Lecture 40,41,43

They are blockers of voltage-gated Na+ channels.

Reduces the slope.
Increases ERP.
Increases APD.

Quinidine, procainamide, and disopyraminde

Reduces the slope.
May decrease ERP.
May decrease APD.

A brief duration of blockade (during the off rates)
Negligible interaction with K+ channels
Doesn't slow down rhythm much during sinus rhythm but performs important Na blockade at rapidly discharging rates. This is how it interacts selectively with INACTIVATED Na channels.

Lidocane and Mexiletine

Very pronounced decreased slope.
Markedly slow conduction.
Little effect on ERP and APD.

-And a long duration of blockade

Flecainide and Propafenone

Moderate Na channel blockage
Increases ERP

Weak Na channel blockage
Decreases ERP

Strong Na channel blockage
No change in ERP because these drugs do not interact with K channels.

Class 1A because it increases ERP. (A longer refractory period makes is easier for an after depolarization to occur.)

These are beta blockers. (sodium channel blockage also occurs with proponalol).

Slows down SA node and ectopic pacemaking, and can block arrythmia that occurs from exercise or apprehension.
Considered to be, "quinidine-like" because it is safe and effective.

Propanolol, metopreolol, atenolol, soralol, and esmolol.

They are K channel blockers, causing delays in repolarazation and prolonged refractory periods.

amiodarone, ibutilide, bretylium, and dofetilide.

They are calcium channel blockers, slowing down the AV node in patients with atrial fibrillation.

Verapamil and and diliatazam. Verapamil also blocks Na channels and is not very selective.

Class 1B

Class 1C

Inhibits voltage-gated Na channels.
Inhibits delayed rectifier K channels.
A muscarinic receptor antagonist (to increase AV nodal conduction).
An alpha adrenergic receptor antagonist.

Can cause AV flutter/fibrilliaton, increases threshold for excitability and decreases SA node conduction.

Reduces conduction velocity and increases QRS duration. Increases QT interval (delaying repolarization), and vasodilates.

dizziness, tinnitus, syncope, ventricular arryhthmia. Quinidine associated torsades occurs more in women.

To treat ventricular arrhythmia and reduce recurrent atrial fibrillation.

-Its use has diminished because of the high incidence of arrhythmic reactions.

It decreases ectopic automacity.
It does not work during rest because it only blocks open and inactivated Na channels.

It is not useful in atrial arrythmias because the channels are not in the inactivated state long enough.

IV doses administered rapidly can cause seizures.

Tremor, dysarthria, altered levels of consciousness.

Acute therapy for ventricular arrythmia.

Similar to Lidocaine--an oral form. Used to treat ventricular arryhIthmia.

It blocks Na and delayed rectifier K currents with similar potencies. And blocks calcium channels.

dose-related blurred vision,
does NOT cause early after depolarizations or torsades. Increases mortality in patients convalescing (recovering) from an MI.

It slows down sinus node automaticity in patients with supraventricular arrhythmias.

It is a beta-adrenergic blocker and can block Na channels, reduces automaticity of SA node. Also automaticity and conduction are decreased in the AV node, His bundle, purkinje fibers, and ventricles.

Angina and tachycardia upon sudden withdrawal, and bronchospasm.

In supraventricular tachycardia. And unlike flecainide, b-blockers provide beneficial effects to pts after MI.

Amiodarone

Unstable VT, VF, and SVT
Off label use is atrial fibrillation

Pulmonary toxicity and bradyarrhythmias with loading dose.
Bradycardia
Thyroid abnormalities
Skin photosensitivity
Hepatic toxicity
Neurologic

1. Blocks Na channels (Class I effect)
2. Blocks Ca channels (Class IV effect)
3. Blocks b-adrenoceptors (Class II effect)
4. Delays repolarization and increases the refractory period by blocking K channels (Class III effect)
5. Decreases automaticity, slows conduction, and vasodilates.

Early after-depolarization

Amiodarone

For atrial fibrillation suppression. It does not work as well as amiodarone but is less toxic.

May increase mortality in heart failure patients. May increase creatinine levels without reducing renal function, due to inhibition of renal cation transport. This drug is metabolized by CYP enzymes so it reacts often with other drugs.

It prolongs action potentials by inhibiting K+ delayed rectifier channels. The L-enatiomer is a b-adrenergoceptor blocker too.

It is a replacement for pts that cannot handle amiodarone. It is used for VT and AF.
The major adverse effect is torsades de pointe.

It is a K+ rectifier channel blocker and also activates an inward Na current.

It is used for immediate conversion of atrial fib and flutter.

It major adverse effect is torsades de pointe.

It is a selective K+ rectifier channel blocker and can prolong the QT interval (may result in torsades de pointe). Therapy must be initiated in a hospital and monitored for 72 hours.

It maintains sinus rhythm in patients with atrial fibrillation

quinidine, procainamide, sotalol, ibutilide, dofetilide, and amiodarone.

They block the slow inward calcium current and reduce automaticity. Refractory period is increased and conduction velocity decreases in the AV node. Contractility is inhibited (not good for CHF pts), and vasodilation.

flushing, reduced contractility of the heart, AV node conduction defects, and constipation. CCBs are used in supraventricular arrhythmias.