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| [[[[Link title]]]]__NOTOC__
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| {{CMG}} {{AE}} {{mitra}}{{MC}}
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| ==Overview==
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| ==Complications==
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| ===Acute Coronary Syndromes===
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| ===Heart Failure===
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| ====Pathophysiology====
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| *Patients with chronic heart failure (HF) may be at higher risk of developing severe COVID-19 infection due to the advanced age and the presence of multiple comorbidities.
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| *Both de novo acute heart failure and acute decompensation of chronic heart failure can occur in patients with COVID-19.
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| *Presumed pathophysiologic mechanisms for the development of new or worsening heart failure in patients with COVID-19 include: <ref name="pmid32219357">{{Cite pmid|32219357}}</ref> <ref name="pmid32360242">{{Cite pmid|32360242}}</ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref>
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| **Acute exacerbation of chronic heart failure
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| **Acute myocardial injury (which in turn can be caused by several mechanisms)
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| **Stress cardiomyopathy (i.e., Takotsubo cardiomyopathy)
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| **Impaired myocardial relaxation resulting in diastolic dysfunction [i.e., Heart failure with preserved ejection fraction (HFpEF)]
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| **Right-sided heart failure, secondary to pulmonary hypertension caused by hypoxia and acute respiratory distress syndrome (ARDS)
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| ====Symptoms and signs====
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| *Dyspnea: may overlap with dyspnea due to concomitant respiratory involvement and ARDS due to COVID-19 infection
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| *Lower limb edema
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| *Orthopnea
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| *Paroxysmal nocturnal dyspnea
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| *Confusion and altered mentation
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| *Cool extremities
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| *Cyanosis
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| *Syncope
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| *Fatigue
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| *Hemoptysis
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| *Palpitations
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| *Weakness
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| *Wheezing or cardiac asthma
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| *Distended jugular veins
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| *Crackles on auscultation
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| ====Electrocardiography (ECG)====
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| *There is no specific electrocardiographic sign for acute heart failure in COVID-19 patients.
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| *The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors such as ischemia, myocarditis, and arrhythmias.
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| *These ECG findings may include:
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| **Low QRS Voltage
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| **Left ventricular hypertrophy
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| **Left atrial enlargement
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| **Left bundle branch block
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| **Poor R progression
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| **ST-T changes
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| ====Chest x-ray (CXR)====
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| *The Chest x-ray may show evidence of:
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| **Cardiomegaly
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| **Pulmonary congestion
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| **Increased pulmonary vascular markings.
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| *Signs of pulmonary edema may be obscured by underlying respiratory involvement and ARDS due to COVID-19.
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| ====Echocardiography====
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| *A complete standard transthoracic (TTE) has not been recommended in COVID-19 patients considering the limited personal protective equipment (PPE) and the risk of exposure of additional health care personnel. <ref name="pmid32391912">{{Cite pmid|32391912}}</ref>
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| *To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
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| *In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
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| **Cardiac point-of-care ultrasound (POCUS)
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| **Focused cardiac ultrasound study (FoCUS)
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| **Critical care echocardiography
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| *Cardiac ultrasound can help in assessing the following parameters:
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| **Left ventricular systolic function (ejection fraction) to distinguish systolic dysfunction with a reduced ejection fraction (<40%) from diastolic dysfunction with a preserved ejection fraction.
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| **Left ventricular diastolic function
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| **Left ventricular structural abnormalities, including LV size and LV wall thickness
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| **Left atrial size
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| **Right ventricular size and function
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| **Detection and quantification of valvular abnormalities
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| **Measurement of systolic pulmonary artery pressure
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| **Detection and quantification of pericardial effusion
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| **Detection of regional wall motion abnormalities/reduced strain that would suggest an underlying ischemia
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| ====Cardiac biomarkers====
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| *Elevated cardiac troponin levels suggest the presence of myocardial cell injury or death.
