Antiarrhythmic Drugs Lecture PDF Flashcards
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Arrhythmia definition
abnormality in the rhythm of the heart beat that in severe forms can prevent blood from being pumped with two basic types being tachyarrythmias and bradyarrhythmias
Virtually all drugs used to treat arrhythmias can ____ arrhythmias or ____ them
create new, worsen
Myocardial cell (and his-purkinje system) action potential mech of action
- AP propagated down stream causing Na+ voltage gated channels to open
- Na+ influx
- K+ efflux
- Ca2+ influx causing plateau and prolongation
- K+ efflux continues causing repolarization
- Active transporters reset ion conc. to resting potential
Pacemaker cell action potential mech of action
- Spontaneous opening (after leaky channels shift gradient) of Ca2+ channels allowing influx
- K+ efflux repolarizes
- Active transporters reset to “resting” potential that is unstable due to leaky Na and K+ channels
Reentry mechanism
In an area of one way block, the action potential goes from a separate branch and then goes retrograde thru the area of the one way block to continue re-stimulating the muscle cells in that area of the block but at a later moment in time
Antiarrhythmics can have 2 effects on blocks and reentrant mechanisms
- eliminate the block
- convert the block to a 2 way block to prevent reentry mechanism
Sodium channel blockers function, the 3 subclasses, and a drug in each subclass
Include biggest group of antiarrhythmic drugs that produce a blockade of cardiac sodium channels slowing conduction in atria, ventricles, and purkinje system including 1A quinidine, 1B lidocaine, and 1C flecanide
Class ___ antiarrhythmic drugs increase risk of developing new arrhythmia the most
1C
B blockers antiarrhythmic function and 2 examples
Reduce Ca2+ entry during fast and slow potentials reducing automaticity of the pacemaker cells and reducing contractility including propranolol, acebutolol
Drugs that delay repolarization (class III antiarrhythmics)
Blockade K+ channels, delay repolarization of fast channels, prolong AP duration and refractory period, examples include amiodarone, dronedarone
Calcium channel blockers antiarrhythmics 2 examples and function
Verapamil and dilitiazem are only two approved for anti-arrhythmic use, same effect as B blockade to delay conduction and reduce contractility
Digoxin and adenosine function
2 drugs that do not fit into any other classes of antiarrhythmics, both drugs decrease conduction thru AV node and reduce automaticity in SA node
CAST study
Study that saw the use of class 1C drugs (encainide and flecainide) to prevent arrhythmia after MI doubled mortality rate, demonstrated that antiarrhythmics should only be used when benefits outweigh risks
Common mechanism of arrhythmia generation by drugs
Prolongation of QT interval leading to torsades de pointes that can lead to fatal vfib
Which is more dangerous, supraventricular or ventricular arrhythmias?
Ventricular!!
Drug therapy for arrhythmia is highly ___, based on response of patient and not scientific principles
empirical
Supraventricular arrhythmias arise from the __ or ___ (locations)
SA or AV node
Supraventricular arrhythmias can be dangerous if…
…the atrial impulses are likely to pass thru the AV node resulting in excitation of the ventricles
Treatment of supraventricular arrhythmias (5)
- vagotonic maneuvers
- DC cardioversion
- B blockers
- Ca2+ blockers
- Adenosine and digitoxin
Atrial flutter treatment of choice
-DC cardioversion almost always converts to normal sinus rhythm
Atrial fibrillation treatments of choice (2)
-DC cardioversion or antiarrhythmic drugs such as amiodarone
-verapamil, dilitiazem and digoxin are contraindicated in what disease state?
WPW syndrome
Prior to cardioversion for atrial fib, a patient needs to be given ___ 3-4 weeks before and for 1-2 weeks after
anticoagulants
Sustained ventricular tachycardia treatments of choice (3)
-cardioversion
-IV procainamide if fails
-IV lidocaine or amiodarone are alternatives
-
Ventricular fibrillation treatments of choice (2)
- electrical cardioversion
- Amiodarone for acute and long term suppression
PVC in presence of acute MI may dispose patient to v fib. What treatment is DOC?
