In this ECG Cases blog, Jesse McLaren and Rajiv Thavanathan look at how ECG and POCUS can complement each other for patients presenting to the emergency department with shortness of breath or chest pain.

Written by Jesse McLaren and Rajiv Thavanathan; Peer Reviewed and edited by Anton Helman. April, 2024

Nine patients presented with dyspnea and/or chest pain. What do the ECG and POCUS show, how do they complement each other, and how does this guide management?

Case 1: 85 year old, history of lymphoma, with shortness of breath and palpitations. ECG and subxiphoid view:

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Case 2: 85 year old, history of amyloid and atrial flutter, with weakness and shortness of breath. ECG and parasternal long-axis view:

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Case 3: 40 year old with pleuritic chest pain, normal vitals. ECG and parasternal long-axis view:

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Case 4: 55 year old with two weeks bilateral leg swelling, one week chest pain and shortness of breath on exertion now constant for two days. ECG and parasternal long-axis view:

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Case 5: 70 year old previously healthy with 16 hours of chest pain and vomiting, HR 140 and BP 115, sat 94%. Old then new ECG, and parasternal short-axis view:

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Case 6: 60 year old with 90 minutes of chest pain. ECG and parasternal long-axis view:

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Case 7: 90 year old with one hour of chest pain and nausea. ECG and parasternal short-axis view

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Case 8: 85 year old with sudden shortness of breath. RR 30, sat 75%, HR 120, BP 130, Temp 38.0. Old then new ECG, and apical four-chamber view:

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Case 9: 80 year old, history of interstitial lung disease, with shortness of breath. ECG and parasternal short-axis view:

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ECG and POCUS for dyspnea and chest pain

ECG and Point of care ultrasound (POCUS) are two bedside tests that can help rapidly diagnose and risk stratify patients with a variety of emergencies. Unlike comprehensive cardiology performed echocardiography, POCUS is intended to be a focused examination to answer specific clinical questions at the bedside, providing an additional data point to integrate in the clinical assessment. [1] This can be helpful in undifferentiated dyspnea or shock, and can help guide resuscitation and cardiac arrest. [1,2]

Like any test, neither ECG nor POCUS are 100% sensitive or specific but they can provide important and complementary data points to modify pre-test probability. They both have the added challenge of being operator dependent for image acquisition (with ECGs limited by lead placement errors and POCUS limited by poor views) and image interpretation. But both are seeing advances in emergency medicine, including supplementary interpretation by software powered by artificial intelligence.[3,4]

POCUS assessment requires multiple views and a detailed assessment that is beyond the scope of this ECG blog post, but each case here includes one view with a brief discussion to highlight how ECG and POCUS can complement each other – especially for patients with dyspnea and chest pain.

  1. Pericardial effusion and other causes of low voltage

ECG findings of pericardial effusion include sinus tachycardia, low voltage and electrical alternans (beat to beat variation in QRS amplitude). None of these findings are sensitive or specific. [5] But if any are present in a patient with dyspnea, the ECG can help identify patients requiring POCUS to confirm or exclude pericardial effusion and associated tamponade. The diagnosis of tamponade is a clinical one, with a spectrum of sonographic findings including a dilated IVC progressing to right-sided chamber collapse. [6] If the IVC is NOT plethoric/non-varying with respiration, tamponade becomes less likely and should prompt a careful search for other causes of instability.

Low ECG voltage has a differential – including adipose/breast tissue, hyperinflated lungs, pleural effusion, pericardial effusion, and cardiomyopathy [7] – and POCUS can help identify other causes. For example, while confirming the echo characteristics of cardiac amyloidosis is generally well outside the scope of POCUS, there are some clues: increased left ventricular (LV) and right ventricular (RV) wall thickening associated with low-voltage criteria on ECG. There may also be biatrial enlargement or PCE. If there is marked symmetric hypertrophy (meaning both the LV septal and lateral walls) +/- the addition of RVH it should make you consider cardiac amyloidosis.[8]

  1. Pericarditis: diagnosis of exclusion

Pericarditis is a diagnosis of exclusion, and POCUS can complement the ECG in assessing for other causes of chest pain first (eg occlusion MI, PE, dissection), in looking for complications of pericarditis (eg myocarditis, pericardial effusion and/or tamponade), or in excluding the diagnosis of pericarditis altogether (eg normal variant ST elevation, with no pericardial effusion on POCUS).

