Evaluation and Management of

New Onset Atrial Fibrillation

Dr. Amanda Khosravi

Subjective: HPI
Pt is 54 y/o male with PMH of protein S deficiency with h/o unprovoked DVT x 2
(1997, 2005) and heavy EtOH use x 30 years presents from Bear Valley Hospital
with palpitations and associated SOB. Palpitations were intermittent for 2 weeks
then became constant for the past week. SOB exacerbated by exertion and lying flat
x 5 days. Pt admits to typical CP. Pt denies HA, fever, chills, nausea, vomiting,
LOC.

Subjective: History
PMH: BPH, DVT x 2, Venous Stasis with RLE ulcer
PSH: Splenectomy 2/2 MVA (1997), exploratory laparotomy 2/2 stab wound
Medications: Terazosin
Allergies: NKA
Family: Brother- DVTs, unknown protein deficiency. Sister- unknown protein
deficiency
Social: Tobacco/smoking quit 20 years ago, THC daily, 6 beers per day

ER Course
VS: BP: 125/96, P: 121, RR: 19, T: 98.1, O2: 98% RA
Cardizem 20 mg IV x 2
Cardizem 30 mg PO
Labs:

145
3.7

109
22

15
0.9

8.8 73
112

13.3
13.37
46.1

284

TSH 1.7, lipase 13, CPK 74, Troponin <0.3

CXR: Mild pulmonary vascular congestion
EKG:
1. Atrial fibrillation with RVR, Rate of 114
2. Atrial flutter (3:1-2:1), rate of 75

6.5 106
3.9 61
0.4

Objective
VS: BP: 105/72, P: 98, RR: 18, O2: 99% on 2L
Gen: WDWN. NAD. Lying comfortably
HEENT: EOMI, PERRLA, oral mucosa moist
Neck: Supple, No LAD + ND??
Resp: decreased bibasilar breath sounds, b/l apical crackles
CV: irregular irregular. No m/g/r. Peripheral pulses erratic
GI: Soft. NTND. Normoactive Bowel Sounds x 4.
Ext: 1+ pitting edema LLE, 2+ pitting edema RLE w venous stasis ulcer
Neuro: No focal defecits. CN II-XII grossly intact b/l. Gross sensation intact. Muscle Strength 5/5 b/l.

Assessment and Plan

Hospital Course: Day 1

Etiology
Abnormalities or damage to the hearts structure -- most common cause
Other possible causes
HTN
MI
CAD
Structural valve disease
Congenital heart disease
Hyperthyroidism

CHA2DS2-VASc
- Estimation of Ischemic Stroke Rate http://www.mdcalc.com/cha2ds2-vasc-score-for-atrial-fibrillation-stroke-risk/

Chronic Heart Failure: 1pt

Hypertension: 1pt
Age 75yo<: 2pts
DM: 1pt
Prior stroke or TIA: 2pts
Age 65-74yo: 1pt
Gender: Male 1pt, Female 0pt

CHA2DS2VASc acronym

Unadjusted ischemic
stroke rate (% per
year)*

0.2%

0.6%

2.2%

3.2%

4.8%

7.2%

9.7%

11.2%

10.8%

12.2%

Algorithm

Management of Hemodynamically unstable AFib

DC cardioversion with synchronized shock!!

Protein S deficiency

Background
Protein S is mainly synthesized in hepatocytes, but also in megakaryocytes,
osteoblasts, and endothelial, Leydig and vascular smooth muscle cells.
The major function of protein S is as a cofactor to facilitate the action of activated
protein C (APC) on its substrates, activated factor V (FVa) and activated factor
VIII (FVIIIa). Protein S deficiencies are associated with thrombosis.
A deficiency can be inherited or acquired due to vitamin K-antagonist therapy, oral
contraceptives, pregnancy and various disorders, such as liver disease, nephritic
syndrome, disseminated intravascular coagulation and chronic infections (e.g. HIV).
Protein S has both APC-dependent and independent anticoagulant properties and
is an important regulator of thrombin generation and fibrinolysis.

