ACUTE ATRIAL FIBRILLATION

Introduction
Incredibly convoluted topic; using primarily the CCS & AHA/ACC
Guidelines
Acute atrial fbrillation: rapid ventricular response due to atrial
fbrillation that causes symptoms requiring intervention
o See defnitions above no! these" they dictate
management
#$% o& all hospital cardiac admissions
Complicates about #'($% o& all )* visits
Alwas t!in" about t!e cause o# t!e AF
o I& the A+ is due to a reversible cause ,i-e-" no ongoing
catecholamine stress" underlying cardiac process. it will
s$ontaneousl revert %&' o# t!e ti(e wit!in )* !ours
+e(odna(ics: A+ reduces cardiac output by ($'/$%" regardless o&
underlying ventricular rate ,maybe atrial ic loss.
Stro"e: (0% o& people !ill have atrial clot a&ter an A+ duration o& 12
hours
3ecogni4e that rhythm control inherently means a component o& rate
control
5rea do!n your patients into stable v- unstable and into duration o&
A+
All the anticoagulation stu6 re&ers to patients not on chronic 7AC
Alwas watc! #or AF , -.- wit! accessor $at!wa ,this is ho!
you 8un your +3 e9am.
All $atients not on $rior OAC t!at need cardioversion /0CC or
$!ar(acolo1ic2 1et !e$arin
Beware o# t!e $atient wit! AF 34&53%&b$( (a be a
$!siolo1ic rate6
A..ROAC+
:he only di6erence in ho! this is presented is that you should start
!ith patient stability at the top o& the paradigm" not duration
o ;uestion o& impending death v- ris o& stroe
7a8or 9uestions to as" oursel# wit! new onset AF:
:uestion S$ecifcall -!
Stable or unstable A5Cs
Cardiogenic shoc ,H3 < (0$.
A=I
Hypo9emic respiratory &ailure
due to cardiogenic pulmonary
edema
:hey !ill die i& you don>t
cardiovert them" nevermind
stroe
Rate;:RS <//$bpm ? ;3S < (/$ms
@ (0$bpm
A+ !ith ABA !ith accessory
path!ay needs electrical
cardioversion 7CDE
Eou may put them into F+ib
arrest !ith AFC blocers
@ (0$bpm G very liely H7:C
not related to A+ liely
physiologic ,loo &or another
reason.
Underlin1 !eart;res$
disease
Ischemic heart disease
CH+
Asthma
Can>t give Class IC drugs to
patients !ith IH*
Care&ul !ith 55 in CH+ or
asthma patients
-! now See precipitants belo! Ceed to treat this" especially
since cardioversion may not
!or until then
0uration @ 12 hours v- < 12 hours See discussion belo!
Stro"e ris" =echanical valves
3heumatic disease
3ecent :IA/stroe
Aill dictate i& you give them
long'term AC a&ter
cardioversion ,i& @ 12 hrs.
S($to(s /i# stable2 *yspnea
Ischemic chest pain ,no
evidence o& A=I.
Syncope
*CC i& you can
Ceed urgent rate control until
cardioversion can be sa&ely
applied
7ANA<E7ENT
Cardioversion
-!at to do Co((ents
.re5treat(ent Amiodarone (0$mg IF
over ($min then
(mg/min 9 H hours then
$-0mg/min 9 (2 hours
Heparin 0$$$ IF bolus
,no evidence.
)vidence that antiarrhythmics reduce rate o&
*CC &ailure
Brimarily indicated inI
+ailure o& initial *CC
Bermanent A+
Jnderlying heart disease
Complications includeI
Barado9ically increases defbrillation
threshold
Increased AF conduction
0irect Current
Cardioversion
/0CC2
+entanyl ($$mcg IF 9 (
?/' =ida4olam /mg q0m
ConsiderI )tomidate 0'
Kmg IF ? Letamine ($'
(0mg
/$$M biphasic !ith sync
Bads AB i& possible
)vidence that higher initial shoc G less
&ailure and no increase ris o& myocardial
damage (Resuscitation 1998;36:193)
)6ective in N0%
Sa&e !ith pacemaers mae appt &or
testing a&ter!ard
=onitor !/ telemetry &or /1'12hrs" esp i& ;:
prolonging agents given
Rate Control for Acute Atrial Fibrillation
0ru1 0ose 7aintenance Co((ents
*iltia4em ,Class
IF.
$-/0mg/g IF over
($min; repeat at
$-#0mg/g
IFI 0'(0mg/hr
B7I (/$'#H$mg
in ;I* dosing
(
st
line agent !ith normal
hearts
Brobably the best one &or
re&ractory A+ ,see belo!"
di6erent dosing.
