Atrial fibrillartion - Covert Flashcards
Dr. Covert EXAM V
Pathophysiology of Afib
-signals from the SA node move in a disorganized way in the atria -> instead of one main contraction there are multiple mini contractions
- seen as small twitching bumps on the ECG and the distance between the QRS is different
instead of being released fast and allowing synchronized (pump) depolarization and contraction of the atrium followed by the ventricles
Why are anticoagulants used for Afib?
-in Afib the blood flow is not as steady (Virchow Triad) -> increasing the risk of forming blood clots
-the blood clots may move to the brain and cause a stroke after a stable contraction of the heart
Causes of Afib
-Heart failure: heart doesn’t pump well, so it is prone to losing its normal rhythm -> arrhythmia; Afib (tachycardia) can also cause Heart failure
-coronary artery disease: due to ischemia (MI) electrical impulses don’t go where they should
-valvular heart disease: valves don’t close as they are supposed to -> impairs the blood flow of the heart
-HTN
-Hyperthyroidism: tachycardia
-sleep apnea
-stimulants/smoking
Afib Signs and symptoms
FYI
-Tachycardia
-Syncope, pass out (heart beats so quick that it doesn’t pump out enough blood)
-Palpitations
-SOB
How are Ischemic and Cardioembolic strokes different?
-Ischemic: blood vessels of the brain are blocked by cholesterol plaque -> platelets will build up there -> Antiplatelets are used to prevent them from sticking + statins
-cardioembolic: blood clot in the atria -> shoots up to the brain; the problem lays on the heart that allows blood clots to form -> thin the blood to prevent blood clots from forming in the atria
What are the two ways that need to be managed in Afib?
-Stagnation of Blood -> causing a blood clot in the atria -> Cardioembolic stroke -> treat with anticoagulants
-rapid ventricular response (RVR), polarization of the ventricles after “every” twitch (tachycardia) -> the heart can’t contract on that pace for long -> cardiac ischemia and heart failure ->
Types of Afib based on Valvular disease
-Valvular Afib:
*moderate to severe mitral or aortic valve stenosis (valve narrows -> less blood goes through -> blood backs up to the atria)
*mechanical heart valve (will need anticoagulant forever)
-> both increase the risk of a blood clot in the heart -> Anticoagulant
-Non-valvular Afib: everyone else
In patients with RVR, what is the goal of treatment?
-Rate control (acute or chronically)
or
-Rhythm control (acute or chronically)
Which way of controlling Afib is preferred?
-Rhythm Control
-outcomes are better when the rhythm is fixed early
-in patients with a new onset of Afib (< 1 year)
-favored in Afib and HFrEF
What are the Rate-controlling drugs
-Beta-Blockers
-Non-DHP-CCBs: Diltiazem, Verapamil
-Amiodarone
-Digoxin
-Goal HR in non HF-patients = <110 bpm (we let the HR be a little higher, bc the side effects of low HR are significant)
What heart rate should a heart failure have?
-lower
-in heart failure we want the heart to pump slowly and as much blood as possible
Factors that favor Rhythm control
-younger age
-shorter history of Afib (new onset)
-more symptomatic
-HR is difficult to control (fe they have tried Diltiazem and they are still tachycardia)
-more LV dysfunction
-AV regurgitation
MOA of BB
-ß1 antagonist -> preventing vasoconstriction -> Vasodilation
-PO,IV
-Caution in asthma and COPD patients -> pick cardio-selective BB
(for Afib alone any BB will work)
-Bisoprolol may cause fatigue
What are the ß-selective BBs?
BEAM
-Bisoprolol (Zebeta)
-Esmolol (Brevibloc)
-Atenolol (Tenormin)
-Metoprolol succiante (Toprolol XL)
MOA of Non-DHP-CCBs
-block the calcium channels to slow conduction to the AV node, slows HR, also negative inotropic effects (decreases the force of contraction)
-Diltiazem (PO, IV, continuous infusion)
-Dont use in HF patients -> the heart is not pumping strong enough -> the negative ionotropic effect is making the heart even weaker -> can be fetal
MOA of Amiodarone
-Class III antiarrhythmic
-Brand name: Pacerone
-blocks K+ channel
-can be used for Rate and Ryhtm control
-PO, CI
ADR of Amiodarone
-corneal deposits, blue-tinged skin
-somewhat QTc prolongation,
-one of the Fab5
-cause hepatotoxicity (hepatic clearance)
-pulmonary fibrosis
-hypothyroidism
-ADR is seen only after long-term use, so used in older patients who can’t tolerate other meds (do not live long enough to experience the side effects)
PK cahracteristic of Amiodarone
-long half-life
-huge Vdoluem of distribution -> gets everywhere, affecting multiple tissues (liver, lungs, thyroid)
MOA of Digoxin
-Brand name: Digitek
-activates Na+ channels and ATPase -> positive inotropic effect
-makes the heart able to contract more completely
bradycardia CAUTION
-last line drug for HF
-works great in patients with fast HR but soft BP -> only lowering the HR and not the BP
ADR:
renally cleared
hyperkalemia,
nystagmus (uncontrolled eye movements)
coma/death
What is the therapeutic concentration of Digoxin?
narrow therapeutic index
HFrEF: 0.5 - 0.9
Afib: 1 - 1.5
Factors determining hemodynamic stability
Rate control
Ability to perfuse their organs well
-is the BP appropriate?
-are they feeling light-headed
-is there an AKI?
