This document defines and discusses various types of arrhythmias (abnormal heart rhythms). It begins by defining types of arrhythmias based on heart rate, such as tachycardia (fast) and bradycardia (slow). It then discusses mechanisms that can cause arrhythmias, including abnormal impulse formation and abnormal conduction. The document goes on to classify and describe specific arrhythmias like sinus tachycardia, atrial fibrillation, ventricular tachycardia, and different types of heart block. Treatment options are provided for many of the arrhythmias.

1. ArrhythmiA
By
cardiovascular department
staff

17. Definition
 It is an abnormalities in heart rhythm as :
1. Tachycardia : heart rate exceeds 100 b/m
2. Bradycardia:heart rate less than 60 b/m .
3. Irregularity of rhythm .
4. Combinationof any of the above as irregular
bradycardia and irregular tachycardia .

18. Mechanisms
1. Abnormal impulse formation :
 Abnormal automaticity : occurs when other cells start firing
spontaneously in stead of SAN
 Triggered activity : occurs due to electrical instability in the
myocardial cell make the heart cells contract twice
although they only have been activated once (after-
depolarization ) for example Torsad De Pointes

19. 2- Abnormal conduction :
 Conduction delay : can cause slow heart rate as happens
during AV conduction block.
 Re-entry : it is a common cause of arrhythmias it can occur
when a conduction path is partly slow down for example VT &
AV –nodal re-entry .

24. Classification of arrhythmias
A. Narrow complex tachycardia (Supraventricular arrhythmias)
Sinus tachycardia, Atrial fibrillation, atrial flutter and SVT
B. Wide complex tachycardia
Ventricular tachycardia, ventricular fibrillation and
Supraventricular arrhythmias with aberration

25. Tachycardia
sinus tachycardia
It means heart rate > 100 b/m. that originates from SAN. Caused
by :
1. In response to increased metabolic needs of the body as
fever , exercise , emotion ,Hge anemia.
2. As a compensatory mechanism in heart disease as in heart
failure , myocarditis , shock
3. Drugs as atropine , adrenaline , ephedrine
Diagnosed by ECG .
Treatment : treat the cause–beta blocker in anxiety

26. ||-Paroxysmal SVT
 This common tachycardia is usually due to re-entry of
excitation wave in the AVN (AVNRT) or due to presence of
accessory pathway as in case of WPW syndrome (atrio-
ventricular reciprocating tachycardia )(AVRT).
 C/P :
1. The attacks may start from childhood
2. The attacks always sudden onset & offset.
3. HR during attacks 150-250 b/m.
4. The duration of each attack varies from few minutes to
hours.

27. 5-The manifestations of low COP can occurs &polyuria .
6- Carotid massage either produces no effect or causes sudden
cessation of the tachycardia.
7- The patient between the attacks complete normal
8-ECG during the attacks show rapid regular tachycardia (150-250
b/m.) with normal QRS complexes but P wave invisible .

28. SVT

29.  Treatment :
* Acute attack : termination of attack by :
1- Reassurance & sedation
2- Increase the vagal tone by carotid sinus
massage or induction of vomiting.
3-Verapamil(isoptin): it is given as 5 mg IV bolus
& can be repeated after 10 min. also adenosine
IV is more effective only on stable patient.
4- DC shock if the patient hemodynamic unstable
or fail of medical treatment

30. * Prevention of recurrence :in between attacks :
1- Avoid the factors that provocation the attacks
as smoking , anxiety & coffee .
2- Use suitable anti-arrhythmic drug as beta
blocker , quinidine , amiodarone
3- In case of resisting medical treatment with
frequent attacks of arrhythmia catheter ablation
therapy should be used , ablation of AVN in case
of AVNRT or accessory pathway on case of AVRT

31. WPW syndrome
 Pre-excitation occurs when ventricular excitation starts earlier
than would be expected using normal AV conduction
pathways.
 This is due to an accessory pathway that connects the atrium to
the ventricle without passing through the AVN ( has a rapid
conduction ).
 It diagnosed by recurrent attacks of SVT .
 ECG : between the attacks show:
* Short PR interval
* Initial slurring QRS (delta wave ).
* Wide QRS.