  1. Heart failure

POCUS can expedite diagnosis in patients presenting with undifferentiated dyspnea, with high sensitivity for heart failure.[9] Even without being able to quantify the exact LV Ejection Fraction (EF%), there are some qualitative clues to severe dysfunction. One common method is the E-point septal separation (EPSS), ie. the distance from the tip of the anterior leaflet of the mitral valve in mid-diastole (open) to the interventricular septum. If the distance is >7mm it suggests severe decrease in global LVEF.[10] Some pertinent causes of false positive are concurrent aortic insufficiency, MV pathology, and regional wall motion abnormalities.

While the ECG is often nonspecific in heart failure, it is important to identify when heart failure is caused by acute coronary occlusion requiring rapid reperfusion – though ACS complicated by cardiogenic shock requires urgent angiography regardless of the ECG.[11]

  1. STEMI(-) Occlusion MI

Patients with Occlusion MI whose ECG meets STEMI criteria, i.e. STEMI(+)OMI, don’t need extra diagnostic time for POCUS before cath lab activation. But as the new American College of Cardiology expert consensus on chest pain explains, STEMI criteria “will miss a significant minority of patients who have acute coronary occlusion. Therefore, the ECG should be closely examined for subtle changes that may represent initial ECG signs of vessel occlusion.”[12] POCUS findings of regional wall motion abnormality (RWMA) can help identify these patients with Occlusion MI whose ECGs don’t meet STEMI criteria, ie. STEMI(-)OMI.[13] RWMA is one of the earliest signs of acute coronary occlusion, and assessment is feasible for the emergency physician and potentially very useful to help expedite care.[14] Think in terms of anatomical segments based on coronary perfusion: anterior (LAD), inferior (RCA), septal (LAD), lateral (Cx). When assessing RWMA look for the thickening of respective LV myocardium, and movement towards the center of the LV in systole.

In a study of stat cardiology consults in the ED for patients suspected of Occlusion MI whose ECGs didn’t meet STEMI criteria, emergency physicians identified RWMA in 87% of patients with confirmed OMI. As the authors summarized, “in a patient presenting with high concern for ACS by history, physical, and ECG, the presence of RWMA should further increase suspicion of OMI. However, the absence of RWMA does not reassure against OMI.”[15]

  1. Right ventricular strain, acute vs chronic

ECG and POCUS can also complement each other for the assessment of right ventricular (RV) strain and pulmonary embolism (PE). Most PE don’t cause RV strain, and RV strain can be from causes other than PE, which limits sensitivity and specificity of ECG and POCUS. But each provides important data points to add to the clinical picture. ECG signs of acute RV strain include sinus tachycardia or new atrial fibrillation, new right bundle branch block, new S1 or right axis, and primary T wave inversion in anterior and inferior leads. None of these are sensitive or specific, but their combination can identify patients suspected of acute RV strain.

There are multiple sonographic/echo signs available to the emergency physician to increase likelihood of PE at the bedside including right ventricular dilation (RV:LV ratio >1) , McConnell’s sign, septal flattening (so called “D-sign”), tricuspid regurgitation, and decreased tricuspid annular plane systolic excursion as a surrogate for impaired RV systolic function (TAPSE<20mm). Although POCUS is never perfect rule-in or rule-out for PE, in patients with abnormal vital signs the absence of any of the above findings should prompt consideration and a diligent investigations for other causes of hemodynamic decompensation.[16] Also don’t forget to consider looking for a DVT at the bedside as well: POCUS has sensitivity and specificity of ~96% each.[17] But RV strain can also be chronic. ECG signs of RV hypertrophy include right axis, tall R waves in 1, persisting S waves in V6, and T wave inversion the anterior leads that are secondary to RVH. There are more advanced POCUS signs of chronic RV strain including thickened RV free wall hypertrophy>5mm, greater right atrial enlargement and greater tricuspid regurgitation.[18]

Back to the cases

Case 1: 85 year old, history of lymphoma, with shortness of breath and palpitations. ECG and subxiphoid view:

  • Heart rate/rhythm: AF with rapid ventricular response
  • Electrical conduction: otherwise normal conduction
  • Axis: normal
  • R-wave progression: slight delay R wave
  • Tall/small voltages: small voltages limb (all <5mm) and precordial (all <10mm)
  • ST/T: no ST/T changes

Impression: AF with rapid ventricular response and low voltage.

