Pulmonary Embolism

Question 1

Just how prevalent is pulmonary embolism?

Answer 1

Evidence of PE is found on 60% of autopsies regardless of their cause of death. So, yeah, you could say it’s prevalent.

Question 2

In the majority of cases, ___ are the source of thrombi that embolize to the lungs

Answer 2

In the majority of cases, the lower extremities are the source of thrombi that embolize to the lungs

Question 3

Factors commonly cited as potential contributors to the genesis of venous thrombosis

Answer 3

1. Hypercoagulability
2. Endothelial dammage
3. Altered bloodflow

aka, Virchow’s triad

Question 4

Risks for thromboembolism

Answer 4

• Stasis (bed rest, long flights, etc)
• Postoperative state
• Congestive heart failure
• Obesity
• Underlying carcinoma
• Pregnancy and post-partum state
• Use of oral contraceptives
• Chronic deep venous insufficiency

Question 5

Pathologic changes that result from occlusion of a pulmonary artery depend to a large extent on . . .

Answer 5

. . . the location of the occlusion and the presence of other disorders that compromise O2 supply to the pulmonary parenchyma

Question 6

Two major consequences of vascular occlusion in the lung parenchyma distal to the site of occlusion

Answer 6

1. Pulmonary infarction and necrosis
2. Hemorrhage and edema (congestive atelectasis)

Question 7

Pleural involvement in thromboembolism

Answer 7

Regardless of type of pathology induced, it reaches all the way to the pleura due to the distribution of arterial supply within the lung.

Thus, pleural involvement and pleural effusion are very common in pulmonary embolism.

Question 8

Recovery from pulmonary embolism

Answer 8

If the embolism results in necrosis, a scar will form, permanently changing lung function.

On the other hand, if congestive atelectasis is the result, it is possible to fully recover lung function.

Question 9

Not all pulmonary emboli . . .

Answer 9

. . . produce infarction or congestive atelectasis.

Many are too small to fully occlude the vasculature, and so instead lead to mild pulmonary ischemia and increased right ventricular afterload. The extent of this depends on 1) how large the thrombus is and 2) how readily it is dissolved by the fibrinolytic system.

If a clot does not dissolve quickly enough, oragnization will ensue.

Question 10

___ is an unusual consequence of pulmonary embolism

Answer 10

Hypercapnia is an unusual consequence of pulmonary embolism.

Mainly because patients routinely increase their minute ventilation after an embolism occurs and more than compensate for the increase in dead space.

In fact, the usual consequence of a pulmonary embolus is hyperventilation and hypocapnia, not hypercapnia

Question 11

Rare situations in which PE results in hypercapnia

Answer 11

When minute ventilation is fixed, such as in an individual with COPD operating at maximal dynamic hyperinflation or someone hooked up to a mechanical ventilator with a set tidal volume and rate.

Question 12

PE-induced cardiogenic shock

Answer 12

When a PE results in substantial increase in RV afterload, the RV may fail, being unable to pump enough blood forward to the LV for the LV to gain a substantial preload.

Thus, the LV cannot pump blood forward to generate a cardiac output that maintains blood pressure, and the patient enter shock.

Question 13

Ischemia in the lung may result in loss of ___ production.

Answer 13

Ischemia in the lung may result in loss of surfactant production.

Atelectasis ensues.

Question 14

Clinical appearance of pulmonary embolism

Answer 14

• Often goes by unnoticed
• Patients usually present with acute onset dyspnea
• Occasionally hemoptysis or pleuritic pain
• Syncopy may occur in a massive embolism, defined as an embolism involving two or more lobes.
• Physical exam may reveal nothing or diminished sounds, wheezing, and crackles

