ATRIAL FIBRILATION
Overview:
Etiology: 1. Atrial dilation, DM, HTN, RH, CAD/MI, Mitral stenosis, myocarditis, S & S : 2. BP in general is stable (unless HTN, MI, etc.).
3. Usually no LOC or syncope (unless some other problem occurred). 4. Pt may c/o anginal pains due to tachycardia DX: Treatment :
1. Atrial rate (>300/min) with slower ventricular rate (<100 - >180).
2. Multiple areas of reentry or multiple atrial ectopic foci producing
400-700 impulses/min, not capable to capture atria as a whole,
are in charge of atrial activity. This gives the characteristic irregular
rate and "fibrillations" on EKG.
age, WPW, CHF. This A.fib is 2ry to structural damage (coronary,
valve, myocardium)
2. Hyperthyroidism, Electrolyte abnormality, PE, stress, coffee, ETOH,
COPD, lung CA, infection. This A.fib is so called "
no underlying heart disease.
3. For more details see "Framingham Study"
1. Tachycardia is common. Pt may c/o palpitations or be asymptomatic.
1.
organized atrial contraction – atrial "kick"), variable heart rate. QRS
complex is generally narrow (<0.12) unless there is underlying BBB in
which case it may be difficult to d.d. from WCT or VT
2. On rare instances it may be difficult to d.d. A.fib from SVT. In these
cases a diagnostic Adenosin 6mg IVP can be given to slow down the
HR and elucidate underlying fibrillation or "brake" the SVT (AVRT or AVNRT)
needed in ER setting. Yet this kind of rhythm response may indicate conduction defect
and pt should be admitted to monitored setting
2.
If ventricular response is > 100/min i.e. "A.Fib with rapid ventricular response" treatment
to slow the rate down is indicated. This, if pt
hemodinamically is stable and symptom free
(no chest pain, no MI, no dyspnea), is achieved in ER with administration of Ca Channel
Blocker (Diltiazem 10-25 mg IV, Verapamil 5 mg) or - blocker (Esmolol infusion at 8-16
mg/min, Metoprolol 5mg IVP). Digoxin 0.5 mg can be added later on followed by 0.25 mg
q6h x 2. Esmolol is short acting – 9 min 1/2 life and can be used in pt's with reactive airway
disease or borderline BP.
3. If pt on the other hand is hemodinamically unstable and c/o chest pain or SOB,
and signs of ischemia pt must be Cardioverted with synchronized mode @ 100 J.
If this is unsuccessful one can cardioversion to 200 J, 300 J, or even 360 J, or give
IV Procainamide and re-attempt with 100 J or higher.
4. If we have pt with documented
new onset A.fib i.e. < 48 hours, one can attempt 6. Pt who has 7. Pt with " 8. Pt with
chemical cardioversion to NSR. Pt's HR must be first slowed down with Ca Channel
Blockers or - Blockers. Class Ia agents such as Procainamide ( or Quinidine ) is then
used for chemical cardioversion once the HR is slowed down. Procainamide is given IV
in order to chemically cardiovert the pt 30-50mg/min IV to max of 17mg/kg. If this is
not successful then synchronized cardioversion is used within 48hrs.
5. If A. Fib is > 48hr., there is a chance of atrial thrombus formation and chance of
thromboembolism and pt should be anticoagulated for 3-4 wk. and Echo should be
done to document the absence of clot and the size of atrium.
narrow or wide complex tachycardia and pose a special problem. These pts should never
be treated with CCB, beta Blocker or Dig i.e. any medication that blocks AV node,since
inhibiting conduction via AV increases conduction through accessory pathway resulting in
1:1 conduction of disorganized atrial impulses and provoking V.fib. These pts are best
treated with
Cardioversion if hemodinamically unstable or very rapid ventricular
response, or IV Procainamide 10-15 mg/kg @ 50 mg/min
if pt is stable and slow-moderate
ventricular response. The disadvantage to Procainamide use is that it can not be
administered rapidly thus delaying therapeutic goal. Like any other WCT (Wide Complex
Tachycardia) of uncertain etiology also A. fib with WPW can be treated with Lidocaine.
While Lidocane is not harmful, it typically will have no effect if WCT is due to WPW with
conduction through accessory pathway
A.fib (C.P., SOB, LOC/Syncope) require monitored bed. .