In this ECG Cases blog we look at 10 patients with shortness of breath, and discuss how the ECG can be used to help diagnose cardiac, respiratory and metabolic emergencies.
Written by Jesse McLaren; Peer Reviewed and edited by Anton Helman. June 2023
10 patients presented with shortness of breath. What’s your ECG interpretation, and your next step in management?
Case 1: 85 year old with one day of shortness of breath and weakness. RR 35, O2 90%, HR 80, BP 120/40.
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Case 2: 45 year old with two days of shortness of breath and diaphoresis. RR 25, O2 87%, HR 110, BP 120/80
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Case 3: 90 year old with one day of shortness of breath, STEMI negative with EMS and treated with puffers for wheezing. RR35, O2 90%, HR 110, BP 110/75. Old then new ECG:
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Case 4: 75 year old, history of COPD, with one day of shortness of breath and wheezing. RR30, O2 80%, HR 110, BP 170/90
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Case 5: 90 year old with few days shortness of breath and lethargy. Old then new ECG. RR 28, O2 84%, HR 120, BP 79/35, temp 35.0
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Case 6: 30 year old, previously healthy, with one day of shortness of breath and syncope. RR 20, O2 95%, HR 110, BP 140/100
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Case 7: 30 year old, history of lupus, with months of exertional dyspnea. Normal vitals
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Case 8: 50 year old, history of lung cancer, with few days fatigue and shortness of breath. RR 20, O2 98%, HR 100, BP 125/75
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Case 9: 80 year old with 3 months exertional dyspnea, increasing bilateral leg edema. R20, O2 95%, HR 50, BP 100/70
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Case 10: 60 year old, history of diabetes, with one day of shortness of breath and weakness. RR 20, O2 100%, HR 90, BP 115/60, glucose 23
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ECG in patients with shortness of breath
The ECG is important for the emergency assessment of shortness of breath, complemented by Point of Care Ultrasound (POCUS). Interpreting ECG changes in the dyspneic patient needs to differentiate between chronic, acute, and incidental changes – and to consider cardiac, pulmonary and metabolic emergencies. These include:
- STEMI/OMI vs demand ischemia
STEMI/Occlusion MI usually presents with chest pain, but shortness of breath is a common anginal equivalent. Patients with acute coronary syndrome without chest pain are more likely to be elderly and have cardiovascular risk factors, more likely to have delayed presentation, more likely to have delayed diagnosis, and more likely to be undertreated even after diagnosis – resulting in worse outcomes.[1,2]
Patients can have coronary occlusion with neither chest pain nor STEMI criteria. But ECG signs of Occlusion MI (OMI) can identify patients with preventable delays to reperfusion,[3] complemented by POCUS findings of regional wall motion abnormalities.[4] So ECG interpretation in the dyspneic patient needs to include looking for STEMI(-)OMI (like many inferior OMI), subacute occlusions with Q waves but ongoing evidence of occlusion, and identifying OMI in the presence of RBBB and LBBB.
On the other hand, dyspneic patients with diffuse ST depression and reciprocal ST elevation in aVR indicates subendocardial ischemia with a broad differential including tachyarrhythmias, cardiac ischemia (including triple vessel disease, left main disease, or acute coronary occlusion), or non-cardiac shock states (including PE, massive GI bleed or sepsis).[5] POCUS is crucial to rapidly work through this differential.
- RV strain, acute vs chronic
Large pulmonary emboli (PE) can sometimes be suspected based on ECG signs of acute RV strain. These include abnormalities in rate/rhythm (sinus tach, new AF), conduction (RBBB), axis (S1 or full right axis deviation), and ST/T changes (primary T wave inversion in anterior and inferior leads). These are not sensitive for PE (because many PE don’t have RV strain), or specific for PE (because RV strain is secondary to pulmonary hypertension, which has a differential). But a patient with acute dyspnea and an ECG showing multiple signs of RV strain can raise suspicion for hemodynamically significant PE,[6,7] complemented by POCUS. RV strain can also be from other causes of pulmonary hypertension, and if chronic this might manifest on the ECG as RV hypertrophy: right axis deviation, early R wave in V1 and deep S wave in V6, and secondary ST depression and T wave inversion.
- Pericardial effusion vs other causes of low voltage
Low voltage on ECG (QRS amplitude <5mm in all limb leads, or <10mm in all precordial leads) might be an early clue that a patient has a pericardial effusion. The classic triad of tamponade is sinus tachycardia, low voltage, and electrical alternans. While most tamponade has at least one of these abnormalities, and the presence of all three is highly specific, the triad has a very low sensitivity.[8] In the dyspneic patient with low voltage on ECG, POCUS can rapidly confirm/exclude pericardial effusion and help differentiate this from other causes of low voltage[9] – some of which can also be associated with shortness of breath, including cardiomyopathy (both ischemic and infiltrative), myxedema, and COPD.
