This document provides an overview of cardiac arrhythmias for medical students. It begins by describing the normal conduction pathways in the heart and ECG patterns. It then classifies arrhythmias as rapid and regular, rapid and irregular, slow and regular, or slow and irregular based on heart rate and rhythm. Common types of arrhythmias are defined such as sinus tachycardia, atrial fibrillation, heart block, and ventricular fibrillation. Causes, characteristics, treatments, and examples of patients with various arrhythmias are outlined. The document also discusses antiarrhythmic drug classifications and indications for procedures like ablation and pacemakers.

1. Arrhythmia for Medical
Students
Samir Rafla, FACC, FESC
Prof. of Cardiology
Alexandria University

2. The pathways of Conduction

3. Anatomy of the AV node (fast and slow pathways)
and the triangle of Koch
Anatomy of the AV node

4. Normal electrical activation of the heart
Sinus node
AV - node
right and
left branch
ECG
(62/min)

5. Normal ECG

7. Classification of arrhythmia:
- Rapid, regular. Sinus tachycardia, supraventricular
tachycardia, atrial flutter, ventricular tachycardia.
- Rapid, irregular. Sinus arrhythmia, multiple
ectopic beats whether atrial or ventricular, atrial
fibrillation.
- Slow, regular. Sinus bradycardia, nodal rhythm,
complete heart block.
- Slow, irregular. Slow atrial fibrillation.

8. Tachycardia Rhythm disturbances
regular irregular
QRS
narr
ow
QRS
wide
Sinus tachycardia
AVNRT
WPW (orthodrom)
AT
VT
SVT with branch
block
WPW (antidrom)
Atrial fib (TAA)
Atrial flutter;
Sinus tachycardia with
SVES
VF
VT (polymorph)
Atrial Fib and WPW
incl- branch block

9. Sinus tachycardia
Cardiac impulses arise in the sinus node at a rate
more than 100/min. 4
Etiology:
A- Physiological: Infancy, childhood, exercise and
excitement.
B- Pharmacological: Sympathomimetic drugs such as
epinephrine and isoproterenol. Parasympatholytic
drugs such as atropine. Thyroid hormones, nicotine,
caffeine, alcohol.
C- Pathological: Fever, hypotension, heart failure,
pulmonary embolism, hyperkinetic circulatory states
as anemia, hyperthyroidism.

10. A 34 year old woman with asthma

11. Sinus Bradycardia
Cardiac impulses arise in the sinus node at a rate less
than 60/min.
Etiology:
A- Physiologic: Athletes, sleep, and carotid sinus
compression.
B- Pharmacologic: Digitalis, propranolol, verapamil
and diltiazem.
C- Pathologic: Convalescence from infections,
hypothyroidism, obstructive jaundice, rapid rise of
the intracranial tension, hypothermia and myocardial
infarction (particularly inferior wall infarction)

12. Benign Arrhythmias
PVC in normal Heart

14. SUPRAVENTRICULAR
TACHYARRHYTHMIAS
SVTs may be separated into three groups based on
duration: brief paroxysms, persistent, and chronic
(permanent).
Arrhythmias that are paroxysmal in onset and offset
(e.g. paroxysmal SVT due to AV nodal reentry or
WPW syndrome, paroxysmal atrial fibrillation,
paroxysmal atrial flutter) tend to be recurrent and of
short duration

15. Mechanism of Reentry
Mechanisms of AVNRT

16. Reentry Arrhythmias
Normal
Re-enterant
Tachycardia

17. PSVT

18. Management of PSVT Due to AV Nodal Reentry
The acute attack: Vagal maneuvers serve as the first
line of therapy. Simple procedures to terminate
paroxysmal SVT
- Carotid sinus massage: If effective the rhythm is
abruptly stopped; occasionally only moderate
slowing occurs
- Cold water splash on face.
- Performance of Valsalva's maneuver (often
effective).

