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FPC2 Exam 7 > Arrhythmia > Flashcards

Arrhythmia Flashcards

1
Q

What at the two types of tachycardia arrhythmias?

A

Supra ventricular

Ventricular

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2
Q

What are the types of supra ventricular arrhythmias? (There are 4)

A

atrial tachycardia,
paroxysmal supraventricular tachycardia
Atrial flutter
atrial fibrillation (most common)

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3
Q

What are the types of ventricular arrhythmias?

A

premature ventricular contractions
ventricular tachycardia
ventricular fibrillation
Torsades de Pointes

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4
Q

What are the risks of afib? What are the treatment goals?

A
  • stroke + tachycardia induced cardiomyopathy. not really fatal on its own
  • relieve symptoms, manage ventricular rate control, restore matinain NSR, prevent stroke
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5
Q

What are the 3 treatment considerations for afib? Which do you hit first?

A

Rate control, rhythm control. anitcoagulation
hit rate first
also this is misleading because you should assess all of these things in afib patients

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6
Q

What are the agents used for afib rate control.

A

Betablockers
Non-dihydropyridine calcium channel blockers
(help the AV node out, block it)
not trying to restore sinus rhythm, just control ventricular rate

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7
Q

What agents are used for rhythm control for afib?

A

antiarrhythmias

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8
Q

What are some agents that block SA and AV nodes? What will you see on ECG?

A

HR down PR interval up

metoprolol, carvedilol, atenolol (don’t use, renal clearance), labetalol, bisoprolol, nadolol, diltiazem, verapamil

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9
Q

What are rate control goals for treatment of afib?

A

stricter rate control (HR<80) in symptomatic. <110 reasoned for asymptomatic and good LV systolic function

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10
Q

The MOA of Digoxin is _________ which __________. What is dosing? What do you need to watch? What reverses it?

A

inhibit Na/K ATPase-> decrease conduction through AV node. does not compensate with activity.
0.125-.25 daily, watch renal.
Digibind reverses it
never been a long term strategy

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11
Q

What is the Vaughan Williams classification and how does it classify?

A

Anti arrhythmia meds. Classify by channel blocked (1 Na, 2 β blocker, 3 K, 4 Ca)
This is an antiquated method

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12
Q

What is going wrong in a fib?

A

atria do not depolarize uniformly (non uniform contraction, can’t pump blood)

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13
Q

What trial was used to look for rate control? qualifications

A

AFFIRM
over 65, no problem with anti-coag
No difference when someone is on rate control drug

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14
Q

Rhythm control medications do what for a patient?

A

control sinus rhythm

used with rate control (if younger, maybe only rhythm)

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15
Q

Which Vaughan Williams classification is rate control? which is rhythm control

A

1 and 3 are rhythm control

2 and 4 are rate control (β block, calcium)

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16
Q

What are the mechanism and effect of class 1 antiarrhythmics?

A

MOA: slow depolarization (1c>1a>1b)
we are looking at the QRS!!!!!
(and QT and PR a bit)

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17
Q

What are the mechanism and effect of class 3 antiarrhythmics?

A 
slow depolarization
QT interval
(drug drug interaction funsies)
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18
Q

All antiarrhythmics can cause what?

A

arrhythmias.

lol

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19
Q

Class 1b agents are used for what?

A

ventricular fibrillation

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20
Q

Are class 1a drugs used in a fib?

A

not really, saved mostly for ventricular fibrillation

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21
Q

Which two classes are used for atrial fibrillation? and what drugs are in the class

A 
Class 1c (propafenone, flecainide)
Class 3 (amiodarone, dofetilide, dronedarone, sotalol)
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22
Q

______ guides choice for a fib drugs?

A

safety, NOT efficacy (process of exclusion)

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23
Q

What makes class 1a, 1b, 1c arrhythmia drugs different?

A

how long they bind to the channel. 1c binds very strongly. also the site of effect (1b only in ventricles)

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24
Q

For class 1c agents there is use dependence, which means?

A

When heart rate fast, drug binds stronger. this is a good thing-> if in afib, drug will be working harder!
try to also put on av nodal blocker

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25
Q

Uses, contraindications, AEs, things to monitor, and interactions for flecainide

A 
Atrial fibrillation (aflutter, PSVT, ventricular arrhythmias)
Contra: structural heart disease
AE: visual, GI, pro arrhythmia
monitor: PR + QRS + do stress test
Interactions: 2d6
26
Q

MOA, use, PK and contra indications for propafenone

A

MOA: Na channel blocker (mild β)
Use: afib (aflutter, v arrhythmias, PSVT, PVC)
PK: 2 active metabolites, 2-10 hrs or 10-32 hrs
Contra: structural heart, sinus node dysfunction/brady

27
Q

AEs, monitoring, and drug interactions for propafenone?

A

AE: dizziness, nausea, metallic taste, arrhythmias

monitor: PR and QRS and stress
interact: 2d6, 3A4, inhibitor 1a2, 2d6, p-gp

28
Q

You should not give flecainide or propafenone in ?

A

structural heart disease

29
Q

What is pill in the pocket therapy?

A

Patient keeps a higher dose of their class 1c drug on hand for when afib happens

30
Q

Class III mechanism of antiarrhythmetics? PK special thing?