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| *Cardiac troponin levels may increase in patients with chronic or acute decompensated HF. <ref name="pmid20863950">{{Cite pmid|20863950}}</ref>
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| *Natriuretic peptides (BNP/NT-proBNP) are released from the heart in response to increased myocardial stress and are quantitative markers of increased intracardiac filling pressure. <ref name="pmid28062628">{{Cite pmid|28062628}}</ref>
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| *Elevated BNP and NT-proBNP are of both diagnostic and prognostic significance in patients with heart failure.
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| *Increased BNP or NT-proBNP levels have been demonstrated in COVID-19 patients.
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| *Increased NT-proBNP level was associated with worse clinical outcomes in patients with severe COVID-19. <ref name="pmid32293449">{{Cite pmid|32293449}}</ref> <ref name="pmid32232979">{{Cite pmid|32232979}}</ref>
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| *However, increased natriuretic peptide levels are frequently seen among patients with severe inflammatory or respiratory diseases. <ref name="pmid18298480">{{Cite pmid|18298480}}</ref> <ref name="pmid16442916">{{Cite pmid|16442916}}</ref> <ref name="pmid28322314">{{Cite pmid|28322314}}</ref> <ref name="pmid23837838">{{Cite pmid|23837838}}</ref> <ref name="pmid21478812">{{Cite pmid|21478812}}</ref>
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| *Therefore, routine measurement of BNP/NT-proBNP has not been recommended in COVID-19 patients, unless there is a high suspicion of HF based on clinical grounds.
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| ====Treatment====
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| *Patients with chronic heart failure are recommended to continue their previous guideline-directed medical therapy, including beta-blockers, ACEI or ARB, and mineralocorticoid receptor antagonists. <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>
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| *Acute heart failure in the setting of COVID-19 is generally treated similarly to acute heart failure in other settings. These may include: <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>
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| **Fluid restriction
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| **Diuretic therapy
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| **Vasopressors and/or inotropes
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| **Ventricular assisted devices and extracorporeal membrane oxygenation (ECMO)
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| *Beta-blockers should not be initiated during the acute stage due to their negative inotropic effects. <ref name="pmid24251454">{{Cite pmid|24251454}}</ref>
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| *Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) should be used with caution in patients with acute heart failure due to their effect on fluid and sodium retention. <ref name="pmid12656651">{{Cite pmid|12656651}}</ref>
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| ===Cardiogenic Shock===
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| ===Myocarditis===
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| ===Pericarditis===
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| ===Arrhythmias ===
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| ==== Pathophysiology: ====
