COVID-19 electrocardiogram: Difference between revisions

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'''For COVID-19 frequently asked inpatient questions, click [[COVID-19 frequently asked inpatient questions|here]]'''<br>
'''For COVID-19 frequently asked outpatient questions, click [[COVID-19 frequently asked outpatient questions|here]]'''<br>
{{COVID-19}}
{{COVID-19}}
{{CMG}}; {{AE}}{{Sab}}; {{HK}}
{{CMG}}; {{AE}} {{Sab}}; {{HK}}; {{Nuha}}


==Overview==
==Overview==
There are no specific [[ECG]] findings associated with coronavirus [[infection]]. Non specific findings can include [[sinus tachycardia]], ST-elevation and diffuse [[T wave]] inversion.
There are no specific [[ECG]] findings associated with [[COVID-19]]. The [[The electrocardiogram|ECG]] findings that have been reported are [[sinus tachycardia]], [[ST elevation|ST-elevation]], diffuse [[T wave]] inversion, [[relative bradycardia]], [[atrial fibrillation]].
 
==Electrocardiogram==
==Electrocardiogram==
*Most of the findings are ST-T abnormalities,and left ventricular hypertrophy, atrial fibrillation,tachy-brady syndrome, and changes consistent with acute pericarditis.<ref name="Amaratunga Corwin2020">{{cite journal|last1=Amaratunga |first1=Eluwana A|last2=Corwin|first2=Douglas S|last3=Moran|first3=Lynn|last4=Snyder|first4=Richard|title=Bradycardia in Patients With COVID-19: A Calm Before the Storm?|journal=Cureus|year=2020|issn=2168-8184|doi=10.7759/cureus.8599}}</ref>
*Non specific findings can include [[sinus tachycardia]], [[ST elevation|ST-elevation]] and diffuse [[T wave]] inversion.<ref name="pmid26922692">{{cite journal |vauthors=Alhogbani T |title=Acute myocarditis associated with novel Middle east respiratory syndrome coronavirus |journal=Ann Saudi Med |volume=36 |issue=1 |pages=78–80 |date=2016 |pmid=26922692 |pmc=6074274 |doi=10.5144/0256-4947.2016.78 |url=}}</ref>
* The [[The electrocardiogram|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|,tachy-brady syndrome]].
**Changes consistent with [[acute pericarditis]]; [[COVID-19]] induced [[pericarditis]] may due to expression of [[Angiotensin-converting enzyme 2|ACE2]] receptors in [[epicardial]] [[Adipocyte|adipocites]].<ref name="Amaratunga Corwin2020">{{cite journal|last1=Amaratunga |first1=Eluwana A|last2=Corwin|first2=Douglas S|last3=Moran|first3=Lynn|last4=Snyder|first4=Richard|title=Bradycardia in Patients With COVID-19: A Calm Before the Storm?|journal=Cureus|year=2020|issn=2168-8184|doi=10.7759/cureus.8599}}</ref>
**[[Complete heart block]], [[acute coronary syndromes]], [[myocarditis]], [[decompensated heart failure]], and [[Pulmonary embolism|pulmonary embolisms]].<ref name="Amaratunga Corwin2020">{{cite journal|last1=Amaratunga |first1=Eluwana A|last2=Corwin|first2=Douglas S|last3=Moran|first3=Lynn|last4=Snyder|first4=Richard|title=Bradycardia in Patients With COVID-19: A Calm Before the Storm?|journal=Cureus|year=2020|issn=2168-8184|doi=10.7759/cureus.8599}}</ref>
**[[Sinus rhythm]] with a [[first-degree atrioventricular block]] (AVB) with SITIIIQIII; [[Sinus tachycardia]] with incomplete [[right bundle branch block]].<ref name="HeWu2020" /><ref name="McculloughGoyal2020" />
 