Diagnosis of Protein S Deficiency

Protein S deficiency is diagnosed using laboratory tests for the protein S antigen
and by using other tests for functional protein S activity.
Free protein S Best initial screen. Can measure free PS specifically using
monoclonal Ab-based assays and ligand sorbent assays.
Total protein S Total PS antigen is measured by various types of immunoassay
techniques.
Functional assays Functional assay methods are based upon PS activity as a
cofactor for the anticoagulant effect of activated protein C (APC).

Diagnosis of Protein S Deficiency

Free protein S
For asymptomatic individuals and those with a first VTE without a positive family history, studies suggest that only
levels of free PS <33 units/dL are clinically significant (ie, predict for an increased risk of thromboembolic
complications).
Total protein S
In absence of genetic data or a strongly positive family history, levels of total or free PS antigen <60 to 65 IU/dL are
generally considered to be in the deficient range.
Functional assays
Use of functional assays can lead to an erroneous diagnosis of functional PS deficiency
Non-specific for PS due to sensitivity to the defects that cause resistance to APC.
Solve by screening plasma samples for APC resistance prior to performance of functional PS assay
Functional PS assay has a larger coefficient of variation and occasional false positives when the factor V Leiden
mutation is present. In practice, it is therefore necessary to perform repeat testing and to take into account family
history to firmly establish the diagnosis of hereditary PS deficiency.

Diagnosis of Protein S Deficiency

Diagnosis of Protein S Deficiency

Genetic testing for PS deficiency not currently possible outside of research setting.
PS deficiency generally restricted to individuals with venous thromboembolism
(VTE) in association with a strong family history of VTE (eg, 1 first degree
relative with VTE <50 yo).
In an individual with PS deficiency and a positive family history of VTE,
appropriate to test first degree relatives for the PS Deficiency.
Asymptomatic individuals or individuals with a first VTE (in absence of a positive
family history) are generally not tested for PS deficiency

False-positives for Lab Results

Erroneous diagnoses can be made due to the influence of acute thrombosis and anticoagulant therapy
Interpretation of PS measurements is obscured in individuals treated with vitamin K antagonists (eg,
warfarin), which substantially lower both antigenic and functional levels of PS.
Preferrable to discontinue oestrogen or a vitamin K antagonist for at least 2 weeks prior to PS Deficiency
studies.
If it is not possible to discontinue warfarin, switch to heparin therapy (does not alter plasma PS levels) to
allow for studies
Newborns Measurement of PS differ among laboratories and the concentrations are substantially lower
in normal newborns and young infants compared with adult values use age-based norms for the specific
laboratory performing the test.

Management
Management of protein S deficiency generally takes place in the event of acute venous
thromboembolism (VTE).
Following an acute thrombosis, administer heparin therapy and then transition to warfarin oral
anticoagulation.
Initial heparin treatment x 5 day minimum may be administered as intravenous unfractionated heparin or as
subcutaneous low molecular weight heparin (LMWH)
Warfarin administration can start on day 1 or 2 of heparin therapy.
After two consecutive International Normalized Ratio (INR) clotting tests and a minimum of 5 days of
heparin therapy, continue on warfarin alone. 6-9 months of initial treatment with warfarin is recommended.

Recommended life long therapy if the first thrombotic event was life threatening or occurred in
multiple or unusual sites (eg, cerebral veins, mesenteric veins)
If precipitated by a strong event (eg, trauma, surgery) and the thrombosis did not meet the
criteria of life threatening or multiple or unusual sites, can perform a trial without warfarin
after 9 months on the basis of low rate of recurrence.

Management
Prophylaxis for Asymptomatic carriers of protein S deficiency
In such patients, avoid drugs that predispose to thrombosis, including oral contraceptives. In these
patients, if surgery or orthopedic injury occurs, prophylaxis with heparin is mandatory.
In pregnancy, experts recommend prophylaxis with heparin; however, the timing is controversial.
Treatment from the second trimester through 4-6 weeks postpartum is generally recommended.
Patient bleeding risks must be assessed on an individual basis for any of these prophylactic
recommendations.