Drugs to treat arrhythmias II Flashcards
Class III MOA
no effect on
phase 0, but they markedly prolong phase
3 and increase the
QT interval.
Why is the use of Amiodiorone limited?
Use is limited due to side effects (incl. tachy arrhythmia)
But it is one of the safest antiarrhythmic agent after B-blockers for oral use
Indications of amiodarone
prophylaxis and treatment of supra ventricular and ventricular arrhythmias
Explain Amiodarone structure
Amiodarone is an organic iodine compound that is structurally related to thyroid hormone
Oral absorption, bioavailability and distribution of Amiodarone
Slow oral absorption with bioavailability of 20-55%
Wide distribution in fat, muscles and Liver.
How long does the therapeutic effect of Amiodarone take?
Therapeutic response may take 3 weeks, with peak effect reached in
1-5 months
After withdrawal of tx with amiodarone, how long do antiarrhythmic effects persist?
Antiarrhythmic effect persist for 10 – 150 days after withdrawal of
long-term treatment
Onset of action of amiodarone
IV 10-15 minutes
Metabolism and excretion of Amiodarone
Extensive hepatic metabolism with biliary excretion (renal excretion
negligible)
Contraindications of Amiodarone (40
Cardiac bradycardia/block, hyperthyroidism, sensitivity to iodine,
hypokalemia
Pregnancy and lactation
Cautions of Amiodarone
Heart failure, hepatic impairment
Drug interactions of Amiodarone
May interact with other drugs for months after
discontinuation of treatment
* Other antiarrhythmics, b-blockers, digoxin, drugs causing QT prolongation,
phenytoin, simvastatin, warfarin, grapefruit juice
Amiodarone adverse effects
May take several weeks to appear and continue for months after
discontinuation of treatment
* Torsades de Pointes
* Hyper/hypothyroidism (thyroid function monitoring necessary)
* Neurotoxicity (including peripheral neuropathies)
* Photosensitivity (warn to avoid exposure to sunlight)
* GI
* Uncommon: pulmonary fibrosis & hypersensitivity pneumonitis
Effects of Class II and Class IV antidysrhythmic drugs
Class II drugs (β-adrenoceptor antagonists) and Class IV drugs (calcium channel blockers) slow phase 4 depolarization in the SA node and increase the PP
interval.
They also slow the atrioventricular (AV) node conduction velocity and increase
the PR interval.
MOA of propranolol (5)
Inhibit sympathetic activation of cardiac automaticity and conduction,
* Slow the heart rate,
* Decrease the AV node conduction velocity, and
* Increase the AV node refractory period,
* Little effect on ventricular conduction and repolarization.
Indications of Propranolol
- Prevent and treat supraventricular dysrhythmias
- Reduce ventricular ectopic depolarizations and sudden death in patients
with myocardial infarction.
MOA of Verapamil (4)
Decrease the AV node conduction velocity and
* Increase the AV node refractory period,
* Smaller effect on the SA node and heart rate,
* Little effect on the ventricular conduction velocity and refractory
period.
Indications of Verapamil
Controlling or converting certain supraventricular dysrhythmias, not
effective in treating ventricular dysrhythmias.
* Control the ventricular rate in patients with atrial fibrillation
ROA of Verapamil
Verapamil can be administered intravenously to terminate paroxysmal
supraventricular tachycardia (PSVT), and it is given orally for chronic
treatment
Adverse effects of Verapamil
Exacerbate wide QRS complex VT and should not be given to patients
with this dysrhythmia.
List 5 miscellaneous antiarrhythmics (ADMIR)
- Adenosine
- Digoxin
- Magnesium sulphate
- Ivabradine &
Ranolazine
What is adenosine used for?
Acute management of paroxysmal supraventricular tachycardias
convert to sinus rhythm
ROA and half-life of Adenosine
Administer as rapid IV bolus
* Half-life <10 seconds
Adverse effects of Adenosine (3)
dyspnoea, flushing, chest pain are an indication the
bolus has reached the heart
Only use when cardiac monitoring and resuscitation is available
What is atrial fibrillation and atrial flutter
disorganized form of re-entry in which atrial cells are continuously re-excited by re-entrant stimuli as soon as they are
repolarized.
The AV node is continuously bombarded with atrial impulses, some of which are conducted to the ventricles, so that the
ventricular rate is often rapid and irregular
What are the objectives of treatment of atrial fibrillation and flutter
- Ventricular rate control to avoid development of cardiomyopathy. Use B-blockers and CCBs which slow AV node conduction velocity and increase its refractory period, so that fewer impulses are conducted to the ventricles.
- Prevent recurrences and maintain normal sinus rhythm -Amiodarone.
3.Anticoagulant (warfarin) to prevent thromboembolism and stroke
What is Torsades de Pointes?
Polymorphic ventricular
tachycardia (VT), associated with
QTc prolongation, which is the heart rate adjusted lengthening
of the QT interval.
What induces Torsade de Pointes? (3)
- Drugs (including tricyclic
antidepressants and
antipsychotic agents ) - Electrolyte abnormalities that
prolong the QT interval and predispose cardiac cells to afterdepolarizations - Congenital prolonged QT syndrome.
Tx of Torsades de Pointes
Withdrawal of the causative agent,
* Correction of any
electrolyte abnormalities,
such as hypokalemia,
* Intravenous administration
of magnesium sulfate IV ,
and
* Cardiac overdrive pacing.
* These treatments act in part by shortening the QT
interval.