19. Management of PSVT Due to AV Nodal Reentry
Intravenous adenosine, Ca channel blockers
(verapamil), digoxin or B-blockers are the choices
for managing the acute episodes.
Adenosine, 6 mg given intravenously, followed
by one or two 6-mg boluses if necessary, is
effective and safe for acute treatment.
A 5-mg bolus of verapamil (isoptin) , followed by
one or two additional 5-mg boluses 10 min apart
if the initial dose does not convert the
arrhythmia

20. short PR interval, less than 3 small squares (120 ms)
slurred upstroke to the QRS indicating pre-excitation (delta wave)
broad QRS
secondary ST and T wave changes
Localising the accessory pathway
An accessory pathway, bundle of Kent, exists between atria and ventricles and causes
early depolarisation of the ventricle. The location of the pathway may be deduced as follows:-
LOCATION V1 V2 QRS axis
left posteroseptal (type A) +ve +ve left
right lateral (type B) -ve -ve left
left lateral (type C) +ve +ve inferior (90 degrees)
right posteroseptal -ve -ve left
anteroseptal -ve -ve normal
Wolf-Parkinson-White syndrome

21. PSVT Due to Accessory Pathways (The Wolff-Parkinson-White
Syndrome)

22. WPW syndrome

23. AVRT
ECG shows:
- Short PR interval
- Delta wave on the upstroke of the QRS complex
►Drug treatment includes flecainide, propafenone,
amiodarone or disopyramide.
►Digoxin and verapamil are contraindicated.
►Catheter radiofrequency ablation is the treatment
of choice.

24. A 25 year old
man with bouts
of tachycardia

25. atrial fibrillation:
Duration
- Paroxysmal Minutes/hours
- Short-lasting Seconds --<1 hour
- Long-lasting >1 hour; -- < 48 hours
- Persistent Two days -- weeks
- Permanent (Chronic) Months / years

26. A 53 year old man with Ischaemic Heart Disease.

27. Causes of atrial fibrillation
With structural heart disease
- Rheumatic mitral valve disease
- Ischemic heart disease
- Hypertension
- Cardiomyopathy: Dilated, Hypertrophic
- Atrial septal defect, - Constrictive pericarditis,
Myocarditis
Without structural heart disease
- Alcohol. Thyrotoxicosis
- Acute pericarditis. Pulmonary embolism
- Sick sinus syndrome, Lone atrial fibrillation

28. A woman with loud first heart sound and mid-diastolic
murmur.

29. AF with AP degenerating to VF

30. • Complications of Atrial Fibrillation:
• 1- Atrial thrombosis due to stagnation of
blood in the fibrillating atria. The formed
thrombi may embolize in the systemic and
pulmonary circulations. Thrombi in left
atrial appendage may embolise to brain
causing stroke or transient cerebral
ischemic attacks; may embolize to retinal
artery causing sudden blindness in one eye;
or embolize to other systems. Right atrial
thrombi may embolize to the lungs causing
pulmonary embolism.

31. • 2- Heart failure due to loss of the atrial
contribution to contractility and the cardiac
output.
• 3- Tachycardia induced cardiomyopathy.
• 4- Complications of treatment as bleeding
from warfarin

32. Treatment of Atrial Fibrillation
Pharmacologic Management of Patients with Recurrent
Persistent or Permanent AF:
- Recurrent Persistent AF:
A) Minimal or no symptoms: Anticoagulation and rate
control as needed.
B) Disabling symptoms in AF:
1- Anticoagulation and rate control
2- Antiarrhythmic drug therapy
3- Electrical cardioversion as needed, continue
anticoagulation as needed and therapy to maintain sinus
rhythm
- Permanent AF: Anticoagulation and rate control as
needed.

33. A 23 year old male with palpitations

36. 36

37. AF management

38. Drugs for Pharmacologic Cardioversion of AF (Rhythm
control)
Drug Route of Admin. And Dosage
Amiodarone Oral: 1.2 to 1.8 g /day then 200 to 400 mg /d maintenance.
IV: 1.2 g /d IV continuous or in divided doses, then 200 to 400
mg /d maintenance
Dofetilide Oral: Creatinine clearance > 60 ml/min: 500 mcg BID
Flecainide Oral 200 to 300 mg
IV: 1.5 to 3 mg /kg over 10 to 20 min
Propafenone Oral: 450 to 600 mg
IV: 1.5 to 2 mg per kg over 10 to 20 min

39. Orally Administered Pharmacological Agents for Heart
Rate Control in Patients with AF
Drug Maintenance dose
Digoxin 0.125 to 0.375 mg daily
Metoprolol* 25 to 100 BID
Propranolol 80 to 360 mg daily in divided doses
Verapamil 120 to 360 mg daily in divided doses
Diltiazem 120 to 360 mg daily in divided doses

