UW PHCOL GE: Arrhythmia and Antiarrhythmic Drugs Flashcards

cardiac action potential
Terms Definitions
Mechanism of action of Class I Antiarrhymic Drugs
Sodium channel blockers
Frequency and voltage dependent
Mechanism of action of Class II Antiarrhymic Drugs
Beta blockers
Mechanism of action of Class III Antiarrhymic Drugs
Potassium channel blockers
Mechanism of action of Class IV Antiarrhymic Drugs
Calcium channel blockers
What are the differences between Class IA , IB, and IC Antiarrhymia Drugs?
IA: Moderate blockade, prolonged ERP, reduced Vmax. Intermediate binding rate.

IB: Weak blockade, decreased ERP, no Vmax change. Fast binding rate.

IC: Strong blockade, prolonged ERP, large reduction in Vmax. Slow binding rate.
What class of drug is quinidine?
Class IA antiarrhythmic
What class of drug is procainomide?
Class IA antiarrhythmic (similar to quinidine, but no action on muscarinic receptors)
What class of drug is verapamil?
Class IV antiarrhymic (calcium channel blocker).
What class of drug is nifedpine?
Class IV antiarrhymic (calcium channel blocker).
What class of drug is diltiazem?
Class IV antiarrhymic (calcium channel blocker).
What class of drug is amiodarone?
Class I/III antiarrhythmic (high affinity potassium channel blocker plus 1A block of sodium channel). Highly lipophilic, slow absorption and elimination.
What class of drug is lidocaine?
Class IB antiarrhythmic.
What class of drug is flecamide?
Class IC antiarrhythmic.
What class of drug is sotalol?
Class II/III (beta blocker and potassium channel antagonist).
What is re-entrant cardiac arrhythmia and what causes it?
Electrical impulses bouncing off ischemic tissue and reversing direction. Due to ischemic (blood and oxygen) deprived tissue that cannot pass along current.
What ion channels are chiefly responsible for initiating diastolic depolarization?
HCN channels.
Define Vmax
The rate of rise in phase 0 of the cardiac action potential.
Which arrhythmia is most acutely dangerous?
Ventricular fibrillation
Drug-induced long-QT syndrome via HERG blockage is a result of what ion channel blockage?
Potassium channels
True/False?
Calcium channels are responsible for the majority of cardiac depolarization in phase 0 of the cardiac action potential.
FALSE
True: Sodium channels
T/F: The conformational change required for sodium channels to recover from inactivation is both time and voltage dependent.
True
T/F: Mutations in sodium channels can lead to long-QT syndromes
True
T/F: The sodium-calcium exchange pump is ATP dependent.
False
The sodium pump is ATP dependent.
The calcium pump is ATP dependent.
The sodium-calcium exchange pump is gradient dependent
What is the primary function of the Sodium/Calcium exchanger?
To maintain low levels of intracellular Calcium.
At what phase of the cardiac action potential do calcium channels open?
Phase 2.
Define Paroxysmal Supreventricular Tachycardia
AV Nodal reentry of electrical impulses
Define Sinus Tachycardia
High heart rate.
Define Effective Refractory Period (ERP)
From BC's Notes: "The minimum interval between two propagated action potentials. Depends on the rate of movement [of the ion channels] from the Inactivated to the Closed states. Related to action potential duration since recovery from Na+ channel inactivation cannot occur until repolarization is essentially complete."
Phase 0 of the cardiac action potential is called ____.
Phase 0 happens with the ____ ion channel is activated, which _____ the cell.
Upstroke
Sodium
Depolarizes
Class IA and Class IB antiarrhytmic drugs differ with respect to:
Effect on ERP
Use in therapy of atrial arrhythmias
The toxic side effect of Class I antiarrhythmic drugs include:
Ventricular tachycardia and fibrillation
Class III antiarrhythmic drugs have the following properties:
1) Block of potassium channels
2) Efficacy of treating atrial arrythmias
3) Toxic side-effects include Long QT syndrome
4) Prolonged ERP
Treatment of atrial arrhythmia would include
A) Verapamil
B) Nifedpine
C) Diltiazem
D) A and B
E) A and C
E) Verapamil and Diltiazem
The use of this drug is limited by hypersensitivity and sometimes systemic lupus erythmatosis.
Procainamide.
The cardiac action potential is conducted rapidly through the
Atria
Phase 1 of the cardiac action potential is called ______.
It involves the activation of the ______ ion channel, which ________ the cell.
Early-Fast Repolarization
Fast, transient K+ channels (out)
Partially Repolarizes
Phase 2 of the cardiac action potential is called _______.
It involves the activation of the ______ ion channel, which ________ the cell.
Plateau
Ca++ channels (influx)
Depolarizes
Phase 3 of the cardiac action potential is called ______.
It involves the activation of the ______ ion channel, which ________ the cell.
Repolarization.
Multiple classes of K+ channels.
Repolarizes
Phase 4 of the cardiac action potential is called ______.
It involves the inactivation of _____ in channels and the activation of the ______ ion channels.
Diastole
inactivation of K+ channels
activation of (HCN) channels as well as activation of Ca++ channels (in SA node and AV node) or Na+ channels (in Purkinje fibers) increasing inward current.
Name an arrhythmia that affects the SA Node.
Sinus tachycardia and brachycardia.
Name arrhythmias that affects the atria.
Premature systoles.

Atrial or supraventricular tachycardia.

Atrial fibrillation.
Name arrythmias that affect the AV Node.
Paroxysmal SupraVentricular Tachycardia (PSVT)

AV block.
Name arrhythmias that affect the ventricles.
Premature ventricular systoles.

Ventricular fibrillation.
Blocking potassium channels (treating with class III antiarrhythmics) ______ the action potential duration.
increases
Because class I antiarrhythmic drugs block the sodium channels, they tend to _______ the Vmax.
decrease
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Term:
Definition:
Definition:

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