34. Paroxysmal VT-|||
 It is rare but much serious & life threatening .
 Started due to hyperexcitable focus on LV that controls the
ventricles at rate (150 -250 b/m.).
 It can be non-sustained (last < 30 sec.) or sustained ( > 30 sec.).
 Causes :
*myocardial diseases as AMI or HOCM.
*toxic dose of anti-arrhythmic drugs as digitalis .
* congenital or acquired long QT interval that produce serious
type of VT (Torsade De Pointes).

36.  C/P : * sudden onset & offset.
* It associated with hemodynamic instability
very low Bl.Pr. & very week pulse or absent.
*If persist for time can cause syncope & shock
and can deteriorate to VF and death.
* AV dissociation is found with it & this is
produce variable first H.S. & canon wave .
* Carotid sinus massage ineffective.
* ECG : show rapid regular rhythm with wide
QRS complexes with no relation to P wave.

37.  Treatment :
A ) Acute attacks :
1. DC shock : in unstable patients & contraindicated in case of VT
due to digitalis toxicity .
2. Lidocaine : is safe & given in stable patient and as
a maintenance after DC.
3. Treatment cause as IHD or hypokalemia.
B ) In between the attacks :
1. Long term anti-arrhythmic drugs as beta blocker or
amiodarone or procainamide.
2. ICD :if medical treatment fail & high recurrence rate

38. lV-Atrial fibrillation (AF)
 It is the most common atrial arrhythmia
 It may be :
*paroxysmal (self terminating within 48 hs.).
*persistent (self terminating in days or weeks
*permanent.
 It produced due to excitation of multiple wavelets presented
on atria that leading to formation of irregular paths about 400-
600 b/m.
 Due to this rapid atrial rate some of this waves blocked at AVN
producing ventricular rate 100-150 b/m. ( pulsus deficit ).

39.  Causes :
1. Any heart diseases can lead to AF that produce dilatation ,
fibrosis or ischemia of the atria (Chron hypertension,
Rheumatic mitral valve disease as mitral stenosis or regurge).
2. Thyrotoxicosis .
3. After surgical operations or trauma.
4. Chronic lung diseases
5. acute pulmonary embolism.
6. Rarely AF may occur without heart disease (lone AF ).

41.  C/P :
1. AF can cause palpitations while some patients become
unaware of the arrhythmia.
2. The HR is usually 100-150 b/m.
3. The pulse is totally irregular on volume & rhythm
4. Absent A wave on neck vein .
5. Pulsus deficit.
6. Systemic embolizations can occurs.
7. ECG : absent P waves are absent and are replaced by
irregular F waves at rate 400-600 / min.& the ventricular rate is
totally irregular .

42. F wave is fibrillatory waves which are
characteristic to AF (Important)

44. Left atrial appendage thrombus

45. Most patients with AF are candidate for
anticoagulation especially patients with
rheumatic mitral stenosis.
There is 2 type of anticoagulation for
thromboembolic prophylaxis
The traditional anticoagulation which is
warfarin but it need regular INR monitoring
The new oral anticoagulants as
rivaroxaban, apixaban, dabigatran and
edoxaban
New oral anticoagulants have the
advantage that they have less bleeding
and no regular follow up INR but they are
expensive

46. VASc is a deigned score system-2DS2CHA
which predict thromboembolic events in
patients with AF

47. Treatment :
A ) Acute attacks : associated with rapid ventricular response
If the attack less than 48 h
* If there is hemodynamic deterioration DC shock should be
given followed by drugs to prevent recurrence as amiodarone
.
* If the patient is hemodynamic stable we can give IV infusion of
amiodarone followed by oral or if the patient has structurally
normal heart we can give propafenone 600 mg oral
If the attack more than 48 h
If TEE is available should be done
LAA is clear, we can proceed to cardioversion
If TEE is not available
We should give the patient anticoagulation for at least 3 weeks
with target INR 2-3 then cardioversion

