1. Cardiac Arrhythmia

2. Skeleton of the lecture  Definition  Sinus Rhythm& Sinus Arrhythmia  Atrial Dysrhythmia & Supraventricular tachycardia  Ventricular Dysrhythmia  Heart Block

3. Definition  The cardiac arrhythmia is a disturbance in the electrical rhythm of the heart; this may be paroxysmal or continuous, and may cause sudden death, syncope, heart failure, lightheadedness, palpitations or no symptoms at all.  Arrhythmias are often a manifestation of structural heart disease but may also occur in the context of an otherwise normal heart.

4. Dysrhythmia Altered conduction  Bradycardia / Tachycardia  Flutter / Fibrillation  Heart blocks

5. Sinus Rhythms  Sinus Rhythms are a class of rhythms which originate at the SA node.  Sinus rhythms generally travel through the entire conduction system without inhibition.

6. The criteria for a Normal Sinus Rhythm is: 1. P-wave before each QRS with an interval of 0.12 to 0.20 seconds in duration. 2. A QRS width of 0.04 to 0.12 seconds 3. Q-T interval of less the 0.40 seconds. 4. The rate for a normal sinus rhythm is 60 to 100 beats a minute

7. 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.

8. E.G.of Sinus Rhythms

9. SINUS ARRHYTHMIA  Phasic alteration of the heart rate during respiration (the sinus rate increases during inspiration and slows during expiration) is a manifestation of normal autonomic nervous activity and is often particularly pronounced in children.

10. E.G.of SINUS ARRHYTHMIA

11. SINUS BRADYCARDIA  A sinus rate of less than 60/min may occur in normal people during sleep and is a common finding in athletes.  Acute symptomatic sinus bradycardia usually responds to intravenous atropine 0.6 mg. In sinus bradycardia the rate must be under 60bpm All complexes are normal in appearance.

12. Bradycardia may be due to  Reduced automaticity (e.g. sinus bradycardia)  Abnormally slow conduction (e.g. atrioventricular block).

13. 1-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 or pathology.  The rate seldom exceeds 160/min, except in infants.  TACHYCARDIA

14.  PAIN  FEVER  ACUTE ANEMIA  HEMORRHAGE  EXERCISE  DRUGS SUCH AS: ATROPINE NICOTINE CAFFEINE AMPHETAMINES COMMON CAUSES FOR SINUS TACHYCARDIA:

15. An arrhythmia may be:  Supraventricular (sinus, atrial or junctional) Supraventricular rhythms usually produce narrow QRS complexes because the ventricles are depolarised normally through the AV node and bundle of His.  Ventricular. ventricular rhythms produce broad bizarre QRS complexes because the ventricles are activated through an abnormal pathway.  However, occasionally a supraventricular rhythm can produce broad or wide QRS complexes due to coexisting bundle branch block or the presence of accessory conducting tiss

16. ATRIAL TACHYARRHYTHMIAS 1-ATRIAL ECTOPIC BEATS (EXTRASYSTOLES, PREMATURE BEATS These usually cause no symptoms but can give the sensation of a missed beat or an abnormally strong beat. In the ECG it is:  Premature.  P wave if present has a different configuration.  Normal QRS complex,there is no compensatory Pause Beyond reassurance no treatment is necessary 

17. ATRIAL ECTOPIC BEATS

18. PAC Not a true dysrhythmia but an individual complex

19. 2-ATRIAL TACHYCARDIA  An ectopic atrial tachycardia due to increased automaticity is rare but is sometimes a manifestation of digitalis toxicity. The ECG shows  An atrial rate of 140-220/min  With abnormal P waves  Often accompanied by atrioventricular block (e.g. 2:1, 3:1 or variable). Management is similar to that for atrial flutter

20. Paroxysmal atrial tachycardia is the sudden onset of tachycardia greater than 151 bpm. Usually triggered by a PAC. Usually not a lethal dysrhythmia but should be monitored closely.

21. SUPRAVENTRICULAR TACHYCARDIA  This term used when the dysrhythmia fits all the characteristics of a PAT but the beginning of the dysrhythmia is not seen.  Originates from an irritable site above the bundle of his with a rate greater than 151.

22. Supraventricular tachycardia  The rate is 180/min and the QRS complexes are normal. unless there is associate BBB

23. Clinical Features It may produce palpitations, syncope, and heart failure depending on the rate and duration of the arrhythmia and the presence and severity of any underlying heart disease.

24. There are two mechanisms of tachycardia 1. Increased automaticity-when the tachycardia is sustained by repeated spontaneous depolarisation of an ectopic focus or single cell 2. Re-entry-when the tachycardia is initiated by an ectopic beat but sustained by a closed loop or re- entry circuit (Most tachyarrhythmias are due to re-entry.