POCUS: large pericardial effusion without RV collapse. The most sensitive window for detecting a gravity-dependent PCE is the subxiphoid view, although in rare cases a complex effusion may be localized to other parts of the pericardium. More views will increase sensitivity! Additionally, this patient is quite tachycardic – although sonographic signs may suggest they are on a spectrum of impending or ongoing cardiac tamponade, the ultimate diagnosis and decision to pursue pericardiocentesis is a clinical one.

Integration: shortness of breath with ECG showing atrial fibrillation with rapid ventricular response and low voltage, which POCUS identified was from a large pericardial effusion without tamponade. The first step in AF with rapid ventricular response is to treat secondary causes of tachycardia, so the patient was initially with fluids, then digoxin and non-urgent pericardiocentesis. Follow up ECG showed larger precordial voltages:

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Case 2: 85 year old, history of amyloid and atrial flutter, with weakness and shortness of breath. ECG and parasternal long-axis view:

  • H: atrial flutter (upright flutter waves in V1) with slow ventricular response
  • E: narrow QRS, long QT
  • A: normal axis
  • R: normal T wave
  • T: low voltages limb and precordial leads
  • S: mild lateral T wave inversion

Impression: atrial flutter with slow ventricular response, and low voltage.

POCUS: tiny pericardial effusion, but marked symmetric LV hypertrophy (septal and lateral wall appear >2cm!), and pleural effusion. As a rough rule-of-thumb, if the LV walls are >1.5cm thickness (as seen here, judging by the 1cm depth-markers at right-side of screen) there’s likely hypertrophy. Particularly if associated with low-voltage QRS on ECG, also present in this case.

Integration: ECG showed low voltage, which POCUS showed was from cardiac amyloid and pleural effusion, with only a trace pericardial effusion. Admitted for heart failure.

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Case 3: 40 year old with pleuritic chest pain, normal vitals. ECG and parasternal long-axis view:

  • H: normal
  • E: normal
  • A: normal
  • R: normal
  • T: tall voltages, cut off at V4, with small J waves V5-6
  • S: proportional ST/T

Impression: early repolarization.

POCUS: good LV function, no pericardial effusion

Integration: chest pain without ECG or POCUS findings. Serial troponin, Dimer and CXR were normal. Patient diagnosed as “pericarditis” based on pain and ECG, but there were no ECG or POCUS signs of pericarditis.

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Case 4: 55 year old with two weeks bilateral leg swelling, one week chest pain and shortness of breath on exertion now constant for two days. ECG and parasternal long-axis view:

  • H: sinus tach, precordial leads high (P wave biphasic in V2)
  • E: normal conduction
  • A: left axis from LAFB
  • R: Q wave V1-2, poor R wave progression
  • T: large voltages V3-4
  • S: no anterior hyperacute T waves, nonspecific T wave inversion V6

Impression: tachycardia and poor R wave progression without acute ischemic changes.

POCUS: Severely reduced global LV systolic function (likely ?dilated LV), with EPSS > 7mm

Integration: subacute CHF, with severe LV dysfunction on POCUS without ECG signs of Occlusion MI. Treated with nitroglycerin and furosemide. Serial troponins in normal range. Non-urgent angiogram found triple vessel disease with 70% lesions, and diagnosed as mixed ischemic/non-ischemic cardiomyopathy.

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Case 5: 70 year old previously healthy with 16 hours of chest pain and vomiting, HR 140 and BP 115, sat 94%. Old then new ECG, and parasternal short-axis view:

  • H: sinus tach
  • E: normal conduction
  • A: left axis from LAFB
  • R: loss of anterior R waves
  • T: normal voltages
  • S: ST elevation V2-3 with hyperacute T waves, ST elevation aVL with inferior reciprocal changes

Impression: subacute proximal LAD occlusion with tachycardia concerning for cardiogenic shock.

POCUS: Tachycardia with anterior RWMA (hypokinetic, nearly akinetic).