*[[COVID-19]] and acute [[myopericarditis]]:
**[[Low QRS voltage|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]].<ref name="InciardiLupi2020">{{cite journal|last1=Inciardi|first1=Riccardo M.|last2=Lupi|first2=Laura|last3=Zaccone|first3=Gregorio|last4=Italia|first4=Leonardo|last5=Raffo|first5=Michela|last6=Tomasoni|first6=Daniela|last7=Cani|first7=Dario S.|last8=Cerini|first8=Manuel|last9=Farina|first9=Davide|last10=Gavazzi|first10=Emanuele|last11=Maroldi|first11=Roberto|last12=Adamo|first12=Marianna|last13=Ammirati|first13=Enrico|last14=Sinagra|first14=Gianfranco|last15=Lombardi|first15=Carlo M.|last16=Metra|first16=Marco|title=Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19)|journal=JAMA Cardiology|year=2020|issn=2380-6583|doi=10.1001/jamacardio.2020.1096}}</ref><ref name="HeWu2020">{{cite journal|last1=He|first1=Jia|last2=Wu|first2=Bo|last3=Chen|first3=Yaqin|last4=Tang|first4=Jianjun|last5=Liu|first5=Qiming|last6=Zhou|first6=Shenghua|last7=Chen|first7=Chen|last8=Qin|first8=Qingwu|last9=Huang|first9=Kang|last10=Lv|first10=Jianlei|last11=Chen|first11=Yan|last12=Peng|first12=Daoquan|title=Characteristic Electrocardiographic Manifestations in Patients With COVID-19|journal=Canadian Journal of Cardiology|volume=36|issue=6|year=2020|pages=966.e1–966.e4|issn=0828282X|doi=10.1016/j.cjca.2020.03.028}}</ref><ref name="Amaratunga Corwin2020" /><ref name="McculloughGoyal2020">{{cite journal|last1=Mccullough|first1=S. Andrew|last2=Goyal|first2=Parag|last3=Krishnan|first3=Udhay|last4=Choi|first4=Justin J.|last5=Safford|first5=Monika M.|last6=Okin|first6=Peter M.|title=Electrocardiographic Findings in Coronavirus Disease-19: Insights on Mortality and Underlying Myocardial Processes|journal=Journal of Cardiac Failure|year=2020|issn=10719164|doi=10.1016/j.cardfail.2020.06.005}}</ref>


*COVID-19 has been associated with complete hart block, acute coronary syndromes, myocarditis, decompensated heart failure, and pulmonary embolisms.<ref name="Amaratunga Corwin2020">{{cite journal|last1=Amaratunga |first1=Eluwana A|last2=Corwin|first2=Douglas S|last3=Moran|first3=Lynn|last4=Snyder|first4=Richard|title=Bradycardia in Patients With COVID-19: A Calm Before the Storm?|journal=Cureus|year=2020|issn=2168-8184|doi=10.7759/cureus.8599}}</ref>
*[[Relative bradycardia]] in patients With [[COVID-19]]:
**The [[pathogenesis]] is poorly understood, [[cardiac pacemaker]] cells may be a target for [[inflammatory]] [[Cytokine|cytokines]] resulting in a change in heart rate dynamics or their responsiveness to [[Neurotransmitter|neurotransmitters]] during [[systemic inflammation]]. Severe deterioration in some patients with [[COVID-19]] being closely related to the [[Cytokine storm|cytokine storm.]]<ref name="YeWang2020">{{cite journal|last1=Ye|first1=Qing|last2=Wang|first2=Bili|last3=Mao|first3=Jianhua|title=The pathogenesis and treatment of the `Cytokine Storm' in COVID-19|journal=Journal of Infection|volume=80|issue=6|year=2020|pages=607–613|issn=01634453|doi=10.1016/j.jinf.2020.03.037}}</ref>
**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]] [[Cytokine|cytokines]], including [[Interleukin 6|IL-6]] directly act on the [[Sinoatrial node|sinoatrial]] ([[SA]]) node.<ref name="Amaratunga Corwin2020">{{cite journal|last1=Amaratunga |first1=Eluwana A|last2=Corwin|first2=Douglas S|last3=Moran|first3=Lynn|last4=Snyder|first4=Richard|title=Bradycardia in Patients With COVID-19: A Calm Before the Storm?|journal=Cureus|year=2020|issn=2168-8184|doi=10.7759/cureus.8599}}</ref>