25. The mechanism of re-entry . Re-entry can occur when there are two alternative pathways with different conducting properties (e.g. the AV node and an accessory pathway, or an area of normal tissue and an area of ischaemic tissue).

27. Supraventricular Tachycardia(SVT)- Treatment In patients without hypotension, vagal maneuvers, particularly carotid sinus massage, can terminate the arrhythmia in 80% of cases. If these maneuvers are unsuccessful,  Adenosine (12 mg intravenously) is the agent of choice  Beta blockers may also be used to slow or terminate the tachycardia but are agents of second choice . Digoxin have a slower onset of action and should not be used for acute therapy  catheter ablation of the bypass tract

28. WANDERING ATRIAL PACEMAKER  originates from at least three different sites above the bundle of his.  size and shape of each individual complex is determined by the site of origin for that complex.  if from the atria, a P wave occurs followed by a QRS complex.

29. Occurs from at least three different sites above the Bundle of His. May include any pacemaker site in the atria, including the SA node, AV node or any combination of these areas.

30. 3-ATRIAL FLUTTER  In this arrhythmia the atrial rate is approximately 300/min.  It is usually associated with 2:1, 3:1, 4:1 atrioventricular block (with corresponding heart rates of 150, 100, 75); however, the degree of AV block often varies and occasionally every beat is conducted, producing a heart rate of 300/min.

31. ATRIAL FLUTTER  A single irritible site in the atria initiates many electrical impulses at a rapid rate.  Normal P waves are not produced& instead flutter waves (f waves) are formed.  Saw-toothed or jagged appearance on the strip.

32. Notice the saw-toothed waves. ↓↓↓

33. . When there is regular 2:1 AV block it may be difficult to distinguish atrial flutter from supraventricular or sinus tachycardia because alternate flutter waves are buried in the QRS complexes.  This should always be suspected when there is a narrow complex tachycardia of 150/min.  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.

34. Atrial Flutter With Variable Block  This is extremely common among A-flutter patients.  There can be as few as a single P-wave or as many as 6 or more P-waves between each QRS complex.

35. Atrial Flutter with Variable Block

36. Management  Drugs can be used to control the ventricular rate) (Digoxin, β-blockers or verapamil  Atrial overdrive pacing  Direct current (DC) cardioversion (most commonly used)

37. ATRIAL FLUTTER-Management  To control the ventricular rate Digoxin, β-blockers or verapamil can be used  To restore sinus rhythm  Direct current (DC) cardioversion It is the best treatment  Drug therapy.( Amiodarone, propafenone or flecainide) Catheter ablation offers a 90% chance of complete cure and is the treatment of choice for patients with persistent and troublesome symptoms

38. Prevention of Recurrence Drugs 1-Drugs: Amiodarone, propafenone or flecainide may be effective and can also be used to prevent recurrent episodes of atrial flutter Radiofrequency catheter ablation 2- Radiofrequency catheter ablation offers a high chance of complete cure and has become the treatment of choice for patients with persistent and troublesome symptoms.

40. 4-ATRIAL FIBRILLATION  It describes a condition in which the atrial tissue randomly generates action potentials from many different regions.  There are no noticable p-waves, and the overall rhythm is irregularly irregular

41.  The atria is not completely depolarized.  The atrial muscle does not forcefully contract.  Only a quivering movement occurs (fibrillatory waves). appear as a wavy line between each QRS complex no true P waves or PR intervals exist

42.  Atrial heart rate of 350 to 500.  If the ventricular rate is usually within normal limits of 60 to 100 impulses it is called controlled atrial fibrillation  If ventricular rate greater than 150 impulses per minute is called uncontrolled atrial fibrillation.

43. ATRIAL FIBRILLATION

45. MANAGEMENT Treatment for AF must take into account:  The clinical situation in which the arrhythmia is encountered,  The chronicity of the AF,  The status of the patient's level of anticoagulation  The risk factors for stroke  The patient's symptoms  The hemodynamic impact of the AF  The ventricular rate.

46. In the absence of hemodynamic compromise that might warrant emergent cardioversion to terminate the AF, the initial goals of therapy are to: (1) Establish control of the ventricular rate. (2) Address anticoagulation status and begin IV heparin treatment if the duration of AF is >12 h and risk factors for stroke as old age,DM,HT,MS with AF are present

47. ATRIAL FIBRILLATION(AF) MANAGEMENT  In acute AF, a precipitating factor such as fever, pneumonia, thyrotoxicosis, &others, therapy should be directed toward their.  If the patient’s clinical status is severely compromised, electrical cardioversion is the treatment of choice.  In the absence of severe cardiovascular compromise, slowing of the ventricular rate becomes the initial therapeutic goal with B–adrenergic blockers and/or calcium channel antagonists  Digitalis preparations are less effective, take longer to act, .