Question 15

Diagnosing pulmonary embolism

Answer 15

• Often challenging
• Relies to some extent on the perceived pretest probability
• D-dimer is often a good place to start
• Checking O₂ sat and ordering CXR are standard, but unfortunately radiography is quite variable, often appearing completely normal
• CXR may reveal Westermark sign or Hampton hump
• Pleural effusion may accompany an embolism. So, if you see an effusion without other explanation, be suspicious of embolism
• Hypocapnia common
• CT angiography now best approach

Question 16

Westermark sign

Answer 16

Focal area of decreased lung markings on CXR

Often the only sign of a pulmonary embolism on CXR, and can be hard to identify

Question 17

Hampton hump

Answer 17

Sometimes visible on CXR

Cone-shaped opacity stretching to the pleura resulting from PE-induced atelectasis

Question 18

False positives on perfusion scans

Answer 18

May result from focal areas of other pulmonary pathology

So, a xenon-based ventilation test is performed for comparison.

Xenon-permeable and radiolabeled-albumin-impermeable areas are likely to be pulmonary embolisms

Question 19

Treating pulmonary embolism

Answer 19

• Anticoagulation: intravenous unfractionated heparin or subcutaneous LMWH, followup with oral anticoagulant (heparin or Xa inhibitor or thrombin inhibitor)
• Fibrinolysis is often employed, especially for patients with large thrombi, however there is no data suggesting it has a survival benefit (streptokinase, urokinase, tPA)
• IVC filter implants
• Prophylaxis: Intermittent pneumatic compression devices for the legs, heparin administered subcutaneously at low dosage

Question 20

IVC filter

Answer 20

Mesh placed in IVC that is intended to capture emboli as they travel to the lungs. Placed in high risk patients

Question 21

Four PE “syndromes”

Answer 21

1. Small or submassive PE
   
   • Dyspnea sometimes w/ cough, pleurisy, or calf/thigh pain, hemodynamically stable, screen w/ D-dimer
2. Pulmonary infarction
   
   • Uncommon due to dual blood supply, usually presents w/ hemoptysis, “Hamptom Hump” sign on CXR
3. Acute massive PE
   
   • Large clot, picture dominated by cardiogenic shock, hypotension w/ tachycardia, RV failure
4. Chronic thromboembolic pulmonary hypertension
   
   • Results in vessel wall remodeling and chronic pulmonary arterial hypertension, RVH

Question 22

Major vasoconstrictor resulting in constriction of pulmonary arteries following embolism

Answer 22

Endothelin-1 released from damaged endothelium

Question 23

Gas exchange changes following pulmonary embolism

Answer 23

1. V/Q mismatch (due to increased dead space), thus widened A-a gradient
2. Hypoxic vasoconstriction in dead space
3. Hyperventilation
4. Shunt physiology may begin to occur 24 hours following embolism due to atelectasis distal to the clut

Question 24

Four most useful tests in pulmonary embolism

Answer 24

1. D-dimer (as a screening method)
2. CT angiography
3. Ventilation-perfusion scan (xenon and radio-iodonated albumin)
4. Pulmonary angiogram (rarely used now)

Question 25

Unless a patient is presenting with an acute massive PE, it is not the clot that is in the lungs that will cause mortality . . .

Answer 25

. . . it’s the clot still sitting in the veins waiting to embolize

So prompt anticoagulation is a must

Question 26

When to use D-dimer test

Answer 26

If the patient has a low pre-test probability, it is a good screening test.

But, in a patient has a high pre-test probability, this may be unnecessary.

Question 27

How can you treat patients with low LV preload due to high RV afterload?

Answer 27

Give fluids to increase the RV preload! This will increase the amount of preload that gets to the LV.

Question 28

Warfarin and heparin overlap

Answer 28

Remember that warfarin therapy starts with ~3-7 day acute increase in clott risk before the chronic reduction in clott risk.

For this reason, patients need to be on heparin during the week they are starting warfarin.

Question 29

Before ordering CT angiography, you should first check. . .

Answer 29

. . . renal function.

They need to be able to get the dye out. If renal function isn’t good enough, do a V/Q test.