AntiArrhythmatic drugs Flashcards
Class I
Na channel blockers
Class II
Beta blockers
Class III
K channel blockers
Class IV
Ca channel blockers
Procainamide
Class IA Slows upstroke of AP, slows conduction, prolongs QRS by non-specific blockade of K channels. used for atrial and ventric arrhythmias. Avoid long term therapy.
AE: Excessive AP and QT prolongation, induces torsades de pointes, and Lupus sx.
PK:
Used in WPW
Quinidine
Class IA, Class IA Slows upstroke of AP, slows conduction, prolongs QRS by non-specific blockade of K channels antimuscarinic effects. Rarely used due to effects
AE: diarrhea N&V, torsades de pointes arrhythmia and syncope.
PK: GI abs, hep met.
Disopyramide
Class IA, Slows upstroke of AP, slows conduction, prolongs QRS by non-specific blockade of K channels antimuscarinic effects. Tx ventricular arrhythmias
AE: atropine like effects, may precipitate heart failure,
PK: hepatic met
Lidocaine
Class IB, Selective depression of conduction in depolarized cells, little effect on ECG. Drug of choice for temination of V-tach and prevention of V fib after cardioversion. Least side effects.
AE: Least, paresthesias, tremor, nausea, slurred speech, convulsions
PK: Extensive first pass, give parenterally
Mexiletine
Class IB. Orally active Lidocaine. elective depression of conduction in depolarized cells, little effect on ECG. Drug of choice for ventricular arrhythmias. Least side effects.
AE: Significant chronic pain reduction due to diabetic neuropathy and nerve injury. Tremor, blurred vision, lethargy.
PK: Hepatic met, longer half life than lidocaine
Tocainide
Not sold in USA
Class IB, lidocaine analog.elective depression of conduction in depolarized cells, little effect on ECG. Drug of choice for ventricular arrhythmias. Least side effects.
AE: Significant chronic pain reduction due to diabetic neuropathy and nerve injury. Tremor, blurred vision, lethargy.
PK:glucuronidation met, longer half life than lidocaine
Flecainide
Class IC, slows upstroke of AP, slows conduction, Potent Na and K channel blocker, slow unblocking kinetics, no AP or QT interval prolonging.
Tx. supraventricular arrhythmias.
AE: makes arhytmia worse when pt has tachyarrhythmias and prior MI and ventricular ectopy
PK: hepatic and renal
Propafenone
Class IC, slows upstroke of AP, slows conduction, Weak B blocker. used for supraventricular arrhythmias. does not prolong AP.
AE: metallic taste, constipation, arrhythmia exacerbation.
PK: hepatic
Moricizine
Not sold in US.
Class IC, slows upstroke of AP, slows conduction, does not prolong AP duration.
Used for ventricular arrhythmias.
AE:
PK: Extensive 1st pass metab.
Propranolol
B blocker (class II) Inhibits sympathetic activity on B1 receptor. Sloppy.
AE: bronchospasm, bradycardia, fatigue
PK: Extensive 1st pass met.
Acebutolol
B blocker (class II), Cardioselective B blocker, better for patients with asthma.
AE: fatigue
PK: 1st pass metabolism, feces.
Esmolol
B blocker (class II), Short acting , used primarily for intraoperative and acute arrhythmias
AE: mild
PK: Metabolized by RBC esterases.
Sotalol
B blocker (class II), nonselective B blockers, prolongs the action potential by slowing outward current of K.
AE: Bronchoconstriction, bradycardia, fatigue
PK: 100% bioavailability, excreted unchanged
Class IA
Na Fast channel blockers, widens QRS, used for a-fib, flutter, super ventricular and ventricular tachyarrhythmias.
Class IB
Weak Na channel blockade, does not affect QRS, shortens AP and refractory period. Used for ventricular tachyarrhythmias.
Class IC
Strongest Na channel blockade, no effect on AP length, shorter QRS. Used for super ventricular tachyarrhythmias, and ventricular tachyarrhythmias.
Class II Drugs
B blockers, prevent sympathetic innervation of the heart.
Class III Drugs
K channel blockers, Prolong repolarization, lengthening the QT interval. Prevents reentry arrythmias are considered pro arrhythmic as well as anti arrhythmic.
Class IV drugs
Blocks L- type Calcium channel blockers on smooth muscle, cardiac myocytes, and SA/ AV nodes. Causes vasodilation, decreased myocardial contractility. Shortened phase 2 of AP in myocytes and lessened force of contraction. In Nodal cells, blocks Ca entry leading to slowed HR, Decreased conduction velocity. Used for angina, block reentry,
Class V drugs
Misc drugs
Amiodarone
Class III,(also a poor Class1,2,4 drug) prolongs AP by K channel blockade used for ventricular tach, and v fib, a fib.
AE: Dose related pulmonary tox. eye probs. Bradycardia of nodal disease, drug accumulation in tissues, blocks production of T3
PK: Hepatic CYP3A4, drug interactions
Dofetilide
Class III, selective K blocker, prolongs AP, prolonged QT from long refractory . in His-purkinje system and ventricles.
A-fib, not for long Qt, bradycardia, hypokalemia
AE: Ventricular arrythmias
PK: 100% bioavailable, CYP3A4
Ibutilide
Class III, prolongs AP, also slows inward Na activator, which delays repolarization, inhibits Na channel inactivation increasing ERP. Used for A-fib and more flutter.
AE: Q-T prolongation and torsades de pointes, v arrhythmias.
PK: hepatic
Class IV Dihydropurines
Smooth muscle selective class IV, used to reduce systemic resistance and treat hypertension, not generally used for angina. All end in -pined
Class IV Non-dihydropurines
Block Ca channels selectively for myocardium, Treat angina, are verapamil, diltiazem
Verapamil
Class IV Blocks activated and inactivated L-type Ca channels, treats supra ventricular tachycardia, a-fib and flutter.
AE: bradycardia peripheral vasodilation. contraindicated in Wolff-P-W, Can cause AV block, constipation, edema.
PK: hepatic
Diltiazem
Class IV Blocks activated and inactivated L-type Ca channels, treats supra ventricular tachycardia, a-fib and flutter.
AE: peripheral vasodilation. contraindicated in Wolff-P-W, Can cause AV block, constipation, edema.
PK: hepatic
Digoxin
Inhibits Na K ATPase which reverses action on Na/Ca exchanger leading to more Ca in cell and inproved cardiac contractility.
Also activates vagal efferents on heart slowing SA rate and AV conduction increasing refractory period
used for a fib and flutter, heart failure. reduces ventricular rate when driven by a high atrial rate.
AE: Extreme AV block, not for AV block patients, WPW, drug interactions
PK: kidney excretion
‘Toxicity= GI distress, hyperkalemia, arrhythmias, av nodal blockade
Adenosine
Activates inward rectifier K channels, inhibits L-type Ca channels. Results in hyperpolarization and suppression of Ca dependent AP.
Drug of choice for paroxysmal supra ventricular tachycardia.
Used therapeutically for SVT.
AE: vasodillation leading to hypotension, flushing, headache, AV block
PK: methyxanthines (caffeine) are competitive antagonizers.
