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A-Fib, Screenshot 2025-04-04 at 10.36.16 PM slide 18, Screenshot 2025-04…
A-Fib
3. Lecture 3 - Arrhythmia Management in AF
rate vs rhythm - evidence
AFFIRM trial
rhythm control offers no survival benefit over rate control. long term AAD dont completely suppress AF, stroke prevention (DOACs) also needed
EAST-AFNET 4
rhythm control beneficial if initiated early (AF onset <1yr)
when to consider rhythm control
younger pts
AF-induced cardiomyopathy
recent onset of AF (<1 year)
poor sx control on rate alone
rhythm control
anti arrhythmic drug classes
(ventricular arrhythmia need higher dosing)
class 1C: flecainide, propafenone
block Na channels
in SA node c/I: pts with hx of MI with non-normal EF and obstructive CAD. may prolong QTc
Class III: amiodarone, dronedarone, sotalol
blocks K channels to prolong refractory period. requires monitoring at baseline, then q3-6 months c/I: CYP3A4 drugs
goal: maintain sinus rhythm
rate control
goal: HR <100 and reducing risk of cardiomyopathy
medications (prolong refractory period
and slow AV node conduction)
non-DHP CCB (first line, avoid in HF with EF)
inhibit Ca influx via L-type channels, and results in negative inotropic, chronotropic, and dromotropic effects
Digoxin (second line, narrow TI, needs renal dose adjustment, can also lead to toxicity)
positive inotropic effects, blocks Na/K ATPase in the myocardium. negative chronotropic and dromotropic effects
beta blockers (first line)
bisoprolol preferred (B1 specific, heart specific)
special approaches
pill-in-pocket
flecainide or propafenone + BB or NDHP-CCB 30 minutes prior
successful if normal sinus rhythm within 6 hours of taking meds
indications: infrequent AF episodes, non-severe sx
electrolyte replacement
K, Mg in AF prevention
initial assessment
hemodynamic stability
determine if pt is in acute AF and whether they are hemodynamically stable or not, then select rate vs rhythm control
rate vs rhythm control strategy
rate control is initiated first for
persistent
AF, but rhythm control is ignited first at onset of AF
non-pharm management
cardioversion (rhythm control tx)
electrical vs pharm
anticoagulation: 2,3,4 rule (shocking the heart back to normal, but
pt needs to be on OAC before the cardioversion
for at least 3 weeks)
potentially causes clotting of pre-existing clots
catheter ablation
minimal invasive procedure where catheter tips remove parts of heart tissue
first line in some 2023 guidelines for:
symptomatic paroxysmal AF where rhythm control is the target
AAD are ineffective
HFrEF
atrial flutter
may require OAC for 2-3 months after procedure or AAD
1. Lecture 1 - Intro to Atrial Fibrillation
diagnosis
ECG findings
irregular rhythm with
absence of P wave and narrow QRS complex
Holter monitoring, loop recorders
Holter: > 24hr continuous ECG monitoring
loop recorders: for rare sx, records up to 3 years, minimally invasive surgery
pulse-based screening
for pts 65y+, it is recommended to screen for AF by manually checking pulse for any irregularities at refills/follow ups
smartwatch data
wearing Apple Watch can tell pts if they have AF
investigations
trans thoracic echo (TTE)
recommended in all pts to identify heart size, dyfxn, heart disease
trans esophageal echo (TEE)
determine identifies heart clot
chest Xray, blood work
signs of heart failure; CBC, coagulation profile, electrolytes, renal/thyroid/liver function tests might determine underlying cause of A-fib
clinical presentation
signs and sx
low energy, fatigue, SOB, fast pulse, pre syncope or syncope, diaphoretic, asymptomatic, palpitations, low exercise tolerance
common presentations
recovering after cardiac surgery, routine follow up with family MD and it gets caught, presents with stroke, presents to ED with racing heart and feeling unwell, presents to pharmacy to check BP
classifications of AF
structural
valvular
AF in the presence of any mechanical heart valve
non-valvular
AF without mechanical heart valve
TTE determines structural classification of AF
pathophysiologic
primary
no precipitating cause
secondary
caused by reversible precipitant (sepsis, surgery)
clinical pattern
persistent
lasting >7 days, stops within a year
permanent
continuous AF, decided to not pursue rhythm restoration
paroxysmal
continuous AF lasting >30 secs but stops within 7 days
definition and overview
pathophysiology
SA node is the heart pacemaker, AV node delays impulse so that A-fib doesn't happen. when a
trigger occurs, rapid atrial firing results in disorganized contractions
, and the heart relies on AV node to filter some of that. the ventricles fill passively and the "atrial kick" aids in filling the ventricles with even more blood. this can then cause the heart to develop fibrosis
risk factors
modifiable
obesity, alcohol, smoking, DM, CKD, HTN, thyroid disease, sleep apnea, CAD, COPD, heart disease
non-modifiable
age, male, Fox, increased height and birth weight
epidemiology
most common cardiac arrhythmia, increases with age
drug-induced AF
stimulants, alcohol, anti-cancer therapy, bisphosphonates
what is AF?
