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24 Cards in this Set

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  • Back
What determines the resting membrane potential?
the K concentration gradient across the membrane
In the fast response action potential - what are the five phases induced from?
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.
What are the two phases in the slow response action potental (SA and AV nodes)?
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)
What two pumps maintain ion concentrations?
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.

Explain how the action potential duration is normally the primary determinant of refractory periods. How do drugs work on this point?
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.
What do tachyarrhymias and premature beats depend on to be initiated?
They depend on the ability of Na channels to recover from inactivation RAPIDLY.
What are the functions of Class I, II, III, and IV antiarrhymics?
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

Why are use- or state-dependant antiarrhymics so wonderful?
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)
Explain the state-dependant effects of Lidocaine:
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.
What do Class I drugs to the number of channels available at any given voltage and the time required for channels to recover?
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.
What do vagal maneuvers do?
Helps to slow conduction through AV node. Used as acute treatment for paroxysmal supraventricular tachycardia (PSVT)
What is responsible for the electrical refractory properties of cardiac muscle?
The duration of the action potential which is both voltage and time dependant
What are the use- or state-dependant actions of Class I drugs?
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.
Using Qunidine as an example, how do Class I drugs block arrhythmias?
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.
Antiarrhythmic drugs that prolong AP's duration are prone to cause what type of arrhythmia?
EAD's, Torsade de Pointes
Which class I drug has a metabolite that exerts class III effects?
Procainamide, its metabolite NAPA can prolong AP duratio as a Class III drug
What are the primary differences in the actions between quinidine and lidocaine?
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
Which Class I drug is not approved in the setting of post-MI?
Which drug is the drug of choice for exercise-induced arrhythmias and why?
Propranolol - because as a Beta blocker it inhibits sympathetic mediated effects, slows sinus and AV rate, increases refractoriness and decreases cardiac work (contractility)
What class III drug causes pulmonary fibrosis?
How do class IV drugs block SVT due to WPW?
They reduce conduction.
Which Ca blocking drug has little anti-arrhythmic action as what is it used for?
Nifedipine - it acts on vascular smth m. to dilate it. This can releave angina and cause hypotension
What is the cellular mechanism of adenosine to block arrhythmias?
Acts on atrial tissue to increase K conductance and inhibit cAMP mediated Ca currents. This slows AV current and increase AV node refractoriness.
What are vagal maneuvers and how do they block PSVT?
They act to slow conduction through the AV node to decrease supraventricular tachycardia.