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