Pulmonary Vascular Disorder Flashcards

1
Q

What is pulmonary hypertension?

What are the measurements that define pulmonary hypertension?

How would you describe the prognosis?

A

Increase in pulmonary arterial pressure from increased pulmonary vascular resistance

Pulmonary artery systolic pressure > 30 mmHg or a mean PAP of > 20 mmHg

Poor prognosis especially in the setting of cor pulmonale

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2
Q

The etiology is extensive for pulmonary hypertension and grouped 1-5. What are the groupings?

5

A
  1. Pulmonary arterial hypertension
  2. Pulmonary hypertension secondary to left heart disease
  3. Pulmonary hypertension secondary to lung disease/chronic hypoxia
  4. Chronic pulmonary thromboembolic disease
  5. Pulmonary hypertension with unclear multifactorial mechanisms
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3
Q

Pulmonary hypertension can be caused by a number of factors but they all lead to what happening?
3

A
  1. Force the right side of the heart to work harder to pump blood to the lungs.
  2. The right chambers may enlarge because of this and struggle to function.
  3. Blood is then forced backward towards the tricuspid valve
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4
Q

Symptoms of Pulmonary Hypertension?

5

A
  1. Dyspnea on exertion
    - -May be at rest in severe cases
  2. Fatigue
  3. Chest pain
    - -Anginal
  4. Syncope with exertion
  5. Nonproductive cough
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5
Q

Signs of pulmonary hypertension?

6

A
  1. Narrow splitting of S2 with loud pulmonary component
  2. Right ventricular hypertrophy
  3. Right atrial enlargement
  4. Enlarged central pulmonary arteries on CXR
  5. JVD
  6. Right sided heart failure symptoms such as Hepatomegaly, LE edema
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6
Q

The workup for pulmonary hypertension may include what?

7

A
  1. CXR
  2. CT of the chest
  3. PFTs
  4. Echocardiography with Doppler flow
  5. Right sided cardiac catheterization with vasodilator challenge
  6. V/Q scanning if suspect disease is from chronic thromboembolic disease
  7. Exclude HIV and collagen vascular disease
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7
Q

What will you see on the chest xray of someone with pulmonary hypertension?
3

A
  1. interstitial pulmonary markings
  2. enlargement of the right and left ventricles and also the right atrium
  3. Large attenuated peripheral pulmonary arteries
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8
Q

Treatment approach for pulmonary hypertension depends on what?

A

Treating the underlying cause first

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9
Q

Treating the underlying cause first for pulmonary hypertension usually with what?
3

A
  1. Vasodilators
  2. Supplemental oxygen if hypoxemia present
  3. May require chronic anticoagulation
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10
Q

What kind of vasodilators would we prescribe for pulmonary hypertension?
4

A
  1. Oral calcium channel blockers (first line therapy)
  2. Oral phosphodiasterase inhibitors (sildenafil, tadalafil)
  3. Oral endothelin receptor antagonists (ambrisentan, bosentan)
  4. Continuous infusion of prostacyclin agents (epoprostenol, treprostinil)
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11
Q

What is cor pulmonale?

What is the prognosis?

What is it most commonly caused by?
3

A

RV systolic and diastolic failure secondary to pulmonary disease or from pulmonary vascular disease

Poor prognosis

Most commonly caused by

  1. Pulmonary hypertension,
  2. COPD or
  3. idiopathic pulmonary fibrosis
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12
Q

Symtpoms of cor pulmonale?

7

A
  1. Chronic productive cough
  2. Exertional dyspnea
  3. Wheezing
  4. Easy fatigability
  5. Weakness
  6. RUQ pain
  7. Dependent edema
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13
Q

Signs of cor pulmonale?

