MVS Pathophysiology: Pulmonary Embolism

community acquired pneumonia | pulmonary embolism | pneumothorax | asthma

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Definition and Classification Etiology and Risk Factors Pathophysiology Clinical Presentation Diagnosis Treatment

A.Definition and Classification

A pulmonary embolism most commonly occurs when a thrombus (a circulating blood clot) lodges in the pulmonary vascular bed and restricts circulation to the corresponding part of lung vasculature. PEs are generally classified as small, medium or large based of the size of the obstruction. Large PEs affect 2 or more lung lobes, medium PE affect 1 lung lobe and small PE affect a fraction of a lung lobe.

B. Etiology and Risk Factors

There are three major risk factors for thromboemboli formation (Virchow's Triad)
1) Stasis
2) Endothelial injury
3) Hypercoagulable states

Most thrombi are derived from the deep veins of the thigh but can arise from other veins, for instance, in the knee, pelvis, upper extremities and also from mural thrombi in the right side of the heart. Surgical procedures that risk intimal injury are a common cause of PE. Bedridden patients subject to long periods of stasis are also at risk. Deep vein thrombosis is not definitively associated with the occurrence of PE.

PE also rarely results from embolization of tumor cells or fragments, fat, amniotic fluid, foreign bodies or air.

C. Pathophysiology

A thrombus that has separated from its site of origin travels through the circulation to the inferior vena cava. The right ventricle pumps this thrombus to the pulmonary arteries where the thrombus finally lodges. PE may occur singly or multiply. They can be microscopic in size or be big enough to occlude the major branches of the pulmonary artery.

The embolus obstructs flow in the pulmonary arteries and thus causes an increase in resistance to blood flow in the pulmonary vessels. Severe pulmonary hypertension, RV strain, and cardiac heart failure occur when more than 50-60% decrease in perfusion. In addition, intrapulmonary reflexes stimulate the relase of humoral substances that lead to vasoconstriction throughout the lungs and thus increases pulmonary vascular resistance.

10% of PE will progress to pulmonary infarction. The lung depends on 3 sources of oxygen (airways, bronchial circulation, pulmonary circulation) and therefore the chance that all 3 sources will be compromised simultaneously are not great.

Recurrent PE may gradually obstruct the pulmonary vasculature and ultimately lead to chronic obstructive pulmonary hypertension and cor pulmonale.

The most important pathophysiological consequence of PE is V/Q mismatch in which there is "dead space" ventilation in some parts of the lung and overperfusion in others. "Dead space" ventilation refers to ventilation of lung segments that have obstructed vascular supply and thus no perfusion. On the other hand, overperfusion and decreased vascular resistance in other parts of the lung leads to right-to-left intrapulmonary shunting with insufficient oxygenation of a large portion of perfused blood.

D. Clinical Presentation

The clinical presentation of a patient with PE is variable and partially depends on the size of the emboli. On auscultation, you will hear percussion dullness and decreased breath sounds over the involved base. Findings are otherwise normal over the other lung segments. Evidence of DVT (deep venous thrombosis) is present in 50% of patients with PE.

E. Diagnosis

1) CXR is frequently normal but may see evidence of atelectasis/infarction or oligemia/decreased vascular markings .

2) ECG most commonly shows sinus tachycardia but may produce S1Q3flippedT3 with a large PE. It is not a specific test for PE but may help to rule out myocardial infarction from the differential diagnosis.

3) ABG: PaO2 (hypoxia) and PaCO2 (hyperventilation) is usually decreased. Low PCO2 and slightly increased pH indicate mild acute respiratory alkalosis. A-a gradient is commonly increased.

4) V/Q scan may reveals areas that are well ventilated but poorly perfused. Results of V/Q scanning must be correlated with the patient's clinical presentation and with CXR results.

5) Pulmonary angiography, although the gold standard for diagnosis of PE, is invasive and should only be considered if surgery is planned or if the risks of long-term anticoagulation are higher than normal.

6) Venous duplex ultrasound or doppler of the lower extremities is non-invasive and may provide corroborative evidence of PE but can produce false positive results.

7) Spiral CT-scan with contrast may show larger, more prominant emboli

F. Treatment

Initial treatment involves administration of oxygen and getting the patient into a sitting position to aid respiration. Thrombolysis can be used for large emboli. Prophylactic anticoagulation therapy with IV heparin proceeding to warfarin should be used to prevent further emboli. An inferior vena cava filter can also be used if anticoagulation is contraindicated or unsuccessful or if another PE would be fatal. Embolectomy is an alternative treatment for patients who cannot maintain effective cardiac output but the survival rate following this procedure is only 10%.

However, the best treatment for PE is prevention. During surgery, the patient should have his legs elevated if possible. In addition, compression boots may be used to increase circulation during surgery. The patient should be encouraged to regain mobility quickly after surgery. If a prolonged recovery is expected, anticoagulation therapy should be maintained after surgery.

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