New Onset Atrial Fibrillation.pptx

7/21/2019 New Onset Atrial Fibrillation.pptx

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Evaluation and Management

New Onset Atrial FibrillationDr. Amanda Khosravi



Subjective !"#

"t is $% &'o male with "M! of (rotein S de)cienc& with h'o un(rovo*

/01123 44$5 and heav& EtO! use - 64 &ears (resents from 7ear +alwith (al(itations and associated SO7. "al(itations were intermittent fthen became constant for the (ast wee*. SO7 e-acerbated b& e-ertion - $ da&s. "t admits to t&(ical 9". "t denies !A3 fever3 chills3 nausea3 :O9.



Subjective !istor&

"M! 7"!3 D+, - 3 +enous Stasis with ;:E ulcer

"S! S(lenectom& ' M+A /011253 e-(lorator& la(arotom& ' stab

Medications ,era<osin

Allergies NKA

Famil& 7rother= D+,s3 un*nown (rotein de)cienc&. Sister= un*nownde)cienc&

Social ,obacco'smo*ing >uit 4 &ears ago3 ,!9 dail&3 ? beers (er da



E; 9ourse+S 7" 0$'1?3 " 003 ;; 013 , [email protected] O 1@ ;A

9ardi<em 4 mg #+ -

9ardi<em 64 mg "O

:abs

,S! 0.23 li(ase 063 9"K 2%3 ,ro(onin B4.6

9C; Mild (ulmonar& vascular congestion

EK0.Atrial )brillation with ;+;3 ;ate of 00%.Atrial 8utter /60=053 rate of 2$

145 109 15

3.7 22 0.9112 13.37

13.3

46.1284

8.8 73

6.5 106

3.9 61

0.4



Objective

+S 7" 04$'23 " 1@3 ;; 0@3 O 11 on :

en DN. NAD. :&ing comfortabl&

!EEN, EOM#3 "E;;:A3 oral mucosa moist

Nec* Su((le3 No :AD NDGG

;es( decreased bibasilar breath sounds3 b'l a(ical crac*les

9+ irregular irregular. No m'g'r. "eri(heral (ulses erratic

# Soft. N,ND. Normoactive 7owel Sounds - %.

E-t 0 (itting edema ::E3 (itting edema ;:E w venous stasis ulcer

Neuro No focal defecits. 9N ##=C## grossl& intact b'l. ross sensation intact. Muscle Strength $'$ b'l.



Assessment and "lan



!os(ital 9ourse Da& 0



9!ADS=+AScCHA2DS2-

VASc acronymUnadjus!sro$! ray!ar()

0 0.2&

1 0.6&

2 2.2&

3 3.2&

4 4.8&

5 7.2&

6 9.7&

7 11.2&

8 10.8&

9 12.2&

- *s"ma"on o+ ,sc#!m"c Sro$! a! -#'//.mdcac.com/c#a2ds2-asc-scor!-+or-ar"a-+"r"a"on-sro$!-r"s$/

C#ron"c H!ar a"ur! 1'

Hy'!r!ns"on 1'

A! 75yo 2's

D 1'

r"or sro$! or ,A 2's

A! 65-74yo 1'

:!nd!r a! 1'; !ma! 0'

http://www.mdcalc.com/cha2ds2-vasc-score-for-atrial-fibrillation-stroke-risk/

http://www.mdcalc.com/cha2ds2-vasc-score-for-atrial-fibrillation-stroke-risk/



Algorithm



Management of !emod&namicall& unstabl

DC cardioversion with synchronized



"rotein S de)cienc&



7ac*ground"rotein S is mainl& s&nthesi<ed in he(atoc&tes3 but also in mega*ar&o

osteoblasts3 and endothelial3 :e&dig and vascular smooth muscle cells.

,he major function of (rotein S is as a cofactor to facilitate the action(rotein 9 /A"95 on its substrates3 activated factor + /F+a5 and activa+### /F+###a5. "rotein S de)ciencies are associated with thrombosis.

A de)cienc& can be inherited or ac>uired due to vitamin K=antagonist

contrace(tives3 (regnanc& and various disorders3 such as liver disease3s&ndrome3 disseminated intravascular coagulation and chronic infectio

"rotein S has both A"9=de(endent and inde(endent anticoagulant (ris an im(ortant regulator of thrombin generation and )brinol&sis.



