Arrhythmias pt 2 Flashcards

tisdale pg 13 - 22 (Afib to goal 1/goal 2 drugs)

1
Q

how many ppl in the US have Afib?

A

around 6 million with prevalence increasing with advancing age
8% of people age 80-89

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how is atrial activity characterized in Afib?

A

chaotic and disorganized
no organize atrial depolarization
atrials are quivering rather than contracting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the ventricular rate associated with Afib?

A

120-180 bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how are P waves and rhythm characterized in Afib?

A

P waves are absent
Rhythm is irregularly irregular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

during Afib, how does blood fill the ventricles?

A

relies on changes of pressure
leads to 70-75% of normal blood filling LV/RV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is stage 1 of Afib?

A

presence of modifiable and nonmodifiable risk factors associated with Afib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is stage 2 of AF?

A

pre-AF
evidence of structural or electrical findings further predisposing a pt –> atrial enlargement, frequent atrial premature beats, atrial flutter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is stage 3 of AF?

A

diagnosed AF
can be 3A, 3B, 3C, or 3D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is stage 3A?

A

paroxysmal AF
most common
starts and stops suddenly and usually resolves within hours
definition - AF that is intermittent and terminates within 7 days of onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is stage 3B?

A

persistent AF
defintion - AF that is continuous and sustained for longer than 7 days and requires interventions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is stage 3C?

A

long-standing persistent AF
definition - AF that is continuous for more than 12 months in duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is stage 3D?

A

successful AF ablation
definition - freedom from AF after percutaneous or surgical intervention to eliminate AF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is stage 4?

A

permanent AF
1/3 of pt progress here
definition - no further attempts at rhythm control after discussion between the pt and clinical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

do antiarrhythmics work in stage 4?

A

no because the pt will never have normal sinus rhythm again

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the MOA of AF?

A

abnormal atrial automaticity
—- pulmonary vein automaticity —-
atrial re-entry (competing waves of depolarization, increase HR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the risk factors of AF?

A

advancing age
cig smoking
sedentary lifestyle
alcohol
obesity
HTN, DM, CAD, HF, CKD
obstructive sleep apnea
valvular HD
familial (genetic)
idiopathic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the etiologies of reversible Afib?

A

hyperthyroidism
Sepsis
thoracic surgery like CABG, lung resection, esophagectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are the symptoms of AF?

A

may be asymptomatic
palpitations
dizziness
fatigue
lightheadedness
SOB
hypotension
syncope
angine
exacerbation of HF symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

if a pt has AF, what are they more likely to develop?

A

stroke/systemic embolism (5x)
HF (3x)
dementia (2x)
mortality (2x)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

why is dementia associated with AF?

A

due to small emboli forming occlusions in the brain

21
Q

what are lifestyle and risk factor modifications of AF?

A

weight loss if overweight or obese (10%)
physical fitness (210 vigorous/week)
smoking cessation
eliminate alc consumption
BP control if HTN
optimal glucose and A1c management in DM

22
Q

what are goals of AF drug therapy?

A

prevent thrombosis and embolism leading to stroke/systemic embolism
slow ventricular response
convert AF to normal sinus rhythm
maintain sinus rhythm (reduce frequency of episodes)

23
Q

how can ventricular response be slowed in AF?

A

by inhibition conduction of atrial impulse to ventricles

24
Q

what are the components of CHADS-VASc score?

A

1pt - congestive HF, HTN, DM, Vascular disease (prior MI, PAD, or aortic plaque), age 65-74, female
2 pt - age 75+, stroke/TIA/TE history

25
when are oral anticoags recommended in AF pts?
CHADS-VASc score over 2 in men and over 3 in women
26
when are oral anticoags reasonable in AF pts?
CHADS-VASc score of 1 in men, 2 in women
27
what is the preferred anticoag treatment in most AF pts?
DOACs exceptions for warfarin
28
when is warfarin only preferred in AF?
in mechanical heart valves (target INR 2.5-3.5) AF associated with heart valve disease (mod-severe mitral valve stenosis, target INR 2-3)
29
when is warfarin or apixaban (eliquis) preferred?
end-stage CKD with CrCl under 15 mL/min hemodialysis
30
what is the antidote of dabigatran?
idarucizumab
31
what is the antidote of rivaroxaban, apixaban, and edoxaban?
andexanet alfa
32
when is rivaroxaban and apixaban CI?
in pts receiving drugs that are combined strong p-glycoprotein and CYP3A4 inducers like rifampin, phenytoin
33
when should normal apixaban dose be lowered?
if SeCr over 1.5 mg/dL over 80 yrs weight under 60 kg
34
how do p-glycoprotein substrate INHIBITORS affect DOACs?
increase plasma concentrations through inhibitors like KTZ, verapamil, amiodarone, dronedarone, clarithromycin
35
how do p-glycoprotein substrate INDUCERS affect DOACs?
reduce plasma concentrations by inducers such as phenytoin, rifampin, carbamazepine, St Johns wort
36
how should anti-coags be monitored in AF?
INR in warfarin therapy at weekly intervals during initiation, when stable monthly at least
37
what drugs are used for ventricular rate control in AF?
diltiazem verapamil BB digoxin amiodarone
38
what are the AE of diltiazem/verapamil?
hypotension HF exacerbation (dont use in HFrEF) bradycardia AV block constipation (oral V only)
39
what are important drug-drug interactions of diltiazem/verapamil?
inhibits CYP3A4 - cyclosporine, statins V also inhibits p-glycoprotein - digoxin/dofetilide
40
what BB are used in AF?
esmolol propranolol metoprolol tart and succ
41
when would BB exacerbate HF in AF pts?
if dose too high or dose increased aggressively
42
what is the MOA of diltiazem, verapamil, and BB in AF?
direct AV node inhibition
43
what is the MOA of digoxin in AF?
vagual stimulation Direct AV node inhibition
44
what is the MOA of amiodarone in AF?
BB and CCB
45
what is the AE of digoxin?
NV anorexia ventricular arrhythmias
46
what are important drug-drug interactions of digoxin?
amiodarone and verapamil inhibit dig elimination
47
what are the AE of amiodarone?
hypotension (IV only) bradycardia blue-grey skin discoloration photosensitivity corneal microdeposits pulmonary fibrosis hepatotoxicity hypothyroidism/hyperthyroidism
48
what are important drug-drug interactions of amiodarone?
inhibits CYP P450 - warfarin, statins inhibits p-glycoprotein - digoxin
49
why is amiodarone not commonly used?
due to long half life (2 months) and a lot of AE