9

A
  1. Cyanosis
  2. Clubbing
  3. Distended neck veins
  4. RV heave or gallop
  5. Prominent lower sternal or epigastric pulsations
  6. Hepatomegaly
  7. Dependent edema
  8. Ascites
  9. Severe lung disease
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14
Q

What would we see in the diagnostic studies for cor pulmonale?
7

A
  1. Polycythemia secondary to chronic hypoxemia
  2. SaO2 of less than 85%
    EKG
    May show RAD, peaked P waves, Deep S waves in V6, may see Q waves in inferior leads b/c of vertically placed heart
    PFTs
    Confirm underlying lung disease
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15
Q

What will the EKG show on cor pulmonale?
4

What will the echo show on a cor pumonale pt?
2

A
  1. May show RAD,
  2. peaked P waves,
  3. Deep S waves in V6,
  4. may see Q waves in inferior leads b/c of vertically placed heart
  5. Should show normal LV size and function
  6. RV and RA dilation and RV systolic dysfunction
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16
Q

How should we treat cor pulmonale?

4

A
  1. Treat chronic respiratory failure
  2. Supplemental O2
    Manage right heart failure symptoms with
  3. Fluid and salt restriction
  4. Diuretics
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17
Q

What does supplemental oxygen help to do in cor pulmonale patients?2

A
  1. May improve survival

2. Helps to decrease RV afterload by reducing the pulmonary vascular resistance

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18
Q

What is the key to treating pulmonary embolism?

A

Key is prevention and always considering this in the differential diagnosis when applicable

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19
Q

PE may be caused by the following:
8

(what is the most common cause?)

A
  1. Air
  2. Amniotic fluid (during active labor)
  3. Fat (long bone fractures)
  4. Foreign bodies (talc in IV drug users)
  5. Parasite eggs
  6. Septic emboli
  7. Tumor cells
  8. Most common cause is a venous thrombus
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20
Q

Where do the clots come from in a pulmonary embolism? 2

What place has the highest risk of developing a PE?

A

have lower extremity DVT (deep vein thrombosis) when evaluated
1. Calf veins
If localized to the calf veins, rarely travel to lungs
20% of thrombi here migrate proximally to popliteal and femoral veins
2. Popliteal and ileofemoral veins
50-60% of patients with thrombi here will develop PE

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21
Q

Risk factors for PE and DVT are the same. What is this called and what is part of it?
3

A

Virchow’s triad

  1. Venous stasis
  2. Injury to the vessel wall
  3. Hypercoagulability
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22
Q

Factors that promote venous stasis that could cause PE

7

A
  1. Immobility
  2. Postoperative state
  3. Obesity
  4. Hyperviscosity
    - -polycythemia
  5. Increased central venous pressure such as
  6. Low cardiac output
  7. Pregnancy
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23
Q

Vessel damage may occur from what three things that could cause PE?
3

A
  1. Prior episodes of thrombosis
  2. Orthopedic surgery
  3. Trauma
24
Q

Factors associated with hypercoagulability that could cause PE
4

A
  1. Surgery
  2. Meds such as hormones
  3. Disease such as malignancy
  4. Genetic
25
Q

What are the genetic factors that could increase the risk of PE?
2

A
  1. Factor V Leiden (most common inherited)
  2. Dysfunction of Protein C, Protein S, Antithrombin III, prothrombin gene mutation, hyper-homocysteinemia, antiphospholipid antibodies (lupus anticoagulant, anticardiolipin antibody)
26
Q

Physiologic changes with PE

3

A
  1. Reflex bronchoconstriction and vasoconstriction from neurohormonal responses
  2. Right ventricular failure
    If massive thrombus
  3. Pulmonary vasculature obstruction
27
Q

Pulmonary vasculature obstruction during a PE causes what?2

A
  1. Increased pulmonary vascular resistance

2. Causes physiologic deadspace (ventilation of the lung without perfusion)

28
Q

What does the presence of dead space (vent without perfusion) lead to?
3

A
  1. Hypoxemia due to R to Left “shunting” of blood
  2. Decreased cardiac output
  3. Surfactant depletion causing atelectasis
29
Q

Pulmonary Embolus symptoms?
8
(What are the two most common?)

