Lung scintigraphy in the diagnosis of pulmonary embolism: pathophysiological and practical evidence

Abstract

The protean clinical presentation of pulmonary embolism (PE) is the consequence of a complex series of haemodynamic and respiratory changes caused by the impact of thrombi within the pulmonary vasculature. Haemodynamic changes result from obstruction of the pulmonary arterial bed leading to increased pulmonary vascular resistances and they are manifested clinically as dyspnoea, engorgement of neck veins, and systemic arterial hypotension. Respiratory changes are characterised by lung volume reduction, hypocapnia and hypoxaemia. Reduced lung volume is mainly due to pulmonary consolidation, atelectasis and decreased distension of the thoracic cage due to chest pain. These pathophysiological changes affect both perfusion and ventilation and could explain the low sensitivity of the ventilation/perfusion (V/Q) mismatch scintigraphic approach in diagnosing PE. Acute PE causes redistribution of pulmonary blood flow from non-perfused areas and, to a lesser extent, of ventilation; this is a further factor arguing against the use of V/Q mismatch for the scintigraphic diagnosis of the disease. Hypoxaemia is primarily the consequence of V/Q abnormalities, namely the development of areas with a low V/Q ratio. On a Q scan this can easily be appreciated from hyperperfused lung areas that, by themselves, are a marker for the scintigraphic diagnosis of PE. In conclusion, a Q scan without a V scan, when properly interpreted according to the prospective investigative study of acute pulmonary embolism diagnosis methodology (presence or absence of wedge-shaped perfusion defects) and combined with the formulation of a pre-test clinical probability, can be used in most patients with clinical suspicion of PE, reducing costs and radiation load, increasing the practicality of the examination, and providing diagnostic accuracy comparable to that of CT angiography.