48. ATRIAL FIBRILLATION(AF) MANAGEMENT  Conversion to sinus rhythm may then be attempted.  Prior to cardioversion, precautions must be taken to reduce the risk of systemic embolization by doing ECHO  Direct-current (DC) electrical cardioversion is a highly effective method to restore sinus rhythm, either as a primary method of therapy or following the failure of antiarrhythmic medications

49. ATRIAL FIBRILLATION(AF) MANAGEMENT  It is unlikely that patients with chronic AF will convert to and remain in sinus rhythm in the presence of long-standing rheumatic heart disease and/or when the atria are markedly enlarged.  The goal of therapy is control of the ventricular response. This can usually be accomplished by beta blockers, calcium channel blockers, or digitalis, singly or in combination

50. In occasional patients, the ventricular response cannot be controlled by pharmacologic therapy alone. In such patients, the creation of complete heart block by radiofrequency catheter ablation of the AV junction followed by permanent pacemaker implantation

51. . Prior to cardioversion, precautions must be taken to reduce the risk of systemic embolization.

52. Prevention of Recurrence If sinus rhythm is restored electrically or pharmacologically, 1- Quinidine or related agents as well as the class IC agents (e.g., flecainide or propafenone) 2-Sotalol, dofetilide, or amiodarone may be used to prevent recurrence.

54. AV_ Node Dysrhythmias

55. PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIAS The most common cause of supraventricular tachycardia is AV NODAL REENTRANT TACHYCARDIA,.. It usually presents as a regular narrow QRS complex tachycardia at rates of 120 to 250 beats/min.

56. Junctional rhythms  The AV node, just like the other cardiac tissue, has automaticity, the AV node is stimulated before it fires by itself.  Occasionally, however, an extra impulse may develop in the junction, thereby spreading up to the atria, and down to the ventricles.

57. WOLFF-PARKINSON-WHITE (WPW) SYNDROME  In this condition there is an abnormal band of atrial tissue which connects the atria and ventricles and can electrically bypass the AV node. 

58.  In normal sinus rhythm conduction takes place partly through the AV node and partly through the more rapidly conducting bypass tract. The ECG shows: 1. shortening of the PR interval 2. and a 'slurring' of the QRS complex called a delta wave

60.  When the ventricles are depolarised through the AV node the ECG is normal  but when the ventricles are depolarised through the accessory conducting tissue the ECG shows a very short PR interval and a broad QRS complex.

61. It May Be in The Form of: A -Sinus rhythm B- Orthodromic tachycardia C- Antidromic tachycardia D -Atrial fibrillation

63. Treatment 1. Carotid sinus massage 2. Intravenous adenosine will often terminate an episode of this form of tachycardia. 3. DC cardioversion Atrial fibrillation is potentially a very dangerous arrhythmia in these patients and may cause collapse, syncope and even death; it should therefore be treated as a medical emergency, usually with DC cardioversion

64. Prophylaxis  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, disopyramide or amiodarone  Digoxin and verapamil increase conduction in the bypass tract and should be avoided.  Transvenous radiofrequency catheter ablation

65. VENTRICULAR TACHYARRHYTHMIAS 1. VENTRICULAR ECTOPIC BEATS(EXTRASYSTOLES, PREMATURE BEATS ) 2. VENTRICULAR TACHYCARDIA 3. VENTRICULAR FIBRILLATION

66. VENTRICULAR ECTOPIC BEATS (EXTRASYSTOLES, PREMATURE BEATS VEBs ) They are frequently found in :  Normal people and their prevalence increases with age.  Subclinical coronary artery disease &AMI  Heart failure  Digoxin toxicity

67. The ECG shows : 1. Premature broad, bizarre QRS complexes 2. No P wave 3. There will be a compensatory pulse

69. TYPES  Unifocal (identical beats arising from a single ectopic focus)  Multifocal (varying morphology with multiple foci-see).  'Couplet' and 'triplet' are terms used to describe two or three successive ectopic beats,  Bigeminy a run of alternate sinus and ectopic beats or ‘ Trigeminy If two normal contractions are followed by a single PVC,

70. Unifocal Multifocal 'Couplet' Bigeminy

71. 2-VENTRICULAR TACHYCARDIA  This is a grave arrhythmia because it is nearly always associated with serious heart disease and may degenerate into ventricular fibrillation

72. Causes 1-Acute myocardial infarction, 2-Myocarditis, 3- Cardiomyopathy 4- Chronic ischaemic heart disease,

74. Clinical Presentation ). Patients may complain of  Palpitation  Symptoms of a low cardiac output, such as dizziness, dyspnoea or even syncope.

