An Electrocardiographic Exigency

ECG Exigency 001

A 23 year-old man is brought in by paramedics after an episode of syncope at home. On arrival he is in severe respiratory distress, extremely pale and dripping with sweat. BP is 125/70, HR is 80bpm, RR 40, SaO2 95% on 15L O2 via NRB. Portable CXR in resus is normal.

His ECG is presented below:

ecg exidency 001


Q1. Describe the ECG

  • Sinus rhythm at 80 bpm
  • Left axis deviation (-70 degrees)
  • RBBB with wide QRS (150ms), tall R wave in V1, RSR’ complexes in leads V1-3
  • Right ventricular strain pattern with deep T wave inversions in V1-3
  • Widespread ischaemic changes with 1-2mm ST elevation and early Q waves in the anterior leads (V2-5) and 1-2 mm ST depression in inferior leads (II, III and aVF). There is also significant ST elevation in leads aVR and aVL with formation of Q waves.

Q2. What is your interpretation of the ECG findings given the clinical context?

  • The combination of new RBBB with signs of right ventricular strain (deep T wave inversions in V1-3) in a patient presenting with dyspnoea and syncope is strongly suggestive of acute pulmonary hypertension secondary to massive PE.
  • Widespread myocardial ischaemia/infarction is likely related to severe global tissue hypoxia from obstructive shock (VBG in this patient showed venous saturations of 10%, venous PO2 10mmHg with a lactate of 8mmol/L).
  • Left axis deviation may represent left anterior fascicular block.

Shortly after this ECG was taken, the patient lost consciousness and had a PEA arrest from which he was unable to be resuscitated. Bedside echocardiogram performed during the resuscitation attempt showed a grossly dilated right ventricle and partially collapsed left ventricle with deviation of the interventricular septum to the left. Post-mortem examination confirmed a large saddle pulmonary embolus with complete obstruction of the pulmonary trunk. Previous hospital notes showed a history of thrombophilia and two previous episodes of venous thromboembolism.

Q3. What other ECG changes may be seen in this condition?

ECG changes are all fairly insensitive for the diagnosis of PE, and in most patients with PE the ECG will be normal.
The following ECG changes may be seen in acute pulmonary embolism:

  • Sinus tachycardia
  • SI QIII TIII – deep S wave in I, Q wave in III, inverted T wave in III
  • Complete or incomplete RBBB
  • Right axis deviation
  • Right ventricular strain pattern: T wave inversions in V1-3, sometimes extending to V4
  • Simultaneous T wave inversions in the inferior (II, III, aVF) and right precordial leads (V1-3).
  • Right atrial enlargement (“P pulmonale”): peaked P wave in lead II > 2mm in height
  • Clockwise rotation: shift of the R/S transition point towards V6, persistent S wave in V6
  • Atrial tachyarrhythmias: AF, flutter, atrial tachycardia

Extreme right axis deviation may occur, with axis between zero and -90 degrees, giving the appearance of left axis deviation (“pseudo left axis”). Simultaneous T wave inversions in the inferior and right precordial leads is the most specific finding for PE, with reported specificities up to 99% in one study. Check out Amal Mattu and William Brady’s excellent ‘ECGs for the Emergency Physician‘ books for some great examples of this.

Q4. What causes ECG changes in this condition?

ECG changes in PE are related to:

  • dilation of the right atrium and right ventricle with consequent shift in the position of the heart
  • right ventricular ischaemia
  • increased catecholamine levels (which drives the tachyarrhythmias)


  • Hampton, JR. The ECG in Practice (5th edition), Churchill Livingstone 2008.
  • Kosuge M, Kimura K, Ishikawa T, Ebina T, Hibi K, Kusama I, Nakachi T, Endo M,  Komura N, Umemura S. Electrocardiographic differentiation between acute pulmonary embolism and acute coronary syndromes on the basis of negative T waves. Am J Cardiol. 2007 Mar 15;99(6):817-21. Epub 2007 Jan 30. PMID: 17350373.
  • Mattu A, Brady W. ECGs for the Emergency Physician 1, BMJ Books 2003.
  • Mattu A, Brady W. ECGs for the Emergency Physician 2, BMJ Books 2008.
  • Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice (6th edition), Saunders 2008.
  • Wagner, GS. Marriott’s Practical Electrocardiography (11th edition), Lippincott Williams & Wilkins 2007.
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  1. Edward Burns says

    I think that the ECG is essentially the changes you would see in LMCA infarct (global ischaemia, anterior infarction, ST elevation in aVR + aVL) superimposed upon the changes of massive PE (RBBB, TWI V1-3). Given that it’s unlikely that this person had simultaneous clots in his LMCA and pulmonary trunk, then the MI changes would have to be secondary to shock and poor oxygen delivery (or at a stretch, LMCA occlusion by a grossly dilated pulmonary trunk pressing on the artery but I’m not sure if that has ever been described). His normal BP may falsely suggest that he was still perfusing his tissues, but it was all peripheral vasoconstriction with critically low cardiac output: he was alabaster white, CRT > 10 seconds, pouring buckets of sweat and had venous sats in his boots with a rising lactate, hence it’s not surprising that he started to infarct his myocardium.

  2. tarang singhal says

    Is there a time limit as to how long after the PE the ECG changes will take place.. I mean if I have to decide between ECG n echo which modality will give me faster [and better] results.