Integration: subacute chest pain with ECG findings of subacute LAD occlusion and corresponding anterior akinesis. Cath lab activated, required intubation and pressors for cardiogenic shock. Angiogram found proximal LAD occlusion, first troponin 15,000 ng/L. Discharge ECG showed return of R waves, and anterolateral reperfusion T wave inversion:

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Case 6: 60 year old with 90 minutes of chest pain. ECG and parasternal long-axis view:

  • H: sinus, borderline bradycardia
  • E: normal conduction
  • A: normal axis
  • R: loss of anterior R waves
  • T: normal voltages
  • S: hyperacute T waves anterolateral and around apex to lead II

Impression: proximal LAD occlusion, STEMI(-)OMI.

POCUS: Story and ECG are concerning for anterolateral OMI/STEMI and POCUS corroborates with an apical RWMA (and suspect distal apex too, hard to tell from this single view). A common pitfall assessing the LV (especially the apex) is “foreshortening”, where the ultrasound beam is not quite cutting through the longest axis of the LV and thus missing the apex. This can lead to overestimation of global LV function, and miss important pathology such as an apical RWMA or LV thrombus

Integration: acute chest pain with ECG showing proximal LAD occlusion with corresponding anteroapical hypokinesis. Cath lab activated: 99% proximal LAD occlusion. First trop 5 ng/L (normal) and peak 200,000.

Discharge ECG showed anterolateral reperfusion T wave inversion, ongoing loss anterior R waves:

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Case 7: 90 year old with one hour of chest pain and nausea. ECG and parasternal short-axis view

  • H: normal
  • E: incomplete RBBB
  • A: normal
  • R: early R wave from incomplete RBBB
  • T: normal voltages
  • S: primary ST depression V2-3 (no rsR’ in these leads) with hyperacute T waves inferolateral

Impression: subtle infero-postero-lateral STEMI(-)OMI.

POCUS: Grossly normal global LV systolic function, with subtle lateral hypokinesis.

Integration: acute chest pain with subtle OMI ECG signs that were recognized, and subtle RWMA that was not recognized. 15 lead ECG had minimal posterior STE but also improved ST depression anterior:

Cath lab activated: 99% circumflex occlusion. First trop 50 ng/L and peak 30,000. Discharge ECG had normalization of inferolateral T waves, tall anterior R wave with residual flat ST segment:

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Case 8: 85 year old with sudden shortness of breath. RR 30, sat 75%, HR 120, BP 130, Temp 38.0. Old then new ECG, and apical four-chamber view:

  • H: sinus tach with PVC
  • E: normal conduction
  • A: normal axis but new S1
  • R: normal R wave progression
  • T: normal voltages
  • S: mild STE and TWI in III along with Q wave

Impression: sinus tach, mild STE in III and S1Q3T3, concerning for acute RV strain.

POCUS: RV dilation (RV:LV > 0.9) and RV mid-free wall hypokinesis sparing the apex (McConnell’s Sign).

Integration: Patient with sudden SOB/hypoxia, with ECG and POCUS signs of RV strain. Treated with empiric heparin, CT chest confirmed extensive PE. First trop 700 n/L and peak 3,000. Admitted to ICU for submassive PE, and recovered without requiring thrombolytics.

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Case 9: 80 year old, history of interstitial lung disease, with shortness of breath. ECG and parasternal short-axis view:

  • H: normal sinus
  • E: normal conduction
  • A: right axis
  • R: late R wave, persist S wave in V6
  • T: normal voltages
  • S: anterior STD/TWI

Impression: right axis, persisting S wave in V6 and anterior TWI, concerning for acute vs chronic RV strain

POCUS: RV dilation with septal flattening aka “D-sign” throughout the cardiac cycle (though worse in systole suggesting RV pressure overload).

Integration: patient with interstitial lung disease and dyspnea, with ECG and POCUS signs of RV strain. CT chest ruled out PE, and patient admitted for ILD flare, with formal echo showing chronic pulmonary hypertension.

