Clinical presentation of Acute Pulmonary Embolism


The clinical signs and symptoms of acute PE are non-specific. In most cases, Pulmonary Embolism is suspected in a patient with dyspnoea, chest pain, pre-syncope or syncope, or haemoptysis. 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. 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.
In some cases, Pulmonary Embolism 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 pre-existing 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. 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 Venous thromboembolism 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. Hypoxaemia is frequent, but ≤40% of patients have normal arterial oxygen saturation (SaO2) and 20% have a normal alveolar–arterial oxygen gradient. 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. Electrocardiographic changes indicative of RV strain—such as inversion of T waves in leads V1–V4, 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;  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.

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