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| Respiratory disease is the chief target of Coronavirus disease 2019 (COVID-19). One-third of patients with severe disease also reported other symptoms including [[Cardiac arrhythmia|arrhythmia]]. According to a study done in Wuhan, China, 16.7% of hospitalized and 44.4% of ICU patients with COVID-19 had arrhythmias.<ref name="WangHu2020">{{cite journal|last1=Wang|first1=Dawei|last2=Hu|first2=Bo|last3=Hu|first3=Chang|last4=Zhu|first4=Fangfang|last5=Liu|first5=Xing|last6=Zhang|first6=Jing|last7=Wang|first7=Binbin|last8=Xiang|first8=Hui|last9=Cheng|first9=Zhenshun|last10=Xiong|first10=Yong|last11=Zhao|first11=Yan|last12=Li|first12=Yirong|last13=Wang|first13=Xinghuan|last14=Peng|first14=Zhiyong|title=Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus–Infected Pneumonia in Wuhan, China|journal=JAMA|volume=323|issue=11|year=2020|pages=1061|issn=0098-7484|doi=10.1001/jama.2020.1585}}</ref> Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) utilizes S-spike to bind to angiotensin-converting enzyme 2 (ACE2) receptors to enter the cells. Type 1 and type 2 [[pneumocytes]] exhibit ACE 2 receptors in the lung. Studies report that coronary [[endothelial cells]] in the heart and intrarenal endothelial cells and renal tubular epithelial cells in the kidney exhibit ACE2. ACE2 is an inverse regulator of the [[renin-angiotensin system]].<ref name="XuShi2020">{{cite journal|last1=Xu|first1=Zhe|last2=Shi|first2=Lei|last3=Wang|first3=Yijin|last4=Zhang|first4=Jiyuan|last5=Huang|first5=Lei|last6=Zhang|first6=Chao|last7=Liu|first7=Shuhong|last8=Zhao|first8=Peng|last9=Liu|first9=Hongxia|last10=Zhu|first10=Li|last11=Tai|first11=Yanhong|last12=Bai|first12=Changqing|last13=Gao|first13=Tingting|last14=Song|first14=Jinwen|last15=Xia|first15=Peng|last16=Dong|first16=Jinghui|last17=Zhao|first17=Jingmin|last18=Wang|first18=Fu-Sheng|title=Pathological findings of COVID-19 associated with acute respiratory distress syndrome|journal=The Lancet Respiratory Medicine|volume=8|issue=4|year=2020|pages=420–422|issn=22132600|doi=10.1016/S2213-2600(20)30076-X}}</ref> The interaction between SARS-CoV2 and ACE2 can bring about changes in ACE2 pathways prompting intense injury to the lung, heart, and [[Endothelium|endothelial cells]]. [[Hypoxemia|Hypoxia]] and [[Electrolyte disturbance|electrolyte abnormalities]] that are common in the acute phase of severe [[COVID-19]] can potentiate [[Cardiac arrhythmia|cardiac arrhythmias]]. Binding of SARS-CoV-2 to ACE2 receptors can result into [[hypokalemia]] which causes various types of [[Cardiac arrhythmia|arrhythmia]]. Elevated levels of [[Cytokine|cytokines]] as a result of the [[Systemic inflammatory response syndrome|systemic inflammatory response]] of the severe [[COVID-19|Coronavirus disease 2019]] (COVID-19) can cause injury to multiple organs, including [[Cardiac muscle|cardiac myocytes]].<ref name="ChenPrendergast2020">{{cite journal|last1=Chen|first1=Mao|last2=Prendergast|first2=Bernard|last3=Redwood|first3=Simon|last4=Xiong|first4=Tian-Yuan|title=Coronaviruses and the cardiovascular system: acute and long-term implications|journal=European Heart Journal|volume=41|issue=19|year=2020|pages=1798–1800|issn=0195-668X|doi=10.1093/eurheartj/ehaa231}}</ref> According to the data based on studies on previous [[Severe acute respiratory syndrome]] ([[Severe acute respiratory syndrome|SARS]]) and the [[Middle East respiratory syndrome coronavirus infection|Middle East respiratory syndrome]] ([[Middle East respiratory syndrome coronavirus infection|MERS]]) epidemic and the ongoing [[COVID-19]] outbreak, multiple mechanisms have been suggested for cardiac damage.<ref name="ClerkinFried2020">{{cite journal|last1=Clerkin|first1=Kevin J.|last2=Fried|first2=Justin A.|last3=Raikhelkar|first3=Jayant|last4=Sayer|first4=Gabriel|last5=Griffin|first5=Jan M.|last6=Masoumi|first6=Amirali|last7=Jain|first7=Sneha S.|last8=Burkhoff|first8=Daniel|last9=Kumaraiah|first9=Deepa|last10=Rabbani|first10=LeRoy|last11=Schwartz|first11=Allan|last12=Uriel|first12=Nir|title=COVID-19 and Cardiovascular Disease|journal=Circulation|volume=141|issue=20|year=2020|pages=1648–1655|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.120.046941}}</ref>
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| ==== Signs and Symptoms: ====
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| Arrhythmia or conduction system disease is the nonspecific clinical presentation of COVID-19. Patients may be tachycardic (with or without palpitations) in the setting of other COVID-19-related symptoms (eg, fever, shortness of breath, pain, etc).
