In this ECG Cases blog we look at 10 patients who presented with cardiorespiratory symptoms. How does the ECG change your initial management and risk stratification, and which patients had pulmonary embolism?

Written by Jesse McLaren; Peer Reviewed and edited by Anton Helman. October 2021

10 patients presented with cardiorespiratory symptoms. How does the ECG change your initial management or pre-test probability, and which patients had PE?

Case 1: 45yo with 5 days of pleuritic chest pain, and shortness of breath on minimal exertion. Normal vitals and chest X-ray

Case 2: 75yo with exertional chest pain and shortness of breath, normal chest Xray/troponins and discharged. Returned with increased shortness of breath, tachypnea and hypoxia. ECG from first and second visits:

Case 3: 85yo with acute on chronic shortness of breath. R24 O2 95% on 5L, HR 95 BP 100/60, afebrile. Large RV on point-of-care ultrasound

Case 4: 80yo with 60 pack-year smoking history, with one month increasing shortness of breath and bilateral leg edema. R24, O2 70%, HR 100, BP 140/80, afebrile. Dilated right ventricle and bilateral pleural effusions on point of care ultrasound. No prior ECG

Case 5: 60yo, history of cancer, with two months shortness of breath on exertion. R18, O2 96%, HR 110 BP 130/70 afebrile

Case 6: 70yo previously well, presented during the first wave of COVID-19 with two weeks of increasing shortness of breath. R35, O2 95% on 15L, HR 110 BP 115/85, afebrile. Dilated RV on point of care ultrasound. Old then new ECG:

Case 7: 75yo previously well, with a few weeks of shortness of breath and fatigue, then syncope. R25, O2 90%, HR 130, BP 130/70, afebrile. No pulmonary edema on point of care ultrasound but prominent RV.

Case 8: 60yo, no history of lung disease, with two days of ongoing shortness of breath without cough or fever, sent to ED for ‘pneumonia’ based on infiltrate on chest x-ray. R20 O2 95% HR 80 BP 110/70 afebrile, troponin 100

Case 9: 60yo with exertional chest pain and shortness of breath, troponin 150. R24, O2 90%, HR 90, BP 110/80, afebrile. Normal portable chest X-ray. Old then new ECG:

Case 10: 40yo with one week intermittent chest pain, normal vitals. Old then new ECG:

Pulmonary embolism and acute RV strain

The ECG can be completely normal in PE, or there can be multiple abnormalities—including rate/rhythm, conduction, axis, R wave progression, voltage and ST/T changes. So it helps to have a systematic approach to ECG interpretation and to correlate it with the underlying pathology. As McGinn and White first explained in their observation of the S1Q3T3 pattern in 1935, “The changes observed clinically and the electrocardiographic variations in cases showing the acute cor pulmonale consequent to pulmonary embolism are due in large part to dilatation and partial failure of the chambers of the right side of the heart.”[1]

The right ventricle is anterior/inferior, smaller than the left ventricle, and contains the right bundle branch. So ECG changes of acute RV strain include:

  • Heart rate/rhythm: sinus tach, atrial fibrillation
  • Electrical conduction: right bundle branch block
  • Axis: S1 (S wave in lead I), or right axis deviation (S>R in I)
  • R-wave: delayed R wave progression
  • Tall/small voltages: small voltages
  • ST/T: Q3T3, primary anterior + inferior T wave inversion, ST elevation in V1 or III, diffuse ST depression with reciprocal STE-aVR (i.e. not a “STEMI-equivalent” but a nonspecific sign of subendocardial ischemia)

None of these changes are sensitive for PE. As a review concluded, “clinicians should not decrease their suspicion for pulmonary embolism according to their absence,” but “several electrocardiographic findings of acute pulmonary hypertension increase the probability of pulmonary embolism in symptomatic ED patients.”[2]

These changes (including S1Q3T3) are also not specific for PE. T wave inversion has a differential (the INVERSION mnemonic), which in the anterior leads including high V2 lead placement, RBBB or RVH with secondary TWI, ischemic primary T wave inversion from PE or reperfused/refractory Occlusion MI, arrythmogenic RV dysplasia, or a normal variant. But combining history, ECG and point-of-case ultrasound (POCUS) can help differentiate these. RV dilation on POCUS can be chronic or acute, but ECG signs of right ventricular hypertrophy (tall R waves in V1 and secondary T wave inversion) suggest chronic, while normal or delayed R wave progression with primary T wave inversion suggest acute. Primary anterior T wave inversion can be from Wellens’ syndrome (LAD reperfusion) or PE: but in the former the symptoms are resolved and the T wave inversion usually does not extend to the inferior leads (unless from wraparound LAD), whereas in PE the symptoms are ongoing and there is T wave inversion in anterior and inferior leads.[3]