48. B) Permenant AF :
1. Decrease the ventricular rate : by drugs as digitalis once daily or
beta blocker as bisoprolol 2.5 mg once daily, inderal 10 mg t.d.s
or verapamil (isoptin 80 mg ) t.d.s.
2. Conversion to sinus rhythm if :
* AF of short duration.
*There is no underlying heart disease.
* The underlying disease has been corrected.
The patient should be anti-coagulated first .
The conversion can be done by DC chock or drugs as propafenone
600 mg once and maintenance dose of either sotalol 80 mg
twice daily or amiodarone once daily or by RF ablation of focus
.
3. Prevention of systemic embolisations by anticoagulant

49. V-Atrial flutter
It is like AF but differ from it by :
*The wave more course the atrial wave 250-350
so can appears on ECG .
*There is regular block on AVN 3-1 or 2-1 block
giving regular ventricular rate (regular
tachycardia 125-175 b/m)

50. Vl-Ventricular fibrillation
 VF is a state of generalized electric activity of the ventricles with
no effective contraction .
 If it is continuous for 3-5 min. leading to permanent brain damage
 Cause :
* IHD & AMI * Advanced heart failure .
* Long QT syndrome .
 C/P :
* Complete loss of consciousness , pulseless
* ECG :irregular undulations without QRS.
 Treatment : cardiopulmonary resuscitation if return to sinus rhythm
give antiarrhythmic drugs as amiodarone.
ICD : in high risk patient

52. Bradycardia
Sinus bradycardia
*hypothermia , hypothyroidism , jaundice.
*drug therapy as beta-blockers , digitalis
*neurally mediated syndromes
*acute ischemia that can affect SAN .
*Chronic degenerative changes as sick sinus syndrome
(episodes of bradycardia or sinus arrest & paroxysmal atrial
tachycardia ( tachy-brady syndrome) .

53. Neurally mediated syndromes
These are due to reflex that may result in both bradycardia and
reflex peripheral vasodilatation.
These syndromes usually present as syncope e.g,
Carotid sinus syndrome :it result from stimulation of carotid sinus
as neck collar(tight collar) or during shaving produce reflex
bradycardia with hypotension .
Vasovagal syndrome : it result from physical & emotional stress
that affect the autonomic nervous system .

55. Heart block
 It is an abnormal heart rhythm where the heart beats too slowly
(bradycardia). In this condition, the electrical signals that tell
the heart to contract are partially or totally blocked between the
upper chambers (atria) and the lower chambers (ventricles)
 It occurs at any level in the conduction system.
Atrio-ventricular block
1. First degree AV block : these electrical changes only leading
to prolonged PR interval without any symptom .
2. Second degree AV block : when P wave conduct & other do
not .
• Mobitz l block (Wenckebach phenomenon): is progressive PR
interval prolongation a P wave fail to conduct .
• Mobitz ll :occurs when QRS dropped suddenly.
• Advanced block: 2:1 or 3:1

56. 3- Third- degree (complete )AV block :
 It occurs when all atrial activity fails to conduct to the ventricles
. In this situation life is maintained by spontaneous escape
rhythm (heart rate 25-40).
 When QRS complex be narrow(<0.12 ) it means that the region
of block lies more proximal to AVN.
 Usually QRS complex be wide (> 0.12 ) it means that the region
of block lies distally to his bundle .

63. Causes of heart block
1. Idiopathic fibrosis of the conductive system.
2. IHD involving conductive system.
3. Myocarditis
4. Rheumatic carditis usually cause first degree.
5. Calcific aortic stenosis may spread to conductive system.
6. Drugs e.g. beta blocker , verapamil ,quinidine ,digitalis
toxicity
7. congenital

64. Clinical features:
 First degree : asymptomatic detected only by ECG
 Second degree : detected by dropped beats.
 Complete heart block:
*symptoms of low COP as fatigue & syncope
*Heart rate is regular and less than 40 / min.
*High systolic & low diastolic blood pressure.
* Large pulse volume .
*Variable intensity of first sound
* Canon waves in the neck veins.
* Adams-Stocks attacks in some cases.

65. Adams-Stocks Attacks :
 It is short and self-limiting attacks of ventricular standstill or VT
or VF.
 Complete or partial heart block can produce it.
 This attacks produce transient cerebral ischemia results in :
1. Pallor .
2. Syncope .
3. Convulsion if the circulatory arrest is prolonged
4. Death may occur if attack > 3 minutes.