Decision: patient has a fast HR (Afib), but is hemodynamically stable
Rate control
-Pharmacologic cardioversion
Does the patient have decompensated HF? (HF due to structural change in the heart)
Yes: IV Amiodarone
No:
BB or Non-DHP-CCBs
Digoxin
Amiodarone
if
What to add if there is an AV nodal block?
Rate control
Magnesium
Decision: patient has a fast HR (Afib), but is not hemodynamically stable
Rate control
Direct-current cardioversion (DCCV) - shock to reset the rhythm
-administering an electrical impulse at a specific time
-the shock is synchronized with the QRS complex to prevent R-onT phenomena -> which could cause cardiac arrest
What are the long-term treatment options?
with HF < 40%: BB or Digoxin
LVEF > 40%: BB or NDCC -> or Digoxin
When is electrical cardioversion preferred?
when hemodynamically unstable, or antiarrhythmics fail
What are the acute Ryhtm Control options?
-Electrical Cardioversion (more effective than pharmacologic alone): when hemodynamically unstable, or antiarrhythmics fail
-Pharmacologic Cardioversion:
Amiodarone
Propafenone (Pill-in-the pocket)
Flecainide (Pill-in-the pocket)
Drug class of Flecainide and Propafenone
-Class Ic (remember Fries Please)
-ats on the Na+ channel
Reminder:
class Ia: Disopyramide, Quinidine, Procainamide (Double, Quarter, Pounder)
class 1b: Lidocaine, Mexiletine (Lettuce, Mayo
class Ic: Flecainide, Propafenone (Fries, Please)
Route/ADR for Flecainide and Propafenone
Acute Rhythm control
!!! Brand name: Flecainide (Tambocor), Propafenone (Rhythmol)
Route: only PO
ADR:
-QTc prolongation
contraindicated in HFrEF patients and MI in the last 2 years
-> fetal arrhythmias, worsening of HFrEF
Which treatment is required before starting Cardioversion?
Acute Rhythm control
3 weeks Anticoagulation -> Cardioversion -> 4 weeks anticoagulation
if someone is acutely unstable and we can’t wait 3 weeks: imaging to see if there is a thrombus in the atria
-if we fix the rhythm of the heart we cause normal contraction of the atrium and ventricles, if there is a clot it will shoot up to the brain -> STROKE
Fill in the pocket
Acute Rhythm control
-patients can cardiovert themselves outpatient when they feel arrhythmia
-they have to be on anticoagulants!
-no HF, no risk for coronary artery disease, no MI
When to use Flecainide and Propafenone?
Acute Rhythm control
-in patients with normal LV function, no MI
-Afib is occurring outpatient
-normal LV function and inpatient:
IV Amiodarone
IV Ibutilide
Rhythm control in patients with HFref <40%
Acute Rhythm control
IV Amiodarone
Chronic Rhythm control with normal LVEF
Class III
-Dofetilide
-Dronedarone
Class Ic
-Flecainide
-Propafenone
Class III
-Amiodarone
Class III
-Solatolol
Chronic Rhythm control with low LVEF, heart disease, or MI
-Amiodarone or Dofetilide
-NYHA III/IV or recent decompensated HF: Dronedarone causes harm and increases death
Which patient population should be treated with Amiodarone?
-patients with HFrEF
-structural heart disease
-don’t use Dronedarone in these patients!!!
If Amiodarone doesn’t work in patients with HF, which drug should be used?
Dofetilide (Tikosyn)
Route: PO
Elimination: renal
-has to be started inpatient bc it has a high risk of QTc prolongation (monitored with ECG)
-in patients with HFreF and structural heart disease
-DDI:
Thiazides
Verapamil
Class I or III anti-arrhythmic (never add two or more class III -> additive risk for QTc)
Bactrim: increases exposure to Dofetilidine
Cimetidine: increases exposure to Dofetilidine
Third line
Role of Sotalol in Afib
-Chronic Rhythm Control in Afib
-3rd line
-renal elimination
-has to be initiated inpatient bc of higher risk of QTc prolongation
What lab to check on before giving anti-arrhythmias?
Electrolytes
-low electrolytes can cause arrhythmias
How to treat patients with Afib where antiarrhythmic drugs are ineffective?
Catheter Ablation
ChadsVasc Score
Cardioembolic stroke
Congestive Heart Failure (1)
HTN (1)
Age >/= 75 y (1)
Diabetes (1)
Stroke or PE (2)
Vascular disease
Age 65-74 (1)
Sex - female (1)
Chads Vasc in men and women
Cardioembolic stroke
for men:
CHADS2VASc >/= 2: Anticoagulation is
recommended
for women:
CHADS2VASc >/= 3: Anticoagulation is
recommended
Which Anticoagulant is preferred for non-valvular Afib (NVAF)?
DOACS: dabigatran, apixaban, rivaroxaban, edoxaban
Which Anticoagulant is preferred for valvular Afib (MV stenosis) or mechanical valve patients?
Warfarin
Apixaban in Cardioembolic stroke
-5 mg PO BID
-If 2/3 risk factors are present, reduce dose to 2.5 mg po BID
*Age > 80 yo
*Weight < 60 kg
*SCr > 1.5 mg/dL
Rivaroxaban in Cardioembolic stroke
-20 mg po daily
*If CrCl 15-50 mL/min, reduce to 15 mg po daily
*ifCrCl < 15, contraindicated
Warfarin in Cardioembolic stroke
-2.5-5 mg po daily
-New start warfarin, bridge with enoxaparin
-Generally, do not bridge for INR excursions
(BRIDGE trial)
INR Goals for Warfarin in Cardioembolic stroke
-Mech MV: INR goal 2.5-3.5
-Mech AV: INR goal 2-3
-MV stenosis: INR goal 2-3
