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115 Cards in this Set
- Front
- Back
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What are the 4 classes of Antiarrhythmic Drugs
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I. Sodium Channel Blockers (Local anesthetics)
II. Beta-Blockers III. Potassium Channel Blockers IV. Calcium Channel blockers * Misc = Adenosine, Potassium ion, Mg2+ ion |
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What is an arrhythmia?
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- Any rhythm that is not a normal sinus rhythm.
- Any rhythm that does not start at the SA node or that is not under the usual ANS control. |
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Arrhythmias are the #1 cause of death in the US after what
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MI
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What are the main types of arrhythmias?
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- Atrial Flutter
- Atrial Fibrillation - Atriventricular Nodal Reentry (a kind of supraventricular tachy) - Premature Ventricular Beats - Ventricular Tachycardia Ventricular Fibrillation |
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What is Torsade de pointes?
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A ventricular arrhythmia caused by a prolonged QT interval.
Induced by some antiarrhythmic drugs |
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What are the NON-pharmacological ways of treatig arrhythmia?
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1.) External Defirillation
2.) Implanted Defibrillators 3.) Implnted pacemakers 4.) Radiofrequency ablation of arrhythmogenic foci via catheter |
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Procainamide =
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IA
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Lidocaine =
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IB
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Flecainide =
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IC
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Porpranolol
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II
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Verapamil =
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IV
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How do arrhythmias form?
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1.) Reentry (MCC) - Infarct casuses slowing down of AP in that area etc.
2.) Enhanced Automaticity - Ectopic pacemaker 3.) Triggered Automaticity - Ischemia, digitalis tox., adrenergic stress |
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What are the 2 types of cardiac tissue in terms of action potential type
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Fast-response: Myocardium & Purkinje cells
Slow-response: SA and AV nodes |
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Stages of Fast-response action potential
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Phase 0 - Rapid Depol:
Na+ channels open, rapid Na+ influx Phase 1 - Partial Repol: Na+ ch inactivate. K+ ch start opening, K+ out, Cl- in. Phase 2 - Plateau: Ca2+ influx, K+ out Phase 3 - Rapid Repol: K+ out, inactivation of Ca2+ ch. Phase 4 - Diastolic Depol: Resting Memb. potential maintained by K+ out and slow Na+ & Ca2+ influx. |
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How is the SLOW-response AP of the SA node and AV node different from the Fast AP?
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AP caused by Ca2+ channels opening.
Has a SLOW, spontaneous uptroke. No Fast Na+ channels Smaller magnitude Very brief plateau |
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What are Class I antiarrhythmics? What are they further classified on?
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Class I's are Local Anesthetics
Classified based on how they affect duration of AP. |
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How do Class IA affect AP?
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Prolong AP duration
by slowing Phase 0 Procainamide |
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How do Class IB affect AP?
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Shorten AP duration
by shortening Phase 3 Lidocaine |
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How do Class IC affect AP?
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No effect on AP duration
Decreased automaticity by increasing threshold potential, thus slowing conduction velocity Flecainide |
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MOA of all Class I's
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Sodium channel blocker
Slow or block conduction in ischemic and depolarized cells and slow/abolish abnormal pacemakers whereever they depend on sodium. |
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Most selective Class I
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Class IB
Have sig. effects on Na channels in ischemic tissue, w/ minimal effect on channels in normal cells |
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Less selective Class I
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IA & IC
Have some effect on normal cells in addition to abnormal cells |
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At what state is the Na channel in when sodium channel blockers block them?
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in the Open/Inactivated state
Arrhythmic ion channels tend to be in the open/inactivated state, therefore can get blocked better by sodium channel blockers |
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What are the 3 kinds of Class IA drugs?
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Quinidine
Procainamide - prototype Disopyramide |
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What class is Amiodarone?
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III and IA
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MOA of Class Ia drugs
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*Affect both Atrial and Ventricular arrhythmias*
Block I Na: - Slow conduction velocity in Atria, Purkinje's, and Ventricular cells - Increased QRS duration - Also slows AV conduction - Slows repol. of Phase 0 - Decreases slope of Phase 4 Block's I K: - Increases AP duration and ERP - Slows conduction velocity and ectopic pacemakers - Increased QT interval |
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Which Class Ia has the greatest AP prolonging effect?
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Amiodarone
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MOA of Class Ib drugs
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*Selectively affect Ischemic/depol'd Purkinje & ventricular tissue*
*no effect on atrial* Blocks Na channels: - Reduces AP duration - Doesn't shorten (may prolong) the REFRACTORY period - Little effect on Normal cardiac cells, so doesn't effect EKG |
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This anticonvulsant is sometimes classified as a Ib b/c it is used to reverse Digitalis-induced arrhythmias
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Phenytoin
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MOA of Class Ic drugs
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* Slow conduction velocity in Atrial and Ventricular cells*
* No effect on AP duration or QT interval* Block Na channels: - in Purkinje cells to shorten the AP duration - Increase QRS duration Block K+ channels: - in ventricular myocytes which prolongs AP Net effect is no change in AP duration. |
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What drugs are classified as Class Ib?