75. ECG Changes  Very broad QRS complexes  Marked left axis deviation.  In addition, there is AV dissociation; some P waves are visible and others are buried in the QRS complexes (arrows).

77.  DIFFERENTIAL DIAGNOSIS ON ECG IS SVT &BBB

78. Management  Prompt action to restore sinus rhythm is required and in most cases should be followed by prophylactic therapy.

79.  DC cardioversion is often the initial treatment of choice but if this is not available or if the arrhythmia is well tolerated,  Intravenous lidocaine (lignocaine) may be given as a bolus followed by an intravenous infusion  Mexiletine, flecainide, disopyramide and amiodarone are suitable alternatives Hypokalaemia, hypomagnesaemia and acidosis must be corrected.

80. 3- Ventricular Fibrillation(VF)  VF is the most common fatal dysrhymia in adult patients. VF represents a chaotic depolarization of random ventricular cells.  A heart in VF literally looks like jiggling Jell-o.  There is no pulse associated with this rhythm. CPR won't do much good either, nor will most drugs. You'd better hope the defibrillator works!

82. Conduction Abnormalities  Heart block can occur anywhere in the specialized conduction system beginning with the sino-atrial connections, the AV junction, the bundle branches and their fascicles, and ending in the distal ventricular Purkinje fibers.

83. SA-NODE BLOCK 1-SA-block Where there is no atrial or ventricular activity 2-Sick sinus syndrome is intermittent tachycardia, bradycardia

85. ATRIOVENTRICULAR (AV) BLOCK  Atrioventricular conduction is influenced by autonomic activity.  AV block can therefore be intermittent and may only be evident when the conducting tissue is stressed by a rapid atrial rate.  Accordingly, atrial tachyarrhythmias are often associated with AV block

86. Atrio-Ventricular (AV) Block Possible sites of AV block:  1- AV node (most common) 2- His bundle (uncommon) 3- Bundle branch and fascicular divisions (in presence of already existing complete bundle branch block)

87. AV Block  First-degree AV block  In this condition AV conduction is delayed so the PR interval is prolonged beyond the upper limit of normal (0.20 seconds). There are no symptoms and the diagnosis can only be made from the ECG

88. Second-degree AV block it is of two types  1-Mobitz type I  2-Mobitz type II

89. In Mobitz type I second-degree AV block  There is progressive lengthening of successive PR intervals culminating in a dropped beat. The cycle then repeats itself.  This is known as Wenckebach's phenomenon It is usually due to impaired conduction proximal to the bundle of His.

90. 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 below the bundle of His and is more serious than Mobitz type I.

91. 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 bundle of His (narrow QRS complexes) or the distal conducting tissues (broad QRS complexes). Distal escape rhythms tend to be slower and less reliable.

92. Adams-Stokes attacks  Episodes of sudden loss of consciousness, Convulsions (due to cerebral ischaemia) can occur if there is prolonged asystole. There is pallor and a death-like it complete heart block or Mobitz type II second-degree AV block, and can also occur in patients with sinoatrial disease

93. Management A-AV block complicating acute inferior myocardial infarction  In 1 st degree heart block – no treatment is needed  Clinical deterioration due to second- degree or complete heart block may respond to atropine (0.6 mg intravenously, repeated as necessary) or, if this fails, a temporary pacemaker. In the vast majority of cases the AV block will resolve within 7-10 days.

94. A-AV block complicating acute anterior myocardial infarction  Second-degree or complete heart block carries a poor prognosis.  Asystole may ensue and a temporary pacemaker should be inserted as soon as possible. 

95. Chronic AV block  *** Patients with symptomatic bradyarrhythmias associated with AV block should receive a permanent pacemaker  *** Asymptomatic first-degree or Mobitz type I second-degree AV block (Wenckebach's phenomenon) does not require treatment.

96.  *** 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. An exception may be made in young asymptomatic patients with congenital complete heart block who have a mean day-time heart rate of more than 50 per minute.

97.  A methodical approach will be much more effective than simply memorizing the appearance of the many dysryhthmias. Always begin you analysis by asking the following questions

98. 1. Is the rate fast or slow? Are the atrial and ventricular rates the same? 2. Are the P-P interval and R-R interval regular or irregular? If the rhythm is irregular, is it consistent or irregular irregularity? 3. Is there a P-wave before each QRS? Is there a QRS before every P-wave? 4. Are the P-waves and QRS complexes identical and normal in configuration? 5. Are the P-R and QRS intervals within normal limits?