Pulmonary thromboemboli occur more commonly in the lower lobes because of the preferential blood flow to these regions. This also applies to the right lung because of the straighter course of the pulmonary artery. Immediately after acute embolism, there is a decrease of perfusion distal to the occluded vessel along with a transient decrease of ventilation to the affected segment. The blood flow is diverted to the other portions of the lung, and pulmonary artery pressure may increase, although cardiac output usually remains stable. The resultant tissue ischemia disturbs certain metabolic functions of the lung such as the production of surfactant. Reduction of the surfactant concentration reduces the alveolar surface tension and may cause the atelectasis that often accompanies embolism. If the embolus completely occludes an artery or an arteriole and the collateral bronchial circulation is insufficient to sustain tissue viability, infarction occurs over 24–48 h. Pulmonary infarction with coagulative necrosis results in an area of radiographic opacity that requires an average of 20 days to resolve but occurs in less than 10–15 % of patients with pulmonary embolism. There is significant inflammatory component in pulmonary infarcts which is the basis behind the reported significant FDG uptake in recent lung infarcts and can cause false-positive interpretation for lung malignancy [8]. More frequently, incomplete infarction with hemorrhage but without necrosis occurs. This type of injury resolves quickly and produces only transient radiographic opacities. Infarction always involves the pleural surface of the lung (peripheral) and more frequently involves the lower lobes than other sites.

The regional decrease in ventilation is due to local bronchoconstriction with a tendency for redistribution of ventilation away from the hypoperfused segment. This probably occurs due to decreased regional alveolar and airway carbon dioxide tension, which is the usual stimulus for bronchodilation. This hypocapnia is corrected quickly, since patients inhale carbon dioxide-rich tracheal “dead space air” into the alveolar zones after the embolic event, raising the alveolar pCO₂ [6]. The release of neurohumoral factors, most importantly serotonin and thromboxane A₂, also causes bronchoconstriction. These factors are released after embolization by activated platelets and mediate bronchospasm of small airways through their effects on the smooth muscles [9]. The ventilation of the hypoperfused areas returns to normal within several hours after acute embolism [10, 11]. This concept is the pathophysiological basis for the scintigraphic interpretation of ventilation and perfusion scans, which show segmental perfusion defects with preserved ventilation as a typical scintigraphic pattern for pulmonary embolism. Those showing only regions of matched perfusion and ventilation defects carry a low probability of pulmonary embolism if no chest X-ray abnormalities are noted at the same sites, since this pattern is more likely associated with nonembolic conditions and is more typical of parenchymal lung disease. Because patients with pulmonary emboli usually arrive at the hospital after normalization of the ventilation at the site of pulmonary emboli, the mismatching pattern is typical of pulmonary emboli. However inpatients may have their V/Q scans within a short time after presentation and matching abnormalities may be associated with pulmonary emboli. This has to be borne in mind, and the duration of symptoms should be a factor in decision-making regarding the management of pulmonary embolism.

Some degree of arterial hypoxemia may also occur, one reason being the widening of the arteriovenous oxygen difference caused by acute right ventricular failure. Another reason is the enhanced perfusion of poorly ventilated or nonventilated lung zones. Loss of pulmonary surfactant may add to the hypoxemia. Hyperventilation almost always occurs and may partly explain the normal levels of oxygen arterial pressure seen in 10–25 % of patients with pulmonary emboli.

An increase in the resistance of the pulmonary arterial circulation, due primarily to mechanical blockage by numerous small emboli in the pulmonary vasculature and also to humorally mediated vasoconstriction, may follow pulmonary emboli. These hemodynamic consequences may include increased pulmonary arterial resistance with elevated pulmonary arterial and right ventricular systolic pressures and hypoxemia. When pulmonary hypertension occurs, it indicates at least 25 % obstruction of pulmonary vascular tree as assessed by angiography [12]. The higher the degree of obstruction, the more severe the abnormalities of the cardiopulmonary hemodynamics become. When over 50 % of the pulmonary vasculature is included (massive pulmonary embolism), acute pulmonary hypertension and/or right ventricular failure (cor pulmonale) occurs [12]. Systemic hypoxemia results from pulmonary arteriovenous shunting and from perfusion of hypoventilated lung segments (V-P imbalances). The AV shunting accounts for the clinical observation that administration of 100 % oxygen will only partially correct hypoxemia induced by pulmonary emboli [11].

