Pulmonary Embolism

FARRUKH MASOOD

NISHTAR MEDICAL COLLEGE

Definition

Pulmonary embolism is a sudden blockage in a lung artery. The blockage usually is caused by a blood clot that travels to the lung from a vein in the leg.

Etiology of emboli

Thrombus, usually formed in the systemic veins or rarely in the right heart (<10% of cases), may dislodge and embolize into the pulmonary arterial system.

Source of thrombi include

Pelvic and abdominal veins DVT Hypercoagulable states Amniotic emboli Fat emboli from long bones

Pathophysiology

As a thrombus clogs pulmonary vessels, there is a decline in perfusion of the lung tissue but ventilation remains intact which results in increased intrapulmonary dead space and impaired gaseous exchange through alveoli.

After some hours the non-perfused lung no longer produces surfactant. Alveolar collapse occurs and exacerbates hypoxaemia.

The primary haemodynamic consequence of pulmonary embolism is a reduction in the cross-sectional area of the pulmonary arterial bed which results in an elevation of pulmonary arterial pressure and a reduction in cardiac output. The zone of lung that is no longer perfused by the pulmonary artery may infarct, but often does not do so because oxygen continues to be supplied by the bronchial circulation and the airways.

Clinical features

Sudden onset of unexplained dyspnea (most common)

Pleuritic chest pain and hemoptysis (if infarct occurs)

On basis of clinical symptoms emboli can be classified as Small/medium pulmonary embolism

Massive pulmonary embolism

Multiple recurrent pulmonary emboli

Small/medium pulmonary embolism

In this situation an embolus has impacted in a terminal pulmonary vessel. 

Symptoms are

pleuritic chest pain and breathlessness.

Haemoptysis occurs in 30%, often ≥3 days after the initial event.

On examination

tachypnoeic with a localized pleural rub and often coarse crackles over the area involved.

An exudative pleural effusion (occasionally blood-stained) can develop. The patient may have a fever, and cardiovascular examination is normal.

Massive pulmonary embolism

This is a much rarer condition where sudden collapse occurs because of an acute obstruction of the right ventricular outflow tract.

Severe central chest pain (cardiac ischaemia due to lack of coronary blood flow) and becomes shocked, pale and sweaty.

Syncope may result if the cardiac output is transiently but dramatically reduced, and death may occur.

On examination the patient is tachypnoeic, has a tachycardia with hypotension

The jugular venous pressure (JVP) is raised with a prominent ‘a’ wave. There is a right ventricular heave, a gallop rhythm and a widely split second heart sound.

Multiple recurrent pulmonary emboli

Increased breathlessness, often over weeks or months accompanied by

Weakness

syncope on exertion and occasionally angina.

The physical signs are due to the pulmonary hypertension that has developed from multiple occlusions of the pulmonary vasculature.

On examination

Right ventricular heave

Loud pulmonary second sound.

Investigation

Small/medium pulmonary emboli

Chest X-ray is often normal, but linear atelectasis or blunting of a costophrenic angle (due to a small effusion) is not uncommon. These features develop only after some time. A raised hemidiaphragm is present in some patients. Previous infarcts may be seen as opaque linear

ECG is usually normal, except for sinus tachycardia, but sometimes atrial fibrillation or another tachyarrhythmia occurs. There may be evidence of right ventricular strain.

Blood tests. Pulmonary infarction results in a polymorphonuclear leucocytosis, an elevated ESR and increased lactate dehydrogenase levels in the serum. Immediately prior to commencing anticoagulants a thrombophilia screen should be checked.

Plasma D-dimer – if this is undetectable, it excludes a diagnosis of pulmonary embolism.

Radionuclide ventilation/perfusion scanning (V̇! /Q̇!  scan) is a good and widely available diagnostic investigation. Pulmonary 99mTc scintigraphy demonstrates underperfused areas which, if not accompanied by a ventilation defect on a ventilation scintigram performed after inhalation of radioactive xenon gas , is highly suggestive of a pulmonary embolus. There are limitations to the test, however. For example, a matched defect may arise with a pulmonary embolus which causes an infarct, or from emphysematous bullae. This test is therefore conventionally reported as a probability (low, medium or high) of pulmonary embolus and should be interpreted in the context of the history, examination and other investigations.

