Cardiogenic shock electrocardiogram
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2] Syed Musadiq Ali M.B.B.S.[3] James Nasr[4]
Cardiogenic shock electrocardiogram
Cardiogenic shock electrocardiogram
Overview
The electrocardiogram is a first-line diagnostic test in suspected cardiogenic shock because it may identify acute coronary occlusion, high-risk ischemic patterns, arrhythmia-mediated shock, right ventricular infarction, conduction disease, or non-ischemic mimics such as myocarditis, stress cardiomyopathy, or cardiac tamponade. The ECG is a core component of the SUSPECT CS bedside diagnostic framework from the 2025 ACC Expert Consensus Statement, which combines ECG and echocardiography into a single diagnostic element (“ECG/Echocardiogram”). The ECG-specific role is to identify acute ischemia, STEMI, STEMI-equivalent patterns, and rhythm disturbances; the echocardiographic portion evaluates regional wall motion abnormalities, LV or RV dilation and systolic dysfunction, and valvular pathology.[1]
A nondiagnostic ECG does not exclude cardiogenic shock. ECG findings should be interpreted with symptoms, physical examination, lactate and end-organ markers, echocardiography, and hemodynamic data when available.[2]
Role of ECG in cardiogenic shock evaluation
Every patient with suspected cardiogenic shock should have an immediate 12-lead ECG. The 2025 ACC/AHA/ACEP/NAEMSP/SCAI Acute Coronary Syndromes Guideline gives a class 1, level B-NR recommendation that a 12-lead ECG should be acquired and interpreted within 10 minutes of first medical contact.[3] ECG evidence of acute ischemia, particularly ST-elevation myocardial infarction, should prompt early triage to a cardiac catheterization laboratory and revascularization when appropriate.[1]
The ECG is used to:
- Identify acute coronary syndrome as the cause of shock
- Detect STEMI, STEMI-equivalent patterns, and high-risk non-ST-elevation ischemic patterns
- Identify left bundle branch block or ventricular paced rhythm with ECG evidence of acute coronary occlusion
- Identify arrhythmias that precipitate or worsen shock
- Detect conduction disease, including high-grade atrioventricular block
- Identify right ventricular involvement in inferior myocardial infarction
- Provide prognostic information, including heart rate, QRS duration, and ST-segment deviation burden
- Monitor for reperfusion, reinfarction, stent thrombosis, recurrent ischemia, and new arrhythmias
In patients who are ultimately diagnosed with STEMI, an initially nondiagnostic ECG may occur. The 2025 ACS guideline notes that 11% of patients ultimately diagnosed with STEMI had an initial nondiagnostic ECG, and 72.4% of these patients had a follow-up ECG diagnostic of STEMI within 90 minutes.[3]
Acute myocardial infarction-related cardiogenic shock
ST-elevation myocardial infarction
ST-segment elevation in contiguous leads is the key ECG finding that identifies acute coronary occlusion and triggers emergent reperfusion. The Fourth Universal Definition of Myocardial Infarction defines new ST elevation at the J point in two contiguous leads with thresholds of ≥1 mm in all leads other than V2-V3. In leads V2-V3, the thresholds are ≥2 mm in men ≥40 years, ≥2.5 mm in men <40 years, and ≥1.5 mm in women.[4]
| ECG finding | Clinical significance in cardiogenic shock |
|---|---|
| ST-segment elevation in two or more contiguous leads | Indicates acute transmural ischemia or infarction and should prompt emergent reperfusion strategy when clinically appropriate.[4] |
| Extensive ST-segment elevation across multiple territories | Suggests large ischemic territory, multivessel disease, or left main involvement; associated with greater shock severity. |
| Hyperacute T waves | May be the earliest sign of acute coronary occlusion before overt ST-segment elevation. |
| Q waves | Suggest established myocardial necrosis; may be present at presentation or develop over time. |
| Reciprocal ST-segment depression | Supports STEMI diagnosis and helps localize culprit territory. |
In the SHOCK trial ECG substudy of patients with cardiogenic shock complicating acute myocardial infarction, ECG abnormalities included ST elevation, Q waves, and ST depression; the ECG was nonspecific in a substantial minority of patients.[5]
