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Atrial Fibrillation
most common sustained cardiac arrhythmia
irregular heartbeat where atria fail to contract rhythmically, causing blood pooling and clot formation
AFib symptoms
racing heart
fluttering
palpitations
SOB
lightheadedness
sometimes asymptomatich
normal heart rate
determined by
normal SA node pacing
bradycardia
tachycardia
determined by
SA node
normal SA node pacing
60 - 100 bpm
bradycardia
< 60 bpm
tachycardia
> 100 bpm
bradycardia
supraventricular arrhythmias
ventricular arrhythmias
bradycardia
atrioventricular blocks
supraventricular arrhythmias
atrial flutter
afib
supraventricular tachycardia
ventricular arrhythmias
vfib
torsades de pointes
asystole
AV blocks: sx increase w/
severity
1st degree AV block
impulse conducts slowed (partial block) at AV node for fixed interbal
asymptomatic
causes
AV nodal block (BB, non-DHP CCB, digoxin)
PNS stimulation
EKG
PR > 0.2 secs
2nd degree AV block
Mobitz Type 1
Mobitz type 2
Mobitz Type 1
conduction slows at AV node, then QRS fails to follow
decreased CO
asymptomatic
causes: AV node blockers, PNS stimulation
Mobitz type 2
block is below AV node; atrial rate regular
symptomatic of bradycardia
unpredictable
3rd degree heart block
complete heart block
AV dissociation
no P waves
symptomatic due to bradycardia
need permanent pacemaker to control ventricular rate
Paroxysmal Supraventricular Tachycardia (PSVT)
sudden, rapid firing of SVT automaticity focus
150 - 250 bpm
PSVT
nonpharm
pharm
radiofrequency ablation
nonpharm
mild to mod = vagal techniques (massage, valsalva, ice water immersion
severe (syncope, angina, HF) = direct current cardioversion (DCC)
pharm
increase vagal tone = digoxin
decrease conduction thru Ca tissue = adenosine, BB, non-DHP CCB
depress conduction thru Na tissue = Quinidine, Procainamide,
radiofrequency ablation
destroy accessory pathway
replaces need for anti-arrhythmic therapy
causes of AF and Aflutter
re-entry
AF = multiple reentrant loops
Aflutter = single dominant reentrant wavelet
structural heart disease
MI, valvular HD, congenital abnormalities
high adrenergic states
thyrotoxicosis, surgery, alcohol, withdrawal, sepsis
other pathways
HTN, CAD, obesity, etc
EKG finding Afib
many atrial foci firing at rapid rates (350 - 450 bpm)
irregularly irregular w/ no p waves
EKG finding Aflutter
atrial impulses faster than SA node impulses (220 - 350 bpm)
single ectopic focus
sawtooth
regular rhythm
occur less frequently than Afib
presentation/symtpoms Afib and Aflutter
fatigue, palpitations, SOB, hypotension, syncope, chest pain
AF w/ RVR (HR > 100 bpm)
can be asymptomatic
AF Classification
paroxysmal
terminates spontaneously or w/ intervention within 7 days of onset
persistent
continuous sustained AF > 7 days
longstanding persistent
continuous AF sustained > 12 months
permanent
no attempts to restore/maintain sinus rhythm
nonvalvular AF
AF in absence of rheumatic mitral stenosis, mechanical heart valve, mitral valve repair
thrombus clot forms in atrium due to
highest risk for clot formation is
most common thromboembolic event is
blood pooling
left atrial appendage (LAA)
ischemic stroke
CHA2DS2-VASc Score
purpose
components (points)
maximum points
interpretation
purpose
calculate stroke risk and determine need for anticoagulation in AF pts
components (points)
1 point
congestive heart failure/LV dysfunction
HTN
diabetes
vascular disease (prev MI, PAD, aortic plaque
age 65 - 74 years old
female
2 points
age ≥ 75 years old
stroke/TIA/thromboembolism
maximum points
9 points
interpretation
higher score = higher stroke risk w/o anticoagulation
HAS-BLED Bleeding Risk Assessment
purpose
components (points)
interpretation
purpose
identify pts at high risk of bleeding on anticoagulation
components (points)
HTN = 1 point
abnormal renal/liver function = 1 or 2 points
stroke = 1 point
labile INR = 1 point
elderly (≥ 65) = 1 point
drugs or alcohol = 1 or 2 points
interpretation
score ≥ 3 = high bleeding risk
CHAD2DS2-VASc score = 0 (men) or 1 (women)
no anticoagulation needed
CHAD2DS2-VASc score = 1 (men) or 2 (women)
anticoagulation therapy may be considered
CHAD2DS2-VASc score = ≥ 2 (men) or ≥ 3 (women)
oral anticoagulation recommended
warfarin (target INR = 2 - 3) or DOACs
DOACs preferred except in cases of mitral stenosis or mechanical heart valves
Warfarin (Coumadin)
1 - 10 mg daily
no P-gp substrate
dose adjustment based on INR
DOACs
preferred over warfarin
superior or non-inferior efficacy and safety
bridging not required unless clot confirmed
DOACs: Dabigatran (Pradaxa)
class
dosing
renal adjusment
interactions
class
DTI
dosing
AF and PE dosing: 150 mg PO BID
