Dysrythmias Flashcards

(57 cards)

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
C/I with classs IC anitarrhythmics
CHF | worse proarrythmic
26
CLass II anitarrhythmics
propranolol metoprolol esmolol
27
what is the MOA of class II antiarrhythmic agents
diminish phase 4 depoloiarization thus depressing automaticity
28
Class III antiarrythmic agents
Sotolol amiodarone dofetilide
29
MOA of class III antiarrythmics
Blocks potassium channels prolonging both repolarization and duration of AP thus lengthening effective refractory period.
30
Indications for class III agents
ventricular and supraventricular arrhythmias.
31
what class II antiarrhytmic agents can result in torsades de pointes?
Sotalol
32
what is dofetilide restricted to for Rx capabilities
MD who have completed manufactuer's training
33
what do amiodarone contain?
Iodine (can mess up a person's thyroid)
34
does amiodarone only have Class III antiarrythmic effects?
No, also has class I, II, IV actions
35
Indications for amiodarone
refractory SVT | ventricular tachyarrhythmias
36
Does amiodarone reduce incidence of sudden death or prolong survival in pt. with CHF
No
37
Why is amiodarone challenging to dose?
Really long 1/2 life (weeks)
38
long term use of amiodarone can result in what?
pulmonary fibrosis (may not be reversible)
39
what color will patietns with amiodarone look like
blue skin discoloration
40
what are class IV agents?
calcium channel blockres
41
indications for class IV agents (CCB)
``` Atrial arrhythmias Reentrant supraventricular tachycardia Reducing ventricular rate in atrial flutter and fibrillation HTN Angina ```
42
contraindications for class IV agents
pts. With preexisting depressed cardiac function due to negative inotropic properties
43
what anitarrhytmic reduces moratlity?
beta blockers
44
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.
Adenosine
45
contraindications for adenosine
2nd and 3rd degree hear block | sick sinus syndrome
46
indications for adenosine
DOC for abolishing supraventricular tachycardia
47
does adenosine have a long or short duration of action
very short duration of action
48
ADRs with adenosine
transient facial flushing chest pain dyspnea bronchospasm
49
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.
Digoxin
50
ADRs with digoxin
VTACH/ VFIB (treat w/ lidocaine)
51
Does acute tx for afib depend on if its paroxysmal or persistent
No
52
is long term anitarrhythmic drug therapy needed for persistnet atrial fibrillation?
No
53
what is DOC if patients are hemodynamically unstable and have severe symptoms of afib?
Direct current cardioversion (DCC)
54
what are initial anticoagulation therapies
UF heparin LMWH then do bridge therapy
55
what meds can be used for ventricular rate control?
digoxin (24-48 hours, if underlying HF) B-blockers, diltiazem, verapmail (better choices w/o heart failure) amiodarone (failure of other drugs)
56
is there improvement in mortality with cardioversion
No
57
what do you give for chronic a-fib therapy for oral anticoagulation?
Warfarin or Dabigatran