In the CULPRIT-SHOCK trial ECG substudy of 665 patients with acute myocardial infarction-related cardiogenic shock, 55.9% had STEMI, 29.3% had NSTEMI, and 14.7% had LBBB-MI. Patients with NSTEMI and LBBB-MI were older and had more comorbidities. After adjustment, ECG presentation was not an independent risk factor for 30-day or 1-year mortality, and ECG presentation did not modify the treatment effect of culprit-lesion-only versus multivessel PCI.[6]
Non-ST-elevation myocardial infarction and left main or multivessel ischemia
Cardiogenic shock may complicate non-ST-elevation myocardial infarction, particularly with left main or severe multivessel coronary artery disease. High-risk ECG patterns include diffuse subendocardial ischemia and STEMI-equivalent patterns.[7]
| ECG pattern | Interpretation |
|---|---|
| ST-segment depression ≥1 mm in six or more leads with ST-segment elevation in aVR or V1 | Suggests diffuse subendocardial ischemia from left main, proximal LAD, or severe multivessel disease; should be treated as a high-risk ischemic pattern in cardiogenic shock.[7] |
| ST-segment elevation in aVR with diffuse ST depression | Suggests global ischemia and severe coronary disease, but is not specific for left main occlusion.[8] |
| De Winter pattern | Tall, prominent, symmetric T waves arising from upsloping ST depression in precordial leads, often with slight ST elevation in aVR; considered a STEMI-equivalent pattern.[7] |
| Dynamic ST depression or T-wave inversion | Suggests active ischemia and should prompt urgent evaluation when shock or instability is present. |
STEMI-equivalent and high-risk occlusion patterns
| Pattern | ECG features | Clinical implication |
|---|---|---|
| Posterior STEMI | Horizontal ST depression in V1-V3, dominant R wave in V2, upright anterior T waves; posterior leads V7-V9 may show ST elevation | Should prompt posterior lead recording and emergent reperfusion when consistent with acute coronary occlusion.[7][4] |
| De Winter pattern | Upsloping ST depression at the J point with tall symmetric precordial T waves, often with aVR elevation | STEMI-equivalent pattern usually associated with proximal LAD occlusion.[7] |
| Left bundle branch block with positive modified Sgarbossa criteria | Positive criteria include any of the following: concordant ST elevation ≥1 mm in leads with a positive QRS complex; concordant ST depression ≥1 mm in V1-V3; or discordant ST elevation ≥1 mm with ST elevation ≥25% of the preceding S-wave depth | New LBBB alone is no longer considered a STEMI equivalent and should not be considered diagnostic of AMI in isolation. LBBB with positive modified Sgarbossa criteria should be treated as acute coronary occlusion when the clinical context is consistent.[7][3] |
| Ventricular paced rhythm with suspected occlusion | Ischemia may be masked; modified Sgarbossa criteria may support diagnosis | Should not delay urgent evaluation when cardiogenic shock and ischemic symptoms are present. |
| Wellens syndrome | Biphasic or deeply inverted symmetric T waves in V2-V3, often after angina | Suggests critical proximal LAD stenosis; may precede large anterior infarction.[7] |
In the modified Sgarbossa derivation study, sensitivity was 91% and specificity was 90% for acute coronary occlusion in the setting of left bundle branch block, compared with 52% sensitivity for the original weighted Sgarbossa criteria.[9] In external validation, modified Sgarbossa criteria had sensitivity of 80% and specificity of 99%.[10]
Right ventricular infarction
Right ventricular infarction is an important cause of cardiogenic shock, especially with inferior myocardial infarction from proximal right coronary artery occlusion. Right-sided ECG leads should be recorded promptly in inferior STEMI because right-sided ST elevation may be transient.[11][12]
| ECG finding | Diagnostic significance |
|---|---|
| ST-segment elevation ≥0.5 mm in V3R or V4R | Supports right ventricular involvement in inferior myocardial infarction; higher threshold may be used in young men according to universal MI criteria.[4] In an autopsy study of 43 patients with acute myocardial infarction, ST elevation in V4R had 100% sensitivity, 68.2% specificity, and 100% negative predictive value for posterior right ventricular infarction.[13] |