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Lidocaine - prototype
Tocainide Mexiletine Phenytoin |
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What drugs are classified as Class Ic?
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Flecainide - prototype
Propafenone Moricizine |
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What kind of arrhythmias are Quinidine, Procainamide and Disopyramide used for?
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Both Atrial and Ventricular
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Which Class I is used for arrhythmias that occur during the acute phase of an MI?
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Procainamide
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NON-cardiac SE of Quinidine
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- GI: D, N, V - common
- CINCHONISM - SYNCOPE: recurr. light-headedness and fainting - Thrombocytopenic Purpura |
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Cardiac SE of Quinidine
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- Torsades de pointes ( prolonged QT)
- Proarrhythmogenic effects: AV block or Asystole |
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How does Quinidine affect OTHER drugs?
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Increases Plasma levels of:
- DIGOXIN & - ORAL ANTICOAGULANTS |
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How do other drugs affect QUINIDINE?
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Phenobarbital adn Phenytoin Decrease Qunidine plasma levels
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Describe the metabolism of Procainamide
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A part of it gets metabolized in the liver to N-acetyl-procainamide (NAPA), which has Class III characteristics, and can cause Torsades de pointes
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SE of Procainamide
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- HYPOtension esp. parenterally
- LUPUS (Reversible) - Pleuritis and pericarditis - May precipitate new arrhythmias - Toxic effects: Asystole, hallucinations, psychosis - Torsades de pointes |
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SE of Disopyramide
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- Anticholinergic effects: Dry mouth, urinary retention, constipation, Glaucoma
- Torsades de pointes - Heart failure in LV dysfxn - Prostatism |
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What condition exacerbates the cardiac tox. of Class I's
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Hyperkalemia
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What would you use to reverse the Class I-induced arrhythmias?
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Sodium Lactate
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What would you used to reverse the Lupus caused by Procainamide?
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Pressor sympathomimetics
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Select project manager
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BEFORE:<NOTHING>
AFTER:Determine company culture and existing systems |
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How is lidocaine administered?
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i.v
Never orally b/c has very high first pass effect and its metabolites are very cardiotoxic |
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SE of Lidocaine
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*Rare*
- CNS effects: drowsiness, numbness, slurred speech, convulsions - Nystagmus = early sign of toxicity |
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Clinical Use of Tocainide
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Ventricular arrhythmias
Orally admin. |
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SE of Tocainide
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- CV effects: brady, tachy, AV block, Hypotension, V-Tach
- Anorexia, nausea - Tremor - Pulm fibrosis, BM aplasia rare |
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Clinical Use of Tocainide
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VEntricular Arrhythmias
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SE of Mexiletine
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Dizziness, nervousness
N, V Blood Dyscrasias Nystagmus, thrombocytopenia Leukopenia, agranulocytosis |
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Clinical Use of Phenytoin
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DOC for tx digoxin-induced A & V arrhythmias
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SE of Phenytoin
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- CNS effects - Nystagmus, ataxia
- GINGIVAL HYPERPLASIA - Serious BM and Derm. rxns can occur |
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Clinical Use for Flecainide
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Life-threatening Ventricular arrhythmias in pts w/out myocardial structural problems
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SE of Flecainide
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- Highest Proarrhythmogenic effects than any other antiarrhythmics (CAST Trial) Thus used only as a last-line agent
- CNS effects: classic local anesthetic effects: blurred vision, Headache - Heart block in pts with conduction problems |
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Clinical Use of Propafenone
& MOA |
A & V arrhythmias
Similar MOA as flecainide, but has Beta-adrenergic blocking effect as well |
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SE of Propafenone
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- Proarrhythmogenic effects
- B-blockade: bronchospasm, bradycardia - Slow metabolizers, drug accumulates in the blood, must monitor plasma levels. |
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Clinical Use of Moricizine
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Tx of Severe Ventricular arrhythmias
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SE of Moricizine
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Proarrhytmogenic effects
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What are the prototype Class II antiarrhythmic beta-blockers?
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Propranolol
Esmolol |
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MOA of Class II antiarrhythmics
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Cardiac Beta-adrenergic blockade
Reduction of cAMP to decreased Ca and Na currents adn suppession of abnormal Pacemakers |
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Which part of the heart is esp. sensitive to beta-blockers?
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the AV node
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Clinical Use for Esmolol
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Acute Surgical Arrhythmias, almost Always.
Very short acting, given i.v. |
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Cinical Use for Propranolol, Metoprolol, Timolol
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Prophylaxis in pts who had an MI
Both A & V arrhythmias |
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What are pts w/arrhythmias more prone to with the use of Beta-blockers
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More prne to teh B-blocker-induced depression of CO
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SE of Class II drugs
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Reduces progression of chronic heart failure
Reduces incidence of potentially fatal arrhythmias in these pts |
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How do Class III drugs affect the AP?
