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Clinical Medicine > Pulmonary Embolus > Flashcards

Pulmonary Embolus Flashcards

1
Q

What is the definition of pulmonary embolism

A

Common, serious, and potentially fatal complication of thrombus formation within the deep venous circulations

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2
Q

What conditions are “two manifestations of the same disease process”

A
  1. Pulmonary embolism
  2. Deep venous thrombus
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3
Q

What is the estimated annual incidence of PE in the US

A

300,000 cases
*most cases not disposed antemortem
*less than 10% of patients with fatal PEs had treatment for them
*90% did not

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4
Q

What is the mortality rate for patients with PE who did not receive treatment

A

30%

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5
Q

What must you do when suspecting someone with a PE

A

Be vigilant, have a systematic approach for understanding risk factors, diagnosis, and to begin therapy
*do not miss diagnosis

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6
Q

What are accurate diagnosis and effective therapy do for mortality rates?

A

Effective therapy (anti coagulation)
*Will be a reduction in mortality rate 2-8% (vs 30%)

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7
Q

What is Virchows triad

A
  1. Venous stasis
  2. Injury to vessel wall
  3. Hypercoagulability
    *causes for PE
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8
Q

What are the risk factors for PE (THROMBOSIS)

A

T: trauma, travel, thromnopillia
H: hypercoagulable state, hormone replacement therapy
R: recreational drugs
O: old age
M: malignancy
B: birth control pills
O: obesity
S: surgery
I: immobilization, iatrogenic
S: serious illnesses

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9
Q

What is venous stasis and what can cause it?

A

Blood that is not flowing as it should
1. Immobility
*prolonged bed rest
2. Major surgery
3. Increased central venous pressure
*pregnancy
*low cardiac output states
4. Hyper-viscosity/hematologic disorder
*polycythemia

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10
Q

What are some causes of “injury to (vessel) wall”

A
  1. History of DVT
  2. Orthopedic surgery
  3. Trauma
  4. Central venous catheters
  5. Chemotherapeutic agents
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11
Q

What can cause hypercoagulability (acquired)

A
  1. Medications
    *oral contraceptives
    *hormone replacement therapy
  2. Pregnancy
  3. Dehydration
  4. Nephrotic syndrome
  5. Sepsis
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12
Q

What types of cancers can cause hypercoagulability (acquired)

A

Highest risk
*adenocarcinoma
*pancreas
*prostate
*breast
*ovary
Intermediate risk
*lung
*GU
*colon

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13
Q

What can cause hypercoagulability (inherited)

A
  1. Most common inherited cause factor V Leiden
  2. Methylenetetrahydrofolate reductase (MTHFR) deficiency
  3. Protein C, S deficiency
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14
Q

What is factor V Leiden deficiency

A
  1. Causes resistance to activated protein C
    *protein C inactivates factor V
    *patients are more likely to clot
  2. Seen in 20-40% of idiopathic venous thrombosis
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15
Q

What is MTHFR deficiency

A
  1. Most common genetic cause of elevated levels of homocysteine in plasma
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16
Q

What is the most common place for a PE to develop

A
  1. Thrombus from lower extremity deep veins
    *proximal DVT up to 60% will have PE
    *20% of calf veins can travel to popliteal and iliofemoral

**many substance can embolize, and travel to the luminary circulation

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17
Q

What are other things that can break off and become emboli

A
  1. Septic emboli (acute infections)
  2. Fat (long bone fractures)
  3. Amniotic fluid (Active labor)
  4. Air
  5. Foreign bodies
  6. Parasite eggs
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18
Q

Majority of patients with a symptomatic PE where has the DVT come from?

A
  1. 50-70% will have confirmed lower extremity DVT
    *will get lodged in the pulmonary artery
    *blood will get sticky and grow a clot, leading to occlusion
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19
Q

What is a PEARL of PE

A
  1. Documentation of a DVT in a patient with a suspected PE establishes need for treatment
    *may preclude further diagnostics
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20
Q

What does a PE increase the likelihood of

A
  1. Acutely increases pulmonary vascular resistance
    *physical obstruction of the vascular bed
    *vasoconstriction from neurohumoral reflexes
  2. Physiologic dead space results in hypoxemia
    *due to right to left shunting, decreased cardiac output and surfactant depletion from atelectasis
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21
Q

What does a PE lead to

A

Increase in wheezing and in effort of breathing
*risk of acute RV failure (massive thrombus possible)

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22
Q

Where is a PE most likely to get stuck

A
  1. Right / left pulmonary artery
    *if stuck in the bifurcation called a saddle
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23
Q

What are the signs and symptoms of aPE

A

Findings are fairly sensitive, not specific
1. Dyspnea
2. Painful inspiration
3. Tachycardia
4. Tachypnea
5. Pleuritic chest pain
6. Hemoptysis