- Severe hyperkalemia
Patients with hyperkalemia commonly present with shortness of breath[10] and often have delayed treatment with calcium despite ECG changes.[11] Signs of hyperkalemia include abnormalities in rate/rhythm (bradycardia, junctional rhythm), conduction (PR prolongation, wide QRS), axis (fascicular block), and ST/T changes (Brugada phenocopy, or diffuse peaked T waves – which are narrow and pointy, as opposed ischemic hyperacute T waves which are broad and tall relative to their QRS). The ECG is not sensitive or specific for hyperkalemia, but the more changes are present, the more likely the patient has severe hyperkalemia and needs calcium.[12]
Back to the cases
Case 1: 85 year old with one day of shortness of breath and weakness. RR 35, O2 90%, HR 80, BP 120/40.
Inferior STEMI(-)OMI plus subendocardial ischemia, rapidly diagnosed
- Heart rate/rhythm: normal sinus
- Electrical conduction: normal intervals
- Axis: normal
- R-wave progression: normal
- Tall/small voltages: normal
- ST/T changes: lead III has Q wave, ST elevation and hyperacute T wave (broad, bulky, as large as QRS), with reciprocal ST depression and T wave inversion in aVL (confirming inferior OMI), with ST depression V2-V6 with reciprocal ST elevation in aVR
Impression: inferior STEMI(-)OMI with subendocardial ischemia. Cath lab activated: 100% RCA occlusion and 80-90% stenosis in LAD and circumflex. First trop 200 ng/L (normal <16 in females and <26 in males) and peak 6,000. Post-cath ECG showed inferior reperfusion T wave inversion and resolution of subendocardial ischemia:
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Case 2: 45 year old with two days of shortness of breath and diaphoresis. RR 25, O2 87%, HR 110, BP 120/80.
Subacute STEMI(+)OMI, treated with puffers before ECG
- H: sinus tach
- E: normal conduction
- A: right axis
- R: poor R wave progression from precordial Q waves
- T: normal voltages
- S: convex ST elevation and hyperacute T waves V3-6, and mild inferior ST elevation with Q waves
Impression: subacute STEMI(+)OMI with ongoing hyperacute T waves. Cath lab activated. 100% LAD occlusion and chronic occlusion of RCA (responsible for inferior Q waves). Troponin 7,000 on arrival. Discharge ECG showed precordial reperfusion T wave inversion:
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Case 3: 90 year old with one day of shortness of breath, STEMI negative with EMS and treated with puffers for wheezing. RR35, O2 90%, HR 110, BP 110/75. Old then new ECG.
RBBB with subacute LAD occlusion, initially treated with puffers
- H: sinus tach
- E: old RBBB
- A: new left axis from inferior Q waves
- R: new precordial Q waves
- T: normal voltages
- S: concordant anterior convex ST elevation and T wave inversion
Impression: subacute LAD occlusion. Initially treated with BIPAP and puffers for wheezing, until first troponin returned at 15,000. Then cath lab activated: 100% LAD occlusion, peak troponin 40,000, and developed cardiogenic shock.
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Case 4: 75 year old, history of COPD, with one day of shortness of breath and wheezing. RR30, O2 80%, HR 110, BP 170/90
COPD exacerbation with LBBB and appropriate discordance, unnecessary cath lab activation.
- H: sinus tach
- E: LBBB
- A: normal axis
- R: delayed R wave progression from LBBB
- T: tall voltages
- S: appropriate discordant ST changes. V2-3 have greater than 5mm ST elevation, but this is proportional to massive voltages, eg V3 has 7mm ST elevation but the S wave is 55mm, so STE/S = 13%
Impression: LBBB with negative Modified-Sgarbossa Criteria, in patient with COPD and wheezing. Unnecessary cath lab activation, and improved with puffers and steroids. Discharge ECG was no longer tachycardic, with secondary ST segments that were less prominent and still proportional:
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Case 5: 90 year old with few days shortness of breath and lethargy. Old then new ECG. RR 28, O2 84%, HR 120, BP 79/35, temp 35.0
Diffuse ST depression and reciprocal ST elevation in aVR from septic shock
- H: AF with rapid ventricular response
- E: otherwise normal conduction
- A: normal axis
- R: mild early R wave progression
- T: normal voltages
- S: diffuse ST depression with reciprocal ST elevation in aVR, with old T wave inversion V4-6 and new T wave inversion I/aVL
Impression: diffuse ST depression with reciprocal ST elevation in aVR, in patient with shortness of breath, lethargy and shock. Diagnosed with pneumonia and septic shock.
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Case 6: 30 year old, previously healthy, with one day of shortness of breath and syncope. RR 20, O2 95%, HR 110, BP 140/100
Acute RV strain from large PE
- H: sinus tach
- E: normal conduction
- A: normal axis but S1
- R: delayed R wave progression
- T: normal voltages
- S: primary T wave inversion anterior and inferior
Impression: multiple signs of acute RV strain. CT chest showed large PE with RV strain, troponin mildly positive at 50
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Case 7: 30 year old, history of lupus, with months of exertional dyspnea. Normal vitals
RVH from chronic pulmonary hypertension
- H: normal sinus rhythm
- E: short PR without delta
- A: right axis
- R: reverse R wave progression with tall R in V1 and deep S in V6
- T: normal voltages
- S: secondary ST depression and T wave inversion anterior/inferior
Impression: RVH with secondary repolarization abnormalities. Diagnosed with chronic pulmonary hypertension secondary to lupus.