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| *'''Palpitations:''' According to a study done in Hubei province,[[Palpitation|palpitations]] were reported as a presenting symptom by 7.3 percent of patients.<ref name="pmid32044814">{{cite journal| author=Liu K, Fang YY, Deng Y, Liu W, Wang MF, Ma JP | display-authors=etal| title=Clinical characteristics of novel coronavirus cases in tertiary hospitals in Hubei Province. | journal=Chin Med J (Engl) | year= 2020 | volume= 133 | issue= 9 | pages= 1025-1031 | pmid=32044814 | doi=10.1097/CM9.0000000000000744 | pmc=7147277 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32044814 }} </ref><ref name="pmid32201335">{{cite journal| author=Driggin E, Madhavan MV, Bikdeli B, Chuich T, Laracy J, Biondi-Zoccai G | display-authors=etal| title=Cardiovascular Considerations for Patients, Health Care Workers, and Health Systems During the COVID-19 Pandemic. | journal=J Am Coll Cardiol | year= 2020 | volume= 75 | issue= 18 | pages= 2352-2371 | pmid=32201335 | doi=10.1016/j.jacc.2020.03.031 | pmc=7198856 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32201335 }} </ref>
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| *'''Prolong QT Interval:''' According to a multicenter study done in New York that involved 4250 COVID-19 patients, 260 patients (6.1 percent) had [[QT interval|corrected QT interval]] (QTc) >500 milliseconds at the time of admittance.<ref name="pmid32320003">{{cite journal| author=Richardson S, Hirsch JS, Narasimhan M, Crawford JM, McGinn T, Davidson KW | display-authors=etal| title=Presenting Characteristics, Comorbidities, and Outcomes Among 5700 Patients Hospitalized With COVID-19 in the New York City Area. | journal=JAMA | year= 2020 | volume= | issue= | pages= | pmid=32320003 | doi=10.1001/jama.2020.6775 | pmc=7177629 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32320003 }} </ref> However, in another study that involved 84 patients who got [[hydroxychloroquine]] and [[azithromycin]], the baseline QTc interval was 435 milliseconds before receiving these medications.<ref name="GiudicessiNoseworthy2020">{{cite journal|last1=Giudicessi|first1=John R.|last2=Noseworthy|first2=Peter A.|last3=Friedman|first3=Paul A.|last4=Ackerman|first4=Michael J.|title=Urgent Guidance for Navigating and Circumventing the QTc-Prolonging and Torsadogenic Potential of Possible Pharmacotherapies for Coronavirus Disease 19 (COVID-19)|journal=Mayo Clinic Proceedings|volume=95|issue=6|year=2020|pages=1213–1221|issn=00256196|doi=10.1016/j.mayocp.2020.03.024}}</ref>
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| *'''Atrial Arrhythmia:''' According to a study, among 393 patients with COVID-19, [[Cardiac arrhythmia|atrial arrhythmias]] were more common among patients requiring invasive [[mechanical ventilation]] than noninvasive [[mechanical ventilation]] (17.7 versus 1.9 percent)<ref name="GoyalChoi2020">{{cite journal|last1=Goyal|first1=Parag|last2=Choi|first2=Justin J.|last3=Pinheiro|first3=Laura C.|last4=Schenck|first4=Edward J.|last5=Chen|first5=Ruijun|last6=Jabri|first6=Assem|last7=Satlin|first7=Michael J.|last8=Campion|first8=Thomas R.|last9=Nahid|first9=Musarrat|last10=Ringel|first10=Joanna B.|last11=Hoffman|first11=Katherine L.|last12=Alshak|first12=Mark N.|last13=Li|first13=Han A.|last14=Wehmeyer|first14=Graham T.|last15=Rajan|first15=Mangala|last16=Reshetnyak|first16=Evgeniya|last17=Hupert|first17=Nathaniel|last18=Horn|first18=Evelyn M.|last19=Martinez|first19=Fernando J.|last20=Gulick|first20=Roy M.|last21=Safford|first21=Monika M.|title=Clinical Characteristics of Covid-19 in New York City|journal=New England Journal of Medicine|volume=382|issue=24|year=2020|pages=2372–2374|issn=0028-4793|doi=10.1056/NEJMc2010419}}</ref>