While ECG signs of acute RV strain are neither sensitive nor specific for PE, they are also more likely in those with hemodynamically significant PE.[4] The combination of ECG signs of right heart strain correlates with a greater risk of adverse events: this includes the Daniel score (a 21 point score including tachycardia, RBBB, anterior T wave inversion, and S1Q3T3,)[5], and the simplified TwiST score (a 10 point score including anterior T wave inversion, S1 and tachycardia).[6] As a meta-analysis of the Daniel score, plus atrial fibrillation and STE-aVR explained, “several of the ECG components (particularly heart rate, inverted T waves in leads V2 and V3, and ST elevation in aVR) had odds ratios higher than echocardiography findings of RV strain, an RV/LV ratio >0.9 on CT scanning, or an elevated troponin I concentration…the six ECG findings provide a composite biomarker of RV failure, and thus provide specific bedside evidence of the need for intensive care services.”[7]

The importance of early bedside detection of acute RV strain can help prevent treatment that could be harmful—for example, aggressive fluid resuscitation in syncope from PE, rate controlling new atrial fibrillation that is rapid secondary to PE, or early intubation for hemodynamically significant PE. ECG findings of acute RV strain can also contribute to risk stratification (the “PE most likely” criteria on the Wells score or YEARS algorithm) and guide empiric treatment. Three-quarter of high pretest probability patients and 85% of patients with confirmed PE do not receive empiric heparin prior to confirmatory imaging, yet the risk of hemorrhagic complications from a dose of heparin is less then 1%.[8] As PE expert Dr. Kline advises, “all patients with a high pretest probability, no contraindication to anticoagulation, and evidence of hemodynamic instability, including recent syncope, any hypotension, hypoxemia, or clinical evidence of right-sided heart strain, should receive immediate empirical heparin.” [9] ECG can complement POCUS in identifying RV strain, contributing to early patient management and risk stratification.

Back to the cases

Case 1: PE with normal ECG

  • H: normal sinus
  • E: normal conduction
  • A: normal axis
  • R: normal R wave progression
  • T: normal voltages
  • S: no ST/T changes

Impression: normal ECG in a patient with a history concerning for PE. Low Wells score so D-dimer was sent, which was 2000. Then CT chest revealed bilateral segmental PE without RV strain. Discharged on oral anticoagulant

Case 2: PE with initially normal ECG then development of RV strain

  • H: sinus tach
  • E: normal conduction
  • A: LAFB + S1
  • R: new late R wave progression
  • T: normal voltage
  • S: new primary anterior + inferior T wave inversion

Impression: return visit with tachycardia, hypoxia and acute RV strain, high pretest probability PE. The emergency physician considered empiric heparin but the patient had a relative contraindication, so waited for expedited CT confirmation: extensive PE with RV strain. Admitted for anticoagulation and monitoring.

Case 3: right ventricular hypertrophy from chronic pulmonary hypertension

  • H: sinus
  • E: normal conduction
  • A: right axis
  • R: tall R wave in V1
  • T: right ventricular hypertrophy
  • S: anterior T wave inversion secondary to RVH

Impression: right ventricular hypertrophy. Patient admitted for exacerbation of chronic pulmonary hypertension.

Case 4: RV strain from COPD and CHF

  • H: sinus rhythm
  • E: incomplete RBBB
  • A: borderline right axis
  • R: delayed R wave progression
  • T: normal voltages
  • S: primary anterior-inferior T wave inversion

Impression: ECG signs of RV strain in chronic smoker with dilated RV and pleural effusions. Treated with diuresis, bronchodilators, BiPAP and empiric heparin. CT chest ruled out PE and patient diagnosed with COPD and CHF, both of which contributed to RV strain.

Case 5: PE with RV strain, delayed heparin

  • H: borderline sinus tach
  • E: normal conduction
  • A: S1
  • R: normal R wave progression
  • T: normal voltages
  • S: Q3T3, primary anterior + inferior T wave inversion

Impression: multiple signs of RV strain, in a patient with risk factors and symptoms of PE. Patient had serial troponins which were mildly positive, then positive Dimer, then CT chest revealing saddle embolism. Heparin started 8 hours after ED arrival, fortunately without any deterioration.

Case 6: PE with RV strain, early diagnosis which changed management

  • H: sinus tach
  • E: RBBB
  • A: LAFB with S1
  • R: poor R wave progression, S>R in V6
  • T: normal voltages
  • S: anterior T wave inversion, secondary to RBBB in V1-2 but primary in V3-4

Impression: patient in respiratory distress with multiple  ECG signs of acute RV strain, and point of care ultrasound revealed large RV, making PE a high pretest probability. Rather than early intubation for respiratory distress (as was common the first wave of COVID), the patient received immediate empiric heparin and ICU consult for presumed PE. CT chest confirmed bilateral PE with RV strain, and troponin was 500 (normal <26). Next day RBBB resolved and R wave progression improved, with ongoing S1 and primary antero-inferior T wave inversion—which resolved on discharge ECG:

Case 7: rapid atrial fibrillation secondary to PE, early diagnosis which changed management

