Cardiac Tamponade in Patients with COVID-19 Infection; A Case Report

Coronavirus disease 2019 (COVID-19) is a novel pandemic that affects the cardiovascular system by various mechanisms. We report two cases of cardiac tamponade in patients with COVID-19, who underwent surgery and had different outcomes. Cardiac complications can occur in patients with COVID-19 that need special attention and may increase mortality and morbidity.

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Case 2
1. An 81-year-old woman was admitted in April 2020 with dry cough, dyspnea, and subjective fever. In January 2019 she travelled to Tehran and was admitted to a hospital because of dyspnea and diagnosed with pericarditis but she left the hospital with her own consent. In medical history, she had hypertension and ischemic heart disease.  Figure 4). The patient was urgently taken to the OR. Although the surgical and anesthesia team was fully protected against COVID-19 with shield and gown. The patient was completely monitored. She took oxygen with mask and SpO2 was 93%. An arterial line with catheter G#20 was installed in the OR under local anesthesia. She underwent general anesthesia with midazolam 2 mg, Fentanyl 100 microgram, etomidate 20 mg, and atracurium 15 mg, then the patient was intubated. After pericardiocentesis, 1500 mL of serosanguinous fluid was drained. Her vital sign was stable (Bp:110/85, PR:80 T:36.8, SpO2:93%), then she was extubated and after that she was transferred to COVID-19 ICU. Cellular and cytological analysis of pericardial fluid revealed presence of inflammatory cells (RBC, PMN and lymphocytes were predominant), while malignant cells were not found. Two days later her hemodynamic parameters worsened, including hypotension and tachycardia and patient developed cardiac arrest. After 45 min of CPR, she expired.
It should be noted that informed written consent was taken from both patients and their companions and the approval of the Ethics Committee (IR.HUMS. REC.1399.040).

Discussion
The most common symptoms of SARS-CoV-2 infection are fever and cough followed by dry cough, headache, fatigue, or shortness of breath (1). In this report both cases presented with cough, dyspnea, tachypnea, and fever. While these clinical manifestations are highly related to the inflammation of the respiratory system, these two cases provide evidence of cardiac involvement as a complication of the viral respiratory infection. This process can be asymptomatic or mild with few interstitial inflammatory cells, diagnosed through pathological findings or can present with overt symptoms with or without respiratory manifestations, similar to this report. A close clinical interplay between SARS-CoV2 and cardiovascular disease processes has been suggested by data from early cohorts with COVID-19. Pre-existing cardiovascular disease has been associated with poor outcomes in affected patients with COVID-19 such as case 2, and though cases are limited, direct cardiovascular effects of the virus have been observed and may be associated with significant morbidity and mortality (4). Coexisting cardiac diseases, are common in patients with COVID-19 and these patients are at higher risk of morbidity and mortality (2). Furthermore, patients with COVID-19 often face diagnostic and therapeutic challenges because respiratory and cardiac pathologies are frequently associated and their clinical manifestations may be similar (2).
In this report, the first case had no history of cardiac disease and was younger, which may be the reason for the better outcome. The second case, was an elderly woman with coexisting heart disease and chronic kidney disease. All of these could be risk factors for adverse outcomes and increased mortality.
Many patients with COVID-19 (>20%) will have cardiac complications leading to increased mortality. Similar cardiovascular complications were also seen in 2003 during the previous SARS epidemic. The exact mechanism is still under study; however, the current belief is that SARS-CoV-2 causes cardiac complications through multiple mechanisms including increased cytokine release, hyperinflammation, adrenergic stimulation, and a hypercoagulable state. Viral infection is usually considered as one of the most common causes of myocarditis, especially in influenza and parvovirus B-19 infection (1). However, the cardiac complications of SARS-CoV-2 infection are less well-known. Myocarditis present as focal or global myocardial inflammation, necrosis, and finally ventricular dysfunction. Focal myocarditis is usually manifested with chest pain after an influenza-like syndrome, clinical evidence such as an acute coronary syndrome on electrocardiography or laboratory testing and evidence of wall motion abnormalities without evidence of coronary artery involvement in coronary angiography (1,5). The pathogenesis of cardiac involvement in SARS-CoV-2 may reveal a process of replication and dissemination of the virus from the respiratory tract through the blood or the lymphatic system. However, to the best of our knowledge, there are no reports of influenza virus or coronavirus RNA in the heart, to date. Alternatively, SARS-CoV-2 could trigger an exaggerated inflammatory response that can cause myocardial injury, and this could favor the use of corticosteroids to attenuate inflammation, as in the present case (1,5). Evidence of significant inflammatory cell mediators, infiltration has been reported in the alveoli of patients with acute pneumonia associated with SARS-CoV-2 infection. Although the exact mechanisms are not certain, a potential binding to a viral receptor of the myocyte can justify the internalization and subsequent replication of the capsid proteins and the viral genome. Moreover, the onset of symptoms several days after the viral infection may reflect these possible mechanisms with a potential myocyte involvement, the activation of the immune and complement system, and, ultimately, clinical presentation of heart failure and cardiac complications (1,5).
It seems that SARS-CoV-2 is able to affect the heart and then potentially cause these cardiac complications: arrhythmias, myocardial infarction (with troponin elevation), STEMI, myocarditis with systolic dysfunction, pericarditis, myopericarditis, pericardial effusion +/-, tamponade, pulmonary embolism. All these cardiac complications are significant and significantly increase morbidity and mortality (5,6).
The best technique for anesthesia management and surgical procedure of these patients is to perform surgery and pericardial window under local anesthesia with sedation especially in patients with unstable hemodynamic condition. However, in these cases we chose general anesthesia and tracheal intubation in coordination with the surgical team and according to the medical history of the patients. Even though cardiac involvement is a rare extra-pulmonary manifestation of COVID-19, it should be kept in mind that intubation and positive pressure ventilation (PPV) can have deleterious hemodynamic effects in patients with cardiac tamponade (2,3)

Conclusion
Because of the increasing prevalence of COVID-19 and its various clinical manifestation, cardiovascular complications should be considered especially in patients with underlying diseases. It should also be noted that coexisting disorders including cardiac and kidney involvement as well as old age can be associated with high mortality and morbidity. Finally, these patients need to be managed carefully by multidisciplinary team work in the ICU under close observation and full monitoring. Research is still in process, and we are slowly learning about new signs and symptoms of the disease. Further related studies are necessary.

Funding
No funding was received.

Disclosure
The authors report no conflicts of interest in this work.