Cardiac arrhythmias can be caused by abnormalities in heart rate, rhythm, origin of impulses, or conduction. The main mechanisms are reentry, automaticity, parasystole, and triggered activity. Reentry requires two pathways that form a loop with a block in one pathway and slow conduction in the other. Common arrhythmias include atrial fibrillation, ventricular tachycardia, and supraventricular tachycardia. First-line drugs for treating arrhythmias include lignocaine, amiodarone, adenosine, beta-blockers, and calcium channel blockers. These drugs work via different mechanisms such as blocking sodium, potassium, or calcium channels to suppress arrhythmias.

4.  Cardiac arrhythmia is an abnormality in:
› Rate
› Rhythm
› Site of origin and,
› The conduction of cardiac impulse
Either - Bradyarrhythmia (<60 beats/min.) or ,
Tachyarrhythmia(>100 beats/min.)

5.  Reentry (Most Common)
 Automaticity
 Parasystole
 Triggered activity

6. Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Reentry Requires…
Electrical Impulse
Cardiac
Conduction
Tissue
1. 2 distinct pathways that come together at
beginning and end to form a loop.
2. A unidirectional block in one of those pathways.
3. Slow conduction in the unblocked pathway.

7. Atrial Reentry
• atrial tachycardia
• atrial fibrillation
• atrial flutter
Atrio-Ventricular
Reentry
• WPW
• SVT
Ventricular Re-entry
• ventricular tachycardia
AV Nodal Reentry
•SVT
Reentry Circuits
SA Node

8.  Heart cells other than those of the SA node
depolarize faster than SA node cells, and take
control as the cardiac pacemaker.
 Factors that enhance automaticity include:
CO2,  O2,  H+,  stretch, hypokalemia and
hypocalcaemia.
Examples: Ectopic atrial tachycardia or multifocal
tachycardia in patients with chronic lung
disease OR ventricular ectopy after MI

9.  Benign type of automaticity problem that
affects only a small region of atrial or
ventricular cells.
 3% of PVCs

10. • Myocardial damage - oscillations of the
transmembrane potential at the end of the action
potential.
• These oscillations, which are called 'after
depolarizations', may reach threshold potential and
produce an arrhythmia.
• The abnormal oscillations can be exaggerated by
pacing, catecholamines, electrolyte disturbances,
and some medications.
• Examples as atrial tachycardias produced by digoxin
toxicity

11. 1. Supraventricular arrhythmias: all arrhythmias above the bundle of His.
› Sinus bradycardia (rate <60 Beats/min.)
› Sinus tachycardia (rate>100 BPM)
› Paroxysmal supraventricular tachycardia (rate: 140-250 BPM)
› Atrial flutter (rate: 240-400 BPM)
› Atrial fibrilation
› Wolff-Parkinson white syndrome
› Premature atrial contraction

12. 2. Ventricular arrhythmias: all arrhythmias originating below the
bundle of His
o Premature ventricular contractions
o Ventricular tachycardia (Torsade de points)
o Ventricullar fibrillation

13. Note : Class IA agents also have class III property; Propranolol
has class I acton as well; Sotalol and bretylium have both class II
and class III actions.

14.  Based on clinical use:
1. Drugs used for supraventricular
arrhythmias: Adenosine, verapamil,
diltiazem
2. Drugs used for ventricular arrhythmias:
lignocaine, mexelitine, bretylium
3. Drugs used for supraventricular as well as
ventricular arrhythmias: Amiodarone, β-
blockers, disopyramide, procainamide

16.  First line drug for the suppression of ventricular
tachycardias.
 Mechanism of action:
inhibit the fast sodium current while shortening the action
potential duration in nondiseased tissue
es the depolarization automaticity and excitability in the
ventricles during the diastolic phase
directly acts on the tissues as the Purkinje network
Acts selectively on diseased or ischemic tissue where they are
thought to promote conduction block, thereby interrupting
reentry circuits.

17.  Indication :
1. Ventricular arrhythmias especially after myocardial
infarction.
2. Cardiac manipulation
 Adverse effect:
1. CNS: tremmor, confusion, restlessness, anxiety, light
headedness, europhoria, apprehension, agitation
2. CVS: cardiac arrest, cardiac dysrhythmia,
hypotension, bradycardia,
3. Respiratory: respiratory depression, respiratory arrest
4. Ear: tinnitus
5. Eye: double vision
6. Methemoglobinemia, seizure, anaphylactic reactions,
malignant hyperthermia

18. Contraindication:
 Hypersensitivity
 Adams-stokes syndrome
 Severe degrees of AV and SA
 Severe heart failure
 Prophyria
 Hepatic failure
 Wolff-parkinson-white syndrome
Drug interaction:
Β-blockers decrease the metabolism of lignocaine
In patients receiving propranolol or halothane the hepatic
clearance of lignocaine is reduced-toxicity