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Case 8: 50 year old, history of lung cancer, with few days fatigue and shortness of breath. RR 20, O2 98%, HR 100, BP 125/75
Low voltage, POCUS confirmed pericardial effusion and identified tamponade
- H: normal sinus rhythm
- E: normal conduction, RSR’ pattern in V2 from high lead placement (biphasic P wave)
- A: normal axis
- R: normal R wave progression
- T: low voltages limb leads (all <5mm) and precordial leads (all <10mm)
- S: nonspecific T wave changes (in V2 from high lead placement)
Impression: low voltages in cancer patient with shortness of breath. POCUS showed large pericardial effusion with diastolic RV collapse (tamponde despite normal blood pressure). Treated with pericardiocentesis
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Case 9: 80 year old with 3 months exertional dyspnea, increasing bilateral leg edema. R20, O2 95%, HR 50, BP 100/70
Atrial flutter and low voltage, POCUS excluded pericardial effusion and identified cardiomyopathy
Impression: atrial flutter and very low voltages. On POCUS there was no pericardial effusion but there were pleural effusions and ventricular thickening with poor function. Admitted with CHF and diagnosed with cardiac amyloid.
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Case 10: 60 year old, history of diabetes, with one day of shortness of breath and weakness. RR 20, O2 100%, HR 90, BP 115/60, glucose 23.
Peaked T waves from severe hyperkalemia, treated with calcium
- H: normal sinus
- E: normal conduction
- A: normal axis
- R: normal R wave progression
- T: normal voltages
- S: diffuse peaked T waves (look pinched, with a sharp point)
Impression: diabetic with hyperglycemia, weakness/dyspnea and peaked T waves. Potassium was 6.8 and peaked T waves resolved after calcium and shifting:
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Take home points for ECG interpretation in shortness of breath
- STEMI/OMI vs subendocardial ischemia: look for STEMI(-)OMI, subacute OMI, and OMI in the presence of LBBB and RBBB, and consider the differential for diffuse ST depression with reciprocal ST elevation in aVR.
- RV strain, acute vs chronic: look for signs of acute RV strain and chronic pulmonary hypertension
- Low voltage: consider pericardial effusion and other causes
- Hyperkalemia: look for multiple signs of hyperkalemia as a guide for empiric calcium
- POCUS complements the ECG: regional wall motion abnormalities in OMI, a differential for diffuse ST depression with reciprocal ST elevation in aVR, RV strain in large PE or chronic pulmonary hypertension, and pericardial effusion or cardiomyopathy in low voltage
References for ECG Cases 43: ECG interpretation in shortness of breath
- Brieger D, Eagle KA, Goodman SG, et al. Acute coronary syndromes without chest pain, an underdiagnosed and undertreated high-risk group. Insights from the Global Registry of Acute Coronary Events. Chest 2004;126:461-469
- El-Menyar A, Zubaid M, Sulaiman K, et al. Atypical presentation of acute coronary syndrome: a significant independent predictor of in-hospital mortality. J of Cardiol 2011 Mar;57(2):165-171
- Meyers, HP, Bracey A, Lee D, et al. Accuracy of OMI ECG findings versus STEMI criteria for diagnosis of acute coronary occlusion myocardial infarction. Int J Cardiol Heart Vasc 2021 Apr 12;33:100767
- Bracey A, Massey L, Pellet AC, et al. FOCUS may detect wall motion abnormalities in patients with ACS, a retrospective study. Am J Emerg Med 2023 Apr 2;69:17-22
- Harhash AA, Huang JJ, Reddy S, et al. aVR ST segment elevation: acute STEMI or not? Incidence of an acute coronary occlusion. Am J Med 2019, 132(5):622-630
- 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
- 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
- Argula RG, Negi SI, Banchs 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 Cariol 2015;38(3):139-144
- Madias J. Low QRS and its causes. J of Electrocardiol 2008 Nov-Dec;41(6):498-500
- Peacock F, Rafique Z, Clark C, et al. Real world evidence for treatment of hyperkalemia in the emergency department (REVEAL-ED): a multicenter, prospective, observational study. J of Emerg Med 2018;55(6):741-750
- Durfey N, Lehnhof B, Bergeson A, et al. Severe hyperkalemia: can the electrocardiogram risk stratify for short-term adverse events. West J of Emerg Med 2017 Aug;18(5):963-971
- Varga C, Kalman Z, Szakall A, et al. ECG alterations suggestive of hyperkalemia in normokalemic versus hyperkalemic patients. BMC Emerg Med 2019 Amy 31;19(1):33
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