The physiological consequences of pulmonary embolism depend on the size of the embolic mass and the general status of the pulmonary circulation. In young individuals with good cardiovascular function and good collateral circulation, thrombi of a large central vessel may be associated with only minimal functional impairment if any. On the other hand, in patients with cardiovascular or severely debilitating diseases, pulmonary embolism may lead to infarction.

Pulmonary emboli may, spontaneously or with treatment, fragment into smaller portions that travel distally and block smaller arterioles (Fig. 13.5). This may create new, smaller perfusion defects that are more peripherally located in comparison to the original defect caused by the original embolus. This pattern should not be mistaken for recurrent pulmonary emboli on a follow-up scan. If this pattern is the only interval change with no other defects seen in areas other than those in the vicinity of the distribution of the original embolus, it does not suggest recurrent emboli [11].

Resolution of pulmonary thromboembolus may start within hours. It can be seen on perfusion scans as early as 24 h and is progressively noted up to 3 months, with insignificant change after 6 months (Fig. 13.6). This is the basis of the recommendation that follow-up ventilation and perfusion scans are performed 3 months after the initial incident for evaluation of resolution and function as a baseline for future incidents to differentiate between acute and unresolved old emboli. This resolution is dependent on the age of the patient, with complete resolution in young age-groups and less complete and less significant resolution in older age-groups [14, 15]. Other factors include age of the thromboembolus or length of time between formation of the embolus and the institution of proper anticoagulation. This is the basis behind the relatively recent trend of starting anticoagulant therapy in most patients with pulmonary emboli who have no contraindication for anticoagulation immediately when a pulmonary thromboembolus is suspected before finishing the workup for the condition. Anticoagulant therapy may then be stopped if the condition is excluded.

Incomplete resolution of acute pulmonary embolism is frequently observed and may rarely result in chronic thromboembolic pulmonary hypertension [16]. Chronic thromboembolic disease is characterized by intraluminal thrombus organization and fibrous stenosis or complete obliteration of pulmonary arteries. The consequence is an increased pulmonary vascular resistance resulting in pulmonary hypertension and progressive right heart failure. Pulmonary endarterectomy is the preferred treatment [17].

Pulmonary thromboemboli recur in up to 50 % of patients [15], although the incidence in treated PIOPED patients was only 8.3 % [18]. The vast majority of deaths among pulmonary embolism patients are due to recurrent emboli. In the PIOPED study population, it was found that nine of ten people who died had a recurrent pulmonary embolus [19]. Recurrence has been reported to occur at the same site as the original thromboembolus [20].

The clinical diagnosis of pulmonary thromboembolism is difficult and unreliable, due to the nonspecificity of its symptoms and signs as well as the laboratory and chest X-ray findings [21, 22]. Chest X-ray however must be obtained since it may show many parenchymal diseases and must be available for lung scan interpretation (Fig. 13.7). Pulmonary embolism may also be asymptomatic. In the literature, only 24 % of fatal emboli were diagnosed antemortem (Table 13.2) [23–31]. Furthermore the presentation is commonly more difficult and atypical in older age group compared to younger patients [32, 33]. Accordingly only 24 % of fatal emboli were diagnosed antemortem (Table 13.2) [23]. Data indicate that the mortality of pulmonary embolism is more than 30 % if untreated. Promptly diagnosed and treated, emboli have a mortality of 2.5–8 % [13, 14, 19]. The mortality of PE was found to vary among patients with or without cardiac disease. Paraskos et al. [34] reported survival rates at a mean follow-up period of 29 months of 19 % among patients with prior congestive heart failure and 86 % for those with no prior congestive heart failure. Pulmonary angiography is the most accurate modality for the diagnosis of pulmonary emboli with an accuracy of 96 % [35]. However, angiography is invasive and is not suitable as a screening imaging modality for the disease.

D-dimer is a fibrin degradation product present in the blood after a thrombus is degraded through fibrinolysis. The blood test to determine D-dimer concentration helps diagnose thrombosis. Although a negative result practically rules out thrombosis, a positive result can indicate thrombosis but does not rule out other potential causes. Its main use, therefore, is to exclude thromboembolic disease where the clinical probability is low.