Cardiac Arrhythmia (Dysrhythmia) Flashcards
→ Definition of Cardiac Arrhythmia (Dysrhythmia)
Disturbance of normal cardiac rhythm
Transmission of Cardiac Rhythm
From Sinoatrial node (SA node) to Atrium to Atrioventricular node (AV node) to Purkinje fibre to Ventricle
Causes of Cardiac Arrhythmias
Ischaemia [shortage of blood supply]
Hypoxia [shortage of blood supply]
which ischemia and hypoxia lead to → Myocardial Infarction (damage/death of heart tissue)
Electrolyte Abnormalities e g hyperkalemia
Autonomic Influences
Drug Toxicity e g digoxin
Infection
Therapeutic Goals of Antiarrhythmic Drugs
Termination of an Ongoing Arrhythmia
Prevention of an Arrhythmia
→ Acute Therapy: Intravenous administration
→ Chronic Therapy: Long term oral use
Approaches of Anti
Arrhythmic Drugs
Alter Autonomic Function
Decreased Ectopic Pacemaker Activity
Decreased Impulse Conduction Rate
Increased Effective Refractory Period ( ERP)[the longest interval at which a premature stimulus
fails to generate a propagated response]
Classification of Anti
Arrhythmic Drugs
Class I Drugs
-sodium channel blockers
Class II Drugs
- β adrenoceptor antagonists
Class III Drugs
- potassium channel blockers
Class IV Drugs
- calcium channel blockers
Characteristics of Class I Anti
Arrhythmic Drugs Sodium Channel Blockers
•
Use Dependence
- binds preferentially to sodium channels which are in the open or inactivated state
→the more frequently the channels are activated, the greater is the degree of block
Name and effect of Subtypes
of Class I Drugs
sodium channel blockers
→ decreased conduction velocity →block tachycardias
Class Ia ::(oldest group)
eg quinidine procainamide disopyramide
Class Ib rapid kinetics
-preferentially block premature beats
e g lidocaine mexiletine
Class Ic slow kinetics
-markedly decreased conduction
eg flecainide encainide propafenone
Name Property and Adverse effect of Class Ib Drugs
e.g. lidocaine , mexiletine
Rapid Kinetics
- dissociate rapidly from sodium channels within the time frame of NORMAL heartbeat
→preferentially block premature beats
Selective for Refractory Channels
→preferentially suppress depolarized cells
(eg in ischaemia)
Adverse Effects
- central nervous system disturbances
(eg nausea, tremor, drowsiness, convulsions)
Name Property and Adverse effect of Class Ic Drugs
flecainide , propafenone
Slow Kinetics
- dissociate slowly from sodium channels
→markedly decreases conduction even at normal heart rates
Adverse Effects
- pro-arrhythmia
→ increases the incidence of sudden death especially in presence of severe heart failure
Propafenone
- structural similarities to propranolol
→weak b adrenergic blocker activity (-ve inotropic)
→→worsen heart failure
Name Property and Adverse effect of Class
Ia Drugs
e.g. quinidine , procainamide , disopyramide
Intermediate Rate of Dissociation from Sodium Channels
→ inhibit increased automaticity
→ moderately decreased conduction
Block Potassium Channels
→ decreased rate of repolarization of cardiac cells
→ increased duration of action potential
→ → increased effective refractory period (ERP)
Adverse Effects of Class
Ia Drugs
Pro-Arrhythmia
→ ectopic beats due to inhibition of potassium channels [→→ polymorphic ventricular
→tachycardia torsades de pointes arrhythmia)]→
Other Adverse Effects
- gastrointestinal disturbances e.g diarrhoea (or constipation), nausea and vomiting
- -less likely with disopyramide
- lupus-related symptoms e g arthralgia and arthritis
- -due to long term use of procainamide
- decreased force of contraction of heart
- disopyramide quinidine procainamide
Effect, class, and Adverseeffect of Class II Anti
Arrhythmic Drugs
Adrenoceptor Antagonists
Oppose b Adrenergic Stimulation
→decreased heart rate
→ increased AV nodal conduction time
→ decreased intracellular calcium overload
Different Subclasses
selective b 1 adrenoceptor antagonists e g metoprolol esmolol [esmolol short half-life because rapidly metabolized by erythrocyte esterases
→intravenous administration primarily used for intraoperative and for acute arrhythmias]
non-selective β adrenoceptor antagonists e g propranolol
-antagonize both b-1 and b-2 adrenergic receptors
Adverse effect
Bronchospasm
→contraindicated in patients with asthma or other forms of obstructive airways
disease
Decreased Force and Rate of Contraction of Heart
→cautious in patients with heart failure
Hypoglycaemia
→contraindicated in patients with diabetes
Name, effect of Class III Anti
arrhythmic Drugs
Potassium Channel Blockers
amiodarone, dofetilide ibutilide sotalol
Decrease Rate of Repolarization of Cardiac Cells
→increased action potential duration
→→ increased effective refractory period
→→→→decreased automaticity
Characteristics and adverse effect of Dofetilide
Potent and “ Potassium Channel Blocker
Risk of Developing Ectopic Beats
[→ polymorphic ventricular tachycardia]
- due to increased action potential duration
- cautious with hypokalemia
- avoided in patients with advanced renal failure or with inhibitors of renal cation transport (e g cimetidine)
Effect and Adverse effect Amiodarone
Highly Effective Anti Arrhythmic Drug
Additional Effects to Potassium Channel Blockade
-block inactivated sodium channels
-weak adrenergic blocking activity
-weak calcium channel blocking activity
→broad spectrum of actions
Low Incidence of Developing Ectopic Beats
[Ie low risk for polymorphic ventricular tachycardia]
Adverser effect
- Pulmonary Fibrosis
- Hypersensitivity hepatitis
-Photosensitivity
→skin rashes and grey blue -skin discoloration following sun exposure
-Corneal Deposits → visual problems
-Thyroid Abnormalities
→hypo or hyper thyroidism due to high iodine content
- Pro Arrhythmia (Bradycardia and Heart Block)
- Drug Interaction [metabolized by liver cytochrome P 450 enzymes]
