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Abbreviations: hs-cTn high sensitivity cardiac troponin, ACS acute coronary syndrome, PE pulmonary embolism, RV right ventricle, CTPA CT pulmonary angiogram
massive PE: Acute PE with sustained hypotension (systolic blood pressure <90 mm Hg for at least 15 minutes or requiring inotropic support not due to a cause other than PE, such as arrhythmia, hypovolemia, sepsis, or left ventricular dysfunction), an absent pulse, or persistent profound bradycardia (heart rate <40 bpm with signs or symptoms of shock).
submassive PE: Acute PE without systemic hypotension (systolic blood pressure ≥90 mm Hg) but with either RV dysfunction or myocardial necrosis. Evidence of RV dysfunction includes RV dilatation on CT or echocardiography or evidence of RV systolic dysfunction on echocardiogram. (details here)
In recent years I have been involved in several cases where investigation of a patient presenting with chest pain syndrome has been misdirected by a failure to realise that PE can result in certain ECG findings which, in our minds, are associated primarily with acute coronary syndrome (ACS). This problem is, in part, a result of the availability of high sensitivity cardiac troponin (hs-cTn) assays. An elevated troponin concentration can blind us to the possibility of diagnostic alternatives to ACS in patients presenting with abnormal ECG findings in the context of a chest pain syndrome. In an appropriate clinical context, PE should at least be considered as a possible cause of certain ECG abnormalities.
chest pain syndrome: a constellation of symptoms which may be related to acute coronary syndrome, eg. chest pain, dyspnoea, syncope etc.
ST segment depression is present on the ECG in a proportion of patients with acute pulmonary embolism. The ECG shown below was recorded from a patient presenting with a one week history of increasing shortness of breath on exertion and a single episode of syncope with loss of consciousness. A submassive pulmonary embolism was confirmed on CTPA.
When present as a result of acute PE, ST depression (arrows) is said to typically occur in the inferior and anterior leads.
The ECG shown below was recorded from a patient with a pulmonary embolism confirmed on CTPA. Right ventricular dilatation was evident on the CT scan.
The S1Q3T3 pattern is associated with the presence of underlying ‘RV strain’. One possible cause of RV strain and this ECG pattern is acute pulmonary embolism. The S1Q3T3 pattern is not specific to PE and may be present in a variety of respiratory and cardiac diseases.
strain: ‘a force tending to pull or stretch something to an extreme or damaging degree’.
Modalities to assess right ventricular function are not readily available. We infer that a pathology is placing a ‘strain’ on the right ventricle, impairing its function, by identifying dilatation or deformity of the RV chamber using imaging methods such as CT scan or echocardiography.
Normal adults may demonstrate inverted T waves in leads V1 and V2 (‘a persistent juvenile pattern’). However, T wave inversion in lead V3 or leads V3 and V4 is abnormal. T wave inversion (arrows on ECG below) in leads V1 to V4 is observed in some cases of acute pulmonary embolism and, in the presence of PE, is indicative of associated RV strain. T wave inversion may be accompanied by ST segment depression in this situation.
New onset incomplete or complete right bundle branch block is a well known ECG finding in acute pulmonary embolism. It is generally observed in either submassive or massive PE. The ECG shown below was recorded from a patient with a submassive PE.
Incomplete right bundle branch block is present on the ECG (qrs duration in upper limit of normal range, late R wave in lead V1). We also note an S1Q3T3 pattern in the standard limb leads (leads I, II and III). The changes in the inferior leads have been misinterpreted by the computer interpretation (CI) as evidence of an inferior infarct.
The ECG shown below was recorded from a patient presenting with central crushing chest pain. The sole abnormality present on the ECG is a rapid heart rate, sinus in origin (99 bpm). Plasma troponin was significantly elevated and twenty four hours post-admission fell to a level below the cutoff value. Investigation for NSTEMI delayed the diagnosis of pulmonary embolism. Remember, PE may be associated with elevated plasma troponin concentration (acute cardiac injury).
Burns E. Life in the Fast Lane. ECG changes in Pulmonary Embolism. (2019) Link
Examples of ECG patterns observed in acute PE
Kas P. The ECGs of Pulmonary Embolism. Resus.com.au (2017) Link
Some wisdom on PE diagnosis
Todd K et al. ECG for the diagnosis of pulmonary embolism when conventional imaging cannot be utilized: A case report and review of the literature. Indian Pacing Electrophysiol J. 2009;9(5):268-75. Link
Useful discussion of ECG changes (including axis deviation) in PE
Levis JT. ECG Diagnosis: Pulmonary Embolism. Perm J. 2011;15(4):75. Link
Example and review of the significance of the S1Q3T3 pattern
Boey E et al. Electrocardiographic findings in pulmonary embolism. Singapore Med J 2015;56(10);533-37. Link
Informative ECGs and literature review.
Bryce YC et al. Pathophysiology of right ventricular failure in acute pulmonary embolism and chronic thromboembolic pulmonary hypertension: a pictorial essay for the interventional radiologist. Insights into Imaging 2019 Link
Interesting discussion of the pathophysiology underlying changes seen on imaging and on the ECG in acute PE.
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