| ST elevation in V4R higher than V1-V3 | Had 100% specificity and 91.7% diagnostic efficiency for posterior right ventricular infarction in the autopsy study by Lopez-Sendon et al.[13] |
| Inferior ST-segment elevation in II, III, and aVF with III > II | Suggests right coronary artery culprit rather than left circumflex occlusion.[11] |
| ST-segment depression in I and aVL | Reciprocal change supporting inferior right coronary artery territory infarction. |
| ST-segment elevation in V1 with inferior ST elevation | May suggest right ventricular involvement. |
| Loss of R wave in V3R or V4R | Additional ECG clue to right ventricular infarction.[12] |
Absence of ST elevation in right-sided precordial leads does not exclude right ventricular infarction, especially when the ECG is obtained late after symptom onset. Imaging and hemodynamic assessment may be needed when the clinical suspicion remains high.[4]
Arrhythmias in cardiogenic shock
Arrhythmias may precipitate cardiogenic shock, worsen established shock, or represent a terminal complication. Continuous telemetry is required in cardiogenic shock, and the 12-lead ECG should be repeated when rhythm changes occur.
| Arrhythmia | Clinical context in cardiogenic shock |
|---|---|
| Ventricular tachycardia or ventricular fibrillation | May precipitate shock or complicate acute myocardial infarction, ischemia, electrolyte derangement, or myocarditis; sustained VT/VF requires immediate defibrillation or cardioversion. |
| High-grade atrioventricular block | May occur with inferior myocardial infarction and right ventricular involvement or with large anterior infarction; can cause profound bradycardia and low cardiac output. |
| Complete heart block | Inferior MI-related block is often nodal and may be transient; anterior MI-related block is usually infranodal and associated with larger infarct territory and worse prognosis. |
| Sinus bradycardia | May occur with inferior MI, right ventricular infarction, or vagal activation and can worsen low-output physiology. |
| Atrial fibrillation | May worsen hemodynamics through loss of atrial contribution and rapid ventricular response. |
| Sinus tachycardia | Common in cardiogenic shock and reflects sympathetic activation, low stroke volume, pain, hypoxemia, or systemic stress. |
Conduction abnormalities
In the SHOCK trial ECG substudy, prolonged QRS duration was associated with 1-year mortality in medically stabilized patients, but not in emergently revascularized patients. Emergency revascularization appeared to eliminate the incremental mortality risk associated with prolonged QRS duration.[5]
| Conduction finding | Clinical significance |
|---|---|
| New or presumed new left bundle branch block | New LBBB alone is no longer considered a STEMI equivalent and should not be considered diagnostic of acute myocardial infarction in isolation. In acute ischemic symptoms with cardiogenic shock, apply modified Sgarbossa criteria and use clinical context to guide emergent catheterization decisions.[7][3] |
| New right bundle branch block | May occur with anterior MI or right ventricular infarction and may reflect larger infarct size or conduction system involvement. |
| Ventricular paced rhythm | May mask acute coronary occlusion; modified Sgarbossa criteria can support diagnosis. |
| Prolonged QRS duration | Associated with worse prognosis in the SHOCK trial ECG substudy among medically stabilized patients.[5] |
| High-grade atrioventricular block | May itself cause or worsen cardiogenic shock and should prompt urgent rhythm-specific management. |
Mechanical complications of myocardial infarction
Mechanical complications usually occur within the first week after myocardial infarction and may present with abrupt hemodynamic deterioration. The ECG may show the infarct territory, recurrent ischemia, arrhythmias, or conduction disease, but it cannot diagnose mechanical complications; urgent echocardiography is required when suspected.[14]
| Mechanical complication | ECG findings | Key limitation |
|---|---|---|
| Ventricular septal rupture | Evolving anterior or inferior MI, Q waves, recurrent ischemia, or ventricular arrhythmias | ECG may identify infarct territory but cannot diagnose septal rupture; echocardiography with color Doppler is required.[15] |
