2. DEFINITION
• Any disturbance in rate, regularity, site of origin, or
conduction of the cardiac electrical impulse
• Any rhythm off the normal sinus rhythm
• General clinical features include palpitation, light
headedness, syncope, angina, CCF
• Normal heart rate- 60-100/min
7. Causes of arrythmias
• Hypoxia
• Ischemia and irritability
• Sympathetic stimulation (hyperthyroidism, CCF, Exercise, etc)
• Drugs e.g. antiarrhythmics
• Electrolyte imbalance e.g. hypokalemia, Ca, Mg
• Bradycardia
• Stretch
8. The basic types
1. Arrhythmia of sinus origin
2. Ectopic beats- (a) sustained Supraventricular
(5 types)
- (b) Ventricular
3. Conduction blocks
4. Pre excitation syndromes
9. 1. Arrhythmias of sinus origin
a) Sinus tachycardia – HR >100, e.g. in CCF,
lung disease, hyperthyroidism, etc
b) Sinus bradycardia – HR <60, occurs in early
signs of acute MI, hypothermia,
hypothyroidism
c) Sinus arrest, asystole
11. 2. Ectopic beats
(extrasystoles, premature beats)
• Can either be supraventricular or ventricular
• Supraventricular arrhythmia originate in the atria
or AV node
• Atrial Premature beats – single ectopic beat that
originates in the atria
• Junctional Premature beats – ectopic beats
originating in the vicinity of AV node
12. • Usually cause no symptoms but can give the
sensation of a missed beat or an abnormally
strong beat.
• A premature but otherwise normal QRS
complex on ECG.
13. (a) Sustained supraventricular
arrhythmias:
i. Paroxysmal supraventricular Tachycardia
ii. Atrial flutter
iii. Atrial fibrillation
iv. Multifocal arterial tachycardia
v. Paroxysmal atrial tachycardia
14. i. Paroxysmal Supra Vent
Tachycardia
• Common, sudden onset and abrupt termination,
• Initiated by a premature supraventricular beat and does not signify
disease.
• Occurs in normal hearts , coffee, or alcohol
• Rate is between 150-250 beats/min
• P- waves usually buried in QRS complex and are difficult to identify
• Carotid massage aborts it, or slows it
15.
16. ii. Atrial Flutter
• Can occur in normal heart or with cardiac
pathology.
• It is regular, saw tooth pattern
• Rate between 250-350/min
• P- waves not seen
• Carotid massage increases block
20. (b) ventricular arrhythmias
i. Premature ventricular contractions (PVCs)
ii. Ventricular tachycardia
iii. Ventricular flutter
iv. Ventricular fibrillation
v. Torsades De pointes
21. Premature ventricular contractions
• Most common ventricular arrhythmia
• QRS complex appears wide in all leads
• A retrograde P-wave may be seen but mostly p waves are missing
• PVC are usually followed by a prolonged compensatory pause
before the next beat appears
• Isolated PVC are common in normal hearts and need no
treatment.
• But Isolated PVC in an MI setting may trigger ventricular
tachycardia or fib- life threatening
23. Ventricular tachycardia
• Three or more successive ventricular complexes
• Can be non sustained (not lasting more than 30 secs) or
sustained
• Generally beats > 100bpm
• Rhythm usually regular
• Width of QRS generally >0.16secs
• Can be monomorphic or polymorphic
• +/- AV dissociation but when present, diagnostic
25. Ventricular flutter
• This is a VT that occurs at a very rapid rate
• Rate often > 220 bpm
• Often no distinctive T waves
• QRS are usually bizarre and usually identical
• No P waves
27. Ventricular fibrillation
• A pre-terminal event, seen in dying hearts
• Frequently encountered arrhythmia in adults who experience sudden
death
• There are no true QRS complexes
• ECG tracing jerks about spasmodically (coarse vent fib) or
undulates gently (fine vent fib)
• The heart generates no cardiac output
• Once seen perform CPR and defibrillation
29. Torsades De pointes
• Simply means twisting of the points
• It’s a unique VT usually seen in pts with prolonged QT interval and
may lead to V.fib
• Prolonged QT found in:
electrolyte imbalance as hypocalcemia, hypomagnesemia,
hypokalemia.
During an acute myocardial infarction
Pharmacologic agents: antiarrhythmic drugs, tricyclic
antidepressants, phenothiazines,
30. .• Some anti-fungals, antihistamines combined with
antibiotics like the erythromycin
• A prolonged QT results from elongation of T
waves
• A PVC falling during the elongated T wave can
initiate torsades de pointes
• Torsade de pointes is xtized by fluctuation of
QRS complexes around the ECG baseline
33. AV BLOCKS
1. First degree AV block
• Xterized prolonged delay in conduction in AV node leading to
prolonged PR interval
• Diagnosis of first degree block is PR interval longer than 0.2 secs
• All atrial impulses eventually make it to AV node and ventricular
contraction
• Every QRS is preceded by a single p wave
• Seen in normal hearts, myocarditis, drug toxicity,
• By itself does not need treatment
34.
35. Second degree AV block
• Not every atrial impulse is able to pass through the AV node.
Some p waves are arrested.
• Two types
a) Mobitz type 1/wenckebach block
b) Mobitz type II
Wenkebach:- Each successive atrial impulse encounters a
longer and longer delay in the AV node usually every 3rd/4th
fails to pass through.
36.
37. Mobitz type II
• Usually due to a block below the AV node
• The ECG shows two or more normal beats with normal
PR interval and then a P wave NOT followed by a QRS
complex
• Diagnosis requires a dropped beat without progressive
lengthening of the PR interval
• Signify serious heart dse and can progress to 3rd degree
heart block
38.
39. Third degree AV block
• The ultimate in heart block, called complete heart block
• Site of block can either be at AV node or lower
• No atrial impulses make it thru to activate the ventricles
• Ventricles respond by generating an escape rhythm, at
slower pace of 30-45 bpm as opposed to atrial rate of
60-100 bpm
41. Management
• Thorough history taking to identify the presenting symptoms
• Physical examination
• Investigations
-12-lead ECG,
-echocardiogram and
- thyroid function tests
42. • AIM of treatment
- identify the cause and treat
- prophylaxis against embolism to prevent
stroke in atrial tachycardia
-SVT- treatment not always necessary
Suitable drugs include β-blockers, flecainide and
digoxin
43. .• Prophylactic 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,
propafenone or amiodarone
44. . Ventricular tachycardia
• Prompt action to restore sinus rhythm is required and in
most cases should be followed by prophylactic therapy.
• DC cardioversion is the treatment of choice if systolic
BP is less than 90 mmHg.
• If the arrhythmia is well tolerated, intravenous
amiodarone may be given as a bolus followed by an
intravenous infusion
