Respiratory disorders : Pulmonary Embolism


Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE) comes under Venous Thromboembolism.
DVT occurs about 3 times more often than PE.
Patients with PE are more likely to suffer recurrent VTE than patients with DVT alone.
Cause of PE: Propagation of lower limb DVT (most common),
Others: amniotic fluid, placenta, air, fat, tumor (choriocarcinoma), septic emboli (endocarditis affecting tricuspid and pulmonary valves) but are rare.
It is a common mode of death in patients with cancer and stroke and remains the most common cause of death in pregnancy.

Risk factors of VTE

Major abdominal/pelvic surgery (Sx)
Hip or Knee Sx
Post operative intensive care


Cardiorespiratory disease
Congestive cardiac failure

Lower limb problems
Varicose veins
Stroke and spinal cord injury

Malignant disease
Abdominal pelvic
Concurrent chemotherapy


Increasing age
Pervious proven VTE
Thrombotic disorders

Clinical features

Dyspnoea (most frequent)
Chest pain (common-due to pulmonary infraction and indicates small PE located distally near the pleura)


Chest radiography: usually non-specific, used to rule out other causes.
Normal radiographic appearances in an acutely breathless and hypoxaemic patient should raise the suspicion of PE.
Bilateral changes in a patient presenting with unilateral pleuritic chest pain.

Features of pulmonary thromboembolism/infarction on chest X-ray

Usually non-specific
Most common findings a sinus tachycardia and anterior T-wave inversion.
Larger emboli may cause: right heart strain revealed by an S1Q3T3 pattern (deep S wave in lead I, Q wave and Inverted T wave in lead III) or the RBBB.
Useful in excluding MI and Pericarditis
Atrial Blood Gas:
Characterised by V/Q mismatch and reduced cardiac output.
A metabolic acidosis may be seen in acute massive PE with cardiovascular collapse.
A low mixed venous oxygen saturation and hyperventilation.
A reduced PaO2 and a normal or low PaCO2

D-dimer and other circulating markers:
D-dimer is a specific degradation product when cross-linked fibrin undergoes fibrinolysis.
High negative predictive value <500ng/ml- suggests absence of PE.
Non-specific elevation of D-dimer is observed in no. of cases other then PE like- Pneumonia, MI and Sepsis.
Imaging: ventilaiton-perfusion scanning (most popular method for PE confirmation)
Normal V/Q scan excludes PE.
High probability scan with a high clinical probability almost certainly diagnoses PE.
CT pulmonary angiography- not only exclude PE but also highlight alternative diagnosis. Has replased simple angiography.
Colour Doppler USG of leg- investigation of choice for DVT.

Acute dilatation of right heart, and thrombus may be visible,
Alternative diagnosis can be established with confidence (eg aortic dissection, LVF, pericardiac temponade)
Pulmonary angiography:
Goldstandard for the diagnosis of PE
Now replaced by CTPE.


General management:
Oxygen to all hypoxic patients,
Opiates to relive pain and stress (use with great caution in hypotensive patients),
Diuretics and vasodilators should be avoided (since cardiac output is reduced in PE) instead hypotension should be treated with IV fluid or plasma expanders.
Resuscitation by external cardiac massage may be successful in the moribund patients by dislodging and breaking up of large central embolus.

Commenced immediately in patients with high probability of PE.
LMW heparin given subcutaneous is easy to administer and as effective as unfractionated heparin (IV)
Heparin- inhibits propagation of the clot and reduces the risk of emboli, must be given for 5 days at least (until INR >2) and must be replaced by oral warfarin.
Six month of warfarin is currently indicated for idiopathic VTE, however the exact duration for other cases is not certain.

Thrombolytics- given in acute massive pulmonary embolism with shock.
Not clear about the advantage over heparin.
Think of risk of intracranial hemorrage before therapy.
Caval filter- in recurrent PE despite adequate anticoagulation or in contraindication of anticoagulant,
Inserted at IVC below the origin of renal vessels.

As high as 9% per year.
Patients with persistent pulmonary hypertension and right ventricular dysfunction are at high risk of developing right heart failure over the next 5 years.