Lecture 68 - Dx and Tx of PE Flashcards

1
Q

what is a DVT? where is it most likely to originate?

A

DVT = Deep venous thrombosis

○ Femoral, popliteal, greater saphenous – most commonly

Pelvic veins

Upper extremity veins – but usually catheter associated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is a PE and how does it kill you? q

A

Pulmonary Embolism

• Results in an anatomical obstruction --- resulting In physiological disruption 

○ Effects on the RV: Increased RV Afterload

○ Death is usually from RV failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the recurrence rate following a thrombo-embolytic event ?

rank the following contexts in which a DVT/PE can occur in terms of likelihood of recurrence: surgically provoked, non surgically provoked, idiopathic

A

Recurrence: Following thromboembolic event – recurrence rate at 8 years is 30%

§ Surgery: highly unlikely to manifest another clot

§ Non-surgical provoked event (eg truama) – higher risk

§ Idiopathic clot – most likely to have recurrence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

PE Physiology: what happens to V/Q?

how do patients typically present ?

what does this mean in terms of blood gas levels?\

A

Creates Dead Space: (High V/Q) (low perfusion, normal ventilation) —

Patients present dyspnea but hyperventilating and able to get expel sufficient CO2 such that they are Hypocapnic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

In what context might patients with PE present with hypercapnea?

A

COPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Is it possible for patients with PE to present with hypoxemia?

Describe this physiology?

A

○ Hypoxemia is Observed – Some areas of the Lung Develop Low V/Q Physiology

  • Bronchoconstriction, areas of atelectasis

§ Loss of surfactant; also leads to atelectasis

§ Pulmonary HTN can lead to shunting –

High RV Pressure can shunt through a Patent Foramen Ovale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Risk Factor for PE: what is virchow’s triad?

A

Increased Clotting Risk: Virchows Triad -

Venous stasis

Vascular/Endothelial Injury

Hypercoagulability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what causes venous stasis?

What causes vascular/endothelial injury?

what types of surgery most commonly lead to DVT/PE?

A

Venous Stasis -Immobility

Vascular/Endothelial Injury – surgery, trauma, post partum, vascular catheters

hip, knee, vascular)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are some inherited Hypercoagulopathies ?

A

Factor V Leiden (protein C resistnace; most common inherited disorder)

□ Antithrombin Deficiency; Protein C deficiency, Protein S deficiency

Prothrombin Gene mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are some acquired hypercoagulopathies?

A

□ Malignancy

□ Hormone replacement

□ Oral Contraceptives

□ Antiphospholipid antibody syndrome

□ Elevated homocysteine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

describe a common presentation for DVT vs PE?

A

§ PE – Sudden onset dyspnea and CP (can be insidious, can be pleuritic in nature);+/- hemoptysis

§ DVT – Asymmetric leg swelling and pain

□ Risk factors: Surgery, OCP, immobilization, catheters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Physical exam findings for DVT?
what is homan’s sign?
Is it useful for diagnosis of DVT?

A

leg edema, warmth, or asymmetry; Palpable cord (indurated, tender subQ vein)

Homan’s = pain in calf with dorsiflexion

Not useful for DVT Dx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Physical exam findings for PE?

A

tachycardic, tachypnic, febrile, hypotensive (severe clot)

Heart Exam – possible loud P2 or tricuspid murmur (LLSB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Best tool for diagnosis of DVT?

what lab is commonly drawn

A

○ Compression Ultrasound – best test; non invasive, quick, accurate

○ D Dimer – a fibrin degradation product
§ Sensitive but not specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Tools for Dx of PE?

which is the current standard evaluative test for PE?

A

EKG, CXR, ECHo, VQ Scan, Pulmonary Arteriogram , CT Scan with IV Contrast

standard: CT Scan with IV Contrast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Classical EKG findings of a PE?

A

S1Q3T3
S1 – S waves in lead 1 = RBBB

Lead III Q waves or T wave inversion = right sided pressure and volume overload causing repolarization abnormalities

17
Q

Classical CXR findings for PE:

A

CXR — A “normal” CXR with someone presenting with sudden onset hypoxemia and SOB is a PE!!!

18
Q

how is an echocardiogram use?

how is V/Q scan used ?

A

Echo – § Can evalutae for Tamponade, aortic disection, MI
§ Can help assess right heart function
Right Ventricular Dilation implies – “submassive” PE

V/Q Scan – § Look for areas that have mismatch
In PE – Getting air but not blood

19
Q

What is the difference between a massive and submassive PE?

A

Some Classifications:
• Massive PE – big enough to effect blood pressure (hypotension)

• "Submassive PE" -- big enough to lead to Right heart strain, dilation 

Clot SIZE visualized on imaging – does not determine massive vs submassive

20
Q

DVT/PE Prophylaxis?

A

• Minimize Risk Factors:
• Low dose prophylactic anticoagulation therapy
○ unfractionated heparin, low molecular weight heparin
• Mechanical
○ venous compression devices

21
Q

Three methods to treat DVT/PE?

A

Anticoagulation – LMW Heparin, Unfractioned Heparin (paraenteral), Wafarin (oral)

Mechanical – IVC filter, Surgical Embolectomy

Thrombolytic Therapy – TPA – only for massive PE

22
Q

when should you initiate treatment for PE?

for how long do you treat?

A

Initiate Treatment (with LMW Heparin) before getting confirmatory results — once it is suspected – or high pre test probability

  • Temporary risk factor — 3 months – surgery, fracture
  • Idiopathic , recurrent or malignancy – life
23
Q

Long term Complications of PE

A

Chronic Thromboembolic Pulmonary Hypertension –

====High clot burden in the pulmonary vasculature; RV can’t handle this resistance… results in Pulm HTN