  • H: atrial fibrillation with rapid ventricular response
  • E: incomplete RBBB
  • A: S1 with borderline right axis
  • R: normal R wave progression
  • T: normal voltage
  • S: T wave inversion anterior + inferior

Impression: new atrial fibrillation + signs of RV strain, in patient with syncope and hypoxia without pulmonary edema. Patient had a high pre-test probability of PE. So rather than getting fluids for syncope or rate control for rapid atrial fibrillation, they received empiric heparin and then CT which confirmed PE with right heart strain. On discharge there was resolution of atrial fibrillation and incomplete RBBB and right axis, but ongoing primary anterior T wave inversion:

Case 8: PE with RV strain, ECG prevented premature closure

  • H: sinus
  • E: normal conduction
  • A: LAFB + dominant S in I
  • R: delayed R wave progression
  • T: normal voltage
  • S: primary T wave inversion anterior (in V2 could be from high lead placement) + inferior

Impression: history inconsistent with pneumonia, and ECG/trop more likely from RV strain than ACS. CT chest revealed bilateral PE with RV strain, started on heparin and admitted.

Case 9: PE, initially misdiagnosed as NSTEMI

  • H: normal sinus
  • E: normal conduction
  • A: S1
  • R: normal R wave progression
  • T: normal voltages
  • S: Q3T3, primary anterior + inferior T wave inversion

Impression: chest pain and positive troponin, but ECG more consistent with PE than ACS. Initially diagnosed as NSTEMI. After a normal angiogram the patient had positive Dimer, then CT revealing bilateral PE. Discharge ECG had resolution of ECG changes:

Case 10: wraparound LAD occlusion with anterior/inferior reperfusion T wave inversion

  • H: normal sinus
  • E: short PR without delta
  • A: borderline left axis
  • R: loss of R waves anteriorly and inferiorly
  • T: low voltage limb leads
  • S: primary antero-inferior convex ST elevation with T wave inversion

Impression: intermittent symptoms with antero-inferior STE and TWI corresponding to wraparound or distal LAD occlusion which is reperfused (but not before loss of R waves, so not Wellens) or refractory. First troponin I was 3,000ng/L and referred to cardiology. Cath lab: 70% LAD occlusion, peak trop 5,000. Discharge ECG resolution of ST elevation, ongoing antero-inferior T wave inversion:

Take home point on ECG in pulmonary embolism and acute right heart strain

  1. ECG signs of acute RV strain include tachycardia, S1 or right axis, new RBBB, and primary T wave inversion in anterior + inferior leads
  2. The differential for anterior T wave inversion high lead placement of V2, RBBB or RVH with secondary TWI, ischemic primary TWI from reperfused/refractory Occlusion MI or PE (more likely PE if anterior + inferior), arrhythmogenic RV displasia, or normal variant.
  3. ECG + POCUS can help detect RV strain at the bedside, contributing to risk stratification and empiric treatment

References for ECG Cases 26: pulmonary embolism and acute RV strain

  1. McGinn S and White PD. Acute cor pulmonale resulting from pulmonary embolism. JAMA 1935 Aug;10(6): 839
  2. Marchick MR, Courtney DM, Kabrhel C, et al. 12-lead ECG findings of pulmonary hypertension occur more frequently in emergency department patients with pulmonary embolism than in patients without pulmonary embolism. Ann Emerg Med 2010;55:331-335
  3. Kosuge M, Ebina T, Hibi K, et al. Differences in negative T waves between acute pulmonary embolism and acute coronary syndrome. Circ J 2014;78: 483-489
  4. Qaddoura A, Digby GC, Kabali C, et al. The value of electrocardiography in prognosticating clinical deterioration and mortality in acute pulmonary embolism: a systematic review and meta-analysis. Clin Cardiol 2017 Oct;40(10):814-824
  5. Daniel KR, Courtney DM, Kline JA. Assessment of cardiac stress from massive pulmonary embolism with 12-lead ECG. Chest 2001 Aug;120(2):474-81
  6. Harihara P, Dudzinski DM, Okechuwku I, et al. Association between electrocardiographic findings, right heart strain, and short-term adverse clinical events in patients with acute pulmonary embolism. Clin Cardiol 2015 Apr;38(4):236-42
  7. Shopp JD, Stewart LK, Emmett TW, et al. Findings from 12-lead electrocardiography that predict circulatory shock from pulmonary embolism: systematic review and meta-analysis. Acad Emerg Med 2015 Oct;22(10):1127-1137
  8. Kline JA, Marchick MR, Kabrhel C, et al. Prospective study of the frequency and outcomes of patients with suspected pulmonary embolism administered heparin prior to confirmatory imaging. Thomb Res 2012 Apr;129(4):e25-8
  9. Kline JA. Pulmonary embolism and deep vein thrombosis. Rosen’s emergency medicine: concepts and clinical practice, 8th edition, 2014. p.1165
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