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Pulmonology > SM 169 Pulmonary Embolism > Flashcards

SM 169 Pulmonary Embolism Flashcards

1
Q

What is the classic presentation for Pulmonary Embolism?

A

There isn’t one; though typical symptoms can include pleuritic chest pain, hemoptysis, and dyspnea

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2
Q

Why is treating Pulmonary Embolism difficult?

A

It produces non-specific symptoms, has high morbidity and mortality if missed, but also lends itself towards over-testing and over-treatment

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3
Q

What are the 3 risk factors that fuel Pulmonary Embolism?

A

Venous stasis, alterations in coagulation, and vascular injury

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4
Q

How does venous stasis promote Pulmonary Embolism?

A

Immobility from lying in a bed, prolonged ravel, or paralysis can promote clot formation in the legs that dislodges and blocks the Pulmonary circulation

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5
Q

How do alterations in coagulation promote Pulmonary Embolism?

A

Hereditary thrombophilias (Factor V), estrogen therapy, and malignancy can predispose clot formation which can block the Pulmonary circulation

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6
Q

How does vascular injury promote Pulmonary Embolism?

A

Surgery, trauma, and childbirth can all injure the vasculature and promote the formation of clots that dislodge and block the Pulmonary circulation

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7
Q

How are the risk factors for Pulmonary Embolism “synergistic”?

A

The risk factors make eachother worse and increase the likelihood of Pulmonary Embolism

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8
Q

Where do most Pulmonary Embolism arise from?

A

Deep veins in a proximal lower extremity, such as the Femoral and Popliteal veins, which then break off and block the Pulmonary circulation

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9
Q

What is a Pulmonary Embolism from a deep vein called?

A

DVT, most common type

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10
Q

What predisposes upper extremity DVT’s?

A

The use of Peripherally Inserted Central Catheters (PICC’s)

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11
Q

Where are the possible areas for a Pulmonary Embolism to cut off circulation?

A 
"Saddle" = at the intersection of the RPA and LPA
"Segmental" = blocking a major Bronchi
"Sub-segmental" = blocking a distal branch of Pulmonary Circulation
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12
Q

What type of Hypoxemia results from blocking a Pulmonary Artery?

A

Dead Space

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13
Q

What type of Hypoxemia results from a Pulmonary Embolism?

A

V/Q Mismatch

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14
Q

What does a sudden increase in dead space indicate in a patient?

A

Pulmonary Embolism, due to sudden loss of perfusion to an area of the lung

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15
Q

Does a Pulmonary Embolism result in hypercapnia or hypocapnia?

A

Pulmonary Embolism results in Hypocapnia, because the loss of blood flow triggers an increase in ventilation to maintain PaO2 leading to decreased PaCO2

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16
Q

Why does Pulmonary Embolism result in hypoxemia?

A

The blood that is cut off by the embolism is shunted to other areas that are not blocked, leading to an increase in flow that overwhelms regional ventilation, precipitating V/Q mismatch

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17
Q

How does Pulmonary Embolism lead to CV collapse?

A

A large Pulmonary Embolism increases afterload on the RV, leading to RV dilation and a shift of the IV Septum into the LV, compressing the LV and lowering LV Preload leading to lower Cardiac Output

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18
Q

How is hypotension in the setting of Pulmonary Embolism treated differently?

A

Normally, acute hypotension is treated by administering fluids; however, in Pulmonary Embolism induced RV failure, pushing fluids increases the strain on the RV by increasing it’s preload, leading to more dilation and worsening Cardiac Output

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19
Q

What sign indicates a Pulmonary Embolism on an echo of the heart?

A

The “D” sign - due to RV compression of LV

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20
Q

How does Pulmonary Embolism effect the RV?

A

Vicious cycle; Increased afterload leads to dilation, but dilation causes LV preload to drop and diminishes CO, leading to further dilation. Additionally, increased RV pressure leads to decreased coronary perfusion, in the setting of increased myocardial O2 demand

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21
Q

Why can Pulmonary Embolism rapidly decompensate?

A

Increased O2 demand by the heart is not met, and actually worsened, by the failing Cardiac Output due to RV dilation and decreased LV Preload

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22
Q

What’s the point of a CXR in a suspected Pulmonary Embolism if it can’t be seen?

A

CXR can be sued to identify alternative diagnoses and rule out other things, allowing diagnosis of Pulmonary Embolism by exclusion

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23
Q

What results from a CXR would raise suspicion for Pulmonary Embolism?

A

Normal CXR with respiratory symptom should raise concern for Pulmonary Embolism

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24
Q

Why is angiography no longer the gold standard for diagnosis of Pulmonary Embolism?

A

Angiography is invasive, requires contrast, specialist involvement, and cannot detect small clots

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25
Q

What is the gold standard for diagnosis of DVT?

A

Compression ultrasound

26
Q

How does a compression ultrasound work?

A

Use an ultrasound to find a major vein, and compress the patient to see the vein close on the ultrasound; if the vein doesn’t close, a clot is present

27
Q

Does a negative lower extremity ultrasound exclude DVT?