A
  1. Dyspnea**
  2. Pleuritic chest pain**
  3. Cough
  4. Leg pain
  5. Hemoptysis
  6. Palpitatins
  7. Wheezing
  8. Anginal pain
30
Q

Pulmonary embolus signs?
10

Whats the most common one?

A
  1. Tachypnea**
  2. Crackles
  3. Tachycardia
  4. S4
  5. S3
  6. Accentuated S2
  7. Low grade fever
  8. Homan’s sign
  9. Pleural friction rub
  10. Cyanosis
31
Q

Diagnostic studies
for a PE?
11

A
  1. EKG
  2. Arterial blood gases
  3. D-dimer
  4. Troponin I or T
  5. BNP
  6. Chest X-ray
  7. CT angiography
  8. Ventilation-perfusion scan (V/Q scan)
  9. Venous ultrasound of the extremities
  10. Pulmonary angiography
  11. MRI
32
Q

PE EKG findings may include:

5

A
  1. Q waves in lead III
  2. R bundle branch block
  3. S wave in lead I
  4. Tachycardia
  5. Inverted T waves in lead III
33
Q

Why would we do an arterial blood gas for a PE?

Hyperventilation would cause what type of metabolic disturbance?

A

Not diagnostic (not sensitive or specific for PE)

  1. May show hyperventilation and/or possibly hypoxemia
  2. alkaline
34
Q

What is a D-dimer lab tell us?

Would it be elevated or decreased?

A

Degradation product of cross-linked fibrin

Elevated in the presence of thrombus
In the setting of thromboembolism
Sensitivity 95-97%
Specificity 45%

35
Q

What in general with cause an increase in the D-dimer?

A

Anything that causes clotting

36
Q

What Cardiac tests would we do for a PE? 3

Would these tests be elevated or decreased and why? 2

What do we need to keep in mind about these tests?

A
  1. Troponin I,
  2. Troponin T and
  3. BNP

May all be elevated due to R ventricular strain and/or acute RV failure

These tests are not helpful for diagnosing PE and may often confuse the matter

37
Q

Radiologic studies for a PE?

6

A
  1. CXR
  2. CT angiogram of the chest
  3. V/Q scan
  4. Lower extremity venous ultrasound
  5. Pulmonary angiography
    - -Previous gold standard but rarely used as there are safer less invasive options
  6. MRI: used primarily in research
38
Q

What will the chest Xray show with a PE?
5

What is the most common finding on a PE XRAY?

A
  1. Wedge shaped peripheral defect (Hampton’s hump) in the setting of pulmonary infarct
  2. Atelectasis
  3. Parenchymal infiltrates
  4. Pleural effusion
  5. Prominent central pulmonary artery (Westermark sign)

The above findings are largely nonspecific
A normal CXR is the most common finding

39
Q

If normal in the setting of acute _______without prior history of lung disease is highly suggestive of PE

A

hypoxemia

40
Q

What is the most sensitive test for detecting PE in larger (proximal) pulmonary arteries?

What are the major risks of these tests?

What if the clot is in distal arteries?

Whats the bottom line to this test?

A

CT pulmonary angiogrpahy

IV contrast and ionizing radiation exposure

May miss as many as 75% of subsegmental defects compared with pulmonary angiography

Bottom line: normal CT scan does not exclude PE in high-risk patients

41
Q

What are we doing in a V/Q scan?

A

Its a nucelar medicine test in which we compared the perfusion scan to the ventilation scan.

42
Q

When is a VQ scan abnormal?

How is it read?

What is the issue with these?

A

Abnormal if there is ventilation without perfusion to the segmental lung area

Read as high, low or intermediate (indeterminate) probability of PE

Helpful if they are read as “normal” or “high probability of PE”
75% of these scans in the PIOPED I study were nondiagnostic

43
Q

In a VQ scan radioactive compounds are inhaled into the airspace of the lung. What will the test look like in a normal lung?