Ultrasound scanning can be performed for the detection of clots in pelvic or iliofemoral veins

CT scans. Contrast-enhanced multidetector CT angiograms (CTA) , have a sensitivity of 83% and specificity of 96%, with a positive predictive value of 92%. These values will increase with the use of 64-multislice scanners.

MR imaging gives similar results and is used if CT angiography is contraindicated.

Massive pulmonary emboli Chest X-ray may show pulmonary oligaemia, sometimes with

dilatation of the pulmonary artery in the hila. Often there are no changes.

ECG shows right atrial dilatation with tall peaked P waves in lead II. Right ventricular strain and dilatation give rise to right axis deviation, some degree of right bundle branch block, and T wave inversion in the right precordial leads . The ‘classic’ ECG pattern with an S wave in lead I, and a Q wave and inverted T waves in lead III (S1, Q3, T3), is rare.

Blood gases show arterial hypoxaemia with a low arterial CO2 level, i.e. type I respiratory failure pattern.

Echocardiography shows a vigorously contracting left ventricle, and occasionally a dilated right ventricle and a clot in the right ventricular outflow tract.

Pulmonary angiography has now been replaced by CT and MR angiography.

Multiple recurrent pulmonary emboli Chest X-ray may be normal. Enlarged pulmonary arterioles with

oligaemic lung fields indicate advanced disease.

ECG can be normal or show signs of pulmonary hypertension

Leg imaging with ultrasound and venography may show thrombi.

V̇!/Q̇!  scan may show evidence of pulmonary infarcts.

Multidetector CT scans can detect small emboli.

Further tests looking for exercise-induced hypoxaemia and catheter studies to estimate pulmonary artery pressures are sometimes required.

Diagnosis

The symptoms and signs of small and medium-sized pulmonary emboli are often subtle and nonspecific, so the diagnosis is often delayed or even completely missed.

Pulmonary embolism should be considered if patients present with symptoms of unexplained cough, chest pain, haemoptysis, new-onset atrial fibrillation (or other tachycardia), or signs of pulmonary hypertension

High clinical probability patients should proceed to multi-detector contrast-enhanced CT angiography (CTA) . A positive test confirms the diagnosis. A negative test but with an elevated D-dimer may require venous ultrasonography. (Patients with renal failure or contrast allergy can have ventilation/perfusion V̇�/Q̇�  scanning).

Low or intermediate clinical risk patients should have a D-dimer assay performed. A negative D-dimer rules out a pulmonary embolism. A positive D-dimer requires further investigation with CTA.

Patients who are haemodynamically unstable (shock, systolic blood pressure <90 mmHg, drop in pressure of ≥40 mmHg) may require urgent CTA or if critically ill with a high clinical probability, an echocardiogram should be performed – right ventricular dysfunction is highly suggestive of a pulmonary embolism – a normal right ventricle should suggest alternative diagnoses.

Treatment

Acute management

All patients should receive high-flow oxygen (60–100%) unless they have significant chronic lung disease. Patients with pulmonary infarcts require bed rest and analgesia.

Patients should be anticoagulated initially with subcutaneous low-molecular-weight heparin or fondaparinux or intravenous unfractionated heparin followed by warfarin therapy.

Massive pulmonary emboli. Intravenous fluids and even inotropic agents to improve the pumping of the right heart are sometimes required, and very ill patients will require care on the intensive therapy unit

Fibrinolytic therapy such as streptokinase (250 000 units by i.v. infusion over 30 min, followed by streptokinase 100 000 units i.v. hourly for up to 12–72 hours, according to manufacturer’s instructions) has been shown in controlled trials to clear pulmonary emboli more rapidly and to confer a survival benefit in massive PE. It should be used in unstable patients and in some stable patients with adverse features, e.g. right ventricular dysfunction.

Surgical embolectomy is rarely necessary, but there may be no alternative when the haemodynamic circumstances are very severe

Prevention of further emboli

Patients should be anticoagulated with vitamin K antagonists for a period of 3–6 months with a target INR of 2.0–3.0.

Patients with cancer or pregnant women should be treated with long-term low-molecular-weight heparin. Occasionally, physical methods are required to prevent further emboli. This is usually because recurrent emboli occur despite adequate anticoagulation, but it is also indicated in high-risk patients in whom anticoagulation is absolutely contraindicated.

The most common method by which pulmonary embolism is treated in this situation is by insertion of a filter in the inferior vena cava via the femoral vein to above the level of the renal veins.

THANK YOU!