|This occurs when material lodges in the pulmonary circulation, impeding pulmonary blood flow. The majority are caused by dislodged deep vein thrombi in the legs or pelvis, but emboli can also consist of amniotic tissue, fat, nitrogen or parasites. Symptoms are variable, and non-specific.
Acute minor pulmonary embolism (PE)
Most often have no signs at all, but some present with:
- Breathlessness 84%
- Pain 74%
- Haemoptysis 30% (some days after initiating event)
Immediate consequences of large PEs are less from occlusion of pulmonary arteries, and more from release of vasoactive mediators and neurogenic reflexes (e.g. 5HT and thromboxane A2). These cause vasoconstriction of pulmonary and coronary arteries and vasodilation of peripheries.
- Increase right ventricular afterload.
- Increase pulmonary arterial pressure leading to right ventricular dilatation.
- Delayed right ventricular emptying, leading to splitting of heart sounds.
- Increase in the jugular venous pressure (JVP).
- Reduced pulmonary blood blow and Bernheim effect (displacement of IV septum into left ventricle, causing a fall in stroke volume) lead to a reduction in CO and hence a fall in blood pressure.
- Collapse with breathlessness and chest pain.
- Equally dyspnoeic in all positions; no abnormal breath sounds.
- JVP engorgement
- Hypotension and gallop rhythm
Chronic repeated PE
Insidious in course; can ultimately progress to pulmonary hypertension and cor pulmonale. Signs as for cor pulmonale.
On clinical grounds, when highly probable. For more accuracy, seek source (as DVT etc.) and evidence of pulmonary involvement:
Arterial blood gases
Unhelpful. Hyperventilation causes hypocapnoea, with hypoxaemia.
Unhelpful, as this is usually normal. There may be vascular shadows and enlarged hilum.
Often shows sinus tachycardia. Can show signs of right ventricular strain, such as the classic S wave in lead 1, Q wave in III, and inverted T in III (S1, Q3, T3).
D-dimer in plasma
This is a degradation product produced by plasmin-mediated proteolysis of cross-linked fibrin. High sensitivity (90%) low specificity (30%) - i.e. anything associated with thrombosis. Not a very useful measurement.
Papers report: In conclusion, the D-dimer enzyme immunoassay is an excellent exclusionary test for deep venous thrombosis.
These results suggest that the D-dimer assay is clearly neither sensitive nor specific enough when used alone to make or exclude the diagnosis of PE. However, it can significantly improve the reliability of excluding PE in patients with a low clinical pre-test probability of PE or with a non-diagnostic lung scan.
Nuclear scintigraphic ventilation perfusion (V/Q) scanning of the lung is the mainstay of hospital diagnostics in PE. It compares the ventilation (V) to perfusion (Q) of the lungs. The inherent inaccuracy of V/Q scans is demonstrated by the imprecision of the reports:
Normal scan rules out significant PE.
High probability scan establishes the diagnosis.
Low probability scan without symptoms would counter the diagnosis.
Medium probability scan, or a low probability scan with PE symptoms, is unhelpful, and the patient may continue in this instance to have pulmonary angiography.
Gold standard of diagnosis of PE, but is not fully available; it is difficult to perform, and carries a mortality of 1%. However, it can be performed easily if there is already a pulmonary catheter in place. Thrombolytic therapy can be given through the catheter afterwards.
Less invasive than pulmonary angiography, more accurate than chest-X-ray.
- Stabilise and resuscitate patient, treat hypotension, pain.
- Anti-coagulation with heparin, aim for activated partial thromboplastin time 2-3 times normal
- Thrombolysis with streptokinase or tissue plasminogen activator.
- Pulmonary embolectomy (unproven), inferior vena cava filter.