rapid heart beat above the ventricles which causes irregular
atrial
activation
life cycle of AF
Stage 1: at risk for AF, Stage 2: pre-AF, Stage 3: AF, Stage 4: permanent AF
consequences of AF
irregular ventricular response
irregular atria impulses sometimes reach the AV node and then the ventricles and cause them to contract at an irregular rhythm (rate or 120-180 bpm)
loss of atrial kick
atrial kick is when the ventricles fill with extra blood. in Afib, the atria are contracting irregularly, which impairs the amount of blood filling the ventricles from the atria (atrial kick)
thrombosis risk
disorganized atrial activity from A-fib and the atria not contracting properly leads to the blood being still; this can cause a clot in the left aftria
2. Lecture 2 - Stroke Prevention in AF
special populations and exceptions
frail elderly
CKD, obesity, CAD with stent, cancer, liver disease
when to choose warfarin over DOACs
mechanical valve replacement, moderate-severe mitral stenosis, antiphospholipid syndrome, left ventricular thrombus, frail elderly pts
antithrombotic therapy
options
warfarin (primary and secondary stroke prevention) INR of 2-3. better than ASA + clopidogrel
DAPT (ASA + clopidogrel) (used for lower risk, not really seen a lot now) major bleeding risk
DOACs: dabigatran, rivaroxaban, apixaban, edoxaban
aspirin (not really seen)
landmark trials
ROCKET-AF (riva)
similar to warfarin in terms of stroke prevention, and similar bleeding risk (but once daily dosing, which some pts like)
ARISTOTLE (apix)
dosed BID; superior to warfarin for stroke AND lower rates of GI bleeding
RE-LY (dabigatran)
was superior to warfarin but had high GI bleed rate
ENGAGE-AF TIMI 48 (edox)
same as warfarin for stroke; but lower rates of bleeding
takeaways
all of the DOACs are better than warfarin for intracranial hemorrhage prevention; dabigatran and apixaban are better for stroke than warfarin; apixaban is best for preventing bleeding
bleeding risk assessment
HAS-BLED score
HTN (systole >160), Abnormal renal fxn or liver, Stroke hx, Bleeding, Labile INR (unstable), Elderly 65+, Drugs (antiplatelet, NSAIDs, steroids), alcohol or abuse
estimates 1 year risk of bleeding for pts on an OAC (score of 3+ = increased risk)
stroke risk assessment
CHA2DS2-VASc
(identifies pts on lower end of stroke risk)
CHF (1), HTN (1), Age75+ (2), Diabetes (1), prior Stroke or TIA (2), Vascular disease (1), Age >65 but <75 (1), Sex criteria female (1). total 9 points
score greater than 2% = tx with anticoagulants
CHADS-65 (not a risk estimate)
age 65+, HTN, diabetes, prior stroke or TIA, heart failure --> start OAC if ANY of these are present
CHADS2
CHF (1), HTN (1), Age75+ (1), Diabetes (1), prior Stroke or TIA (2). total of 6 points
initiation of OACs
SDM tools
ENHANCE-AF
if AF is documented by ECG or if certainty of AF is high CHA2DS2 score of 2 in men and 3 in women
stroke risk in AF
why AF leads to stroke
ineffective atrial contraction leads to still blood in the ventricles; a clot may form in the heart and travel to the brain, causing a stroke
white vs red clots
white
arteries, composed of platelets and strands of fibrin; results in MI/stroke; tx with antiplatelets
red
veins; composed of RBCs in fibrin matrix; leads to DVT,
stroke from AF
; tx with anticoagulant
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