key: cord-0902215-cykzkg33
authors: Ansari, Saad Ali; Ansari, Yusra; Khan, Tahir Muhammad Abdullah
title: COVID-19 and Bradyarrhythmias: A Case Report With Literature Review
date: 2022-01-24
journal: Cureus
DOI: 10.7759/cureus.21552
sha: d4f6243c53a7c2868cdcf1a0bd84bc44a1726859
doc_id: 902215
cord_uid: cykzkg33

We report a case of a 51-year-old male with no past medical history who was admitted for acute hypoxic respiratory failure secondary to COVID-19. During his hospitalization, the patient developed sinus bradycardia and frequent sinus pauses were observed on telemetry. No other cause of his bradyarrhythmia was identified except for his COVID-19 infection. There has been numerous case reports and case series describing different arrhythmias seen in patients infected with COVID-19. We present a case of sinus arrest in a patient with COVID-19 and a review of other case reports describing bradyarrhythmia in COVID-19 patients.

The COVID-19 pandemic due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has affected millions of people worldwide since the emergence of the first case in Wuhan, China, in December 2019. Severe acute respiratory syndrome coronavirus 2 has spike (S) proteins on its surface which are responsible for binding to host cell receptors and fusion of viral and cellular membranes. Angiotensinconverting enzyme 2 (ACE 2) is identified as a functional receptor for the spike protein of SARS-CoV-2. The ACE 2 is expressed in high concentrations in the lung (type II alveolar cells), heart, esophagus, ilium, kidney, and urinary bladder [1, 2] . Patients infected with SARS-CoV-2 manifest symptoms ranging from mild to severe respiratory disease including acute respiratory distress syndrome (ARDS) and can involve multiorgan failure. Although the respiratory system is the most affected organ system, other organ systems involvement has been frequently reported which may manifest as encephalopathy, a hypercoagulable state with thromboembolic disease, deranged liver enzymes, acute kidney failure, and myocardial injury (myocarditis). Cardiac injury (defined as an increase in high sensitivity troponins T or I level more than the 99th percentile upper reference limit and new ECG or transthoracic echocardiographic changes) has been reported in 49% of patients with critical illness secondary to COVID-19. The most frequent abnormalities observed were EKG or echocardiographic signs of left ventricle abnormalities (87%), and right ventricular dysfunction (47%) which was more common than left ventricular dysfunction (13%). Other abnormalities observed were pericardial effusion (43%), new-onset atrial arrhythmias (33%), left ventricular relaxation impairment (33%), and left ventricle (LV) systolic dysfunction (13%) [3] . Among conduction abnormalities, sinus node dysfunction with sinus arrest secondary to COVID-19 is rarely reported in the literature and prognosis and disease course in these patients is unknown yet. We report a case of sinus arrest secondary to COVID-19 infection in a critically ill patient who required a permanent pacemaker.

A 51-year-old Caucasian male patient, active cigarette smoker, unvaccinated for COVID-19, and no prior history of any medical illness, presented with worsening shortness of breath. The patient tested positive for COVID-19 a few days prior to presentation. On presentation, patient had a blood pressure of 137/80 mm Hg, heart rate of 93 beats per minute, he was afebrile and was saturating at 92 % on 15 L of O2 via a non-rebreather mask. He was alert and awake but was showing signs of respiratory distress using accessory respiratory muscle and was tachypneic. Chest auscultation showed bilateral lower lung crackles with no wheezing. Laboratory tests of the patient are given in Table 1 . Chest X-ray (CXR) showed bilateral ground-glass infiltrates consistent with COVID -19 pneumonia and left pleural effusion ( Figure 1 ). The EKG showed no acute ischemic changes, PR interval at 184 milliseconds (ms), QTc of 490 ms ( Figure 2 ) and troponin were elevated to 0.10 ug/mL (0-0.034 ug/mL) which subsequently trended down to normal values. 