66. Treatment of heart block
1. Treatment of underlying cause .
2. If the patient is asymptomatic and the rhythm is stable over 40
b/m. no treatment is needed.
3. If the cause is transient as inferior MI observe but when be
symptomatic start by atropine if still no improvement
temporary pacing is needed.
4. Chronic irreversible symptomatic cases permanent
pacemaker is needed.
5. During Adams-Stocks attacks immediate cardiopulmonary
resuscitation must be done.

67. Types of pacemaker
I. Single chamber VVI
II. Dual chamber DDD
III. CRT
(cardiac resynchornizayion
therapy)
(it has 3 leads and used in case of
systolic dysfunction)

68. Size of pacemaker

69. VVI pacemaker

70. DDD pacemaker

71. CRT pacemaker

72. Chest Xray shows dual chamber pacemaker

73. Bundle branch block
Bundle branch block : block or delay conduction of one of
the bundle branches of the conduction pathway leads to
widening of QRS complex in ECG.
it may be incomplete and produce slight wide QRS but up to
0.11 second & may be complete that produce wide QRS >
0.12 s.
Right bundle branch block : produce late activation of right
ventricle .
Left bundle branch block : produce late activation of left
ventricle .
The left bundle may be complete or divided into left anterior
hemiblock or left posterior hemiblock.
Bifascicular block : it is a block of two from three fascicle: right
bundle branch or left anterior or left posterior .
Trifascicular block : it is bifascicular block plus prolonged PR
interval

74. RBBB

75. LBBB

76. Management of arrhythmia
A) Anti-arrhythmic drugs .
B) Ablation therapy
it is radiofrequency ablation of ectopic focus in the heart to
resore normal rhythm as in case of:
* SVT
* AF & FLUTTER
* VT
A) Device therapy (ICD )
For recurrent cases of serious arrhythmias as VT & VF.

77. ICD: implantable cardiac defibrillator which
gives the patients intrinsic shocks to save him if
ventriculat tachycardia or fibrillation ocuured
(Life saving)

78. arrhythmic drugs-Anti
1- Block Na channels ( class l ) : as
1a : Quinidine (AF ),procainamide (VT)
1b : lidocaine , mexilitine (VT)
1c : propafenone, fleicainide. (AF)
2- Block beta-adrenergic receptors ( class ll ) .
3- Prolong the refractory period ( class lll ) , as amiodarone ,
dronedarone, ibutilide and sotalol . (Broad spectrum )
4- Block calcium channels ( class lV ) as verapamil (SVT).
5- others digoxin

79. MCQ

80. 1- PSVT, A-fib, and sinus tachycardia are types of:
A. Supraventricular arrhythmias
B. Ventricular arrhythmias
C. Conduction blocks
D. Normal physiological variations

81. 2- Which of the following are class IA drugs?
A. Quinidine
B. Lidocaine
C. Flecainide
D. Disopyramide

82. 3- A patient presents with the most common
arrhythmia. It is due to a chaotic rhythm with multiple
ectopic foci in atria firing randomly and multiple
reentrant loops. His atrial rate is 350-600 bpm and his
ECG shows no identifiable p wave. He has recently
fainted. He has hypertension and heart failure
already. What is his diagnosis?
A. A fib
B. V fib
C. PSVT
D. Heart block

83. 4- regarding the previous patient, is he at an
increased risk of thrombotic stroke??
A. True
B. False

84. 5- Which of the following are class III agents?
A. Amiodarone
B. Digoxin
C. Propafenone
D. Flecainide

85. 6- Atrial fibrillation is associated with:
A. normal p wave morphology
B. systemic thromboembolic events like stroke
c. Accessory pathway
D. fever

86. 7- The following conditions can cause heart block
except:
A. IHD
B. Degenerative
C. Drug induced
D. Anemia

87. 8- Narrow complex tachycardia include the
following except
A. AF
B. SVT
C. VT
D. Sinus tachycardia

88. 9- Wide complex tachycardia include the following
except
A. AF
B. VF
C. VT
D. AF with aberration

89. 10. ECG criteria of wolf Parkinson white WPW
syndrome include the following except:
A. Short PR interval
B. Initial slurring QRS (delta wave ).
C. Wide QRS.
D. F wave

90. Thank you