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.)
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.
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
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
15.
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.
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
19.
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.
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
28.
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.