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Pharm II > Dysrythmias > Flashcards

Dysrythmias Flashcards

1
Q

imbalance of what can lead to dysrhythmias

A

potassium

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2
Q

what do class I antiarrhythmics do?

A

Block Na

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3
Q

what do class Ia Na blockers do?

A

slow Phase 0 depol

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4
Q

What do phase IB Na do?

A

shortens Phase 3 repol

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5
Q

What do phase IC Na blockers do?

A

slow Phase 0 depolarization (better than phase Ia)

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6
Q

what is the prototype of class IA antiarrhythmic?

A

Quinidine

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7
Q

what does quinidine help with

A

inhibit ventircular arrhythmias
ectopic arrhytmias
prevent re-entry arrythmias

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8
Q

contradincations for class IA antiarrhythmic agents

A 
Great block
SA node dysfunction
cardiogenic shock
uncompensated heart failure
SLE w/ procainamide also schizophrenia
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9
Q

what inhibits the metabolism of quinidine

A

cimetidine

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10
Q

what induces quinidine

A

rifampin
barbituates
phenytoin

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11
Q

what is a ADR of quinidine that results in blurred vision, tinnitus, HA, disorientation, psychosis

A

Cinchonism

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12
Q

Clas I A antiarrhythmic that is a derivative of local anesthetic.

A

procainamide

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13
Q

what is procainamide metabolized to

A

N-acetylprocainamide (NAPA) which prolongs duration fo AP (Class III properties)

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14
Q

ADRs with procainamide

A

HPOTN
reversible lupus like symptoms
asystole or ventricular arrhtymias at toxic concen
depression, hallucinations, psychosis

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15
Q

similar to quinidine. C/I with HF or peripheral vasoconstriction. Used to treat ventricular arrhythmias.

A

Disopyramide

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16
Q

ADRs with dispyramide

A

anticholinergic

proarrhythmic

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17
Q

What is the class IB prototype and DOC for cardiac arrhythmias

A

Lidocaine

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18
Q

MOA of lidocaine

A

shortens phase 3 reporalization and decrease the duration of the action potential. Suppresses arrhythmias caused by abnormal automaticity

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19
Q

indications for liocaine

A 
administer IV (fist pass metabolism avoided)
ventricular arrhythmias post MI or arising from MI
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20
Q

what are other class IB meds?

A

Mexiletine and TOcainide (PO)

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21
Q

what is a concert with tocainide?

A

pulmonary fibrosis

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22
Q

prototype of class IC antiarrhythmic

A

flecainide

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23
Q

MOA of flecanide

A

blocks sodium channels

slow phase 0 depolarization

24
Q

indications for class IC anitarrhythmics

A

refractory ventricular arrhythmias (PVCs)

25
Q

C/I with classs IC anitarrhythmics

A

CHF

worse proarrythmic

26
Q

CLass II anitarrhythmics

A

propranolol
metoprolol
esmolol

27
Q

what is the MOA of class II antiarrhythmic agents

A

diminish phase 4 depoloiarization thus depressing automaticity

28
Q

Class III antiarrythmic agents

A

Sotolol
amiodarone
dofetilide

29
Q

MOA of class III antiarrythmics

A

Blocks potassium channels prolonging both repolarization and duration of AP thus lengthening effective refractory period.

30
Q

Indications for class III agents

A

ventricular and supraventricular arrhythmias.

31
Q

what class II antiarrhytmic agents can result in torsades de pointes?

A

Sotalol

32
Q

what is dofetilide restricted to for Rx capabilities

A

MD who have completed manufactuer’s training

33
Q

what do amiodarone contain?

A

Iodine (can mess up a person’s thyroid)

34
Q

does amiodarone only have Class III antiarrythmic effects?

A

No, also has class I, II, IV actions

35
Q

Indications for amiodarone

A

refractory SVT

ventricular tachyarrhythmias

36
Q

Does amiodarone reduce incidence of sudden death or prolong survival in pt. with CHF

A

No

37
Q

Why is amiodarone challenging to dose?

A

Really long 1/2 life (weeks)

38
Q

long term use of amiodarone can result in what?

A

pulmonary fibrosis (may not be reversible)

39
Q

what color will patietns with amiodarone look like

A

blue skin discoloration

40
Q

what are class IV agents?

A

calcium channel blockres

41
Q

indications for class IV agents (CCB)

A 
Atrial arrhythmias
Reentrant supraventricular tachycardia
Reducing ventricular rate in atrial flutter and fibrillation
HTN
Angina
42
Q

contraindications for class IV agents

A

pts. With preexisting depressed cardiac function due to negative inotropic properties

43
Q

what anitarrhytmic reduces moratlity?

A

beta blockers

44
Q

Endogenous nucleoside that acts at tissues in the lungs, afferent nerves, and platelets.
MOA: high doses decreases conduction velocity, prolongs the refractory period and decreases automaticity in the AV node.

A

Adenosine

45
Q

contraindications for adenosine

A

2nd and 3rd degree hear block

sick sinus syndrome

46
Q

indications for adenosine

A

DOC for abolishing supraventricular tachycardia

47
Q

does adenosine have a long or short duration of action

A

very short duration of action

48
Q

ADRs with adenosine

A

transient facial flushing
chest pain
dyspnea
bronchospasm

49
Q

Indicated for control of ventricular rate in Afib and a flutter. MOA: shortens refractory period in atrial/ventricular cells while prolonging effective refractory period and decreasing conduction velocity in Purkinje fibers.

A

Digoxin

50
Q

ADRs with digoxin

A

VTACH/ VFIB (treat w/ lidocaine)

51
Q

Does acute tx for afib depend on if its paroxysmal or persistent

A

No

52
Q

is long term anitarrhythmic drug therapy needed for persistnet atrial fibrillation?

A

No

53
Q

what is DOC if patients are hemodynamically unstable and have severe symptoms of afib?

A

Direct current cardioversion (DCC)

54
Q

what are initial anticoagulation therapies

A

UF heparin
LMWH
then do bridge therapy

55
Q

what meds can be used for ventricular rate control?

A

digoxin (24-48 hours, if underlying HF)
B-blockers, diltiazem, verapmail (better choices w/o heart failure)
amiodarone (failure of other drugs)

56
Q

is there improvement in mortality with cardioversion

A

No

57
Q

what do you give for chronic a-fib therapy for oral anticoagulation?

A

Warfarin or Dabigatran

Pharm II (16 decks)

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