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24
Q

What symptoms can a massive PE lead to

A
  1. Syncope
  2. Hypotension
  3. PEA
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25
Q

Why can diagnosing a PE be difficult

A
  1. Depends on the size of the embolus and the cardiopulmonary status of the patient
    *pre-existing comorbidities greatly affect the PE’s S/sx
  2. Signs are non-specific
    *no single symptoms or sign or combination of clinical findings is specific findings is specific to confirm a PE
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26
Q

What must you do the diagnosis a PE

A
  1. Must establish pre-diagnostic study probability
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27
Q

What is an initial approach to diagnose a PE

A
  1. Use clinical likelihood of pulmonary embolus or venous thromboembolism derived from clinical prediction rule and results of diagnostic tests
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28
Q

What are the three type of decision that can be made about the diagnosis of a PE

A
  1. Confirmed venous thromboembolism
    *either DVT or PE
  2. Exclude venous thromboembolism with enough evidence and the patient may discontinue anticogaultion
  3. Additional testing needed for confirmation
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29
Q

What happens when a patient has a score of <4 and meets ALL of the following criteria

A
  1. Age <50
  2. HR <100bpm
  3. Oxyhemoglobin saturation on room air >95%
  4. No prior history of venous thromboembolism
  5. No recent trauma or surgery requiring hospitalization
  6. No presenting hemoptysis
  7. No estrogen therapy
  8. No unilateral leg swelling
    *PE can be excluded (low risk PT)
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30
Q

What does a chest radiograph aid in?

A
  1. Assist with interpretation of V/Q scan
    *does not establish diagnosis of PE
31
Q

What will a EKG show for a PE

A
  1. Abnormal in 70% of PT
    *sinus tachycardia
    *non-specific ST and T wave changes
    *possible, but not common P pulmonale, RVH, R axis deviation, RBBB
32
Q

What will the Arterial Blood gas (ABG) show for a PE

A
  1. Shows acute respiratory alkalosis
  2. Supportive of diagnosis of PE, especially with
    *normal chest x-ray
    *no previous history of pulmonary disease
    *profound hypoxia
  3. Not diagnostic
33
Q

What is a d-diner

A
  1. Degradation product of cross-linked fibrin
34
Q

What will high levels of a D-diner show

A
  1. High in the presence of thrombus or PE
    *elevation: no established diagnostic thresholds and does not establish diagnosis of VTE/PE
35
Q

What does a PE under 500 indicate

A
  1. Strong evidence against VTE in patients with low pertest probability of a PE
36
Q

What is the initial diagnostic test of choice for a PE

A
  1. Pulmonary CT-angiography (CT-PA)
    *termed the “gold standard diagnostic study in North America”
  2. Useful for intermediate or high pretest probability, increased D dimer
  3. High sensitivity and specificity
  4. Non invasive
37
Q

Does a normal helical CT-PA help with excluding a PE in a high-risk patient

A

No
*has a 15-20% false negative rate
*clinical pretest probability improves the accuracy

38
Q

What are other reasons to use a CT-PA

A
  1. May monitor with CT-PA who are off therapy
  2. CT-PA vs V/Q results are roughly comparable
  3. Other pulmonary diagnoses are made frequently with CT-PA
39
Q

What is the Ventilation/Perfusion scan (V/Q scan)

A
  1. Alternative for CT-PA if CI
  2. Patient is injected with radiolabeled proteins in venous system, particles travel to pulmonary capillaries
  3. Patient will breathe in radioactive gas or aerosol while distribution of radioactivity in lung fields is recorded
40
Q

What does a + perfusion / + ventilation mean

A

+Perfusion defect represents decreased blood flow
+Ventilation defect represents decreased air flow
*not specific for PE only helpful is normal / negative

41
Q

What do normal and high probability results of a V/Q scan mean?

A

Normal = excludes clinically significant PE
*negative predictive value 91%
High-probability = >2 segmental perfusion defects in the presence of normal ventilation
*positive predictive value for PE 88%

42
Q

What does a non-diagnostic V/Q scan result mean?

A

Still cannot confirm diagnosis
*low probability
*intermediate probability

43
Q

How can clinical assessment of pre-test probability be combined with V/Q results

A
  1. Low pretest probability + low probability scan = very low probability of PE
  2. High + high = very high
44
Q

How can venous ultrasound / doppler be used to detect a PE

A

Test of choice to detect proximal DVT
1. Inability to compress femoral or popliteal veins is diagnostic
2. 70% of patients with a PE have a +DVT

45
Q

What is contrast venography used for?

