Z-Pharm Antiarryth I And Ii

Front 1

What determines the resting membrane potential?

Back 1

the K concentration gradient across the membrane

Front 2

In the fast response action potential - what are the five phases induced from?

Back 2

Phase 0 = upstoke, activation of fast Na channel
Phase 1 = transcient outward K current and inactivation of Na channels
Phase 2 = plateau, slow inward Ca current and decrease in K permiabilty
Phase 3 = repolarization, increase in K permeability and inactivation of Ca channels
Phase 4 = resting membrane potential, K permiability high again.

Front 3

What are the two phases in the slow response action potental (SA and AV nodes)?

Back 3

Upstroke - activation of slow inward Ca channels (as in Phase 2)

Repolarization - inactivation of Ca channels and increase in K permiabilty (as in phase 3)

Front 4

What two pumps maintain ion concentrations?

Back 4

1. Na-K pump - maintains Na and K concentration gradients. Na pumped out and K pumped in

2. Na-Ca exchange - maintains low intracellular Ca conc.

Front 5

VIP

Explain how the action potential duration is normally the primary determinant of refractory periods. How do drugs work on this point?

Back 5

Under normal conditions as the action potential repolarizes (voltage) the Na channels recover very quickly from inactivation. There for the action potential duration (voltage) is the primary determinant of refractory periods. Some anti-arrythmic drugs can increase the time required for the Na channels to recover from inactivation and therefore increase the refractory period. By doing so this blocks tachycardia and premature beats from occuring.

Front 6

What do tachyarrhymias and premature beats depend on to be initiated?

Back 6

They depend on the ability of Na channels to recover from inactivation RAPIDLY.

Front 7

What are the functions of Class I, II, III, and IV antiarrhymics?

Back 7

I: block Na channels
II: beta adrenergic receptor blockers
III: prolong repolarization to then prolong AP and effective refractory period
IV: block slow inward calcium current

Front 8

VIP

Why are use- or state-dependant antiarrhymics so wonderful?

Back 8

Because they have a high affinity for activated Na or Ca channels (phase 0) or inactivated Na or Ca channels (phase 2) and low affinity for resting channels. This is great because these drugs won't effect nL tissue, instead will only effect electically active tissue or tissue with positive resting membrane potentials (like ischemic tissue)

Front 9

Explain the state-dependant effects of Lidocaine:

Back 9

Lidocaine acts by blocking Na channels. It blocks more Na channels as membrane potential becomes more positive. As more Na channels are blocked, activity of the tisse ceases.

Front 10

What do Class I drugs to the number of channels available at any given voltage and the time required for channels to recover?

Back 10

Class I drugs reduce the # of Na channels available and increase the time needed for Na channels to recover from inactivation, especially prominent at more postiive voltages.

Front 11

What do vagal maneuvers do?

Back 11

Helps to slow conduction through AV node. Used as acute treatment for paroxysmal supraventricular tachycardia (PSVT)

Front 12

What is responsible for the electrical refractory properties of cardiac muscle?

Back 12

The duration of the action potential which is both voltage and time dependant

Front 13

What are the use- or state-dependant actions of Class I drugs?

Back 13

Class I drugs block Na channels that activated (quidine) and those that are both activated and inactivated (Lidocaine) thus making them specific to unruly cardiac tissue.

Front 14

Using Qunidine as an example, how do Class I drugs block arrhythmias?

Back 14

Lip p199
Quinidine decreases normal automaticity which inhibits ectopic arrhythmias and ventricular arrhythmias. It also prevents reentry of arrhythmias by producing a bidirectional block from its effect on decreasing membrane responsiveness and prolonging refractory period.

Front 15

Antiarrhythmic drugs that prolong AP's duration are prone to cause what type of arrhythmia?

Back 15

EAD's, Torsade de Pointes

Front 16

Which class I drug has a metabolite that exerts class III effects?

Back 16

Procainamide, its metabolite NAPA can prolong AP duratio as a Class III drug

Front 17

What are the primary differences in the actions between quinidine and lidocaine?

Back 17

Lidocaine causes the inactivation of both activated and inactivated Na channels allowing it to be specific for damaged tissue. It only really increases the refractory period of partially depolarized tissue and thus does not have the effects of increasing AP duration overall (as Quinidine does) which can cause v-fib or v-tac and EAD's.

Lidocaine is the drug of choice for supression of v-tach or v-fib and is used for arrhythmias following an MI. Quinidine on the other hand is used more for a-flutter or a-fib

Front 18

Which Class I drug is not approved in the setting of post-MI?

Back 18

Flecainide

Front 19

Which drug is the drug of choice for exercise-induced arrhythmias and why?

Back 19

Propranolol - because as a Beta blocker it inhibits sympathetic mediated effects, slows sinus and AV rate, increases refractoriness and decreases cardiac work (contractility)

Front 20

What class III drug causes pulmonary fibrosis?

Back 20

Amidarone

Front 21

How do class IV drugs block SVT due to WPW?

Back 21

They reduce conduction.

Front 22

Which Ca blocking drug has little anti-arrhythmic action as what is it used for?

Back 22

Nifedipine - it acts on vascular smth m. to dilate it. This can releave angina and cause hypotension

Front 23

What is the cellular mechanism of adenosine to block arrhythmias?

Back 23

Acts on atrial tissue to increase K conductance and inhibit cAMP mediated Ca currents. This slows AV current and increase AV node refractoriness.

Front 24

What are vagal maneuvers and how do they block PSVT?

Back 24

They act to slow conduction through the AV node to decrease supraventricular tachycardia.