| Papillary muscle rupture with acute mitral regurgitation | Recent inferior or posterior MI pattern; sinus tachycardia may be present | ECG contribution is limited; echocardiography is essential.[16] |
| Free wall rupture | New ST elevation from pericardial irritation, sinus bradycardia, junctional or idioventricular rhythm, complete heart block, electromechanical dissociation | Often presents as sudden collapse; echocardiography is required to identify tamponade or hemopericardium.[14] |
Non-acute myocardial infarction causes of cardiogenic shock
| Condition | ECG findings | Diagnostic caveat |
|---|---|---|
| Acute myocarditis | ST-segment elevation, ST-T wave changes, T-wave inversion, PR depression, low voltage, ventricular arrhythmias, or atrioventricular block | ECG may mimic acute myocardial infarction; diagnosis requires clinical, biomarker, imaging, and sometimes tissue integration.[17] |
| Stress cardiomyopathy | ST-segment elevation, deep T-wave inversion, QTc prolongation, and dynamic ECG evolution over days | ECG is abnormal in most cases but often overlaps with acute coronary syndrome; coronary evaluation and imaging are commonly required.[18] |
| Cardiac tamponade | Sinus tachycardia, low QRS voltage, electrical alternans, and diffuse ST elevation or PR depression if pericarditis is present. Electrical alternans has high specificity but very low sensitivity for tamponade; reported sensitivity ranges from 16% to 23%, and specificity may approach 98% in pericardial effusion cohorts.[19][20] | ECG findings are supportive but not definitive; echocardiography confirms hemodynamic tamponade.[21] |
Prognostic ECG findings
The SHOCK trial ECG substudy identified several ECG parameters associated with prognosis in cardiogenic shock complicating acute myocardial infarction.[5]
| ECG parameter | Prognostic significance |
|---|---|
| Higher heart rate | Baseline heart rate was higher in nonsurvivors than survivors in the SHOCK trial ECG substudy. |
| Prolonged QRS duration | Associated with higher 1-year mortality in medically stabilized patients; emergency revascularization appeared to eliminate this incremental risk. |
| Greater sum of ST depression | In inferior AMI, greater ST depression burden was associated with higher 1-year mortality in medically stabilized patients, but not in emergently revascularized patients. |
| Diffuse ST depression with aVR elevation | Suggests left main, proximal LAD, or severe multivessel ischemia and should be treated as a high-risk ECG pattern. |
| QTc prolongation | Particularly relevant in stress cardiomyopathy and drug-related causes; QTc >500 ms increases risk for torsade de pointes. |
Serial ECG monitoring
Serial ECG recording is important because cardiogenic shock and acute ischemia evolve over time. Serial ECGs may identify reperfusion, reinfarction, stent thrombosis, dynamic ischemia, arrhythmia, conduction disease, and QTc prolongation.[4]
Repeat ECG should be obtained when there is:
- Persistent or recurrent chest pain
- Worsening shock or new hemodynamic instability
- New arrhythmia or conduction abnormality
- Concern for reinfarction or stent thrombosis
- Initial nondiagnostic ECG with ongoing suspicion of acute coronary syndrome
- New murmur or abrupt deterioration after myocardial infarction
- QT-prolonging drug exposure or suspected stress cardiomyopathy
When the initial ECG is nondiagnostic and suspicion for acute coronary syndrome remains high, serial ECGs at 15- to 30-minute intervals during the initial evaluation may help identify evolving ischemia.[4] Continuous telemetry monitoring is required in all patients with cardiogenic shock.
Practical ECG approach
- Obtain and interpret a 12-lead ECG within 10 minutes of first medical contact in every patient with suspected cardiogenic shock.
- Identify STEMI, posterior STEMI, de Winter pattern, LBBB or ventricular paced rhythm with positive modified Sgarbossa criteria, diffuse ST depression with aVR elevation, and other high-risk ischemic patterns.
- Activate emergent catheterization when STEMI or a STEMI-equivalent/acute occlusion pattern is present with cardiogenic shock.
