PE/DVT Flashcards

1
Q

Sources of Emboli?

A

pelvic veins
upper extremity veins
DVT in legs (90%)

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2
Q

Non blod clot emboli sources?

A
Air
Tumor
Amniotic fluid
Talc
Fat
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3
Q

Virchow’s Triad

A

Stasis
Hypercoagulability
Endothelial injury

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4
Q

6 congenital causes of hypercoagulability?

A
Factor V Leiden mutation***
Prothrombin "G" mutation 
Protein C  & Protein S deficiency
Antithrombin III deficiency
Dysfibrinogenemia 
Homocystinemia
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5
Q

9 acquired causes of hypercoagulability?

4 more important

A
estrogen*
pregnancy (hormonal)*
malignancy*
nephrotic syndrome*
thrombocytosis
DIC
HIT
antiphospholipid antibody syndrome
PNH
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6
Q

4+ DVT risk factors are associated with a confirmed DVT rate of ___%;
3 risk factors&raquo_space; ___%
0 risk factors&raquo_space; ___%

A

100
50
11

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7
Q

What factors determine the extent of physiologic consequences of PE?

A

The size of the embolus
Cardiopulmonary status/reserve
Neurohormonal substances

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8
Q

Compensation by the circulation (due to PE)?

How does this help?

A

Vasodilatation of uninvolved vasculature –>

  • helps to decrease pulm vasc resistance
  • improves V/Q in uninvolved areas
  • improves overall oxygenation
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9
Q

What are the physiologic consequences of PE?

A
  1. increased pulm vasc resistance
  2. impaired gas exchange
  3. alveolar hyperventilation
  4. increased airway resistance (bronchoconstriction)
  5. decreased pulm compliance
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10
Q

What causes increase in pulm vasc resistance in PE?

A
  1. Vascular obstruction

2. Neurohumoral agents (serotonin, Endothelin)

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11
Q

What causes impaired gas exchange in PE?

A
  1. Increased alv dead space from vasc obstr (V/Q mismatch)
  2. Impaired carbon monoxide transfer (low DLCO) due to loss of gas exchange surface
  3. Right-to-left shunting (in massive PE)
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12
Q

What causes alveolar hyperventilation in PE?

A

reflex stimulation of irritant receptors

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13
Q

What are possible causes of decreased pulm compliance in PE?

A

lung edema, lung hemorrhage or loss of surfactant

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14
Q

Gas exchange abnormalities resulting from PE?

A

hypocapnia
hypoxemia
widened A-a gradient

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15
Q

What causes tachypnea associated with PE?

A

increased minute ventilation

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16
Q

What causes hypoxia associated with PE?

A

V/Q mismatch

shunting (if massive PE)

17
Q

What are the consequences, in terms of circulation + cardiac symptoms, of PE? (6)

A
Tachycardia
Decrease in cardiac output
Systemic hypotension
Pulmonary hypertension and cor pulmonale
Pulmonary infarction
Bradycardia (sometimes)
18
Q

Diagnostic Measures for PE

A
Clinical signs and symptoms
Laboratory data (ABG/BNP/Troponin)
EKG
CXR
V/Q Scan
Pulmonary angiography
Helical CT (CT Pulmonary angiography)
19
Q

What happens to the clot (micro path) following PE? Which is most favorable?

A
  1. Fibrinolyis (most favorable outcome)
  2. Organization of clot
  3. Partial resolution /compensation via opening of arterial, collateral circ, increased alv ventil
20
Q

Common signs and symptoms in PE

A
dyspnea
pleuritic CP
tachypnea
tachycardia
loud P2

(increase HR/RR; decrease CO2/O2)

21
Q

Abn lab data in PE?

A

Widened A-a gradient
Nml or elevated WBC
elevated d-dimer
elevated LDH and bilirubin

22
Q

EKG findings in PE

A

Nonspecific ST-T abnormalities
Tachycardia
S1Q3T3 – found in a minority of patients***
Atrial arrhythmias

23
Q

Chest Radiography in PE (8)

What’s most common?

A
Normal CXR (most common)
Cardiomegaly
Hampton’s hump
Westermark’s sign
Sausage sign
Discoid atelectasis 
Elevated diaphragm
Pleural effusion (small when present)
24
Q

Do we need to learn Well’s criteria?

A
Previous DVT or PE  
Immobil/ Surg with in 4 weeks
Tachy HR > 100  per minute 
Cancer 
Hemoptysis 
Edema/Symp of DVT 
Diagnosis other than PE less likely
25
Q

Why is Lung Scan Interpretation combined with Clinical Assessment ?

A

high clinical suspicion + high prob V/Q scan = confirms PE

low + low = excludes

26
Q

V/Q Scanning - Pitfalls: (4)

A
  1. 15 sec breath hold to complete test!
  2. Better results in patients w/o structural disease
  3. 30% observer variability
  4. Majority of the scans are indeterminate
27
Q

What is the “gold standard test” for PE? How will a PE look on this test?

A

Pulmonary angiography

  • filling defect
  • cutoff sign
28
Q

What can establish or exclude the diagnosis of DVT?

A

Serial noninvasive studies (ultrasound)

29
Q

Primary diagnostic modality of choice for PE?

A

helical CT

Note: If a PE is excluded: provides alternate diagnosis in about 70% of patients

30
Q

Clinical manifestations of DVT

A
Swelling of the leg		
Duskiness
Homan’s sign - 50:50
Palpable deep thrombi
Dilated superficial veins (collaterals)
Tender cord in the femoral triangle
31
Q

Diagnostic Measures for DVT

A

Ascending contrast venography (invasive)

Real-time (B-mode) ultrasonography (US) ***

32
Q

Prevention of DVT (Prophylaxis)
normal patients?
sedated/sick?

A

Early mobilization

if sedated or sick:

  1. TED hose stockings
  2. Intermittent external pneumatic compression of the calf and thigh
  3. anti-coags
33
Q

How are PE treated?

A
  1. thrombolysis (tPA)
  2. radiological intervention (clot disrupted w catheter or embolectomy)
  3. surgical (Pulm embolectomy, thromboendarterectomy)
34
Q

Prognosis, if PE treated?

A
  1. death = uncommon
  2. pulm hemodynamics return to nml in 2-8 weeks
  3. very fe develop pulm HTN
35
Q

“triad” associated with fat embolism?

A

Mental status changes
Thrombocytopenia
Petechiae in the chest and neck