Antiarrhythmic Drugs Flashcards
What are the two targets of mechanisms of antiarrythmics
§Abnormal automaticity (pacemaker activity)
§Abnormal propagation of electricity through the myocardium
Mechanisms of AAD
Decrease excitability of cardiac tissue (CALM down)
Decrease pacemaker activity (SLOW down)
Inhibit conduction (BLOCK)
AADs classifications (and pneumonic)
“Some Block Potassium Channels”
Vaughn-Williams Classification:
I –Na blocker (Sodium)
II – Beta blocker, blocks catecholamines (Beta blocker)
III –K channel blocker, prolong AP and repolarization, (Potassium)
IV – block L-type calcium channels (Calcium)
Effect of Class 1 drugs
Decrease the slope of phase 0
Increase Effective Refractory Period (ERP)
Slow conduction of the action potential –Increasing QRS duration
Differences between class 1 types
Class 1 mechanism
Block re-entry by increasing ERP
Convert uni-directional block to bi-directional block
Class 1a drugs and treatment
Quinidine, Procainamide
Can by used to treat atrial or ventricular arrhythmias
Quinidine target, adverse effects, contraindication
Blocks Na+ current, but also Ikr, Iks, IKATP, and Ito
Prolongs PR, QRS, and QTc
Contraindicated if ischemic heart disease
Adverse Effects:
GI (most common): Nausea, anorexia, diarrhea
Tinnitus, hearing loss, visual disturbance, confusion (cinchonism)
Thrombocytopenia, hemolytic anemia (in G6PD deficiency), anaphylaxis
Anti-cholinergic effects
Procainamide target, adverse effects, contraindication
Use: Drug of choice for atrial fibrillation in WPW (preexcited afib). Blocks accessory pathway muscle conduction and His-Purkinje system.
Contraindicated if ischemic heart disease
Adverse Effects:
GI side effects
Vasculitis, Raynaud’s phenomenon
Agranulocytosis
Hypotension, bradycardia, QT prolongation, torsades de pointes (Idiosyncratic)§Anti-cholinergic effects
Drug-induced lupus ~ 30% (+ ANA in 80%)
Class 1b drugs and treatment
Lidocaine, Mexelitine
Shortens action potential duration, thus, no torsades risk
Used for ventricular tachycardia, especially if caused by ischemia
Lidocaine special use, metabolism, and side effects
Lidocaine causes voltage dependent Na+ channel block ( bigger effect in ischemic tissue)
Metabolism depends on hepatic blood flow
Side effects: Neurological (delerium, seizures, tremors)
Why do 1Bs work well in ischemic tissue
Class 1c drugs and treatment
Flecainide, propafenone
Used to maintain or restore sinus rhythm in atrial fibrillation
Class 1c mechanisms and causes
Most potent Na+ channel blockers and greatest use-dependence
Increases QRS duration (decrease slope phase 0)
No change in QTc
Flecainide contraindication and adverse effects
CONTRAINDICATED if structural heart disease (↓EF) or recent MI/ischemic heart disease
§Adverse effects: Dizziness, visual disturbance, marked negative inotropic effects – worsen HF
How can 1c drugs cause arrythmia
Class 1 effects on QTc, PR, QRS
Increase PR and QRS
- IA drugs prolong QTc
- IB drugs shorten QTc
- IC drugs primarily decrease slope phase 0 (increases QRS)
Class III mechanism of action
K Channel blocker
blocks re-entry by increasing ERP duration so it is longer than conduction time
Class III drug and treatment
Amiodarone (multiple class effects), Ibutilide,Dofetilide, Sotalol
Can be used for atrial and ventricular arrhythmias (dirty job, dirty drug)
Mostly used for converting Afib to NSR or maintaining NSR after cardioversion
Class III effect on EKG
Increase action potential duration (QTc)
Prolong repolarization - refractory period
No change in QRS (phase 0 not affected)
May not increase risk of Torsades
Amiodarone dosing and metabolism
P450 inhibitor – can increase many drug levels
Large volume of distribution; lipid soluble; >10 gms needed to saturate fat stores; Half-life 13-103 days
Amioderone side effects
Also has class I, II, and IV effects (dirty job, dirty drug) – but most side effects are due to accumulation outside heart!
Hyperthyroidism: Need to stop drug
Hypothyroidism: Most common! Supplement T4; usually don’t need to stop
Pulmonary: Appears like pulmonary edema on CXR
Photosensitivity, gray/blue skin discoloration
What to monitor on amioderone
annual eye exams, liver function tests, thyroid studies, pulmonary function tests (LFT, TFT, PFT)
Class II drugs MOA
Class II effects on EKG
↓HR
↑PR interval
Decreased ventricular rate in Afib
No change in QRS or QTc
Beta Blockers common use
Use: Most tachyarrhythmias (atrial and ventricular)
Only anti-arrhythmics shown to reduce arrhythmic mortality post-MI (okay for ischemic or structural heart disease)
Beta blockers side effects
Caution in systolic heart failure due to negative inotropy (especially with IV)
Possible bronchospasm with nonselective
Can cause heart block, bradycardia
Class II drugs
Class IV mechanisms
Block activated and inactivated L-type calcium channels
Prolongs phase 4 of nodal AP, much like beta blockers, decreasing pacemaker activity
increases AV node refractory period duration (blocks AV node reentry)
reduces Ca2+ entry preventing Ca2+ overload (prevents DADs)
Class IV effect on EKG
Decrease HR and increase PR interval
Class IV drugs and treatment
Diltiazem, Verapamil
Used for rate control of atrial fibrillation
Class IV adverse effects
bradycardia, hypotension, heart block, worsen heart failure due to negative inotropy
Potency of class 1 drugs
Intensity of sodium channel blockade: IC>IA>IB
Digitalis (Digoxin) MOA
Digoxin use
Anti-arrhythmic use: ONLY for rate control of Afib when all else fails or is contraindicated (systolic heart failure)
Narrow therapeutic window
Digoxin toxicities and what to give
Competes for binding site with K – toxicity aggravated by hypokalemia
Toxicity: nausea, vomiting, bradycardia, ECG changes
Pro-arrhythmic effects due to high intracellular Na (higher resting potential): Increased automaticity, Ventricular Tachycardia, AV block, ST segment abnormalities
Treat with Digibind (Ab)
Digoxin toxicity on EKG
Adenosine use and MOA
Drug of choice for termination of SVTs that depend on AV node
Activates K channels à K out à takes cell longer to depolarize
Blocks Ca influx
Inhibits AV node reentry = BLOCKS AV node conduction
Half life is second – transient
Adenosine side effects and contraindication
Side effects: flushing via endothelial-dependent relaxation of smooth muscle, av block, nausea, shortness of breath
Caution: Can trigger Afib by changing atrial refractoriness. Contraindicated for pre-excited Afib(WPW)
