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FPC2 Exam 7 > Arrhythmia > Flashcards

Arrhythmia Flashcards

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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
Uses, contraindications, AEs, things to monitor, and interactions for flecainide
``` Atrial fibrillation (aflutter, PSVT, ventricular arrhythmias) Contra: structural heart disease AE: visual, GI, pro arrhythmia monitor: PR + QRS + do stress test Interactions: 2d6 ```
26
MOA, use, PK and contra indications for propafenone
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
AEs, monitoring, and drug interactions for propafenone?
AE: dizziness, nausea, metallic taste, arrhythmias monitor: PR and QRS and stress interact: 2d6, 3A4, inhibitor 1a2, 2d6, p-gp
28
You should not give flecainide or propafenone in ?
structural heart disease
29
What is pill in the pocket therapy?
Patient keeps a higher dose of their class 1c drug on hand for when afib happens
30
Class III mechanism of antiarrhythmetics? PK special thing?
delay depolarization, watch QT interval | reverse use dependance (slower->bind more->slow more-> ruh roh)
31
Drug drug interactions for class III antiarrhythmics
fluoroquinolone, macrolides, azoles, amphotericin (basically think about how I'm going to be fighting the cardiologists one day) also diuretics, conivaptan
32
MOA for amidarone? Use? Distribution?
K, β, Na, and Ca block ventricular arrhythmias, atrial fibrillation half life is 53 days, extensive tissue distribution
33
Contraindications and drug interactions for amiodarone
sinus node dysfunction, 2nd or 3rd degree av block | literally so many drug interactions (all the major cyp450)
34
What are 4 systems to monitor for amiodarone?
pulmonar, hepatic, thyroid, ocular
35
MOA of Dofetilide? uses? PK special?
K channel blocker. no effect on contractility or BP. Use: afib or aflutter reverse use dependence
36
Where is dofetilide metabolized? Where is it eliminated?
hepatic (3a4) | urine (glomerular filtration) half life 10 hours
37
There has been no increase in ___ or ___ in people taking dofetilide?
MI and CHF
38
Dosing for dofetilide is based on ___ and ___
CrCl and QTc. cannot use if QTc is >440
39
Adverse effects of dofetilide? what to monitor?
headache, dizziness, TdP (type of arr) | monitor: QTc electrolytes, renal function
40
Where is dofetilide eliminated + metabolized?
renal elimination CYP3a4-> increase concentrations. (watch verapamil, azaleas,) watch for anything prolonging QT interval
41
MOA of Sotalol (D vs L)? Uses?
D: Class III, L: Class III and β use: atrial fibrillation/flutter, ventricular arr reverse use dependance
42
Where is sotalol eliminated? Where is it metabolized?
renal (t1/2 8-12 hours) | no metabolism
43
Contraindications and AEs of Sotalol?
Brady cardia, QTc>450msec | AEs: Brady, bronchospasm, TdP
44
Drug interactions of sotalol and what to monitor?
look for AV blocking and qt prolong. there is no hepatic metabolism monitor: QTc, electrolytes, renal function
45
How long should someone be monitored for based on sotalol?
hosptialized for 3 days. initiate 80mg and max dose 160mg | dosing based on afib vs VT
46
MOA of Dronedarone and uses?
MOA is a bit ? but has properties of all 4 classes | Use: persistent AF or AFL. does not cardiovert
47
Metabolism of Dronedarone? Elimination? distribution?
CYP3a4 t1/2 13-19 hours, fecal elimination steady state 4-8 days
48
Dronedarone is contraindicated in ___
``` Class IV HF or class II or III HF with reduced decompensation strong 3A4 inhibitors ```
49
AEs of dronedarone
Gi effects, QT prolong, SCr (compete with creatine for clearance) monitor LFTs!!!
50
What drugs will cardiovert?
Class I: clecainide, dofetilide, propafenone | Class III: amiodarone
51
What does the patient need to be after they are cardioverted?
anticoagulated for 4 weeks. | usually want to make sure they are anticoagulated beforehand as well
52
There is a higher risk of stroke with afib is?
Left appendage, blood collect, thrown out during afib, stroke!
53
What does CHA2DS2-VASc score look at? What is it?
Congestive, Hypertension, Age (>75), Diabetes, Stroke, Vascular disease, Age (65-74), Sex (female) chance of having a stroke
54
Guidelines for anticoagulation based on CHADVASC
2 in men, 3 in women
55
______ is the preferred agent over warfarin for anticoagulation
DOAC (direct oral anticoagulant)
56
What are premature ventricular complexes (PVCs)? How to treat?
ectopic impulses originating in ventricular tissue (increase in sympathetic NS activity) common in MI Treat: β block, CCB, antiarrhythmics, ablation
57
What is a Torsades de Pointes?
Proarrhythmic situation that is a concern for antiarrhymtic drugs. Polymorphic VI, prolonged QT interval
58
What are drugs indicated for VT/VF?
absolute number 1 is β blocker (metoprolol, carvedilol) | amidarone, sotalol, lidocaine, mexiletine, procainamide
59
Lidocaine mechanism?
Class 1B, inhibits influx of Na+ (up recovery period, suppress automaticity in His-purkingie) act preferentially on ischemic tissue
60
What are adverse effects of lidocaine?
CNS (dizziness, drowsiness, vision change) | Cardiac (Brady, hypotension, proarr)
61
What is the oral equivalent of lidocaine?
mexiletine. | has the same adverse effects.
62
What is MOA of procainamide? What is it used for?
Block NA channels in atria and ventricles. | used in refractory VT

FPC2 Exam 7 (4 decks)

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