We also inject it into the vein and this will travel to the lung tissue in blood vessels. If there is a pulmonary embolus what will it show?

What combination gives us a high risk test for pulmonary emolbism?

A

the compound will distribute evenly

No injected material will reach this space of the vasculature in the lung

mismatch of inhaled and injected compounds onthe lung scan images

44
Q

What is lower extremity venous ultrasonagrpahy useful for?
2

When is it less accurate?
2

A
  1. Helpful for ruling out/in DVT of the lower extremities
  2. Quite accurate for the detection of proximal LE DVT (common femoral or popliteal veins)
  3. Distal or recurrent thrombi
  4. Asymptomatic patients
    (low positive predictive value)
45
Q

What is the gold standard for a daignosis of PE?

What is its role in the daignosis of a PE?
2

A
Pulmonary angiography
(definitive diagnosis in 97% of patients with DVT)
  1. If the diagnosis of PE is in doubt when there is a high clinical pretest probability of PE
  2. When the diagnosis of PE must be established with certainty
46
Q

Work up for PE may include:

6

A
  1. D-dimer
  2. EKG
  3. CXR
  4. Doppler ultrasound of the lower extremities
  5. *CT angiogram of the chest with PE protocol
  6. *V/Q scan
    * Do not routinely order a CT angiogram AND V/Q scan; pick one of the two
47
Q

What is the PERC rule for a PE?

8

A
  1. 50 or over
  2. HR is 100 or over
  3. O2 below 95%
  4. History of venous thromboembolism
  5. trauma or surgery within 4 weeks
  6. hemoptysis
  7. Exogenous estrogen
  8. unilateral leg swelling
48
Q

Wells criteria for a DVT?

9

A
  1. Active cancer
    Treatment or palliation within 6 months
  2. Bedridden recently ≥3 days or major surgery within 12 weeks
  3. Calf swelling >3 cm compared to the other leg
  4. Collateral (nonvaricose) superficial veins present
    - —Measured 10cm below tibial tuberosity
  5. Entire leg swollen
  6. Localized tenderness along the deep venous system
  7. Pitting edema, confined to symptomatic leg
  8. Paralysis, paresis, or recent plaster immobilization of the lower extremity
  9. Previously documented DVT

Alternative diagnosis to DVT at least as likely

49
Q

PERC will rule out a PE if what criteria arent met?

A

if no criteria ar present and pre-test probabilty is below 15%

50
Q

Wells Criteria can be used to help aid in the workup
Unlikly?
Likely?

A

Unlikely (score ≤4)

Likely (score less than 4)

51
Q

If the wells criteris is equal to or greater than 4 what should we do?
2

A
  1. D-dimer > 500 ng/mL proceed to imaging study (CTA or VQ scan)
  2. HOWEVER if high probability score > 6 can skip the D-dimer and go directly to imaging
52
Q

If the wells score is less than 4 what should we do?

A

D-dimer

53
Q

PERC is only used for patients with what?

How should we apply this?
2

A

Only for patients with low probability of PE

Patient with low likelihood of PE but need to rule out

  1. If all 8 criteria are met, no further testing needed
  2. If not meeting all 8 criteria then further testing with D-dimer or imaging is needed
54
Q

Treatment of PE?

A
  1. Hospitalization
  2. Supplemental oxygen
  3. Heparin (LMWH, UFH)
  4. Assess for fibrinolytics
  5. Outpatient anticoagulation for 3-6 months depending on the clinical situation
  6. Inferior vena cava filter
55
Q

When should we think of using a inferior vena cava filter? 2

When would we want to use fibrinolytics?
2

A
  1. if large clot burden or
  2. unable to anticoagulate as an outpatient

if significant hemodynamic compromise (shock or syncope)