Take home points for ECG-PoCUS approach to chest pain and dyspnea

  1. Pericardial effusion: tachycardia and low voltage ECG requires POCUS to assess for pericardial effusion and tamponade
  2. STEMI(-)OMI: subtle ECG signs of occlusion and POCUS signs of regional wall motion abnormality can identify Occlusion MI in the absence of STEMI criteria
  3. RV strain: ECG and POCUS can show signs of RV strain, which can be acute or chronic

* For interactive online and live ECG interpretation courses for medical students, residents, paramedics, and emergency physicians, visit heartsECGcourse.com

References for ‘ECG Cases 49 – ECG/PoCUS in dyspnea and chest pain’

  1. Chenkin J, Atzema CL. Contemporary application of point-of-care echocardiography in the emergency department. Can J Cardiol 2018 Feb;34(2):109-116
  2. Kim DJ, Atkinson P, Sheppard G, et al. POCUS literature primer: key papers on POCUS in cardiac arrest and shock. CJEM 2024 Jan;26(1):15-22
  3. Herman R, Meyers HP, Smith SW, et al. International evaluation of an artificial intelligence–powered electrocardiogram model detecting acute coronary occlusion myocardial infarction, European Heart Journal – Digital Health, 2023;, ztad074, https://doi.org/10.1093/ehjdh/ztad074
  4. Motazedian, P., Marbach, J.A., Prosperi-Porta, G. et al. Diagnostic accuracy of point-of-care ultrasound with artificial intelligence-assisted assessment of left ventricular ejection fraction. npj Digit. Med. 6, 201 (2023). https://doi.org/10.1038/s41746-023-00945-1
  5. Argula RG, Negi SI, Bacnhs J, et al. Role of a 12-lead electrocardiogram in the diagnosis of cardiac tamponade as diagnosed by transthoracic echocardiography in patients with malignant pericardial effusion. Clin Cardiol 2015 Mar;38(3):139-44
  6. Alerhand S, Adrian RJ, Long B, et al. Pericardial tamponade: A comprehensive emergency medicine and echocardiography review. Am J Emerg Med. 2022 Aug;58:159-174
  7. Madias JE. Low QRS voltage and its causes. J Electrocardio 2008 Nov-Dec;41(6):498-500
  8. Cuddy SAM, Chetrit M, Jankowski M, et al. Practical Points for Echocardiography in Cardiac Amyloidosis. J Am Soc Echocardiogr. 2022 Sep;35(9):A31-A40
  9. Zanobetti M, Scorpiniti M, Gigli C, et al. Point-of-care ultrasonography for evaluation of acute dyspnea in the ED. Chest 2017 Jun;151(6):1295-1301
  10. McKaigney CJ, Krantz MJ, La Rocque CL, et al. E-point septal separation: a bedside tool for emergency physician assessment of left ventricular ejection fraction. Am J Emerg Med. 2014 Jun;32(6):493-7
  11. Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC guideline for the management of patients with non-ST elevation acute coronary syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014 Dec 23;64(24):e139-e228
  12. Kontos MC, de Lemos JA, Deitelzweig SB, et al. 2022 ACC expert consensus decision pathway on the evaluation and disposition of acute chest pain in the emergency department: a report of the American College of Cardiology solution set oversight committee. J Am Coll Cardiol 2022 Nov;80(20):1925-1960
  13. Xu C, Melendez A, Nguyen T, et al. Point-of-care ultrasound may expedite diagnosis and revascularization of occult occlusive myocardial infarction. Am J Emerg Med 2022 Aug:58:186-191
  14. Croft PE, Strout TD, Kring RM, Director L, Vasaiwala SC, Mackenzie DC. WAMAMI: emergency physicians can accurately identify wall motion abnormalities in acute myocardial infarction. Am J Emerg Med. 2019 Dec;37(12):2224-2228
  15. Bracey A, Massey L, Pellet A, et al. FOCUS may detect wall motion abnormalities in patients with ACS. Am J Emerg Med 2023 Jul:69:17-22
  16. Daley JI, Dwyer KH, Grunwald Z, et al. Increased Sensitivity of Focused Cardiac Ultrasound for Pulmonary Embolism in Emergency Department Patients With Abnormal Vital Signs. Acad Emerg Med. 2019 Nov;26(11):1211-1220
  17. Pomero F, Dentali F, Borretta V, et al. Accuracy of emergency physician-performed ultrasonography in the diagnosis of deep-vein thrombosis: a systematic review and meta-analysis. Thromb Haemost. 2013 Jan;109(1):137-45
  18. Alerhand S, Adrian RJ. What echocardiographic findings differentiate acute pulmonary embolism and chronic pulmonary hypertension. Am J Emerg Med 2023 Oct;72:72-84