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55 Cards in this Set
- Front
- Back
What are the two basic cellular mechanisms that cause arrythmias?
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altered impulse formation
altered impulse conduction |
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What is overdrive suppression?
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Rapid discharge from the sinus node causes suppression of purkinje fiber automaticity.
Causes membrane to become hyperpolarized to -85mV. After cessation of overdrive, the next action potential is delayed by the extra negative charge. |
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How do purkinje and ventricular cells express automaticity?
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When stimulated, the faster SA impulse causes normal firing.
When cells are not stimulated, they exhibit spontaneous depolarization. |
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How does decreased resting potential cause abnormal automaticity?
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Sodium channels become inactivated at -65 to -50 mV and current becomes carried by calcium channels. The potential can resemble pacemaker cells. If it becomes faster than the SA node, it takes over.
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What are causes of decreased resting potential that potentiates arrhythmia?
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Hypoxia
Hypokalemia Myocardial stretch |
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What factors can suppress abnormal automaticity?
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Calcium channel blockers.
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What are the effects of hypokalemia on automaticity?
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Potassium causes outward flow of potassium, which causing an increase in firing rate.
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What are early after-depolarizations? what are they involved with?
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Depolarization that occurs before the AP has repolarized. Caused by imbalance of calcium and potassium in phase 3.
Involved with long QT syndrome. |
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What are delayed after-depolarizations? What worsens them?
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Depolarization that occurs after full repolarization.
Worsened by tachycardia. |
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How does ischemia/ hypoxia cause arrhythmia?
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Decreased ATP causes opening of potassium channels. Potassium leaves the cell and increases resting potential. Fewer sodium channels are reactivated to lengthen the AP.
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What are the requirements for a reentry arrhythmia to occur?
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Unidirectional block
Time to travel circuit must exceed the refractory period. Circuit length is greater than conduction velocity * refractory period. |
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What factors promote antiarrhythmia in circus reentry? What factors promote proarrhythmia?
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Anti- faster conduction, longer ERP, shorter circuit path.
Pro- slowed conduction, shorter ERP, longer circuit path. |
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What are the four major types of antiarrythmic drugs?
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Sodium channels blocker
Beta adrenergic blockers Potassium channel blocker Calcium channel blocker |
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Where do class I antiarrhythmics work? What are the effects?
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Block fast Na channels.
Decreases slope of phase 0 and amplitude of AP. |
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Where do class IA antiarrythmics work?
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Moderate effects on sodium effects. Binds to open state.
Inhibits potassium efflux during phase 3. Inhibit vagal activity. |
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What is the mechanism of quinidine?
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Increased threshold and decreased automaticity. Prolong AP duration. Blocks alpha-adrenergic receptors.
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What are the adverse effects of quinidine?
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Torsade de pointes
Anticholinergic effects Enhance digoxin toxicity Cinchonism |
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What is the mechanism of procainamide? What is the use?
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Increased threshold and decreased automaticity. Prolonged AP duration. Blocks alpha-adrenergic receptors.
Acute management of SVT and ventricular arrhythmias. |
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What are adverse effects of procainamide?
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QT prolangation
Lupus-like syndrome |
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What are the adverse effects of disopyramide?
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Negative inotropic effects
Torsade de pointes Anticholingergic side effects |
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Where do class IB antiarrhythmics bind? What are the effects?
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Inhibition of fast sodium channels to inactive state.
Increase potassium channels. |
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What is the use of lidocaine? What are the adverse effects?
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Ventricular arrhythmias.
May cause seizures. |
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What is the use of mexiletine? What are the adverse effects?
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Treat ventricular arrhythmias.
Tremor, nausea. |
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Where do IC antiarrhythmias work? What are the effects?
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Strong inhibition of sodium channels.
Reduction in amplitude of phase 0, no change in ERP |
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What is the use of flecainide? What are the adverse effects?
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Prevention of PSVT and a-fib.
Induce new or worsen arrhythmias. |
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What is the use of propafenone? What are the adverse effects?
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Prevention of PSVT and a-fib.
Can precipitate atrial flutter, increase digoxin, negative inotropic effects. |
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What are the effects of class II antiarrhythmics?
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Reduced heart rate.
Decreased calcium overload. Inhibits automaticity. Prevents hypokalemia. Slows AV conduction. |
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What are the indications for class II antiarrhythmics?
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SVT
Atrial flutter Atrial fibrillation PST |
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What are adverse effect of class II antiarrhythmics?
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Bradycardia
Heart failure Hypotension Bronchoconstriction Decreased plasma glucose |
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What are actions of class III antiarrhythmics? What are effects?
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Block delayed rectifier potassium currents.
Delays repolarization. Increased AP duration. Suppress reentrant arrhythmias. Increased QT interval |
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What are the mechanisms of amiodarone?
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Blocks potassium channels
Blocks sodium channels blocks alpha and beta receptors Calcium channel blocker |
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What is the use of amiodarone?
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A-fib
V-tach V-fib |
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What are the adverse effects of amiodarone?
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Pulmonary fibrosis
Ocular microdeposits Hyper or hypothyroidism Drug interactions |
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What is the use of dronedarone? What are the adverse effects?
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A-fib and atrial flutter.
GI side effects. |
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What is the use of dofetilide? What are the adverse effects?
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A-fib
Torsade de points. |
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What is the use for ibutilide? What are the adverse effects?
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A-fib or flutter
Prolongs QT and causes torsade |
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What is the use for sotalol? What are the adverse effects?
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Severe v-tach and a-fib.
May increase EAD and increase torsade de pointes. |
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What is the mechanism for class IV antiarrhythmias?
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Inhibits calcium channels in slow response tissues.
Inhibits AV node. |
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What are the adverse effects of class IV?
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Hypotension
Sinus bradycardia Raise serum digoxin contraindicated in WPW |
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What is the mechanisms for adenosine?
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Activates potassium current to decrease automaticity, increase ERP and decrease AV conduction.
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What is the use of adenosine? What are the adverse effects?
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Terminating supraventricular arrhythmia.
Facial flushing, transient dyspnea, hypotension, bronchoconstriction. |
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How does digitalis work in arrhythmia?
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Slows AV nodal conduction by decreased AV nodal automaticity.
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What are the adverse effects of digoxin?
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Nausea, congnitive disturbance, yellow vision.
Arrythmias. |
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What are the uses of magnesium salt?
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Prevention of torsade de points and treatment of digitalis arrhythmias.
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When are arrhythmias treated?
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Decrease cardiac output
Predispose to more serious arrhythmias Precipitae an embolism |
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Which drugs are used to treat sinus tachycardia?
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II, IV
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Which drugs are used to treat a-fib/flutter?
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Ia, Ic, II, III, IV
Digitalis Adenosine |
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Which drugs are used to treat paroxysmal supraventricular tachycardia?
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Ia, Ic, II, IIi, IV
Adenosine |
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Which drugs are used to treat ventricular tachycardia?
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I, II, III
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Which drugs are used to treat premature ventricular complexes?
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II, IV
Magnesium salts |
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What drugs are used to treat digitalis induced arrhythmias?
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Ib
Magnesium salts KCl |
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Which drugs are used to treat long QT syndrome?
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Beta blockers
ICD |
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What are the treatment goals of a-fib?
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Prevent stroke
Control ventricular rate Restore normal sinus rhythm |
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Which drugs are used to control rate in a-fib?
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Beta blockers (acute)
Digoxin, beta blockers, calcium antagonists (chronic) |
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What is teh drug of choice for atrio-ventricular nodal reentry tachycardia?
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adenosine
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