20.  Bioavailability: 35% (PO)
 Onset: IV 45-90 sec
 Duration : 10-20 min
 Protein bound: 60-80%
 Vd: 119 L
 Metabolism- dependent on hepatic blood flow
 Extensive first pass effect (so requires iv
administration).
 Half-life: 8 min. distributive and 2 hrs for elimination
(prolonged in CHF, Liver disease)
 Excretion: urine (90%)

21.  Dose of lignocaine :
› 1-1.5 mg/kg slow IV bolus over 2-3 min

22.  Alert box:
› Lignocaine hydrochloride 2% injection for cardiac
arrhythmias has a different formulation and should
not be confused with lignocaine for anaesthesia.
› Lignocaine intravenous agent :used only for
ventricular dysrrhythmias.
› It’s preparation is intended for IV administration
and contain no preservative or catecholamines
› Preparation containing epinephrine or another
catecholamines must never be administered
intravenous. If so that can cause severe
hypertension and life threatening dysrrhythmias.

23.  Mechanism of action:
Inhibits movement of calcium ions across the cell
membrane into vascular smooth muscles and
myocytes
Causes relief of angina by decreasing myocardial
oxygen demand, similarly slow the sinus rate,
increases PR and QT intervals, and decreases
peripheral vascular resistance.

24.  Indication :
› Life threatening ventricular arrhythmias
unresponsive to conventional therapy with less
toxic agents.
› Supraventricular arrhythmias unresponsive to
conventional therapy.

25.  Adverse effect:
› CNS: headache, dizziness, fatigue, malaise,
poor concentration, tremor, involuntary
movement
› CVS: pinresistant bradycardia, worsening of
arrhythmias, sinus arrest, AV block
› GIT: nausea, vomiting, anorexia, constipation
› Respiratory: pulmonary fibrosis, interstitial
pneumonitis, pulmonary oedema
› Endocrine: disturbances in thyroid function,
increased triglycerides
› Liver: liver damage increased liver enzymes
› Muscular: phototoxicity

26. Drug interaction:
› It inhibits cytP450 enzymes and may increase
plasma concentrations of digoxin,
methotrexate, theophylline, procainamide,
warfarin, and phenytoin resuliting in toxicities.
Contraindication:
 Severe sinus node dysfunction
 2nd and 3rd degree heart block
 Marked sinus bradycardia
 Cardiogenic shock
 Thyroid disease
 Severe respiratory failure

27. Bioavailability: 35-65% (PO)
Effective plasma concentration: 1.2 mcg/ml
Slow onset 2 days to several weeks.
Duration of action= weeks to months
Protein bound: 96%
Vd: 4620 L
Metabolism: liver with enterohepatic
recirculation
Half-life = 26 to 107 days
Not dialyzable by hemodialysis or peritoneal
dialysis
Elimination: bile, urine

29.  Dose of Amiodarone:
› IV: 150 mg IV over 10 min; Repaeted as needed
to a maximum of 2.2g/24 hr
› Oral:
 Loading dose: 800-1600mg PO OD for 1-3 week;
reduce dose to 600-800mg/day for 1 month
 Maintenance dose: 400mg PO OD

30.  MECHANISM OF ACTION:
 Ubiquitous in the body, in combination with phosphate
(cyclic AMP)
 2 types of specific adenosine receptor A1 and A2.
 A1: inhibition of AV nodal conduction, reduction of
contractility, inhibition of neurotransmitter release in
CNS and PNS, renal vasoconstriction and
bronchoconstriction.
 A2: vasodilation, inhibition of platelet aggregation and
stimulation of nociceptive neurones.
 It restores normal sinus rhythm by interrupting re-
entrant pathways in the atrio ventricular node and also
slow conduction time through the atrio ventricular node.

31. Indication:
› Rapid reversion to sinus rhythm of paroxysmal
supraventricular tachycardia.
Adverse effect:
CNS: headache, lightheadedness, dizziness,
numbness, irritability, apprehension
CVS: transient arrhythmia, heart block,
haemodynamic disturbances, palpitation, chest
pain hypotension, bradycardia
GIT: nausea, tightness in throat
Respiratory: dyspnoea, hyperventilation
Blood: flushing

32.  Drug interaction:
› Dipyridamole inhibits Adenosine uptake.
› Aminophylline or Caffeine is potent inhibitors of
adenosine.
Contraindication:
 2nd and 3rd degree heart block
 Sick sinus syndrome
 Asthma

33.  Half-life : <10 sec
 Duration: 60- 90 sec
 Onset: 20-30 sec
 Metabolism: blood and tissue
 Total body clearance: 30 sec

35. Drugs F
(PO)
Half-
life
Onset Vd Metabolis
m
Elimination
Lignocaine 35% 8 min
(IV)
45-90
sec(IV)
119L liver urine
Amiodarone 35-
65%
26-
107
days
Several
weeks
4620L liver Bile, urine
Adenosine
(IV)
- <10
sec
20-30
sec
- Blood and
tissue
sweat