- Record right-sided leads V3R and V4R in inferior STEMI to assess for right ventricular infarction.
- Do not treat new LBBB alone as diagnostic of acute myocardial infarction; apply modified Sgarbossa criteria and integrate clinical context.
- Identify rhythm-mediated shock, including ventricular tachycardia, ventricular fibrillation, high-grade atrioventricular block, complete heart block, and rapid atrial arrhythmias.
- Repeat ECGs serially when symptoms or hemodynamics evolve.
- Integrate ECG findings with echocardiography, laboratory findings, and hemodynamics.
Common pitfalls
- Treating new left bundle branch block alone as a STEMI equivalent despite current guideline language
- Failing to apply modified Sgarbossa criteria in left bundle branch block or ventricular paced rhythm
- Failing to obtain right-sided leads in inferior STEMI
- Missing posterior STEMI because only standard anterior leads are reviewed
- Missing de Winter pattern or diffuse ST depression with aVR elevation
- Delaying reperfusion in cardiogenic shock with clear STEMI or STEMI-equivalent/acute occlusion pattern
- Assuming a normal or nondiagnostic ECG excludes cardiogenic shock
- Trying to diagnose mechanical complications by ECG instead of urgent echocardiography
- Over-relying on electrical alternans to exclude tamponade despite its low sensitivity
- Failing to monitor QTc in stress cardiomyopathy
- Interpreting ECG findings without integrating clinical, laboratory, echocardiographic, and hemodynamic data
References
References
- ↑ 1.0 1.1 Sinha SS, Morrow DA, Kapur NK, Kataria R, Roswell RO (2025). “2025 Concise Clinical Guidance: An ACC Expert Consensus Statement on the Evaluation and Management of Cardiogenic Shock”. Journal of the American College of Cardiology. 85 (16): 1618–1641. doi:10.1016/j.jacc.2025.02.018.
- ↑ van Diepen S, Katz JN, Albert NM; et al. (2017). “Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association”. Circulation. 136 (16): e232–e268. doi:10.1161/CIR.0000000000000525.
- ↑ 3.0 3.1 3.2 3.3 Rao SV, O’Donoghue ML, Ruel M; et al. (2025). “2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes”. Journal of the American College of Cardiology. 85 (22): 2135–2237. doi:10.1016/j.jacc.2024.11.009.
- ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 Thygesen K, Alpert JS, Jaffe AS; et al. (2018). “Fourth Universal Definition of Myocardial Infarction (2018)”. Journal of the American College of Cardiology. 72 (18): 2231–2264. doi:10.1016/j.jacc.2018.08.1038.
- ↑ 5.0 5.1 5.2 5.3 White HD, Palmeri ST, Sleeper LA; et al. (2004). “Electrocardiographic Findings in Cardiogenic Shock, Risk Prediction, and the Effects of Emergency Revascularization: Results From the SHOCK Trial”. American Heart Journal. 148 (5): 810–817. doi:10.1016/j.ahj.2004.05.012.
- ↑ Zeitouni M, Akin I, Desch S; et al. (2021). “Clinical Outcomes According to ECG Presentations in Infarct-Related Cardiogenic Shock in the Culprit Lesion Only PCI Versus Multivessel PCI in Cardiogenic Shock Trial”. Chest. 159 (4): 1415–1425. doi:10.1016/j.chest.2020.10.089.
- ↑ 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 Kontos MC, de Lemos JA, Deitelzweig SB; et al. (2022). “2022 ACC Expert Consensus Decision Pathway on the Evaluation and Disposition of Acute Chest Pain in the Emergency Department”. Journal of the American College of Cardiology. 80 (20): 1925–1960. doi:10.1016/j.jacc.2022.08.750.
- ↑ Gibbs MA, Leedekerken JB, Littmann L (2019). “Evolution of Our Understanding of the aVR Sign”. Journal of Electrocardiology. 56: 121–124. doi:10.1016/j.jelectrocard.2019.07.014.
