Managing Hypertension in Patients with Viral Illness
Continue all existing antihypertensive medications during acute viral illness unless hemodynamic instability or specific contraindications develop. 1
Key Management Principles
Medication Continuation During Viral Illness
Do not discontinue RAAS inhibitors (ACE inhibitors or ARBs) during viral infections, including COVID-19. Growing evidence demonstrates these medications are safe and may provide protective effects during viral illness 1
Maintain all guideline-directed medical therapy (GDMT) for hypertension during acute viral illness unless the patient develops hemodynamic instability requiring intravenous vasopressors or inotropes 1
Abrupt discontinuation of antihypertensive therapy can precipitate acute hypertensive crisis and worsen cardiovascular outcomes 1
Blood Pressure Targets During Viral Illness
Target BP remains <130/80 mmHg in most hypertensive patients, even during acute viral illness 1
For elderly patients (>65 years), target <140/80 mmHg is acceptable 1
In patients with heart failure or hemodynamic compromise from severe viral illness, temporarily accept higher BP values (systolic 120-140 mmHg) until clinical stability returns 1
Specific Considerations for COVID-19 and Viral Respiratory Illnesses
Hypertension emerged as a common comorbidity in hospitalized COVID-19 patients, though its role as an independent risk factor remains unclear after adjusting for age and other comorbidities 1. The evidence shows:
SARS-CoV-2 binds to ACE2 receptors, raising initial concerns about RAAS inhibitor safety 1
Multiple clinical groups and studies have confirmed the safety of continuing ACE inhibitors and ARBs in COVID-19 patients 1
Some evidence suggests potential protective effects of RAAS inhibitors in COVID-19, though data are limited 1
ACE inhibitor treatment specifically was associated with dampened COVID-19-related hyperinflammation and increased antiviral responses 2
Monitoring and Follow-Up
Monitor BP more frequently during acute viral illness (every 1-2 weeks if possible via telemedicine or home BP monitoring) as viral infections can affect BP control 1
Check for signs of volume depletion if the patient has reduced oral intake, fever, or gastrointestinal symptoms—may require temporary diuretic dose reduction 1
Assess for drug-drug interactions if new medications are prescribed for viral illness treatment (e.g., antivirals, antibiotics) 1
Common Pitfalls to Avoid
Do not stop antihypertensive medications based solely on concerns about viral infection or ACE2 receptor interaction 1. This misconception led to widespread inappropriate medication discontinuation during the COVID-19 pandemic.
Do not aggressively lower BP in patients with severe viral illness and hemodynamic compromise. Viral infections, particularly severe respiratory infections, can cause myocardial depression and require permissive hypertension temporarily 1
Do not ignore new-onset hypertension or worsening BP control during or after viral illness. Emerging evidence shows viral infections (including CMV and SARS-CoV-2) can cause persistent BP elevation requiring new or intensified treatment 3, 4, 5
Post-Viral Illness Considerations
Reassess BP control 2-4 weeks after viral illness resolution as some patients develop new-onset hypertension or require treatment intensification 3
COVID-19 survivors show a 65% increased risk of new-onset hypertension compared to controls, with 9% developing new hypertension post-infection 3
The mechanism involves viral interaction with ACE2 receptors and renin-angiotensin system dysregulation 4, 5
Medication Selection if Initiating or Adjusting Therapy
If BP remains uncontrolled during viral illness and medication adjustment is necessary:
First-line agents remain ACE inhibitors or ARBs plus calcium channel blockers and/or thiazide-like diuretics 1, 6
Avoid abrupt initiation of beta-blockers in patients with acute respiratory viral illness unless specific indications exist (e.g., acute coronary syndrome, heart failure) 1
Consider loop diuretics instead of thiazides if significant volume overload or renal impairment (eGFR <30 mL/min/1.73m²) develops 1