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| *'''Ventricular Arrhythmia:''' According to a study done in Wuhan, China. among 187 hospitalized patients with [[COVID-19]], 11 patients (5.9 percent) developed [[Ventricular arrhythmias|ventricular tachyarrhythmias]].<ref name="pmid32219356">{{cite journal| author=Guo T, Fan Y, Chen M, Wu X, Zhang L, He T | display-authors=etal| title=Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19). | journal=JAMA Cardiol | year= 2020 | volume= | issue= | pages= | pmid=32219356 | doi=10.1001/jamacardio.2020.1017 | pmc=7101506 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32219356 }} </ref>
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| *'''Cardiac Arrest:''' According to a Lombardia Cardiac Arrest Registry (Lombardia CARe) of the region Lombardia in Italy. Out of 9806 cases of [[COVID-19]], 362 cases of out-of-hospital [[cardiac arrest]] were reported during the study time frame in 2020. During a similar period in 2019, 229 cases of out-of-hospital [[cardiac arrest]] were reported, which means an increment of 58% was observed in 2020 among [[COVID-19]] patients.<ref name="BaldiSechi2020">{{cite journal|last1=Baldi|first1=Enrico|last2=Sechi|first2=Giuseppe M.|last3=Mare|first3=Claudio|last4=Canevari|first4=Fabrizio|last5=Brancaglione|first5=Antonella|last6=Primi|first6=Roberto|last7=Klersy|first7=Catherine|last8=Palo|first8=Alessandra|last9=Contri|first9=Enrico|last10=Ronchi|first10=Vincenza|last11=Beretta|first11=Giorgio|last12=Reali|first12=Francesca|last13=Parogni|first13=Pierpaolo|last14=Facchin|first14=Fabio|last15=Bua|first15=Davide|last16=Rizzi|first16=Ugo|last17=Bussi|first17=Daniele|last18=Ruggeri|first18=Simone|last19=Oltrona Visconti|first19=Luigi|last20=Savastano|first20=Simone|title=Out-of-Hospital Cardiac Arrest during the Covid-19 Outbreak in Italy|journal=New England Journal of Medicine|year=2020|issn=0028-4793|doi=10.1056/NEJMc2010418}}</ref> According to the records from a tertiary care hospital in Wuhan. Out of 761 patients with severe [[COVID-19]], 151 patients developed in-hospital [[cardiac arrest]]. 136 patients received resuscitation. Out of 136 patients, 119 patients had a respiratory cause. 10 patients had a cardiac cause. 7 patients had other causes. Ventricular fibrillation or pulseless ventricular tachycardia was observed in 8 patients (5.9%), [[Pulseless electrical activity]] in 6 patients (4.4%), and [[asystole]] in 122 [[COVID-19]] patients (89.7%).<ref name="ShaoXu2020">{{cite journal|last1=Shao|first1=Fei|last2=Xu|first2=Shuang|last3=Ma|first3=Xuedi|last4=Xu|first4=Zhouming|last5=Lyu|first5=Jiayou|last6=Ng|first6=Michael|last7=Cui|first7=Hao|last8=Yu|first8=Changxiao|last9=Zhang|first9=Qing|last10=Sun|first10=Peng|last11=Tang|first11=Ziren|title=In-hospital cardiac arrest outcomes among patients with COVID-19 pneumonia in Wuhan, China|journal=Resuscitation|volume=151|year=2020|pages=18–23|issn=03009572|doi=10.1016/j.resuscitation.2020.04.005}}</ref>
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| ==== Diagnostic Testing: ====
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| *'''ECG:'''
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| ==References ==
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| <references />
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