Flashcards in Antiarrhythmic Class IV, Digoxin, adenosine, magnesium and A-fib Deck (26)
Class IV drugs include Diltiazem and Verapamil. This class of drugs are the cardiac selective Ca channel blockers. What is their MOA?
Decrease Ca dependent action potentials in slow response tissues (Decrease rate of phase 4)
--this decreases the rate of automaticity, slow conduction velocity, and prolong the effective refractory period.
--heart rate is slowed and PR interval lengthened
--prolonged repolarization at the AV node
What are the clinical applications for Class IV drugs?
Reduction of ventricular rate in atrial fibrillation and flutter
--2nd line to adenosine for conversion of PSVT to normal sinus rhythm
What are the adverse effects of Class IV calcium channel blockers?
Impaired electrical conduction
What are the contraindications for Class IV calcium channel blockers?
--contraindicated in patients with preexisting depressed cardiac function
The next drug to speak about is a cardiac glycoside called Digoxin. What is the main clinical application of this drug?
Control of ventricular response rate in atrial fibrillation and flutter with impaired left ventricular function or heart failure
What is the MOA for digoxin?
Actives vagal efferent nerves to the heart ---- reduction in the conduction of electrical impulses within the AV node.
--therefore fewer impulses reach the ventricles and ventricular rate falls
What are the major side effects of digoxin?
--esp atrial tachycardias and AV block
Next drug to discuss is Adenosine. What is the clinical application?
Drug of choice for abolishing acute supraventricular tachycardia
What is the MOA for adenosine?
Opens K channel
--inhibits SA nodal, atrial, and AV nodal conduction
Inhibits cAMP mediated Ca influx therefore depresses action potentials
--AV node much more sensitive
What are the pharmacokinetics and adverse effects of adenosine?
--lasts about 15 seconds, use IV
--effects blunted by theophylline and caffeine
--flushing, hypotension, chest pain, sense of impeding doom and bronchospasm
The next drug is Magnesium, what are the clinical applications of this drug?
torsades de pointes
digitalis induced arrhythmias
prophylaxis of arrhythmia in acute MI
What is the mechanism of action of Magnesium?
--prevents the influx of Ca2+ into the cell
The next drug is Atropine, what is the clinical use?
--decrease vagal tone
What is the mechanism for Atropine?
Muscarinic receptor antagonist
--inhibits the effects of excessive vagal activation on the heart
Finally the last topic will be drug therapy for Atrial Fibrillation. What are the three objectives when managing a patient with a-fib?
1) Slowing the ventricular rate
2) prevention of thromboembolism
3) correction of the rhythm disturbance
First lets discuss rate control in a-fib. What is the goal?
Slow the ventricular rate
--allows more time for the ventricles to fill with blood and increased cardiac output
Drugs that are used to control ventricular rate are drugs that are able to slow down conduction at the AV node. Which include?
First-line rate control:
--B-blockers, verapamil or diltiazem (used for tx of atrial fibrillation with rapid ventricular response)
How are beta blockers used for rate control in a-fib?
Acute and chronic control of ventricular rate
--particularly if excess catecholamines are suspected
Should not be used to acutely control the ventricular response in patients with HF or patients with COPD
Digoxin are the least effective in controlling rate of A-fib, when is digoxin indicated?
Reduced EF or CHF
How is amiodarone used as a rate control in A-fib?
Patients who are refractory or have contraindications to beta-blockers, Ca channel blockers or digoxin
--use for critically ill patients with CHF
Now after treatment with AV nodal blocking drugs and successful response, the patient needs their rhythm restored to sinus rhythm, if a-fib persists
In patients with heart failure of other hemodynamic compromise attributable to new onset a-fib, restoration of normal sinus rhythm is indicated
If sinus rhythm is to be restored, anticoagulation therapy should be initiated prior to what?
--because return of atrial contraction increases the risk of thromboembolism
Patients with a-fib for longer than 48 hours or an unknown duration should receive what?
Warfarin for at least 3 weeks prior to cardioversion and return of normal sinus rhythm
There are two methods for restoring sinus rhythm in a-fib. The first is direct current cardioversion (DCC). What is this?
---small risk of complications