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Definately PROLONG the AP duration
Block K channels, reducing the force for repolarization, thus elongating the depol.'d state Prolong the Effective refractory period |
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What effect do Class III's have ont eh EKG
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Prolong QT interval
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Clinical Use of Sotalol
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A & V arrhythmias
Reduces mortality in these pts too |
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SE of Sotalol
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Torsades de pointes
XS Beta-blocking effects - brady, asthma |
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Clinical uses of Ibutilide and Dofetilide
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Atiral Flutter and Fibrillation
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SE of Ibutilide and Dofetilide
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Torsades de pointes
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Which drug is considered the most efficacious of all antiarrhythmics?
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Amiodarone
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MOA of Amiodarone
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Blocks Sodium, Calcium, Potassium, and Beta-adrenoceptors
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Clinical Use of Amiodarone
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Has lost of toxicities so only used for Arrhythmias that are resistant to other drugs.
Still in used very extensively |
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SE of Amiodarone
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Its structurally similar to Thyroid hormone
- Microcrystalline deposits in Cornea, Skin - Thyroid Dysfxn: Hypo/hyper - Paresthesias - Tremor - Pulmonary Fibrosis - Blue skin b/c of Iodine accumulation - PFT's, LFT's and Thyroid function tests should be done/monitored |
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What are the drugs that belong to Class IV drugs?
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Verapamil - prototype, has greatest effect
Diltiazem - not used for arrhythm Nifedipine - not used for arrhythm |
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MOA of Class IV drugs
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Block "L-Type calcium channels"
--- - Decrease both SA node automaticity and AV nodeal conduction - Decrease the rate of Phase 4 spontaneous depol. - AV conduction velocity is decreased - Increase refractory period adn PR interval |
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Clinical Use of Class IV drugs
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- Conversion of AV nodal reentry to normal sinus rhythm/
- Mainly to prevent nodal arrhy's in pts prone to recurrence |
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SE of Class IV drugs
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Bradycardia
CHF HYPOtension Dizziness Constipation |
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MOA of Digoxin
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Inhibits Na/K ATP-ase pump in myocardial cell membranes
Increases refractory period and decreases conduction time of the AV node |
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Clinical Use of Digoxin
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Atrial arrhythmias and CHF
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SE of Digoxins
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Most commonly atrial tachycardia
Atrial or ventricular dysrhtymias |
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Tx for Digoxin toxicity
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Digoxin antibodies
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Clinical use of Adenosine
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Markedly slows or completely blocks conductions in the AV node, hyperpolarizing it
Great to abolish AV nodal arrhythmias, DOC, low toxicities |
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Clinical Use of Potassium for arhhythmias
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Depresses ectopic pacemakers even those form digitalis toxicity
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Clinical use of Magnesium Sulfate
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Torsades de pointes
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SE of Mg Sulfate
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Bradycardia
Respiratory paralysis Flushing Headache |
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What are the NON-pharmacologic treatments of arrhythmias?
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1. External defibrillator
2. Implanted defibrillators 3. Implanted pacemakers 4. Radioofrequency ablation or arrhythmogenic foci via catheter |
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* MOA of Class IA (Procainamide), Class IB (Lidocaine), Class IC (Flecainide) Antiarrhythmics
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* Sodium Channel Blockers
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* SE of Procainamide
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* Lupus like syndrome
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* Limiting side effect of Quinidine
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* Prolongs QT interval
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* Other side effects of Quinidine
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* Thombocytopenic purpura & CINCHONISM
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* Major drug interaction with Quinidine
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* Increases concentration of Digoxin
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* DOC for management of acute ventricular arrhythmias
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* Amiodarone
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* DOC for digoxin induced arrhythmic
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* Phenytoin
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* SE of phenytoin
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* Gingival hyperplasia
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* Class of anti-arrhythmics that has a pro-arrhythmic effect (CAST trial), therefore are used as LAST line agents
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*Class IC (flecainide, propafenone, moricizine)
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* Class II antiarrhythmics are
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* Beta-blockers
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* Antiarrhythmics that exhibit Class II and Class III properties
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* Sotalol
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* SE of Sotalol
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* prolongs QT & PR Intervals
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* Used i.v. for acute arrhythmias during surgery
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* Esmolol
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* Antiarrhythmics that decrease mortality
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* Beta-blockers
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MOA of Class III antiarrhythmics
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* Potassium channel blockers
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* Class III antarrhythmic that exhibits properties of all four classes
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* Amiodarone
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* Specific pharmacokinetic characteristic of amiodarone
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* prolonged Half life, up to 6 weeks
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* Antiarrhythmic effective in most types of arrhythmia
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* Amiodarone
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* SE of Amiodarone
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* Cardiac dysfxn
photosensitivity skin (blue smurf syndrome) pulmonary fibrosis thyroid & corneal deposits |
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* MOA of Class IV antiarrhythmics
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* Calcium channel blockers
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* Life threatening event that prolonged QT leads to
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* Torsades de pointes
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* Agent to treat Torsades de pointes
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* Magnesium Sulfate
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* Drug used for digoxin
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* Digoxin
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* DOC for paroxysmal supraventricular tachycardia (PSVT)
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* Adenosine
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* Adenosine's MOA
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* Activation of inward K+ current and inhibition of Ca++ current resulting in marked hyperpolarization
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* Anti-arrhythmic with 15 sec duration of action
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* Adenosin
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