- ↑ Smith SW, Dodd KW, Henry TD, Dvorak DM, Pearce LA (2012). “Diagnosis of ST-elevation Myocardial Infarction in the Presence of Left Bundle Branch Block With the ST-elevation to S-Wave Ratio in a Modified Sgarbossa Rule”. Annals of Emergency Medicine. 60 (6): 766–776. doi:10.1016/j.annemergmed.2012.07.119.
- ↑ Meyers HP, Limkakeng AT, Jaffa EJ; et al. (2015). “Validation of the Modified Sgarbossa Criteria for Acute Coronary Occlusion in the Setting of Left Bundle Branch Block: A Retrospective Case-Control Study”. American Heart Journal. 170 (6): 1255–1264. doi:10.1016/j.ahj.2015.09.005.
- ↑ 11.0 11.1 Wagner GS, Macfarlane P, Wellens H; et al. (2009). “AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram: Part VI: Acute Ischemia/Infarction”. Circulation. 119 (10): e262–e270. doi:10.1161/CIRCULATIONAHA.108.191098.
- ↑ 12.0 12.1 Goldstein JA, Lerakis S, Moreno PR (2024). “Right Ventricular Myocardial Infarction-a Tale of Two Ventricles: JACC Focus Seminar 1/5”. Journal of the American College of Cardiology. 83 (18): 1779–1798. doi:10.1016/j.jacc.2023.09.839.
- ↑ 13.0 13.1 Lopez-Sendon J, Coma-Canella I, Alcasena S, Seoane J, Gamallo C (1985). “Electrocardiographic Findings in Acute Right Ventricular Infarction: Sensitivity and Specificity of Electrocardiographic Alterations in Right Precordial Leads V4R, V3R, V1, V2, and V3”. Journal of the American College of Cardiology. 6 (6): 1273–1279. doi:10.1016/S0735-1097(85)80213-8.
- ↑ 14.0 14.1 Damluji AA, van Diepen S, Katz JN; et al. (2021). “Mechanical Complications of Acute Myocardial Infarction: A Scientific Statement From the American Heart Association”. Circulation. 144 (2): e16–e35. doi:10.1161/CIR.0000000000000985.
- ↑ Cubeddu RJ, Lorusso R, Ronco D; et al. (2024). “Ventricular Septal Rupture After Myocardial Infarction: JACC Focus Seminar 3/5”. Journal of the American College of Cardiology. 83 (19): 1886–1901. doi:10.1016/j.jacc.2024.01.041.
- ↑ Gong FF, Vaitenas I, Malaisrie SC, Maganti K (2021). “Mechanical Complications of Acute Myocardial Infarction: A Review”. JAMA Cardiology. 6 (3): 341–349. doi:10.1001/jamacardio.2020.3690.
- ↑ Ammirati E, Moslehi JJ (2023). “Diagnosis and Treatment of Acute Myocarditis: A Review”. JAMA. 329 (13): 1098–1113. doi:10.1001/jama.2023.3371.
- ↑ Medina de Chazal H, Del Buono MG, Keyser-Marcus L; et al. (2018). “Stress Cardiomyopathy Diagnosis and Treatment: JACC State-of-the-Art Review”. Journal of the American College of Cardiology. 72 (16): 1955–1971. doi:10.1016/j.jacc.2018.07.072.
- ↑ Roy CL, Minor MA, Brookhart MA, Choudhry NK (2007). “Does This Patient With a Pericardial Effusion Have Cardiac Tamponade?”. JAMA. 297 (16): 1810–1818. doi:10.1001/jama.297.16.1810.
- ↑ Argula RG, Negi SI, Banchs J, Yusuf SW (2015). “Role of a 12-Lead Electrocardiogram in the Diagnosis of Cardiac Tamponade as Diagnosed by Transthoracic Echocardiography in Patients With Malignant Pericardial Effusion”. Clinical Cardiology. 38 (3): 139–144. doi:10.1002/clc.22370.
- ↑ Wang TKM, Klein AL, Cremer PC; et al. (2025). “2025 Concise Clinical Guidance: An ACC Expert Consensus Statement on the Diagnosis and Management of Pericarditis”. Journal of the American College of Cardiology. 86 (25): 2691–2719. doi:10.1016/j.jacc.2025.05.023.
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