A

delay depolarization, watch QT interval

reverse use dependance (slower->bind more->slow more-> ruh roh)

31
Q

Drug drug interactions for class III antiarrhythmics

A

fluoroquinolone, macrolides, azoles, amphotericin
(basically think about how I’m going to be fighting the cardiologists one day)
also diuretics, conivaptan

32
Q

MOA for amidarone? Use? Distribution?

A

K, β, Na, and Ca block
ventricular arrhythmias, atrial fibrillation
half life is 53 days, extensive tissue distribution

33
Q

Contraindications and drug interactions for amiodarone

A

sinus node dysfunction, 2nd or 3rd degree av block

literally so many drug interactions (all the major cyp450)

34
Q

What are 4 systems to monitor for amiodarone?

A

pulmonar, hepatic, thyroid, ocular

35
Q

MOA of Dofetilide? uses? PK special?

A

K channel blocker. no effect on contractility or BP.
Use: afib or aflutter
reverse use dependence

36
Q

Where is dofetilide metabolized? Where is it eliminated?

A

hepatic (3a4)

urine (glomerular filtration) half life 10 hours

37
Q

There has been no increase in ___ or ___ in people taking dofetilide?

A

MI and CHF

38
Q

Dosing for dofetilide is based on ___ and ___

A

CrCl and QTc. cannot use if QTc is >440

39
Q

Adverse effects of dofetilide? what to monitor?

A

headache, dizziness, TdP (type of arr)

monitor: QTc electrolytes, renal function

40
Q

Where is dofetilide eliminated + metabolized?

A

renal elimination
CYP3a4-> increase concentrations. (watch verapamil, azaleas,)
watch for anything prolonging QT interval

41
Q

MOA of Sotalol (D vs L)? Uses?

A

D: Class III, L: Class III and β
use: atrial fibrillation/flutter, ventricular arr
reverse use dependance

42
Q

Where is sotalol eliminated? Where is it metabolized?

A

renal (t1/2 8-12 hours)

no metabolism

43
Q

Contraindications and AEs of Sotalol?

A

Brady cardia, QTc>450msec

AEs: Brady, bronchospasm, TdP

44
Q

Drug interactions of sotalol and what to monitor?

A

look for AV blocking and qt prolong. there is no hepatic metabolism
monitor: QTc, electrolytes, renal function

45
Q

How long should someone be monitored for based on sotalol?

A

hosptialized for 3 days. initiate 80mg and max dose 160mg

dosing based on afib vs VT

46
Q

MOA of Dronedarone and uses?

A

MOA is a bit ? but has properties of all 4 classes

Use: persistent AF or AFL. does not cardiovert

47
Q

Metabolism of Dronedarone? Elimination? distribution?

A

CYP3a4
t1/2 13-19 hours, fecal elimination
steady state 4-8 days

48
Q

Dronedarone is contraindicated in ___

A 
Class IV HF or class II or III HF with reduced decompensation
strong 3A4 inhibitors
49
Q

AEs of dronedarone

A

Gi effects, QT prolong, SCr (compete with creatine for clearance)
monitor LFTs!!!

50
Q

What drugs will cardiovert?

A

Class I: clecainide, dofetilide, propafenone

Class III: amiodarone

51
Q

What does the patient need to be after they are cardioverted?

A

anticoagulated for 4 weeks.

usually want to make sure they are anticoagulated beforehand as well

52
Q

There is a higher risk of stroke with afib is?

A

Left appendage, blood collect, thrown out during afib, stroke!

53
Q

What does CHA2DS2-VASc score look at? What is it?

A

Congestive, Hypertension, Age (>75), Diabetes, Stroke, Vascular disease, Age (65-74), Sex (female)
chance of having a stroke

54
Q

Guidelines for anticoagulation based on CHADVASC

A

2 in men, 3 in women

55
Q

______ is the preferred agent over warfarin for anticoagulation

A

DOAC (direct oral anticoagulant)

56
Q

What are premature ventricular complexes (PVCs)? How to treat?

A

ectopic impulses originating in ventricular tissue (increase in sympathetic NS activity)
common in MI
Treat: β block, CCB, antiarrhythmics, ablation

57
Q

What is a Torsades de Pointes?

A

Proarrhythmic situation that is a concern for antiarrhymtic drugs.
Polymorphic VI, prolonged QT interval

58
Q

What are drugs indicated for VT/VF?

A

absolute number 1 is β blocker (metoprolol, carvedilol)

amidarone, sotalol, lidocaine, mexiletine, procainamide

59
Q

Lidocaine mechanism?

A

Class 1B, inhibits influx of Na+ (up recovery period, suppress automaticity in His-purkingie)
act preferentially on ischemic tissue

60
Q

What are adverse effects of lidocaine?

A

CNS (dizziness, drowsiness, vision change)

Cardiac (Brady, hypotension, proarr)

61
Q

What is the oral equivalent of lidocaine?

A

mexiletine.

has the same adverse effects.

62
Q

What is MOA of procainamide? What is it used for?

A

Block NA channels in atria and ventricles.

used in refractory VT

FPC2 Exam 7 (4 decks)

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