The masquerade of massive pulmonary embolism

Massive pulmonary embolism often presents without the classical symptoms of pleuritic chest pain, acute dyspnoea or haemoptysis and overlaps significantly with the symptoms of cardiac disease.

Case 1

A 76-year-old man with a past history of myocardial infarction (MI), type II diabetes mellitus and a recent strangulated ventral hernia repair, presented following two episodes of sudden and transient loss of consciousness. He denied symptoms of chest pain, breathlessness or palpitations. On admission, he was haemodynamically stable and oxygen saturations were 97% on room air. Examination was unremarkable. 12-lead resting electrocardiogram (ECG) showed evidence of old inferior MI with new T wave inversion in leads V1-V4 and a prolonged QT interval of 518 ms (

Figure 1

a. 12-lead ECG: a prolonged QT interval of 518 ms with T wave inversion in precordial leads (V1-V3) and inferior leads (III, aVF); b. echocardiography (parasternal short axis view): dilated right ventricle, with flattening of the inter-ventricular septum (arrow) and a ‘D’ shaped left ventricle; c. CTPA: massive pulmonary embolism involving the main pulmonary artery and extending into the branches (arrows)

Figure 1a). He was treated for possible acute coronary syndrome. Subsequent investigations confirmed normal electrolytes; Troponin T levels were undetectable.

Over the next 48 hours, he had two syncopal episodes – on climbing a flight of stairs and while straining on the toilet. On the second occasion, his blood pressure dropped to 80/60 mmHg and he was tachycardic at 120 bpm. Blood gases confirmed severe hypoxia. Bedside echocardiogram revealed a dilated right ventricle and a flattened, dyskinetic inter-ventricular septum with normal left ventricular systolic function (Figure 1b). There was mild–moderate tricuspid regurgitation. He was commenced on treatment dose low molecular weight heparin for possible massive pulmonary embolism and an urgent CT pulmonary angiogram requested, which confirmed massive pulmonary embolism in the main pulmonary artery and extending into the proximal branches (Figure 1c). He was subsequently anticoagulated.

Case 2

A 73-year-old woman, with a past medical history of hypertension and hypercholesterolaemia, presented with a five-day history of exertional dyspnoea and mild orthopnoea. Her exercise tolerance was limited to 100 yards and she had difficulty in climbing stairs. She denied chest pain, palpitations or paroxysmal nocturnal dyspnoea.

On examination, she was hypoxic with saturations of 93% on room air. The blood pressure measured 170/83 mmHg and she had a sinus tachycardia of 110 bpm. The jugular venous pressure (JVP) was elevated at 5 cm, there was minimal pedal oedema and a pan-systolic murmur suggestive of tricuspid regurgitation was audible at the left sternal edge. The rest of the examination was normal.

ECG on admission showed a sinus tachycardia with peaked T waves in leads V1-V3 and T wave inversion in inferior leads (

Figure 2

a. 12-lead ECG: T wave inversion and q waves in the inferior leads (III, aVF). This pattern was also observed in right-sided chest leads (V3R, V4R); b. lung ventilation perfusion scan: segmental and subsegmental defects in both lungs (arrows)

Figure 2a). Chest X-ray was unremarkable. Troponin T levels were marginally elevated at 0.03 µg/L (<0.01) and D-dimer levels were significantly raised at 1.08 µg/ml (<0.19).

Although her presentation was suggestive of congestive cardiac failure, the hypoxia in the presence of normal lung fields and clinical evidence of right heart strain, prompted a bedside echocardiogram which confirmed severe tricuspid regurgitation and elevated pulmonary artery pressures (>60 mmHg). Both left and right ventricular systolic function was normal and there was no suggestion of pericardial pathology.

The patient was treated for massive pulmonary embolism, which was subsequently confirmed by lung ventilation perfusion scan (Figure 2b).

Discussion

Massive pulmonary embolism remains a diagnostic challenge for the clinician. It is reported that less than one-third of patients with massive pulmonary embolism are detected prior to autopsy. 1, 2 In a large multicentre trial of 2392 patients, untreated massive pulmonary embolism was associated with a mortality of 52%. 3 The mortality is six-fold greater when massive pulmonary embolism is missed. 4

The PIOPED II study, a trial of over 900 patients with small and massive pulmonary embolism (excluding the critically-ill and patients with cardiac and lung pathology), provides valuable insights into the reasons for misdiagnosis. 5 Pleuritic chest pain was absent in >50% of acute pulmonary embolism, while haemoptysis was rare and tended to be scanty. More importantly, massive pulmonary embolism overlapped significantly with congestive cardiac failure in presentation with dyspnoea at rest or on exertion being the most frequent symptom (>90%) while a proportion of patients had >2 pillow orthopnoea. Dyspnoea was insidious in onset (over days) in one-fifth of patients while >10% had a raised jugular venous pressure on examination. Circulatory collapse was found in 8% although other autopsy series suggest a higher incidence (24%). 4

ECG changes in pulmonary embolism tend to be non-specific and include sinus tachycardia, ST segment/T wave abnormalities, RBBB and a prolonged QT interval. Ferrari et al. reported T wave inversion in precordial leads V1-V3 as a frequent and reliable indicator of massive pulmonary embolism which resolved after thrombolysis. 6 This may arise from mechanical compression of the right coronary artery in the atrio-ventricular groove as a result of right ventricular pressure overload, which also explains the inferior T wave inversion seen in 50% of massive pulmonary embolism. 6

Current guidelines advocate the use of echocardiography in massive pulmonary embolism, although not as a routine screening tool. 7 Echocardiographic findings in massive pulmonary embolism include RV dilatation and systolic dysfunction (sometimes sparing the apical region – McConnell's sign), tricuspid regurgitation and pulmonary arterial hypertension. 8 Thrombolysis is the recommended first-line therapy in massive pulmonary embolism. 7

Conclusion

The majority (two-thirds) of pulmonary angiograms are negative for pulmonary embolism where the diagnosis was initially suspected suggesting that clinicians tend to over-diagnose pulmonary embolism presenting with chest pain/pleuritic symptoms. 9, 10 However, we propose that massive pulmonary embolism is often under-diagnosed. Our case series illustrates the varied clinical presentation of massive pulmonary embolism and the role of bedside imaging in rapid diagnosis. Case 1 presented with recurrent circulatory collapse and ‘ischaemic’ ECG changes (T wave inversion and a prolonged QT interval), which prompted the initial diagnosis of acute coronary syndrome. Case 2 had an insidious onset of dyspnoea suggestive of congestive cardiac failure; however clinical signs in keeping with right heart overload prompted further assessment. A high index of suspicion and bedside echocardiography enabled rapid and accurate diagnosis in both instances.

Learning points

Massive pulmonary embolism is an under-diagnosed condition, which has a varied and often atypical clinical presentation.

Careful analysis of the ECG is required in the recognition of massive pulmonary embolism, particularly in the presence of ‘ischaemic’ patterns such as T wave inversion/prolonged QT interval.

Bedside echocardiography is of value in the rapid identification of massive pulmonary embolism, and should be undertaken promptly when clinical signs are suggestive of right-heart strain.

Footnotes

DECLARATIONS

Competing interests None declared

Funding None

Ethical approval Not applicable

Guarantor UK

Contributorship Both authors contributed equally

Reviewer Charlene Pius