Anti-Arryhthmics

Question 1

Arrhythmias result from abnormalities of what

Answer 1

impulse conduction and impulse initiation

Question 2

Automaticity is

Answer 2

the ability of the heart to undergo spontaneous action potentials

Question 3

NSR stands for

Answer 3

normal sinus rhythm

Question 4

it is critical for the ventricles to be what

Answer 4

relaxed while the atria are filling

Question 5

Things that cause ectopic foci

Answer 5

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

Question 6

the most common conduction abnormalities involve

Answer 6

conduction blocks

Question 7

Usually conduction abnormalities are caused by

Answer 7

localized or regional hypoxia from decreased coronary blood flow

Question 8

Effective refractory period

Answer 8

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

Question 9

Classification of antiarrhythmics

Answer 9

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

Question 10

Class Ia

Answer 10

Procainamide, Quinidine, disopyramide

Question 11

What do all class 1a drugs do

Answer 11

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

Question 12

Non-nodal

Answer 12

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

Question 13

Quinidine other use

Answer 13

for RLS

Question 14

MOA of class 1a

Answer 14

decreases myocardial excitability and conduction velocity by increasing threshold for firing

Question 15

Class 1a used for

Answer 15

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

Question 16

Class 1a NOT recommended for

Answer 16

Vfib or hemodynamically unstable V tach

Question 17

ADRs of class1a

Answer 17

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

Question 18

Disopyramide (3)

Answer 18

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

Question 19

Class 1B

Answer 19

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

Question 20

Lidocaine (Xylocaine) (5)

Answer 20

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

Question 21

Mexiletine (Mexitil) (4)

Answer 21

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

Question 22

Class 1C

Answer 22

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

Question 23

Propafenone (Rythmol) (5)

Answer 23

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

Question 24

Flecainide (tambocor) (5)

Answer 24

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

Question 25

Class II MOA

Answer 25

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

Question 26

Effect of Class II

Answer 26

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

Question 27

Metoprolol (lopressor, toprol XL) (5)

Answer 27

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

Question 28

Class III

Answer 28

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

Question 29

K is responsible for

Answer 29

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

Question 30

a prolonged action potential duration has what effect

Answer 30

increases ERP

Question 31

Classic effect of Class III

Answer 31

prolonged QT, prolonged time the cells is not excitable

Question 32

Amiodarone (Cordarone, Nexterone) (3)

Answer 32

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

Question 33

MOA of amiodarone

Answer 33

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

Question 34

ADRs of amiodarone

Answer 34

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

Question 35

Dronedarone (Multaq) (5)

Answer 35

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

Question 36

Contraindications of Dronedarone (Multaq)

Answer 36

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

Question 37

Sotalol (Betapace) (3)

Answer 37

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

Question 38

Dofetilide (Tikosyn) (5)

Answer 38

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

Question 39

Ibutilide (Corvert (3))

Answer 39

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

Question 40

Class IV

Answer 40

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

Question 41

Diltizem (Cardizem)

Answer 41

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

Question 42

Digoxin (lanoxin)**

Answer 42

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

Question 43

Adenosine (Adenocard)

Answer 43

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

Question 44

Magnesium and Potassium

Answer 44

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

Question 45

Atropine

Answer 45

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

Question 46

Most important anti-Arrhythmic

Answer 46

amiodarone