Diagnosis of "rotein S De)ci"rotein S de)cienc& is diagnosed using laborator& tests for the (rotei

and b& using other tests for functional (rotein S activit&.

Free protein S L 7est initial screen. 9an measure free "S s(eci)callmonoclonal Ab=based assa&s and ligand sorbent assa&s.

Total protein S L ,otal "S antigen is measured b& various t&(es of

techni>ues.Functional assays L Functional assa& methods are based u(on "S acofactor for the anticoagulant eIect of activated (rotein 9 /A"95.



Diagnosis of "rotein S De)ciFree protein S

For as&m(tomatic individuals and those with a )rst +,E without a (ositive famil& histor&3 studielevels of free "S B66 units'd: are clinicall& signi)cant /ie3 (redict for an increased ris* of thrombcom(lications5.

Total protein S

#n absence of genetic data or a strongl& (ositive famil& histor&3 levels of total or free "S antigen Bgenerall& considered to be in the de)cient range.

Functional assays

se of functional assa&s can lead to an erroneous diagnosis of functional "S de)cienc&

Non=s(eci)c for "S due to sensitivit& to the defects that cause resistance to A"9.Solve b& screening (lasma sam(les for A"9 resistance (rior to (erformance of functional "S assa

Functional "S assa& has a larger coecient of variation and occasional false (ositives when the famutation is (resent. #n (ractice3 it is therefore necessar& to (erform re(eat testing and to ta*e intohistor& to )rml& establish the diagnosis of hereditar& "S de)cienc&.



Diagnosis of "rotein S De)ci



Diagnosis of "rotein S De)cienetic testing for "S de)cienc& not currentl& (ossible outside of res

"S de)cienc& generall& restricted to individuals with venous thrombo/+,E5 in association with a strong famil& histor& of +,E /eg3 0 )rsrelative with +,E B$4 &o5.

#n an individual with "S de)cienc& and a (ositive famil& histor& of +a((ro(riate to test )rst degree relatives for the "S De)cienc&.

As&m(tomatic individuals or individuals with a )rst +,E /in absencefamil& histor&5 are generall& not tested for "S de)cienc&



False=(ositives for :ab ;esulErroneous diagnoses can be made due to the in8uence of acute thrombosis and anticoagula

#nter(retation of "S measurements is obscured in individuals treated with vitamin K antagwarfarin53 which substantiall& lower both antigenic and functional levels of "S.

"referrable to discontinue oestrogen or a vitamin K antagonist for at least wee*s (rior studies.

#f it is not (ossible to discontinue warfarin3 switch to he(arin thera(& /does not alter (lasallow for studies

Newborns L Measurement of "S diIer among laboratories and the concentrations are su

in normal newborns and &oung infants com(ared with adult values P use age=based normslaborator& (erforming the test.



ManagementManagement of (rotein S de)cienc& generall& ta*es (lace in the event of acute venou

thromboembolism /+,E5.Following an acute thrombosis3 administer he(arin thera(& and then transition to wanticoagulation.

#nitial he(arin treatment - $ da& minimum ma& be administered as intravenous unfractionsubcutaneous low molecular weight he(arin /:M!5

arfarin administration can start on da& 0 or of he(arin thera(&.

After two consecutive #nternational Normali<ed ;atio /#N;5 clotting tests and a minimum

he(arin thera(&3 continue on warfarin alone. ?=1 months of initial treatment with warfarin

;ecommended life long thera(& if the )rst thrombotic event was life threatenimulti(le or unusual sites /eg3 cerebral veins3 mesenteric veins5

#f (reci(itated b& a strong event /eg3 trauma3 surger&5 and the thrombosis didcriteria of life threatening or multi(le or unusual sites3 can (erform a trial withoafter 1 months on the basis of low rate of recurrence.



Management"ro(h&la-is for As&m(tomatic carriers of (rotein S de)cienc&

#n such (atients3 avoid drugs that (redis(ose to thrombosis3 including oral contrace(atients3 if surger& or ortho(edic injur& occurs3 (ro(h&la-is with he(arin is mandato

#n (regnanc&3 e-(erts recommend (ro(h&la-is with he(arinQ however3 the timing is ,reatment from the second trimester through %=? wee*s (ost(artum is generall& rec

"atient bleeding ris*s must be assessed on an individual basis for an& of these (ro(recommendations.

New Onset Atrial Fibrillation.pptx

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