renal adjustment
CrCl 15 - 30 ml/min → 75 mg PO BID
interactions
P-gp substrate
reduce dose/avoid w/ 3A4/P-gp inhibitors and inducers
DOACs: Rivaroxaban (Xarelto)
class
dosing
renal adjustment
interactions
class
factor Xa
dosing
AF = 20 mg Po daily with food
VTE = 15 mg PO BID x 3 weeks, then 20 mg PO daily
renal adjustment
CrCl15 - 30 ml/min → 15 mg PO daily w/ food
interactions → avoid inhibitors and inducers
CYP3A4/5
P-gp substrate
DOACs: Apixaban (Eliquis)
class
dosing
renal adjustment
interactions
class
factor Xa
dosing
AF = 5 mg POBID
VTE = 10 mg PO BID x 1 week, then 5 mg PO BID
renal adjustment
2.5 mg PO BID if 2 of 3 criteria met:
over 80 years old
< 60 kg
Scr ≥ 1.5 mg/dL
interactions
CYP3A4, p-gp → avoid inducers and inhibitors
DOACs: Edoxaban (Sayvaysa)
class
dosing
interactions
class
factor Xa
dosing
AF and VTE = 60 mg PO daily
interactions
avoid Rifampin (inducer)
rate control strategy
goals
symptom control, increase ventricular filling time
100 110 bpm at rest
meds
BBs
non-DHP CCBs
digoxin
BBs
1st line
preferred for
HF w/ low EF: carvidolol, metoprolol, bisoprolol
CAD
non-DHP CCBs
diltiazem, verapamil
if BB use is limited
digoxin (Lanoxin)
indication
MOA
effect
dosing
PK
therapeutic index
s/sx of toxicity
indication
systolic HF,
hypotension
sedentary pts
MOA
bind to Na-K-ATPase
positive inotrope
negative chronotrope
effect
slow HR at rest only
dosing
0.125 - 0.5 mg daily
PK
renally excreted
narrow therapeutic index
HF = 0.5 - 0.8 ng/ml
arrhythmia = < 1.2 ng/ml
toxicity risk = > 2ng/ml
s/sx of toxicity
anorexia
n/v/d
yellow halos
HAs
PVC
AV block
vtach, vfib
acute managment of AF w/ RVR: hemodynamically unstable
direct current cardioversion
acute managment of AF w/ RVR: hemodynamically stable
meds based on underlying conditions
no decompensated HF → IV non-DHP CCBs, IV BB, IV digoxin, IV amiodarone
decompensated HF → IV amiodarone, digoxin
ryhthm control
meds
catheter ablation
surgery
rhythm control strategy
goal
cardioversion
goal
cardioversion
restore and maintain sinus rythm
direct current cardioversion
pharm cardioversion
post cardioversion
direct current cardioversion (DCCV)
pharm cardioversion
post cardioversion
electrical shock - efficacy 80 - 90%
meds - efficacy 40 - 60%
require AADs to maintain NSR
DCCV
emergent indication
elective indication
emergent
hemodynamically unstable
elective
rate control ineffective
younger pts (< 60)
poor exercise
anticoagulation for cardioversion
risk
visual
TE seen
post cardioversion
risk
TE risk if AF duration > 2 days (or unknown)
visual
Transeoesophageal echo (TEE) > TTE
TE seen
therapeutic anticoagulation needed for at least 3 weeks before cardioversion
post cardioversion
anticoagulant for at least 4 weeks after cardioversion
AADs for Pharmacological Cardioversion: drugs (proven efficacy)
amiodarone (Cardarone, Pacerone)
dofetilide (Tikosyn)
ibutilide (IV only)
flecainide
propafenone
AADs: Normal LV function, no prior MI or structural HD
amiodarone, ibutilide
procainamide
AADs: prior MI or structural HD
-amiodarone
dofetilide
AADs for Maintenance of NSR
amiodarone, dronedarone, dofetilide, Sotalol, flecainide, propafenone
depends on underlyinh structural HD, renal function, toxicities
Amiodarone (Cordarone, Pacerone)
MOA
PK
efficacy
toxicity
DDIs
MOA
class 3, activity from all 4 classes
prolong QT, refractoriness, slow HR, AV node conduction, intracardiac conduction
PK
long t ½ = 60 days
efficacy
most effective
toxicity
most toxic → pulmonary fibrosis, thyroid dysfunction, blue-gray, etc
DDIs
extensive die to CYP inhibition and P-gp inhibition
Dronedarone (Multaq)
MOA
PK
ADR
BBW
MOA
class 3, activity from all 4 classes
PK
less lipophilic
shorter t ½
ADR
not as much as amiodarone
BBW
increased risk of death w/ decompensated HF or permanent HF
Sotalol (Betapace AF)
MOA
use
precautions
monitoring
CI
MOA
class 3, non-selective BB
use
not for HTN or rate control
precautions
avoid in systolic HF
monitoring
renal function, QT porlongation
CI
QT interval > 450 msec
dofetilide (Tikoysn)
MOA
risk
intitiation
use
monitoring
DDIs
MOA
class 3
risk
torsades de pointes
intitiation
prev rquired hospitalization for 1st 5 doses
use
cardioversion
maintanence of NSR
monitoring
renal function
QT interval
drug interactions
DDIs
QT-prolonging drugs
Flecainide (Tambocor) and Propafenone (Ryhtmol)
MOA
CI
clinical pearl
MOA
class 1 agents
CI
structural heart disease
clinical pearl
pill in pocket
catheter ablation
pulmonary vein isolation
AV node ablation
indications
pulmonary vein isolation
can be curative for AF symptoms
AV node ablation
leads to permanent pacemaker
indications
AAD ineffective, CI, intolerant
1st line in younger pts