-B blocker
Torsades des pointes can be caused by class ___, ___, and ____ antiarrhythmics, and is treated with _____ plus _____
IA, III, and IV magnesium, cardioversion
Digoxin toxicity
Mimics most types of ventricular arrhythmias, done by increasing automaticity in atria, ventricles, and his purkinje system as well as decreasing conduction thru the AV node
Nonsustained vs sustained arrhythmia treatment
Nonsustained generally only require intervention when symptomatic, sustained are dangerous benefits to treat generally outweigh risks
Asymptomatic vs symptomatic arrhythmia treatment
No evidence of benefit in treating asymptomatic conditions
Supraventricular vs ventricular arrhythmia treatment
Supra are usually benign, treatment goal to terminate arrhythmia or prevent excessive atrial beats from reaching ventricles, ventricular arrhythmias need to be treated
Minimizing risks of antiarrhythmic drugs methods (3)
- low dose and titrate upward
- use of holter monitor
- monitor plasma drug levels
Class I antiarrhythmic agents nickname
Local anasthetic antiarrhythmic agens
Quinidine drug class and function, ADR’s (3), drug interactions
- Class IA
- Drug most commonly used to treat supraventricular tach and atrial flutter/fib, blockades sodium channels, slows impulse of conduction delaying depolarization, strongly anticholinergic blocking vagal imput on heart and thus must be pre-treated with AV conduction suppressant such as verapamil, or B blocker
Adverse effects include diarrhea, cinchonism (tinnitus, headache, etc with one dose), QT prolongation, require pretreatment with anticoagulants
Intensifies effect of atropine, can double digoxin levels
Procainamide function
Class IA agent Similar to quinidine but CAN terminate vtach and vfib, but has serious side effects such as SLE like syndrome, blood dyscrasia, QT prolongation
Disopyramide function
Class IA agent Actions similar to quinidine, but ADR’s such as anticholinergic response common and limits use
Class IB agents differ from class IA in these ways…
…they accelerate repolarization instead of delay it, and have little effect on EKG
Lidocaine drug class, function, ADR’s (3)
- Class IB agent
- IV agent only used against ventricular arrhythmias only
- ADR’s include more common in elderly drowsiness and parasthesias
Phenytoin (dilantin) function
Antiseizure drug used to treat digoxin induced arrhythmia, reduces automaticity in ventricles, has little or no effect on EKG, differs in that it increases AV nodal conduction
Mexiletine (mexitil) function and ADR’s (2)
Oral agent of lidocaine, used to treat symptomatic ventricular arrhythmias indicated for PVC’s and sustained ventricular tach, does not alter EKG,
ADR’s include GI disturbances and neurologic disorders
Flecainide drug class and function
- Class IC agent
- active against ventricular and supraventricular arrhythmias, decreases cardiac conduction and increases absolute refractory period, prolongs the PR interval and widens QRS complex, pro-arrhythmic effects such as in patients with asymptomatic vtach associated with MI, can precipitate heart failure so should not be combined with other agents that decrease contractile effect, should be used for situations without safer drug options
Propafenone (rhymthol) drug class and function
- Class IC antiarrhythmic
- similar to flecainide actions and uses, possesses proarrhythmic properties and has b adrenergic blocking properties but reserved for patients not responding to safer drugs
4 B blockers approved as antiarrhtyhmics
- Propranolol
- Acebutolol
- esmolol
- Sotalol
Propranolol (inderal LA) drug class, function, and ADR’s (4) (arrhythmic)
- B blocker
- used for arrhythmias caused by excessive stimulation of heart
- ADR’s include HF, AV block, sinus arrest, hypotension
Acebutlolol function
Cardioselective B blocker for oral therapy of PVC’s similar to propranolol
Esmolol function
Cardioselective B blocker with short IV half life of 9 min for immediate control of ventricular rate in patients with afib and atrial flutter, ADR’s similar to propranolol
Amiodarone drug class, function, and ADR’s (3)
- Repolarization delayer class III antiarrhythmic
- lasts for a long time and higly effective against all types of arrhythmia, approved for long term therapy for 2 life threatening ventricular arrthymias in patients who have not responded to other agents, most effective drug for Afib even tho not approved for this use to convert to sinus rhtynm and maintain it
- ADR’s include pulmonary toxicity, sinus bradycardia, and thyroid toxicity (T4 to T3 conversion)
Dronedarone (multaq) function
Derivative of amiodarone that is noniodinated but also less effective, approved for PO treatment of aflutter and paroxysmal or persistent afib but not permanent atrial fib, doubles risk of death in patients with hf or permanent afib
Sotalol function
B blocker that delays repolarization and has combined class II and III properties, used for ventricular arrhythmias that are life threatening, not approved for HTN or angina, used in highly symptomatic patients
Ibutilide (corvert) function
IV agent to terminate aflutter and afib of recent onset, cardioversion to sinus rhythm during infusion, more effective on afib than flutter, risk of torsades des pointes formation
only 2 Ca2+ blockers approved for treatment of arrhythmia’s
Verapamil and diltiazem
Verapamil and dilitiazem drug class, function, ADR’s (4), and drug interactions (2) (anti-arrhythmic)
- Class IV antiarrhythmic agent
- Reduce SA node automaticity, delay av conduction, reduce myocardial contractility, slows ventricular rate in pats with atrial fib or flutter, terminates supraventricular tach cause by av nodal reentrant circuit
- ADR’s include hypotension and vasodilation, bradycardia, AV block
- Drug interactions with digoxin amplify it, B blockers are contraindicated because they produce exaggerated effect when combined
Adenosine (adenocard) DOC for what condition
IV drug of choice for terminating paroxysmal supraventricular tach
Adenosine administration fun fact
Adenosine needs to be injected as close to heart as possible, initial dose is 6 mg, if no response in 1-2 min then 12 mg may be repeated once, otherwise then no dice
