Pharm 14 Drugs Used In Cardiac Arrhythmias

Front 1

2 major mechanisms for arrhythmias?

Back 1

abnml automaticity
abnml (reentrant) conduction

Front 2

what is Torsade de pointes?

Back 2

ventricular arrhythmia often induced by antiarrhythmic drugs that prolong the QT interval

looks like polymorphic v.tach on ECG, QRS amplitude rises and falls

Front 3

which ion(s) cause phase 0 and is(are) the main determinant of conduction velocity?

Back 3

Na

Front 4

which ion(s) cause the AV node upstroke and conduction velocity?

Back 4

Ca

Front 5

which ion(s) cause phase 2?

Back 5

Ca and K
(plateau)

Front 6

which ion(s) cause phase 3?

Back 6

K
(rapid repolarization)

Front 7

what factors determine the refractory period length?

Back 7

rapidity of Na channel recovery
membrane potential (varies w/ repol time and extracellular [K])
actions of Na channel blocking drugs

Front 8

what are the four classes of antiarrhythmics?

Back 8

I - Na channel blockers
II - beta blockers
III - K channel blockers
IV - Ca channel blockers
(miscellaneous - adenosine, K+, Mg+)

Front 9

Electrical effect of all Class 1s?

Back 9

slow/block conduction in ischemic and depolarized cells
slow/abolish abnml pacemakers (if they depend on Na channels)

Front 10

Class 1As?

Effects?

Back 10

Procainamide, quinidine, disopyramide

Block both A & V arrythmias by slowing conduction velocity in atria, Purkinjes and ventricular cells (block Na channels)
increase AP duration and refractory period (block K channels)

Front 11

Class 1B's?

Effects?

Back 11

Lidocaine (IV), Mexiletine (oral)

selectively affects ischemic or depolarized Purkinje and ventricular tissue
slow phase 0, long refractory , shortens AP

Front 12

what drug can be used to reverse digitalis arrythmias because it has class 1B-like actions?

Back 12

Phenytoin

Front 13

Class 1C's?

Effects?

Toxicity?

Back 13

Flecainide, Encainide, Propafenone

slow phase 0 and long refractory period, but no change in AP duration

effective in A & V arrhythmias

Tox: greatest proarrhythmic effect; anesthetic-like CNS toxicity

Front 14

Mechanism of Class II's in arrhythmias?

Back 14

cardiac b-adrenoceptor blockade and reduction of cAMP (reduces Na and Ca currents)

AV node is most sensitive (Ca-dependent conduction)

Front 15

Very short-acting IV b-blocker?

Back 15

Esmolol

Front 16

B-blockers used as prophylaxis in pts with hx of MI?

Back 16

propanolol, metoprolol, timolol

Front 17

Toxicity of Class II's?

Back 17

depresses contractility and reduces CO

Front 18

Class III's?

Effects?

Back 18

Sotalol, ibutilide, dofetilide, amiodarone

Increase AP duration (slow repol, long refractory)

Front 19

Significant toxicity of Class II's?

Back 19

Torsade de pointes

Front 20

MOA of Amiodarone?

Back 20

blocks Na, Ca and K channels and B-adrenoceptors

Front 21

toxicity of Amiodarone?

Back 21

microcrystalline deposits in cornea and skin
thyroid dysfxn
paresthesias
tremor
pulmonary fibrosis

Front 22

Class IV's?

Effects?

Back 22

Verapamil, Diltiazem

Effective against arrhythmias that must traverse the AV node
Slows AV conduction velocity, long refractory, long PR

Front 23

Toxicity of Class IV's?

Back 23

significant depresssion of contractility, AV conduction, and BP

Front 24

Adenosine MOA?

Back 24

slows/blocks AV node conduction (by hyperpolarizing via K-block, and blocking Ca currents)

Front 25

Drug of choice for AV nodal arrhythmias?

Back 25

Adenosine

Front 26

What should always be checked when treating arrhythmias and why?

Back 26

serum potassium

hypokalemia = arrhythmias
hyperkalemia = depressed conduction and reentry arrhythmias