COVID-19 electrocardiogram
For COVID-19 frequently asked inpatient questions, click here
For COVID-19 frequently asked outpatient questions, click here
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sabawoon Mirwais, M.B.B.S, M.D.[2]; Syed Hassan A. Kazmi BSc, MD [3]; Nuha Al-Howthi, MD[4]
Overview
Overview
There are no specific ECG findings associated with COVID-19. The ECG findings that have been reported are sinus tachycardia, ST-elevation, diffuse T wave inversion, relative bradycardia, atrial fibrillation.
Electrocardiogram
Electrocardiogram
- Non specific findings can include sinus tachycardia, ST-elevation and diffuse T wave inversion.[1]
- The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors, such as ischemia, myocarditis, and arrhythmias.
- Most of the findings are:
- ST-T changes, atrial fibrillation,tachy-brady syndrome.
- Changes consistent with acute pericarditis; COVID-19 induced pericarditis may due to expression of ACE2 receptors in epicardial adipocites.[2]
- Complete heart block, acute coronary syndromes, myocarditis, decompensated heart failure, and pulmonary embolisms.[2]
- Sinus rhythm with a first-degree atrioventricular block (AVB) with SITIIIQIII; Sinus tachycardia with incomplete right bundle branch block.[3][4]
- COVID-19 and acute myopericarditis:
- Low voltage in the limb leads, ST-segment elevation and an ST-segment depression with T-wave inversion; Severe stages of COVID-19 have been attributed to possible hypoxia and inflammatory damage incurred by the virus.[5][3][2][4]
- Relative bradycardia in patients With COVID-19:
- The pathogenesis is poorly understood, cardiac pacemaker cells may be a target for inflammatory cytokines resulting in a change in heart rate dynamics or their responsiveness to neurotransmitters during systemic inflammation. Severe deterioration in some patients with COVID-19 being closely related to the cytokine storm.[6]
- The inflammatory cytokines released during the stage of overwhelming immune response, acting on the cardiac pacemaker cells could possibly contribute to bradycardia. It may be that the high levels of pro-inflammatory cytokines, including IL-6 directly act on the sinoatrial (SA) node.[2]
- Medication induce prolongation of PQ interval,particularly in those with co-morbidities and in those who are treated with other QT-prolonging medications.[7]
QTc Assessment Guidelines
QTc Assessment Guidelines
Table 1. Risk Score For Drug-Associated QTc Prolongation[8]
| Risk Factors | Points |
|---|---|
| Age ≥68 y | 1 |
| Female sex | 1 |
| Loop diuretic | 1 |
| Serum K+ ≤3.5 mEq/L | 2 |
| Admission QTc ≥450 ms | 2 |
| Acute MI | 2 |
| ≥2 QTc-prolonging drugs | 3 |
| sepsis | 3 |
| Heart failure | 3 |
| One QTc-prolonging drug | 3 |
| Maximum Risk Score | 21 |
| K+ indicates potassium; and MI, myocardial infarction. |
A Tisdale score of ≤ 6 predicts low risk, 7-10 medium risk, and ≥ 11 high risk of drug-associated QT prolongation (Table 2).
| Table 2. Risk Levels For Drug-Associated QT Prolongation |
|---|
| Low risk = ≤6 points |
| Moderate risk = 7-10 points |
| High-risk = ≥11 points |
References
References
- ↑ Alhogbani T (2016). “Acute myocarditis associated with novel Middle east respiratory syndrome coronavirus”. Ann Saudi Med. 36 (1): 78–80. doi:10.5144/0256-4947.2016.78. PMC 6074274. PMID 26922692.
- ↑ 2.0 2.1 2.2 2.3 Amaratunga, Eluwana A; Corwin, Douglas S; Moran, Lynn; Snyder, Richard (2020). “Bradycardia in Patients With COVID-19: A Calm Before the Storm?”. Cureus. doi:10.7759/cureus.8599. ISSN 2168-8184.
- ↑ 3.0 3.1 He, Jia; Wu, Bo; Chen, Yaqin; Tang, Jianjun; Liu, Qiming; Zhou, Shenghua; Chen, Chen; Qin, Qingwu; Huang, Kang; Lv, Jianlei; Chen, Yan; Peng, Daoquan (2020). “Characteristic Electrocardiographic Manifestations in Patients With COVID-19”. Canadian Journal of Cardiology. 36 (6): 966.e1–966.e4. doi:10.1016/j.cjca.2020.03.028. ISSN 0828-282X.
- ↑ 4.0 4.1 Mccullough, S. Andrew; Goyal, Parag; Krishnan, Udhay; Choi, Justin J.; Safford, Monika M.; Okin, Peter M. (2020). “Electrocardiographic Findings in Coronavirus Disease-19: Insights on Mortality and Underlying Myocardial Processes”. Journal of Cardiac Failure. doi:10.1016/j.cardfail.2020.06.005. ISSN 1071-9164.
- ↑ Inciardi, Riccardo M.; Lupi, Laura; Zaccone, Gregorio; Italia, Leonardo; Raffo, Michela; Tomasoni, Daniela; Cani, Dario S.; Cerini, Manuel; Farina, Davide; Gavazzi, Emanuele; Maroldi, Roberto; Adamo, Marianna; Ammirati, Enrico; Sinagra, Gianfranco; Lombardi, Carlo M.; Metra, Marco (2020). “Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19)”. JAMA Cardiology. doi:10.1001/jamacardio.2020.1096. ISSN 2380-6583.
- ↑ Ye, Qing; Wang, Bili; Mao, Jianhua (2020). “The pathogenesis and treatment of the `Cytokine Storm’ in COVID-19”. Journal of Infection. 80 (6): 607–613. doi:10.1016/j.jinf.2020.03.037. ISSN 0163-4453.
- ↑ Chorin, Ehud; Dai, Matthew; Shulman, Eric; Wadhwani, Lalit; Bar-Cohen, Roi; Barbhaiya, Chirag; Aizer, Anthony; Holmes, Douglas; Bernstein, Scott; Spinelli, Michael; Park, David S.; Chinitz, Larry A.; Jankelson, Lior (2020). “The QT interval in patients with COVID-19 treated with hydroxychloroquine and azithromycin”. Nature Medicine. 26 (6): 808–809. doi:10.1038/s41591-020-0888-2. ISSN 1078-8956.
- ↑ Tisdale, James E.; Jaynes, Heather A.; Kingery, Joanna R.; Mourad, Noha A.; Trujillo, Tate N.; Overholser, Brian R.; Kovacs, Richard J. (2013). “Development and Validation of a Risk Score to Predict QT Interval Prolongation in Hospitalized Patients”. Circulation: Cardiovascular Quality and Outcomes. 6 (4): 479–487. doi:10.1161/CIRCOUTCOMES.113.000152. ISSN 1941-7713.
Looking for the patient version?
© 2026 MyEClinic – IFTM Institut für Telematik in der Medizin GmbH