*on>t use i& you no! they
have any CH+
)smolol ,Class II. $-/0'$-0$mg/g IF
over ( min
IFI 0$ug/g/min Jltra short acting
*on>t use i& asthmatic or
A*CH+
Jse i& really unsure i& they>ll
tan their pressure
*C3 patient !ith so&t pressures
=etoprolol ,Class
II.
0mg IF over / min;
repeat q0m 9 #
B7I /0'($$mg in
5I* dosing
*on>t use i& asthmatic or
A*CH+
Bre&erred i& ischemia !ith A+
but no H7:C
*igo9in $-H/0mg IF 9 ( then
$-/0mg IF 9 /
separated by qHh
B7I $-(/0mg B7
7*
:aes at least #$min be&ore
onset
Jseless in acute
Cot bad &or synergy !ith 55
later
Unstable (Cest! "##9; 13$:8%9&8$9)
Cardioversion
Indications &or emergent cardioversion ,see ACDS.I
o s5B @ K$'2$ and/or symptomatic hypotension ,altered D7C" shoc. due to rapid
A+
o Active" ongoing ischemia
o Contribution to decompensation o& CH+
o Bre'e9citation syndrome contributing to a H3 < /$$
:his re&ers to the acutely crumping patient because o& A+
:here does e9ists the patient !ho is unstable" but not li&e'threateningly
unstable and/or does not !ant ACDS ,code level. see discussion
belo!
Cardioversion overview
o Bretreatment
o )lectrical ,*CC. frst line
o Shoc +ailure
o Anticoagulation
.retreat(ent sip this is they are acutely crashing
0irect Current Cardioversion /0CC2 ,see above.
S!oc" Failure
o *CC !ill not restore CS3 ,/0%." reverts bac to A+ a&ter brie&
CS3 ,($%. or reverts bac to A+ over ne9t &e! !ees ,($%.
o Add Amiodarone i& not already done
o Increase energy to #H$M
o Co beneft to continue *CC i& &ailure a&ter /
nd
attempt see
3e&ractory Acute A+ belo!
Anticoa1ulation
o Heparin bolus in all patients ,J+H G D=AH; consensus based
statement.
o = )* !ours
High ris F:) &eatures ,mechanical valve" recent
stroe/:IA" rheumatic valves. G treat lie < 12 hours
Co high ris F:) &eatures G no long'term 7AC
o > )* !ours
Heparin bridge to 7AC
7AC &or minimum 1 !ees
+/J and assessment &or permanent 7AC
Atrial Fibrillation in Se$sis
Co evidence
=y thoughtsI
o H3 @ (0$bpm ? H7:C is very liely physiologic- I- *o C7: slo! them do!n
o H3 < (0$bpm ? H7:C is a Oudgment call- I>m inclined to *CC these patients-
I& they are =( and/or don>t !ant/&ailed *CC !ith H3 < (0$ and H7:C
o Bush dose pressor ,($$mcg o& phenyl.
o Amiodarone (0$mg IF bolus then in&usion
o ACJ:) rate controlI *ilt or )smolol
*ilt and )smolol may not !or in very high catecholamine states and Amio seems
e6ective &or acute rate control ? H$% conversion rate (A' ( Cardiol 1998;81:$9%&$98)
:he issue !ith Amio is that it can tae < #$ min &or onset- I& you are in *I3) need o&
rate control ,i-e-" their rate is < (K$ and they are taning" consider a special *ilt drip
,see belo!.
) %8 ours
I# ou can?t ascertain duration@ !eart disease@ $reci$itant RATE control t!ese
$atients until ou can sa#el cardiovert t!e(A
<et i($ortant in#o /in addition to above2
o Code status" !ishes reI *CC/ICJ
Unstable but not li#e5t!reatenin1 OR stable wit! s($to(s
o Agree to *CC shoc
o Co *CCI
Transient AF: rate control
Non5transient" un"nown $reci$itant@ new onset: rate
control Amio" *ilt. until acute pharmacologic conversion
,see above.
o Anticoa1ulation
High ris same as < 12hr strategy
Do! ris nothing
Stable
o Bharmacologic conversion
o I& &ails rate control and &ollo!'up &or 7AC
= )* !ours
o .er(anent or un"nown status o# AF
<et a TEE i# ou can ASA.
No TEE B rate control until :)) or 7AC 9 # !ees then
decide on pharmacologic
TEE B $!ar(acolo1ic conversion ,see table above.
=ae sure you fgure out i& the heart is abnormal
o Transient AF ,identifable stressor" post'operative.
3ate control ,see table.
=onitor on tele 9 /1'12hrs until resolution
I& no resolution" treat lie permanent A+
> )* !ours or un"nown
o :hese patients almost never convert to CS3
o Eou !ill