A

No, it just says there’s no clot in the vein on the ultrasound, and the clot may have already migrated elsewhere

28
Q

How is Type IV Pulmonary Hypertension diagnosed?

A

V/Q scan

29
Q

How does a V/Q scan work?

A

Inject and inhale radiolabeled isotopes to look for V/Q defects without contrast

30
Q

What are the limits of a V/Q Scan?

A

Doesn’t work well on patients with chronic lung disease

31
Q

Why does a V/Q scan detect Pulmonary Embolism?

A

Pulmonary Embolism results in increased flow through regions without the embolism and absent flow in the blocked region, causing a V/Q mismatch

32
Q

What is the best test for Pulmonary Embolism?

A

PE-CT

33
Q

How does a PE-CT scan work?

A

A bolus of contrast is inserted into the Pulmonary circulation, which should spread through the vasculature if unobstructed by Pulmonary Embolism

34
Q

What are the pro’s of PE-CT?

A

Fast, widely available, and high diagnostic accuracy

35
Q

What are the con’s of PE-CT?

A

Radiation, contrast, and less accurate for sub-segmental thrombi

36
Q

What are the test characteristics of the D-dimer?

A

High sensitivity but low specificity

37
Q

Is a D-dimer a rule out or a rule in test?

A

Rule’s out Pulmonary Embolism due to high sensitivity and NPV, but can’t rule in due to low specificity and low PPV

38
Q

How does a D-dimer work?

A

Measures a fibrin degradation product which is present after a clot or embolism forms

39
Q

What makes for an ideal diagnostic algorithm?

A

Low miss rate and avoids expensive tests

40
Q

What is a Wells Score?

A

Uses subjective and objective criteria to score a patient’s risk for PE; Well’s > 4 = PE likely

41
Q

What is the cutoff on a Wells Score?

A

Score > 4 makes PE likely, Score =< 3 makes PE unlikely

42
Q

What does the Wells Score do, statistically?

A

Sets pre-test probability

43
Q

What was the Christopher study?

A

Investigated the use of Wells Score + D-dimer to predict Pulmonary Embolism; extremely successful algorithm

44
Q

What was the Christopher study algorithm to predict Pulmonary Embolism?

A 
In a suspected PE, first calculate Well Score
If Well Score > 4, PE likely, do CT-PA
If Well Score =< 3, D-dimer test
If D-dimer elevated, PE likely, run CTPA
If D-dimer low, PE unlikely
45
Q

Why is a Well Score > 4 sufficient to initiate CTPA?

A

Because a Well Score > 4 has a high pretest probability of Pulmonary Embolism

46
Q

What are the acute treatment options for Pulmonary Embolism?

A

Heparin or Systemic Fibrinolytic Therapy, depending on severity

47
Q

What sets the treatment used for Pulmonary Embolism?

A

Severity of Pulmonary Embolism; for most patients, Heparin or LMWH are acceptable, but for PE + Shock/Cardiac Arrest, use a Systemic Fibrinolytic

48
Q

How does Heparin treat Pulmonary Embolism?

A

Infused via IV to help prevent clot formation, but requires lab monitoring

49
Q

How do LMWH’s treat Pulmonary Embolism?

A

SubQ injections that do not require lab monitoring help prevent clot formation

50
Q

How is Pulmonary Embolism in the setting of shock or cardiac arrest managed?

A

Use a systemic fibrinolytic to immediately break of the embolism and restore cardiac output

51
Q

What are the risks of systemic fibrinolytic therapy?

A

Higher risk for internal bleeding, including intracranial hemorrhage

52
Q

How should treatment of PE begin in the setting of high pre-test probability for PE?

A

Start anticoagulants while you evaluate

53
Q

What is the treatment for PE if anti-coagulants are contraindicated?

A

Insert an IVC filter to catch emboli before they reach the heart

54
Q

What is Submassive Pulmonary Embolism and how is it treated?

A

Pulmonary Embolism with RV dysfunction but without shock or cardiac arrest, treated with anticoagulants

55
Q

What are the treatment options for chronic Pulmonary Embolism?

A

Vitamin K antagonists (Warfarin)
LMWH (Enoxaparin)
Novel Oral Anticoagulants (RABE)

56
Q

What are the pro’s and con’s of Warfarin?

A 
Pro's = low cost, reversible, safe in renal disease
Con's = life long blood monitoring
57
Q

What are the pro’s and con’s of LMWH?

A 
Pro's = no lab monitoring
Con's = harder to reverse, hard to use in renal failure
58
Q

What are the pro’s and con’s of Direct Oral Anticoagulants?

A

Pro’s = no lab monitoring

Con’s expensive, limited reversal agents

59
Q

What are the 3 types of chronic Pulmonary Embolism?

A

Provoked, unprovoked, and Associated w/ Malignancy

60
Q

How is Provoked Pulmonary Embolism treated?

A

3 months of therapy

61
Q

How is Unprovoked Pulmonary Embolism treated?

A

3 months of therapy at a minimum, possibly indefinite depending on bleeding risk

62
Q

How is Pulmonary Embolism associated with Malignancy treated?

A

3 months minimum, until cancer is treated

Pulmonology (22 decks)

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