Pulmonary Embolism Flashcards
Just how prevalent is pulmonary embolism?
Evidence of PE is found on 60% of autopsies regardless of their cause of death. So, yeah, you could say it’s prevalent.
In the majority of cases, ___ are the source of thrombi that embolize to the lungs
In the majority of cases, the lower extremities are the source of thrombi that embolize to the lungs
Factors commonly cited as potential contributors to the genesis of venous thrombosis
- Hypercoagulability
- Endothelial dammage
- Altered bloodflow
aka, Virchow’s triad
Risks for thromboembolism
- 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
Pathologic changes that result from occlusion of a pulmonary artery depend to a large extent on . . .
. . . the location of the occlusion and the presence of other disorders that compromise O2 supply to the pulmonary parenchyma
Two major consequences of vascular occlusion in the lung parenchyma distal to the site of occlusion
- Pulmonary infarction and necrosis
- Hemorrhage and edema (congestive atelectasis)
Pleural involvement in thromboembolism
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.
Recovery from pulmonary embolism
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.
Not all pulmonary emboli . . .
. . . 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.
___ is an unusual consequence of pulmonary embolism
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
Rare situations in which PE results in hypercapnia
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.
PE-induced cardiogenic shock
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.
Ischemia in the lung may result in loss of ___ production.
Ischemia in the lung may result in loss of surfactant production.
Atelectasis ensues.
Clinical appearance of pulmonary embolism
- 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
Diagnosing pulmonary embolism
- 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
Westermark sign
Focal area of decreased lung markings on CXR
Often the only sign of a pulmonary embolism on CXR, and can be hard to identify
Hampton hump
Sometimes visible on CXR
Cone-shaped opacity stretching to the pleura resulting from PE-induced atelectasis
False positives on perfusion scans
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
Treating pulmonary embolism
- 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
IVC filter
Mesh placed in IVC that is intended to capture emboli as they travel to the lungs. Placed in high risk patients
Four PE “syndromes”
-
Small or submassive PE
- Dyspnea sometimes w/ cough, pleurisy, or calf/thigh pain, hemodynamically stable, screen w/ D-dimer
-
Pulmonary infarction
- Uncommon due to dual blood supply, usually presents w/ hemoptysis, “Hamptom Hump” sign on CXR
-
Acute massive PE
- Large clot, picture dominated by cardiogenic shock, hypotension w/ tachycardia, RV failure
-
Chronic thromboembolic pulmonary hypertension
- Results in vessel wall remodeling and chronic pulmonary arterial hypertension, RVH
Major vasoconstrictor resulting in constriction of pulmonary arteries following embolism
Endothelin-1 released from damaged endothelium
Gas exchange changes following pulmonary embolism
- V/Q mismatch (due to increased dead space), thus widened A-a gradient
- Hypoxic vasoconstriction in dead space
- Hyperventilation
- Shunt physiology may begin to occur 24 hours following embolism due to atelectasis distal to the clut
Four most useful tests in pulmonary embolism
- D-dimer (as a screening method)
- CT angiography
- Ventilation-perfusion scan (xenon and radio-iodonated albumin)
- Pulmonary angiogram (rarely used now)
Unless a patient is presenting with an acute massive PE, it is not the clot that is in the lungs that will cause mortality . . .
. . . it’s the clot still sitting in the veins waiting to embolize
So prompt anticoagulation is a must
When to use D-dimer test
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.
How can you treat patients with low LV preload due to high RV afterload?
Give fluids to increase the RV preload! This will increase the amount of preload that gets to the LV.
Warfarin and heparin overlap
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.
Before ordering CT angiography, you should first check. . .
. . . renal function.
They need to be able to get the dye out. If renal function isn’t good enough, do a V/Q test.