*COVID-19 and acute myopericarditis:
*Medication induce prolongation of PQ interval,particularly in those with [[Comorbidities|co-morbidities]] and in those who are treated with other [[QT-prolongation|QT-prolonging]] medications.<ref name="ChorinDai2020">{{cite journal|last1=Chorin|first1=Ehud|last2=Dai|first2=Matthew|last3=Shulman|first3=Eric|last4=Wadhwani|first4=Lalit|last5=Bar-Cohen|first5=Roi|last6=Barbhaiya|first6=Chirag|last7=Aizer|first7=Anthony|last8=Holmes|first8=Douglas|last9=Bernstein|first9=Scott|last10=Spinelli|first10=Michael|last11=Park|first11=David S.|last12=Chinitz|first12=Larry A.|last13=Jankelson|first13=Lior|title=The QT interval in patients with COVID-19 treated with hydroxychloroquine and azithromycin|journal=Nature Medicine|volume=26|issue=6|year=2020|pages=808–809|issn=1078-8956|doi=10.1038/s41591-020-0888-2}}</ref>
**low voltage in the limb leads, minimal diffuse ST-segment elevation (more prominent in the inferior and lateral leads), and an ST-segment depression with T-wave inversion in lead V1 and aVR.<ref name="InciardiLupi2020">{{cite journal|last1=Inciardi|first1=Riccardo M.|last2=Lupi|first2=Laura|last3=Zaccone|first3=Gregorio|last4=Italia|first4=Leonardo|last5=Raffo|first5=Michela|last6=Tomasoni|first6=Daniela|last7=Cani|first7=Dario S.|last8=Cerini|first8=Manuel|last9=Farina|first9=Davide|last10=Gavazzi|first10=Emanuele|last11=Maroldi|first11=Roberto|last12=Adamo|first12=Marianna|last13=Ammirati|first13=Enrico|last14=Sinagra|first14=Gianfranco|last15=Lombardi|first15=Carlo M.|last16=Metra|first16=Marco|title=Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19)|journal=JAMA Cardiology|year=2020|issn=2380-6583|doi=10.1001/jamacardio.2020.1096}}</ref>
=='''[[QTc]] Assessment Guidelines'''==
'''Table 1. Risk Score For Drug-Associated [[QTc]] Prolongation'''<ref name="TisdaleJaynes2013">{{cite journal|last1=Tisdale|first1=James E.|last2=Jaynes|first2=Heather A.|last3=Kingery|first3=Joanna R.|last4=Mourad|first4=Noha A.|last5=Trujillo|first5=Tate N.|last6=Overholser|first6=Brian R.|last7=Kovacs|first7=Richard J.|title=Development and Validation of a Risk Score to Predict QT Interval Prolongation in Hospitalized Patients|journal=Circulation: Cardiovascular Quality and Outcomes|volume=6|issue=4|year=2013|pages=479–487|issn=1941-7713|doi=10.1161/CIRCOUTCOMES.113.000152}}</ref>
<br />
{| class="wikitable" style="border: 0px; font-size: 90%; margin: 3px;" align="center"
! rowspan="1" style="background: #4479BA; padding: 5px 5px;" |'''Risk Factors'''
! colspan="1" style="background: #4479BA; padding: 5px 5px;" |'''Points'''
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Age ≥68 y


**ECG signs of acute pericarditis concave ST elevation and PR depression throughout most of the limb (I, II, III, aVL, aVF) and precordial (V2-V6) leads, reciprocal ST depression and PR elevation in aVR, and a ST segment/T wave ratio> 0.25. COVID-19 induced pericarditis might reflect the expression of ACE2 receptors in epicardial adipocites, mediating the cell entry of SARS-CoV-2 and possibly triggering local inflammation.<ref name="Amaratunga Corwin2020">{{cite journal|last1=Amaratunga |first1=Eluwana A|last2=Corwin|first2=Douglas S|last3=Moran|first3=Lynn|last4=Snyder|first4=Richard|title=Bradycardia in Patients With COVID-19: A Calm Before the Storm?|journal=Cureus|year=2020|issn=2168-8184|doi=10.7759/cureus.8599}}</ref>
| style="padding: 5px 5px; background: #F5F5F5;" |1


* There are no specific [[ECG]] findings associated with coronavirus [[infection]].
|-
* Non specific findings can include [[sinus tachycardia]], ST-elevation and diffuse [[T wave]] inversion.<ref name="pmid26922692">{{cite journal |vauthors=Alhogbani T |title=Acute myocarditis associated with novel Middle east respiratory syndrome coronavirus |journal=Ann Saudi Med |volume=36 |issue=1 |pages=78–80 |date=2016 |pmid=26922692 |pmc=6074274 |doi=10.5144/0256-4947.2016.78 |url=}}</ref>
|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.
|
|}__NOTOC__
A Tisdale score of ≤ 6 predicts low risk, 7-10 medium risk, and ≥ 11 high risk of drug-associated QT prolongation (Table 2).
{| class="wikitable"
!'''Table 2. Risk Levels For Drug-Associated QT Prolongation'''
|-
|Low risk = ≤6 points
|-
|Moderate risk = 7-10 points
|-
|High-risk = ≥11 points
|}
<br />


==References==
==References==
{{reflist|2}}
{{reflist|2}}

Latest revision as of 15:42, 8 July 2020

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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

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

  • 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

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

  1. 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. 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. 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. 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.
  5. 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.
  6. 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.
  7. 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.
  8. 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.