Anti-arrhythmia drugs Flashcards
What is occurring during phase 0 of action potential in cardiac electrical system fast response fibers?
Activate NA channels open and Na moves into the cell
What is occurring during phase 1 of action potential in cardiac electrical system fast response fibers?
Na channels inactivated and K moves outward
What is occurring during phase 2 of action potential in cardiac electrical system fast response fibers?
Ca inward balanced by K outward - plateau
What is occurring during phase 3 of action potential in cardiac electrical system fast response fibers?
Inactivation of Ca channels
Repolarization –> K outward
What is occurring during phase 4 of action potential in cardiac electrical system fast response fibers?
Resting membrane potential by Na/K ATPase pump
What is occurring during phase 0 of action potential in cardiac electrical system slow response fibers?
Activation of L-type Ca channels –> Ca inward
What is occurring during phase 3 of action potential in cardiac electrical system slow response fibers?
K outward –> repolarization
What is occurring during phase 4 of action potential in cardiac electrical system slow response fibers?
Na and Ca inward –> K outward
Pacemaker current
4 properties of the electrophysiology of the heart
Responsiveness
Conductance
Automaticity
Refractoriness
Equation that illustrates measure of refractoriness of the heart electrical system
ERP/APD
ERP = effective refractory period
APD = action potential duration
Result of increase SyNS activity in SA node
Tachycardia
Result of increase PsNS activity in the SA node
Bradycardia
General mechanism of Vaughn Williams class I antiarrhythmic drugs
Na channel blockers
Mechanism of Vaughn Williams class Ia antiarrhythmic drugs
Block activated Na channel to decrease Vmax and prolong ADP
Anticholinergics
Anticholinergic effect on the heart
Increase HR and conduction
Adverse effects of quinidine
Cinchonism
Increase QT interval –> Torsades de pointes
Displace digoxin –> decrease VD
Antacids increase absorption
Symptoms of cinchonism
Tinnitus
Hearing loss
GI upset
Diplopia
Adverse effects of procainamide
Agranulocytosis
SLE like syndrome –> slow acetylators
Drugs included in Vaughn Williams class Ia antiarrhythmic drugs
Quinidine - also an alpha blocker
Procainamide - least anticholinergic
Disopyramide - most anticholinergic
Mechanism of Vaughn Williams class Ib antiarrhythmic drugs
Decrease APD and no effect on Vmax
Increase threshold of V fib
Slow conduction in hypoxic and ischemic tissue
Preference for ischemic tissue
Drugs included in Vaughn Williams class Ib antiarrhythmic drugs
Lidocaine –> least cardiotoxic
Tocainide
Mexiletine
Cardiovascular uses of lidocaine
V tach after MI
Digitalis toxicity
Adverse effects of lidocaine
Drowsiness
Paresthesia
Convulsions –> toxic doses
Mechanism of Vaughn Williams class Ic antiarrhythmic drugs
Both Na channels to markedly decrease Vmax with no effect on APD
Drugs included in Vaughn Williams class Ic antiarrhythmic drugs
Flecainide
Propafenone
Moricizine
Clinical uses of Vaughn Williams class Ic antiarrhythmic drugs
Life threatening V tach or V fib
Refractory SVTs
Adverse effects of Vaughn Williams class Ic antiarrhythmic drugs
Pro-arrhythmic effect
Increase risk for sudden death and cardiac arrest by decreasing LV function after MI
Mechanism of Vaughn Williams class 2 antiarrhythmic drugs
Beta-blocker that decrease SA and AV node conduction –> decrease slope of phase 4 depolarization
Clinical uses of Vaughn Williams class 2 antiarrhythmic drugs
Prophylaxis for ventricular arrhythmias post MI
SVTs
Adverse effects of Vaughn Williams class 2 antiarrhythmic drugs
Proarrhythmic
Can cause AV block
Mechanism of Vaughn Williams class 3 antiarrhythmic drugs
K channel blockers that increase ADP and ERP. Prolong repolarization and lengthen phase 2.
Drugs included in Vaughn Williams class 3 antiarrhythmic drugs
Amiodarone
Dofetilide
Ibutilide
Sotalol
Dronedarone
Mechanism of amiodarone
Binds to and inactivates Na channel
Blocks K and Ca channels
Non-competitive inhibition of beta receptors
Half-life of amiodarone
25-60 days
Clinical uses of amiodarone
A fib
V tach
Use with anticoagulant
Adverse effects of amiodarone
Pulmonary fibrosis
Hepatotoxicity
Bluish discoloration of skin
Hypothyroidism in 5%
Hyperthyroidism in 25%
Torsades de pointes
Mechanism of dofetilide and ibutilide
Selectively block outward K channel (delayed rectifier K channel). Results in prolonged ventricular repolarization and increase QT interval.
Uses of dofetilide and ibutilide
Pharmacological cardioversion –> A fib and A flutter
Mechanism of sotalol
Beta blocker and K channel blocker - Decrease HR and AV conduction
- Prolongs APD and ERP
Antiarrhythmic uses of sotalol
A fib
Life threatening ventricular arrhythmias
Adverse effects of sotalol
Torsades de pointes
HA
Depression
Impotence
Contraindication of sotalol
Asthma
Ca channel blockers used for arrhythmias
Diltiazem
Verapamil
Mechanism of Ca channel blockers in arrhythmia
Decrease SA and AV nodal conduction
Decrease slope of phase 4
Anti-arrhythmic use of Ca channel blockers
PSVT due to AV nodal reentry
Adverse effects of Ca channel blockers
Orthostatic hypotension
Reduce CO
Lower extremity edema
Constipation
Drug interactions of verapamil
Displaces digoxin, increasing its toxicity
Drug interaction of Ca channel blockers
Pro-arrhythmic AV block is used with beta blockers
Condition in which Ca channel blockers should be used with caution
A tach due to WPW
Rapid acting AV nodal blocker with a half-life of 30 seconds
Adenosine
Adenosine receptors and their effect
A1 –> Gi coupled –> decrease SA and AV nodal rate
A2a –> Gs coupled –> vasodilate
A2b –> Gq coupled –> bronchoconstrict
Clinical use of adenosine
Drug of choice for PSVT
Antagonist of adenosine
Theophylline
Adverse effects of adenosine
Flushing
SOB
Burning sensation in chest
Anti-arrhythmic uses of digoxin
Control ventricular rates in A fib and A flutter
Arrythmias caused by drugs that prolong QT intervals
Torsades de pointes
Treatment for Torsades de pointes
Discontinue causative agent
Magnesium sulfate and potassium
Some drugs that can cause torsades de pointes
Amiodarone
Quinidine
Sotalol
Thioridazine
TCAs
