What could explain bradycardia in a patient hospitalized with COVID-19 and Influenza A, requiring high flow oxygen (O2) therapy, with normalized blood pressure (BP) and no arrhythmias?

Bradycardia in COVID-19 and Influenza A Co-infection

The bradycardia in this patient is most likely multifactorial, with direct viral myocardial involvement, systemic inflammation, and steroid therapy (if administered) being the primary contributors, particularly given the normalized blood pressure and absence of arrhythmias on ECG. 1, 2

Primary Mechanisms to Consider

Direct Viral Cardiac Effects

• Both COVID-19 and influenza can cause direct myocardial injury through viral localization in cardiac tissue, leading to bradyarrhythmias that are otherwise rarely described during viral illness 3
• Atrioventricular block has been specifically reported in hospitalized COVID-19 patients as a recognized cardiac complication 3
• The heart rate of 45-50 bpm with no compensatory tachycardia despite hypoxemia (requiring 5L O2) represents relative bradycardia, a recognized clinical feature of COVID-19 where patients fail to mount an appropriate HR response to fever and hypoxemia 4

Steroid-Associated Bradycardia (Critical Consideration)

• If this patient received dexamethasone or other corticosteroids for COVID-19 respiratory management, this is a significant risk factor for bradycardia 2
• A 2024 study demonstrated that steroid use in COVID-19 patients was significantly associated with bradycardia (OR: 3.67; 95% CI: 1.12-11.96, P=0.031) 2
• The incidence of bradycardia in COVID-19 patients receiving steroids was significantly higher than in influenza patients (P=0.007) 2
• This is particularly relevant given the patient's normalized BP, suggesting the bradycardia is not hemodynamically compromising and may be medication-related rather than shock-related 2

Myocardial Inflammation and Injury

• COVID-19 can cause acute myocardial injury through imbalance of oxygen demand and supply associated with increased breathing work and severe hypoxemia 3
• Check high-sensitivity cardiac troponin (hs-cTnT) - slight elevations have been documented in COVID-19 patients with bradycardia and may indicate myocardial involvement 5, 4
• SARS-CoV-2 infection has the potential to induce durable myocardial changes predisposing to arrhythmias through direct pathophysiological, histological, and structural cardiac alterations 3

Clinical Context Supporting Benign Course

Hemodynamic Stability Indicators

• The normalization of blood pressure from initial hypotension suggests recovery rather than deterioration 5
• Absence of arrhythmias on ECG rules out high-grade AV block or other malignant rhythms 3
• Oxygen saturations of 95-96% on 5L indicate adequate oxygenation despite respiratory involvement 5

Self-Limiting Nature

• COVID-19-associated bradycardia typically appears suddenly on days 5-14 of illness with minimal heart rates of 32-44 bpm and is self-limiting in most cases, lasting 3-11 days 5
• This bradycardia often correlates with decreasing inflammatory markers (IL-6 and CRP significantly lower at bradycardia onset compared to admission) 5
• Most patients do not require temporary pacing or specific intervention 5

Recommended Diagnostic Workup

Essential Monitoring

• Obtain cardiac biomarkers (hs-cTnT) to assess for myocardial injury, reserving comprehensive echocardiography for patients with elevated troponin or hemodynamic instability 3
• Check inflammatory markers (IL-6, CRP) - declining levels may paradoxically coincide with bradycardia onset 5
• Continuous telemetry monitoring is reasonable given the acute illness, vital sign abnormalities, and potential for clinical deterioration 3

Medication Review

• Review all medications for bradycardic effects, particularly corticosteroids (dexamethasone), remdesivir, and any cardiovascular medications 2, 5
• Assess for QT-prolonging medications that may complicate arrhythmia risk, though this patient has bradycardia rather than tachyarrhythmia 3, 6

Echocardiographic Evaluation (Selective)

• Reserve comprehensive echocardiography for patients with elevated troponin, ECG ischemic changes, or hemodynamic instability to reduce infection exposure risk 3
• If performed, assess for pericardial effusion (found in some COVID-19 bradycardia cases), left ventricular function, and regional wall motion abnormalities 5

Management Approach

Observation Strategy

• Most COVID-19-associated bradycardia is self-limiting and requires only observation 5
• Intervention is typically unnecessary unless the patient becomes symptomatic (lightheadedness, syncope, hemodynamic compromise) 5
• The normalized blood pressure and stable oxygen saturations support conservative management 5

When to Intervene

• Consider atropine or orciprenaline only if bradycardia becomes symptomatic with hemodynamic compromise 5
• Temporary pacing is rarely required and should be reserved for persistent symptomatic bradycardia unresponsive to medical therapy 5
• If steroids are being administered, consider whether dose reduction or discontinuation is feasible based on respiratory status 2

Key Clinical Pitfalls

• Do not assume bradycardia requires immediate intervention - most cases in COVID-19 are self-limiting despite impressive heart rate reductions 5
• Avoid attributing bradycardia solely to hypoxemia or respiratory failure when steroid therapy may be contributory 2
• Relative bradycardia (lack of compensatory tachycardia despite fever/hypoxemia) is a specific COVID-19 finding and should not be mistaken for medication effect alone 4
• The combination of COVID-19 and influenza A may have additive cardiac effects, though specific data on co-infection bradycardia is limited 1