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............................................................................ As an immediately life-threatening situation, high-risk PE requires an emergency diagnostic (upon suspicion) and therapeutic (upon confirmation or if the level of suspicion is sufficiently high) strategy, as outlined in section 7. However, the absence of haemodynamic instability does not exclude beginning (and possibly progressing) RV dysfunction, and thus an elevated PE-related early risk. In this large population, further assessment (outlined in sections 5 and 7) is necessary to determine the level of risk and adjust management decisions accordingly. 4 Diagnosis The increased awareness of venous thromboembolic disease and the ever-increasing availability of non-invasive imaging tests, mainly computed tomography (CT) pulmonary angiography (CTPA), have generated a tendency for clinicians to suspect and initiate a diagnostic workup for PE more frequently than in the past. This changing attitude is illustrated by the rates of PE confirmation among patients undergoing diagnostic workup: these were as low as 5% in recent North American diagnostic studies, in sharp contrast to the approximately 50% prevalence reported back in the early 1980s.71 Therefore, it is critical that, when evaluating non-invasive diagnostic strategies for PE in the modern era, it is ensured that they are capable of safely excluding PE in contemporary patient populations with a rather low pre-test probability of the disease.72 Conversely, a positive test should have an adequate specificity to set the indication for anticoagulant treatment. 4.1 Clinical presentation The clinical signs and symptoms of acute PE are non-specific. In most cases, PE is suspected in a patient with dyspnoea, chest pain, presyncope or syncope, or haemoptysis.7375 Haemodynamic instability is a rare but important form of clinical presentation, as it indicates central or extensive PE with severely reduced haemodynamic reserve. Syncope may occur, and is associated with a higher prevalence of haemodynamic instability and RV dysfunction.76 Conversely, and according to the results of a recent study, acute PE may be a frequent finding in patients presenting with syncope (17%), even in the presence of an alternative explanation.77 In some cases, PE may be asymptomatic or discovered incidentally during diagnostic workup for another disease. Dyspnoea may be acute and severe in central PE; in small peripheral PE, it is often mild and may be transient. In patients with preexisting heart failure or pulmonary disease, worsening dyspnoea may be the only symptom indicative of PE. Chest pain is a frequent symptom of PE and is usually caused by pleural irritation due to distal emboli causing pulmonary infarction.78 In central PE, chest pain may have a typical angina character, possibly reflecting RV ischaemia, and requiring differential diagnosis from an acute coronary syndrome or aortic dissection. In addition to symptoms, knowledge of the predisposing factors for VTE is important in determining the clinical probability of the disease, which increases with the number of predisposing factors present; however, in 40% of patients with PE, no predisposing factors are found.79 Hypoxaemia is frequent, but <_40% of patients have normal arterial oxygen saturation (SaO2) and 20% have a normal alveolararterial oxygen gradient.80,81 Hypocapnia is also often present. A chest X-ray is frequently abnormal and, although its findings are usually non-specific in PE, it may be useful for excluding other causes of dyspnoea or chest pain.82 Electrocardiographic changes indicative of RV strain—such as inversion of T waves in leads V1V4, a QR pattern in V1, a S1Q3T3 pattern, and incomplete or complete right bundle branch block—are usually found in more severe cases of PE;83 in milder cases, the only abnormality may be sinus tachycardia, present in 40% of patients. Finally, atrial arrhythmias, most frequently atrial fibrillation, may be associated with acute PE. 4.2 Assessment of clinical (pre-test) probability The combination of symptoms and clinical findings with the presence of predisposing factors for VTE allows the classification of patients with suspected PE into distinct categories of clinical or pre-test probability, which correspond to an increasing actual prevalence of confirmed PE. This pre-test assessment can be done either by implicit (empirical) clinical judgement or by using prediction rules. As the post-test (i.e. after an imaging test) probability of PE depends not only on the characteristics of the diagnostic test itself but also on the pretest probability, this is a key step in all diagnostic algorithms for PE. The value of empirical clinical judgement has been confirmed in several large series.84,85 Clinical judgement usually includes ................................................ Table 5 The revised Geneva clinical prediction rule for pulmonary embolism Items Clinical decision rule points Original version91 Simplified version87 Previous PE or DVT 3 1 Heart rate 7594 b.p.m. 3 1 >_95 b.p.m. 5 2 Surgery or fracture within the past month 2 1 Haemoptysis 2 1 Active cancer 2 1 Unilateral lower-limb pain 3 1 Pain on lower-limb deep venous palpation and unilateral oedema 4 1 Age >65 years 1 1 Clinical probability Three-level score Low 03 01 Intermediate 410 24 High >_11 >_5 Two-level score PE-unlikely 05 02 PE-likely >_6 >_3 b.p.m. = beats per minute; DVT = deep vein thrombosis; PE = pulmonary embolism. Downloaded from academic.oup.com/eurheartj/article/41/4/543/5556136 by guest on 07 October 2026