Patient developed respiratory distress in the emergency room and arterial blood gas (ABG) showed PH 7.33, partial pressure of carbon dioxide (PaCO2) at 51, partial pressure of oxygen (PaO2) at 56, on 100% fraction of inspired oxygen (FiO2). The patient was intubated and supported with lung protective strategy of mechanical ventilation. Deep tracheal aspirates were sent for gram stain and culture, and BioFire® FilmArray® (BioFire Inc., Salt Lake City, UT, USA) pneumonia (PN) panel testing post which the patient was initiated on dexamethasone 10 mg twice a day and broad-spectrum antibiotics with linezolid and cefepime. When the sputum culture and pneumonia polymerase chain reaction (PCR) panel did not suggest bacterial infection, the patient was given one dose of 400 mg of sarilumab, and antibiotics were discontinued. Intravenous (iv) propofol and fentanyl infusions were used for sedation and analgesia, and he required a low dose of norepinephrine for sedation induced mild hypotension. Proning protocol was implemented.

Over the following week, the patient developed sinus bradycardia necessitating change of sedatives from propofol to midazolam, and intermittent iv fentanyl for adequate analgesia. Two weeks into his admission, patient developed ventilator associated bacterial pneumonia (VAP) with pan sensitive Escherichia coli which was further complicated by left side pneumothorax warranting placement of 14 French-size pigtail catheters and iv ceftriaxone for VAP. Unfortunately, the patient developed worsening sinus bradycardia with heart rate as low as 27 with frequent sinus pauses observed on telemetry ( Figure 3 ) with largest pause of 12 seconds along with loss of arterial pulse waveform. A transvenous pacemaker was placed.

Telemetry strips showing sinus pauses of approximately 2.2 and 3.6 s.

The EKG showed mild LV hypertrophy with LV ejection fraction of 60% to 65% and no regional wall motion abnormality. After treatment of VAP, requirement of supplemental oxygen improved but he could not be liberated from mechanical ventilator due to excessive respiratory secretions. Bedside percutaneous tracheostomy was performed without complication, and due to persistent intermittent dependence of transvenous pacemaker, a permanent pacemaker ( Figure 4 ) was placed without complication as per discretion of electrophysiologist. The patient was later transferred to long term acute care facility (LTAC) for weaning from ventilator and physical and occupational therapy. Unfortunately, the patient's condition was complicated by bilateral lower extremities deep venous thrombosis requiring anticoagulation therapy and later by the second event of ventilator associated pneumonia with Stenotrophomonas maltophilia with bacteremia and septic shock. The patient's family opted for comfort care and he succumbed to his illness.

We reviewed a total of 30 case reports/case series involving a total of 67 patients utilizing advanced search on PubMed. Keywords used for literature review were: "COVID-19", "bradyarrhythmias", "bradycardia", "sinus arrest", "sinus pauses", "atrioventricular (AV) block", "heart block", "complete heart block (CHB)", "sinus node dysfunction". Case reports from the start of the pandemic till January 2022 were reviewed. Out of a total of 67 patients, 54% were males (36/67) while 46% were females (31/67 We presented a case of a patient without any major comorbidities who was admitted to the hospital for COVID-19 pneumonia and later during hospitalisation developed sinus bradycardia with frequent sinus pauses for which a permanent pacemaker had to be placed. In our patient who had no significant cardiac risk factors, sinus bradycardia and pauses are possibly related to conduction abnormalities caused by COVID-19. COVID-19 has been associated with myocarditis, myocardial infarction, hypercoagulable state, arrhythmias, and conduction abnormalities [34] . From our literature review, it is evident that a lot of patients with COVID-19 who develop bradyarrhythmia have little or no cardiac risk factors. The extent of respiratory compromise or critical illness does not always correlate with conduction abnormalities as only 19% of patients who developed bradyarrhythmia in our review were intubated and put on ventilatory support. Long term effects of COVID-19 on the conduction system is still to be studied. In the majority of patients, only transient bradycardia or conduction abnormalities were noted. However, up to 30% of patients did end up getting permanent pacemaker placement. Outpatient follow-ups of patients who develop arrhythmias while hospitalized for COVID-19 infection is necessary to study the long term effects on the cardiac conduction system.

In conclusion, COVID-19 is associated with wide-ranging cardiac manifestations including bradyarrhythmias. These bradyarrhythmias do not always correlate with severe COVID-19 infection and can present in individuals without any cardiac risk factors. In the majority of patients, these are only transient and resolve as COVID-19 infection subsides, but further study is required to determine the long-term effects of COVID-19 on the conduction system of the heart.

Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work.

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