Pulmonary thromboembolism Flashcards

1
Q

What is a pulmonary thromboembolism?

A

A condition in which one (or more) blood clots (thrombi), typically from the deep veins of the legs, travel to the lung and obstruct pulmonary arteries.

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2
Q

Name the key signs and symptoms of a pulmonary thromboembolism (8)

A
  • Dyspnea (SOB)
  • Pleuritic chest pain
  • Tachycardia
  • Hypotension
  • Signs of deep vein thrombosis (swelling and pain in the leg)
  • Hemoptysis
  • Palpitations
  • Syncope
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3
Q

What is one of the main causes of pulmonary thromboembolism

A

Deep vein thrombosis (usually in the leg): about 95% of pulmonary thromboembolism results from DVT

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4
Q

What are some risk factors for pulmonary thromboembolism? (10)

A
  • Surgery
  • Pregnancy
  • COPD
  • Congestive heart failure
  • Varicose veins
  • Fractures
  • Malignant disease
  • Age
  • Immobility
  • Thrombotic disorders
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5
Q

Describe the Virchow’s triad, i.e. the 3 primary risk factors for thrombosis

A
  1. Hypercoagulability
  2. Abnormal blood flow (stasis and turbulence)
  3. Endothelial injury/dysfunction
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6
Q

What are some risk factors for endothelial injury? (3)

A
  1. Trauma
  2. Surgery (post-operative injury)
  3. Previous venous thromboembolism
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7
Q

What are some risk factors for blood stasis? (2 main ones)

A

Immobility:
* Post-operative (surgery)
* Medical illness (congestive heart failure, stroke)
* Travel (economy flight syndrome)

Obstruction to venous flow:
* Pregnancy
* Previous venous thromboembolism
* Malignancy
* “May Thurner” syndrome (anatomic)

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8
Q

What are some risk factors for hypercoagulability (5)?

A
  • Hormones (pregnancy, contraceptive pill)
  • Malignancy
  • Medications
  • Medical illness
  • Congenital mutations of factors involved in the coagulation cascade
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9
Q

How does a pulmonary thromboembolism disrupt the pressures in the vasculature and what are the 2 consequences of the cardiovascular system?

A
  1. Pulmonary artery blockage results in an increase in pulmonary vascular pressure
  2. Increase in vascular pressure leads to the back flow of blood to the right side of the heart
  3. Back flow leads to increase in the right ventricular pressure: right ventricle becomes dilated and weakened
  4. Dilation of the right ventricle can cause right-sided heart failure
  5. Right-sided heart failure results in a decreased stroke volume, decreased cardiac output and overall decreased blood pressure

Net Result
Hypotension (low BP) Tachycardia (compensatory mechanism for low CO)

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10
Q

A pulmonary thromboembolism will cause abnormal gas exchange because the obstruction of pulmonary vessels causes… (2)

A

V-Q mismatch (ventilation-perfusion mismatch) and inflammation

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11
Q

During a PTE, how does inflammation in the lung result in hyperventilation?

A

Inflammation stimulates bronchoconstriction by the release of various cytokines. This leads to a decrease in oxygen (hypoxemia), which will stimulate hyperventilation.

Note that hyperventilation during a PTE is also a compensatory mechanism for increased dead space due to decreased perfusion

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12
Q

What is the consequence of hyperventilation during a PTE?

A

Hypocapnia (decrease in carbon dioxide)

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13
Q

Hyperventilation and inflammation during a PTE ultimately result in….

A
  • Hypocapnia (decrease in blood CO2)
  • Hypoxemia (decrease in blood O2)

Together, these conditions result in RESPIRATORY ALKALOSIS

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14
Q

As you know, PTE causes hyperventilation, but the blood vessels are unperfused (V/Q>1). This leads to…

A

an increased alveolar dead space.

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15
Q

Unusual case:
A patient has a pulmonary thromboembolism. However, their minute ventilation is fixed, because they are unconscious and anesthetized, and their ventilation is controlled by a mechanical ventilator. How might their PCO2 be affected?

A

Decreased perfusion without hyperventilation will still lead to an increase in alveolar dead space. However, in this case, the patient may develop hypercapnia (high CO2 in blood) and hypoxemia because fewer areas of the lungs can participate in gas exchange.

Respiratory acidosis

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16
Q

Name 3 mediators released by platelets in the thrombus contributing to bronchoconstriction.

A

serotonin
prostaglandins
histamine

17
Q

What is the Wells score?

A

A scoring method used to evaluate a patient’s risk for deep vein thrombosis.

Score >6 : High probability of PE
Score 2-6: Moderate probability of PE
Score <2: Low probability of PE

18
Q

What are two CXR patterns that may indicate a PE?

A

Hampton’s Hump
Westermark Sign

Both are very difficult to see and it is almost impossible to diagnose a PE by CXR

19
Q

What are some diagnostic tests used to diagnose a PE? Which is the most common and reliable one?

A
  • CXR
  • V/Q Scanning
  • Compression ultrasonography (leg)
  • Computerized tomographic pulmonary angiography (CTPA)

Most common and reliable diagnostic test: CTPA

20
Q

What are some advantages (4) and disadvantages (2) of computerized tomographic pulmonary angiography?

A

Advantages:
* Non-invasive
* Readily available
* May give alternative diagnosis
* Good at ruling in and out

Disadvantages:
* Requires contrast (which not everyone can tolerate)
* Requires expert reading

21
Q

Historically, what is the gold standard for PE diagnosis?

A

Conventional pulmonary angiography (now replaced by CT angiography)

22
Q

When should a physician begin therapy for a PE? Why?

A

A physician should begin therapy when diagnosis is suspected, while waiting for diagnostic test results.
Reason: A PE can be life-threatening and obtaining results can take some time!

23
Q

What is the main treatment for a PE? What is the mechanism behind it?

A

Anticoagulant drugs
* Heparin
* Warfarin
* Direct oral anticoagulants (DOAC): most commonly used!

These drugs stop the PROPAGATION of the blood clot, but cannot dissolve the existing thrombus!

24
Q

What type of therapy is administered to patients with critical cases of PE? (3)

A
  • Thrombolysis (therapy that dissolves thrombus, BUT increases risk of bleeding)
  • Catheter-based therapies
  • Surgery (embolectomy)
25
Q

How long does PE therapy last?

A

At least 3-6 months, but may be lifelong depending on the case

26
Q

Low molecular weight heparin (3)

A
  • Quick onset of action
  • Subcutaneous injection
  • No need for monitoring level of anti-coagulation
27
Q

Warfarin (3)

A
  • Oral Vitamin K antagonist
  • Longer onset of action (4-7 days)
  • Needs careful monitoring
28
Q

Direct oral anticoagulants (DOAC) (3)

A
  • Factor Xa inhibitors (taken orally)
  • No need for monitoring
  • Minimal interactions with other medications
29
Q

Direct oral anticoagulants (DOAC) are contra-indicated with…

A

renal failure