A
  1. Detect intraluminal filing defects
  2. Not used frequently
46
Q

What hinders the results of the MRI

A
  1. Cardiac and pulmonary artifacts
47
Q

What is a pulmonary angiography used for

A
  1. Historical reference standard for diagnosis of EP
    *definitive diagnosis = intraluminal defect in >1 view
    *minor complications; contrast allergic reaction
    *expensive, high radiation dose invasive
48
Q

What is the more current use of pulmonary angiography

A
  1. Catheters-directed thrombolytic therapy or mechanical embolectomy
  2. Confirm diagnosis of a chronic PE in chronic thromboembolic Pulm HTN
49
Q

What are the 3 possible outcomes after determining pre-test probability and completing diagnostics

A
  1. Confirm diagnosis of PE or DVT
    *will treat both
  2. Conclusively rule out PE or DVT
  3. Unable to rule in or rule out PE/DVT
    *refer for pulmonary angiography
50
Q

What happens once PE is confirmed

A

Risk stratification needs determined (completed for every patient with confirmed PE)
*high risk
*low risk
*intermediate risk

51
Q

Who is in the high risk category

A
  1. Massive PE
  2. Hemodynamic compromised
  3. Cardiac arrest
52
Q

Who is in the intermediate risk of PE

A
  1. Submissive PE
  2. Hemodynamically stable
  3. Signs of dysfunction
53
Q

Who is in the low risk category

A
  1. Normotension
  2. No signs of dysfunction
54
Q

What is the treatment

A
  1. Anticoagulation
    *heparin followed by oral anticoagulants (secondary prevention)
  2. Thrombolytic therapy
  3. Vena cava filters
  4. Pulmonary embolectomy
55
Q

What is the mainstay of treatment for a PE and VTE

A
  1. Anticoagulation (Low molecular weight heparin)
    *blunts additional thrombus formation
    *allows endogenous fibrinolytic mechanisms to lose existing thrombus
    *initiated if highly suspected, even before confirmed
56
Q

What is unfractionated heparin

A
  1. Binds and accelerates the ability of antithrombin to inactivate thrombin, factor Xa and factor Ixa
57
Q

What are the different types of low molecular weight heparin

A
  1. Dalteparin
  2. Enoxaparin
  3. Tinzaparin
  4. Fondaparinux
58
Q

What is the second line tx for a PE

A

Direct oral anticoagulants (DOACs)
1. First-line oral anticoagulant option for most patients

59
Q

What are the advantages / disadvantages of DOAC

A

Advantages
1. Do not need blood test monitoring during use
2. Not affected by food or ETOH
Disadvantages
1. May need twice-daily dosing
2. More expensive than warfarin

60
Q

What are the complications of Anticoagulation therapy

A
  1. Hemorrhage
    *risk factors include, intensity of Anticoagulation, duration of therapy patient characteristics
  2. Bleeding, bruising (minor)
61
Q

How long should you use an anticoagulation for P

A
  1. Can stop as little as three months
  2. Usually 6 months
    *however case by case basis
62
Q

What is Coumadin effected by?

A
  1. Effect mediated by inhibition of synthesis of vitamin K-dependent factors
    *vitamin K antagonist
    *II, VII, IX, X
63
Q

When does peak effect of Coumadin happen?

A
  1. Does not occur until 36 to 72 hours after initiation of drug
    *effect is delayed until the clotting factors are eliminated
64
Q

What are the complications of Coumadin

A
  1. Hemorrhage
  2. INR >4.0 = high risk
65
Q

What is the target INR when on Coumadin

A

2.0 to 3.0

66
Q

What is thrombolytic therapy for a PE

A

Catheter-directed thrombolysis
*delivers thrombolytics directly into PE, which will reverse right ventricle dilation fast
*for high-risk PE
*intermediate risk or sub-massive PE no mortality benefit

67
Q

What does thrombolytic therapy increase

A
  1. Increases plasmin levels
    *lyses intramuscular thrombi, accelerates resolution of emboli
68
Q

When is thrombolytic therapy CI

A
  1. Active bleeding
  2. Stoke within 3 months
    *incrases risk of major hemorrhagic complications
69
Q

What are the thrombolytic meds

A
  1. Streptokinase
  2. Urokinase
  3. Recombinant tissue plasminogen activator
70
Q

When is mechanical pulmonary embolectomy or surgical extraction indicated

A
  1. For patients who are CI or have failure of thrombolysis
71
Q

What is the indications for inferior vena cava filter placement?

A
  1. Major CI for anticoagulation
  2. Recurrent thromboembolism despite anticoagulation
    • PE and +Free-floating proximal end DVT
72
Q

What are the complications of PE/VTE

A
  1. Reoccurrence
  2. Pulmonary infarction
  3. Arrhythmias
  4. Pleural effusion
  5. Pulm HTN
  6. Mortality
73
Q

How to prevent PE and DVTs

A
  1. Receive pharmacolgic thromboprophylaxis (LMWH) prophylactically prior to surgery
  2. All patients receive non-pharmacogic therapies
    *early Ambulation
    *compression devices
74
Q

What is the prognosis of PE

A

When recognized and treated prognosis is good
*dependent on underlying illness
*perfusion usually can be fully restored

Clinical Medicine (164 decks)

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