His–Purkinje system and carries a risk of asystole. .

48. Third-degree (complete) AV block When AV conduction fails completely, the atria and ventricles beat independently (AV dissociation, ) Complete AV block -produces a slow (25–50/min), regular pulse that,. . Cannon waves may be visible in the neck and the intensity of the firstheart sound varies due to the loss of AV synchrony

49. Aetiology of complete AV block
Congenital Acquired • Idiopathic fibrosis • MI/ischaemia • Inflammation Acute (e.g. aortic root abscess in infective endocarditis) Chronic (e.g. sarcoidosis, p. 708; Chagas disease, p. 354) • Trauma (e.g. cardiac surgery) • Drugs (e.g. digoxin, β-blocker)

50. Stokes–Adams attacks Episodes of ventricular asystole may complicate complete heart block or Mobitz type II second-degree AV block, or occur in patients with sinoatrial disease This may cause recurrent syncope or ‘Stokes– Adams’ attacks.A typical episode is characterised by sudden loss of consciousness that occurs without warning and results in collapse..

51. AV block complicating acute MI Acute inferior MI is often complicated by transient AV block because the RCA supplies the AV node. if the patient remains well, no treatment is required. Symptomatic second- or third-degree AV block may respond to atropine(0.6 mg i.v., repeated as necessary) or, if this fails, a temporary pacemaker. In most cases the AV block will resolve within 7–10 days. Second- or third-degree AV heart block complicating acute anterior MI indicates extensive ventricular damage involving both bundle branches and carries a poor prognosis.

52. Bundle branch block and hemiblock
Conduction block in the right or left bundle branch can occur as a result of many pathologies, including Ischaemic or hypertensive heart disease or cardiomyopathies . This causes delayed conduction into the LV or RV, broadens the QRS complex (≥ 0.12 s) and produces the characteristic alterations in QRS morphology

53. Right bundle branch block (RBBB can occur in healthy people but left bundle branch block (LBBB) often signifies important underlying heart disease. The combination of right bundle branch and left anterior or posterior hemiblock is known as bifascicular block

54. Common causes of bundle branch block
Right bundle branch block • Normal variant • Right ventricular hypertrophy or strain, e.g. pulmonary embolism • Congenital heart disease, e.g. atrial septal defect • Coronary artery disease Left bundle branch block • Hypertension • Aortic valve disease • Cardiomyopathy

55. Anti-arrhythmic drug therapy

56. Classification of anti-arrhythmic drugs according to effect on the intracellular action potential
Class I: membrane-stabilising agents (sodium channel blockers) (a) Block Na+ channel and prolong action potential • Quinidine, disopyramide (b) Block Na+ channel and shorten action potential • Lidocaine, mexiletine (c) Block Na+ channel with no effect on action potential • Flecainide, propafenone Class II: b-adrenoceptor antagonists (b-blockers) • Atenolol, bisoprolol, metoprolol, I-sotalol Class III: drugs whose main effect is to prolong the action potential • Amiodarone, d-sotalol Class IV: slow calcium channel blockers • Verapamil, diltiazem N.B. Some drugs (e.g. digoxin and adenosine) have no place in this classification, while others have properties in more than one class: e.g. amiodarone, which has actions in all four classes.

57. Other anti-arrhythmic drugs
Atropine sulphate (0.6 mg i.v., repeated if necessary to a maximum of 3 mg).

58. Adenosine. Must be given intravenously
Adenosine. Must be given intravenously. It produces transient AV block lasting a few seconds. Adenosine is givenas an intravenous bolus, initially 3 mg over 2 seconds If there is no response after 1–2 minutes, 6 mg should be given; if necessary, after another 1–2 minutes, the maximum dose of 12 mg may be given. Patients should be warned that they may experience short-lived and sometimes distressing flushing, breathlessness and chest pain. Adenosine can cause bronchospasm and should be avoided in asthmatics; its effect are greatly potentiated by dipyridamole and inhibited by theophylline and other xanthines.

59. Response to intravenous adenosine
Arrhythmia Response Supraventricular tachycardia Termination Atrial fibrillation, atrial flutter Transient AV block Ventricular tachycardia No effect

60. Digoxin. A purified glycoside from the European foxglove, Digitalis lanata, which slows conduction and prolongs the refractory period in the AV node.. Digoxin is largely excreted by the kidneys, and the maintenance dose should be reduced in children, older People and those with renal impairment. It is widely distributed and has a long tissue half-life (36 hours), so that effects may persist for several days after th last dose..

61. Therapeutic procedures
External defibrillation and cardioversion This will interrupt any arrhythmia and produce a brief period of asystole -that is usually followed by the resumption of sinus rhythm. Defibrillators deliver a DC, high-energy, short-duration shock via two metal paddles coated with conducting jelly or a gel pad, positioned over the upper right sternal edge andthe apex. Modern units deliver a biphasic shock, during which the shock polarity is reversed mid-shock. This reduces the total shock energy required to depolarise the heart.

62. Electrical cardioversion
This is the termination of an organised rhythm such as AF or VT with a synchronised shock, usually under general anaesthesia. The shock is delivered immediately after detection of the R wave, High-energy shocks may cause chest wall pain post-procedure, so if there is no urgency it is appropriate to begin with a lower- amplitude shock (e.g. 50 joules), going on to larger shocks if necessary. -

63. Catheter ablation
The technique has revolutionised the management of many arrhythmias and is now the treatment of choice for AVNRT and AV re-entrant (accessory pathway) tachycardias, when it is curative in > 90% of cases. Focal atrialtachycardias and atrial flutter can also be eliminated by radiofrequency ablation,

64. Temporary pacemakers
. Permanent pacemakers

65. Implantable cardiac defibrillators (ICDs)
Primary prevention • After MI, if LV ejection fraction < 30% • Mild to moderate symptomatic heart failure on optimal drug therapy, with LV ejection fraction < 35% Secondary prevention • Survivors of VF or VT cardiac arrest not due to transient or reversible cause • VT with haemodynamic compromise or significant LV impairment (LV ejection fraction < 35%)

66. Cardiac resynchronisation therapy (CRT)
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%.’

67. Quiz
What are the treatment of SVT ? Enumerate the causes of complete heart block?

68. Thanks a lot