Anti-Arryhthmics Flashcards Preview

Pharmacology > Anti-Arryhthmics > Flashcards

Flashcards in Anti-Arryhthmics Deck (46):
1

Arrhythmias result from abnormalities of what

impulse conduction and impulse initiation

2

Automaticity is

the ability of the heart to undergo spontaneous action potentials

3

NSR stands for

normal sinus rhythm

4

it is critical for the ventricles to be what

relaxed while the atria are filling

5

Things that cause ectopic foci

electrolyte disturbances, ischemia, excessive myocardial stretch, drugs, toxins

6

the most common conduction abnormalities involve

conduction blocks

7

Usually conduction abnormalities are caused by

localized or regional hypoxia from decreased coronary blood flow

8

Effective refractory period

period of time a new action potential cannot be initiated, limits rapid depolarization, target of antiarrhythmetic drugs, prolonged ERP effective for abolishing reentry currents

9

Classification of antiarrhythmics

Vaughan Williams; class 1- Na channel blockers, class II- B blockers, Class III- k channel blockers, Class IV- Ca channel blockers; miscellaneous- atropine, adenosine, digoxin, electrolyte

10

Class Ia

Procainamide, Quinidine, disopyramide

11

What do all class 1a drugs do

selectively block Na channels undergoing depolarization of non-nodal action potential at a high rate, INCREASE ERP, slow conduction velocity through His purkinje, depresses automaticity

12

Non-nodal

drugs active in atrial and ventricular myocytes and purkinje cells; depolarization of nodal cells occurs via Ca channels

13

Quinidine other use

for RLS

14

MOA of class 1a

decreases myocardial excitability and conduction velocity by increasing threshold for firing

15

Class 1a used for

atrial or ventricular arrhythmias, A fib, a flutter, PSVT, PVCs, Vtach

16

Class 1a NOT recommended for

Vfib or hemodynamically unstable V tach

17

ADRs of class1a

can cause dyscrasisas such as agranulocytosis, lupus like syndrome, hypotension, arrhythmias; lot of drug interactions

18

Disopyramide (3)

rarely used, last line therapy, strong anticholinergic activity, can be used for atrial or ventricular arrhythmias

19

Class 1B

lidocaine, mexiletine, decrease ERP, not active with K channels,

20

Lidocaine (Xylocaine) (5)

Can be given ET tube, decreases erp, used for PVC, Vfib, hemodynamically staple V tach, cause bradycardia and arrythmias, not used in WPW syndrome

21

Mexiletine (Mexitil) (4)

oral form of lidocaine, used for PVC in pt with pacemaker, significant hepatotoxicity in some, lots of drug interactions

22

Class 1C

Flecainide, propafenone, very little effect on action potential duration, no change in ERP, used more

23

Propafenone (Rythmol) (5)

blocks fast Na channel, Ca and BB activity, prevents recurrence of Afib, on BEERS list, Lots of drug interactions

24

Flecainide (tambocor) (5)

slows conduction in cardiac tissue, slight prolong ERP, used for life threatening ventricular arrhythmias (can also induce them!), WPW syndrome, BEERS list, don't use with CAD pt

25

Class II MOA

bind to B receptor and block activity of epinephrine or norepinephrine, blocks B receptors in SA/AV nodes, conducting system and contracting myocytes

26

Effect of Class II

increase SA node automaticity, increase sinus rate, abort reentry circuits by decreasing conduction velocity, also affect non-pacemaker action potentials, increase ERP

27

Metoprolol (lopressor, toprol XL) (5)

A fib, SVT contol, acute not chronic arrhythmias, DOC for BB, only use if hemodynamically stable, caution with CHF, WPW

28

Class III

K channel blockers; Work both nodal and non nodal tissue; Amiodarone, Dronedarone, sotalol, dofetilide, ibutilide

29

K is responsible for

repolarization, slow in nodal tissue, fast in non-nodal tissue

30

a prolonged action potential duration has what effect

increases ERP

31

Classic effect of Class III

prolonged QT, prolonged time the cells is not excitable

32

Amiodarone (Cordarone, Nexterone) (3)

iodine allergy, VERY long half life, used for Afib (DOC)

33

MOA of amiodarone

active on Na, Ca, K channels and prolongs action potential, lengthens ERP, slows SA function and AV conduction

34

ADRs of amiodarone

brady, hypotension, hypothyroidism, slate blue skin, pulmonary toxicity

35

Dronedarone (Multaq) (5)

only available PO, very similar to amiodarone (no iodine), used for paroxysmal Afib, no CHF or pulmonary impaired pts, BEERS

36

Contraindications of Dronedarone (Multaq)

double risk of death in pt with permanent Afib, and in pt with CHF

37

Sotalol (Betapace) (3)

only PO, MOA- non selective BB, also K channel blocker- prolong PR and QT interval, used for stable Vtach and prevention of Afib

38

Dofetilide (Tikosyn) (5)

only PO, EKG monitored x 3 days, pt who have failed others or high risk SVT, few providers allowed to prescribe, MOA: blocks cardiac ion channel carrying rapid component of K current

39

Ibutilide (Corvert (3))

rarely used, NK MOA, usually one time dose to convert

40

Class IV

only non-dihydropyridines, blocks Ca channels in cardiac nodal tissue, cause peripheral vasodilation, NO USE IN CHF, slows AV conduction, increase time for each beat, decreases myocardial demand

41

Diltizem (Cardizem)

IV for acute afib or flutter, DOC for arrythmias, rate control not rhythm, only for hemodynamically stable pts

42

Digoxin (lanoxin)**

a cardiac glycoside from foxglove plant, TDM required, used for heart failure, A fib; CANNOT give to atrial tachyarrhythmias, Inhibits Na/K ATPase, increases intracellular Ca, increased contractility

43

Adenosine (Adenocard)

very short half life (10 secs); proximal vein administration, used for PVST, causes inhibition of L-type Ca channels, reduces HR and conduction in AV node

44

Magnesium and Potassium

low Mg and K can induce arrhythmias, also make digoxin toxicity worse

45

Atropine

increases phase 4 depolarization, increase firing rate, used for brady, post procedurally, does not improve overall outcomes

46

Most important anti-Arrhythmic

amiodarone