anti-arrythmics Flashcards Preview

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Flashcards in anti-arrythmics Deck (24):
1

What is the only drug that slows heart rate but does not affect contractility?

ivabradine - slows SA node firing by selectively inhibiting sunny sodium - slowing and prolonging phase 4 depolarization

2

what effect do verapamil and diltiazem have on myocardial action potentials?

type 4 calcium channel blockers - inhibit L-type calcium channels during phase 2 depolarization which prolongs the AP.

slows sinus rate
prolong conduction through AV node
decrease contractility

3

what effect do class 1A antiarrythmics have on myocardial action potential?

How does this profile contrast

Class 1A anti-arrythmics (disopyramide, qunidine, procainamide) decrease the slope of phase 0 depolarization, and slow conduction

Specific features of Class1A
1) INCREASED ACTION POTENTIAL DURATION
2) increased effective refractory period in ventricular action potential
3) prolonged QT interval (prolonged phase III repolarization)

(Class 1A drugs also depress contractility)

By contrast, class 1B (lidocaine and mexiletine) cause:
1)DECREASED ACTION POTENTIAL DURATION and preferentially affect ischemic or depolarized perkinje or ventricular tissue making them particularly suitable for threatment of post-MI arrhythmias (DOC=lidocaine)

4

What are the class IC antiarrythmics? What effect do they have on APs?

Flecainide and prpafenone

specifically prolong the effective refractory period in the AV node and accessory bipass tracts but have no effect on action potential duration in kurkinje and ventriuclar tissue?

5

What effect do potassium channel blockers have on cardiac action potentials?

class III anti-arrythmics act on phase 3 slow delayed rectifier potassium channels

They delay and prolong repolarization
prolong AP duration
prolong refractory period

NOT USED FOR CHF!

6

what class of antiarrythmic is used for atrial and ventricular arrythmias particularly re-entrant and ectopic SVT and VT

Class 1A - atrial and ventricular arrythmias particularly re-entrant and ectopic SVT and VT

7

what class of antiarrythmic is used for acute ventricular arrhythmia especially post-MI

Class 1B - used for acute ventricular arrhythmia especially post-MI because specifically affects ischemic tissue

8

what class of antiarrythmic is used for atrial fibrillation (and only as last resort used for VT)

Class 1C - atrial fibrillation (and only as last resort for VT)

specifically prolong the effective refractory period in the AV node and accessory bipass tracts but have no effect on action potential duration in kurkinje and ventriuclar tissue?

9

what class of antiarrythmic is used for afib, aflutter, VT
and produce a significantly prolonged AP with increased effective refractory perior and prolong QT interval?

Class III - afib, aflutter, VT (amiodorone or sotalolol only)

10

what are class 1A used for? Why?

atrial and ventricular arrythmias particularly re-entrant and ectopic SVT and VT

because prolonged ventriuclar AP (and also some effect of prolonged phase 3 repolaization) slows the rate of ventricular contraction in setting of tachy independently from pacemaker activity

11

what drugs should not be used in a patient with CHF?

flecainide and propafenone - contraindicated with CHF

12

pt receives a medication and later reports corneal deposits and blue/grey deposits on their skin. what was the drug?

amiodarone

13

what are the main side effects of amiodarone?

pulmonary fibrosis
hepatotoxicity
hyperthyroidism/hypothyroidism (40% iodine by weight)
bradycardia, heart block, heart failure

14

Pt is treated for tachycardia and later develops dislipidemia. what was the drug?

metropolol

15

what is the treatment for betablocker overdose?

saline, atropine and glucagon

16

after treatment for ventricular arrythmia a patient presents with reversible SLE-like syndrome. What was the drug?

procainamide

17

which anti-arrythmic can cause impotence?

beta-blockers

18

what class of anti-arrythmics would phentoin fall into?

class IB

19

rank the strenth of inhibition of phase 0 depolarization from the class I antiarrhythmics from strong to weak

1C>1A>1B

20

rank the degree of prolongation of the action potential from the class I antiarrhythmics from long to short

1A(prolonged)>IC(no change)>IB(shortened)

21

what is the MOA for adenosine on cardiac cells?

adenosine activates potassium channels and increases the K+ conductance by interacting with A1 receptors. This results in:

hyperpolarization
transent slowing of the sinus rate
increased AV nodal conduction delay

ADENOSINE DOES NOT MODULATE THE VENTRICULAR MYOCYTE AP

22

how does digoxin exert antiarrhythmic effects?

digoxin increases vagal output to the AV node and conduction system which results in decreased conduction velocity

DIGOXIN DOES NOT MODULATE THE VENTRICULAR MYOCYTE AP however it does increase intracellular Ca2+, increasing contractility

23

Flecainide has a high affinity for sodium channels and exhibits a slow rate of receptor dissociation, which makes it more effective at higher rates of depolarization. What is this effect called?

use dependence

24

what is the primary site of action of beta blockers?

AV node
Beta blockers do not affect the ventriclar myocyte AP!

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