Antiarrhythmic Drugs Flashcards Preview

Cardio > Antiarrhythmic Drugs > Flashcards

Flashcards in Antiarrhythmic Drugs Deck (12)
Loading flashcards...
1

arrhythmia

• Abnormalities of cardiac impulse formation and/or conduction

• Rhythm is NOT normal sinus

• Pharmacologic therapies

• Nonpharmacologic therapies

Intracardiac devices

Ablation Cardioversion

•Arrhythmias are disorders of cardiac impulse formation and /or conduction that result in a rhythm that is not normal sinus rhythm. The resulting heart rates may be outside of the normal of 50 to 100 beats per minute.

2

the goal of antiarrhythmic drugs

•The goal of antiarrhythmic therapy may be to restore normal cardiac function or alleviate symptoms or prevent sudden cardiac death Unfortunately, antiarrhythmic drugs may not only help control arrhythmias but also can cause them, even during long-term therapy

•Available antiarrhythmic drugs suppress arrhythmias by blocking flow through specific ion channels or by altering autonomic function.

• RESTORE NORMAL HT FUNCTION

 • ELIMINATE SYMPTOMS

• PREVENT SUDDEN DEATH &HEMODYNAMIC COLLAPSE

• REDUCE OTHER RISKS ASSOCIATED WITH ARRHYTHMIA (stroke in atrial fibrillation)

• The drugs work because they act specific ion channels or alter autonomic function

3

mechanisms of arrhythmia

• Enhanced automaticity

• Triggered automaticity

Early – slow heart rate, hypokalemia

Delayed – Ca²⁺ excess

• Reentry Anatomically defined

– a bypass tract Functionally defined

– electrical problem
 

4

reentry

The prototypical example of reentry is the WPW syndrome in which patients have an accessory connection between the atrium and ventricle. With each sinus node depolarization, impulses can excite the ventricle via the normal structures (AV node) or the accessory pathway, and this often results in an unusual and characteristic QRS complex in normal sinus rhythm. Importantly, the electrophysiological properties of the AV node and accessory pathways are different:

Accessory pathways usually consist of nonnodal tissue with longer refractory periods and without decremental conduction. Thus, with a premature atrial beat (e.g., from abnormal automaticity), conduction may fail in the accessory pathway but continue, albeit slowly, in the AV node and then through the His-Purkinje system; there the propagating impulse may encounter the ventricular end of the accessory pathway when it is no longer refractory. The likelihood that the accessory pathway is no longer refractory increases as AV nodal conduction slows, demonstrating how slow conduction enables reentry. When the impulse reenters the atrium, it then can reenter the ventricle via the AV node, reenter the atrium via the accessory pathway, and so on

 

• Reentry is the electrophysiological mechanism responsible for most of the clinically important arrhythmias: Atrial fibrillation Atrial flutter AVNRT AV reentry with a bypass tract VT after MI VF Reentry occurs when a propagating impulse fails to die out after normal activation of the heart and persists to reexcite the heart after the refractory period has ended.

• Impulses propagate by >1 path between 2 points

• The pathways may be:

 Anatomically defined - a bypass tract

Functionally defined - cell-cell EP differences

5

6

amiodarone

•block K+ channels, also blocks Na+ and Ca++ channels and beta adrenergic receptors

•atrial and ventricular arrhythmias

•side effects: QT prolongation, pulmonary fibrosis, hypo and hyper thyroidism, blue grey skin changes (blue man syndrome), liver toxicity, corneal deposits, increased liver density on CT scan

 

Class III Mechanism – Unknown

A thyroid hormone analog

Ion channel block – Na+, K+ & Ca2+

Alpha & beta adrenergic receptor block(noncompetitive)

CYP3A4, 2C19 & P-gp disposition

An inactivated state blocker

Electrophysiology

Action potential duration Prolonged

Refractory period Prolonged

Conduction velocity Slowed

PR, QRS & QT intervals Prolonged

 

USES - A drug with life threatening side effects for life threatening arrhythmias Refractory ventricular arrhythmia termination: VT or VF Atrial fibrillation used when there is structural heart disease Not FDAapproved

•side effects:

Cutaneous Eye- corneal deposits optic neuritis

Lung - fibrosis

Cardiac - VT,VF

Liver - hepatitis

Thyroid - hypo & hyper

AMIODARONE DRUG INTERACTIONS

Pharmacokinetic

Warfarin- inhibits P-450

Digoxin- P-gp inhibition

Pharmacodynamic

Catecholamines

Diltiazem

Propranolol

Ledipasivir/sofosbuvir (Harvoni®) Sx- bradycardia

7

atrial fibrillation

8

metorprolol

Beta Adrenergic Blockers

-CLASS II

EP Actions relevant to atrial fibrillation

Automaticity in SA and AV Node

– Decreased AV Nodal Conduction

– Slowed AV Nodal Refractory Period

- Prolonged Net effect: cardiac slowing

•also for hypertension, ischemic heart disease, heart failure

 

BETA BLOCKERS for ARRHYTHMIAS

Atrial arrhythmias to control ventricular rate

Atrial fibrillation with RVR

Atrial flutter Paroxysmal supraventricular tachycardias

Post- myocardial infarction & HFrEF

Improved survival

•side effects:

CNS Cardiovascular Bad dreams

Aggravation of severe CHF

Depression

Aggravation of occlusive arterial disease

Slow A-V conduction

Pulmonary Bronchospasm in severe asthmatics

Drug interactions

Drugs that impair A-V conduction (digoxin and some calcium channel blockers ( V & D)

9

verapamil

diltiazem

•Ca++ channel blockers

Calcium channel blockers:

EP Actions relevant to atrial fibrillation

AV Nodal Conduction

– Slowed AV Nodal Refractory Period - Prolonged

Net effect: cardiac slowing

 

Class IV – Calcium Channel Blocking

 

•also for ischemic heart disease, hypertension

EP Actions relevant to atrial fibrillation

Activated and inactivated calcium channels blocked

- Rapidly firing tissues

- Incompletely polarized tissues at rest

- Tissues depending only on calcium channels

AV Nodal conduction is slowed and refractory period is prolonged

Net effect is cardiac slowing

Therapeutic Use

Supraventricular tachycardia- to slow ventricular rate

Atrial fibrillation – to slow ventricular rate

•side effcets:

Common (< 10%)

Mild hypotension

Nausea, vomiting

Dizziness

Constipation

Non - cardiogenic edema

 

Toxicity CARDIAC

- Negative inotropic

- AV block (Digoxin and beta-blockers)

- Hypotension

Drug Interactions - Digoxin plasma levels – Increased (V)

10

adenosine

•adenosine receptor agonist

•produces transient AV block- diagnosis of arrhythmias

•bronchospasm

 

•A DIAGNOSTIC AND THERAPEUTIC DRUG FOR THE INITIAL ASSESSMENT and TREATMMENT of reentrant SVTs

Action – Adenosine receptor A1 agonist KACh activated in sinus & AV nodes

- Potassium conductance – increased -

Inhibition c-AMP induced calcium influx

EP Actions

- AV node refractoriness – increased

- AV nodal refractory period – increased

Net effect: slowing, asystole sometimes

Toxicity - Flushing-broncoconstriction

11

lidocaine

•Na+ channel blocker

12

digoxin

•inhibits na+/K+ ATPase, positivev ionotropic effect, slows AV conduction by vagal effect

•atrial fibrillation, heart failure

•side effects: arrhythmias, nausea/vomiting, confusion, blurred vision, yellow vision, hyperkalemia