40. Anticoagulation of Patients with Atrial
Fibrillation: Indications
Rheumatic mitral valve disease with recurrent or
chronic atrial fibrillation.
Dilated cardiomyopathy with recurrent persistent or
chronic atrial fibrillation.
Prosthetic valves.
Prior to (>3 weeks) elective cardioversion of
persistent or chronic atrial fibrillation, and also for 3
weeks after cardioversion (because of atrial
stunning).
Coronary heart disease or hypertensive heart disease
with recurrent persistent or chronic atrial fibrillation

42. Atrial Fibrillation Management
• Long-term management of atrial fibrillation include two strategies:
– Rhythm control: antiarrhythmic drugs plus DC cardioversion plus
warfarin
– Rate control: AV nodal slowing agents plus warfarin
• Recurrent paroxysms may be prevented by oral medication; class Ic agents
are employed in patients with no significant heart disease and class III
agents are preferred in patients with structural heart disease.
• Rate control is usually achieved by a combination of digoxin beta-blockers
or calcium channel blockers (diltiazem or verapamil).
• Anticoagulation (target INR 2.0-3.0) This is indicated in patients with AF
and one of the following major or two of the moderate risk factors:
• Major risk factors: Prosthetic heart valve, Rheumatic mitral valve disease,
Prior history of CVA/TIA, Age > 75 years, Hypertension, Coronary artery
disease with poor LV function
• Moderate risk factors: Age 65-75 years, Coronary artery disease but normal
LV function, Diabetes mellitus.

43. Atrial Flutter

45. Treatment of Cardiac Arrhythmias with Catheter
Ablative Techniques
Radiofrequency ablation destroys tissue by
controlled heat production. Catheter ablation is
used to treat patients with four major
tachyarrhythmias:
atrial flutter/fibrillation, AV nodal reentry,
accessory pathways and ventricular tachycardia.

46. A woman with Romano-Ward Syndrome

47. QTc
Normal QTc
• Men < 0.43
– borderline o.43-0.45
– prolonged >0.45
• Women < 0.43
– borderline o.43-0.47
– prolonged >0.47

48. VENTRICULAR
TACHYCARDIA

50. 6

52. A 60 year old man with IHD

53. Ventricular fibrillation (VF)
• 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.
• The ECG shows shapeless, rapid oscillations and there is no
hint of organized complexes
• A person in VF requires prompt defibrillation to restore the
normal rhythm and function of the heart. It may cause sudden
cardiac death. Basic and advanced cardiac life support is
needed
• Survivors of these ventricular tachyarrhythmias are, in the
absence of an identifiable reversible cause, at high risk of
sudden death. Implantable cardioverter-defibrillators (ICDs)
are first-line therapy in the management of these patients

54. Ventricular Fibrillation

55. AV HEART BLOCK

56. Mobitz type I (Wenckebach) block
Mobitz Type II second degree heart block

57. 10

58. Atrioventricular (AV) Block
Second degree A-V Block
Mobitz type I (Wenchebach 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.
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

61. 18
10 year old girl who is asymptomatic and found to have this
ECG. Q: What are the ECG findings?

62. A 73 year old woman with dizziness.

63. A 70 year old man with exercise intolerance.

64. An 82 year old lady with dizzy spells

65. Sudden Cardiac Death
Definition: unexpected natural death due to
cardiac cause within one hour from the onset of
symptoms .

66. SD in
Athletes

67. Your diagnosis please?
20

69. Phase 0
Phase 1
Phase 2
Phase 3
Phase 4
R.M.P
(Plateau Phase)
Class I:
Na + channel blockers.
- Pacemaker potential
-
-
-
Class III:
K + channel blockers
-
Class IV:
Ca ++ channel blockers
Class II:
Beta blockers
Classification of Anti-Arrhythmic Drugs

70. Classification of Antiarrhythmic Drugs
based on Drug Action
CLASS ACTION DRUGS
I. Sodium Channel Blockers
1A. Moderate phase 0 depression and
slowed conduction (2+); prolong
repolarization
Quinidine,
Procainamide,
Disopyramide
1B. Minimal phase 0 depression and slow
conduction (0-1+); shorten
repolarization
Lidocaine
1C. Marked phase 0 depression and slow
conduction (4+); little effect on
repolarization
Flecainide
II. Beta-Adrenergic Blockers Propranolol, esmolol
III. K+ Channel Blockers
(prolong repolarization)
Amiodarone, Sotalol,
Ibutilide
IV. Calcium Channel Blockade Verapamil, Diltiazem