Low blood pressure, or hypotension, is a recognized complication that can occur during and after a COVID-19 infection. Hypotension is defined as blood pressure insufficient to circulate blood effectively to the body’s organs. This condition can lead to inadequate tissue perfusion, potentially resulting in serious consequences like acute kidney injury or shock in severe cases. Understanding the relationship between the SARS-CoV-2 virus and blood pressure regulation is important for timely medical intervention.
Low Blood Pressure During Acute Infection
Hypotension is a frequent observation in patients hospitalized with an active COVID-19 infection, with studies reporting a prevalence between 30% and 40% in some cohorts. A drop in blood pressure often signals a shift toward more severe disease, particularly when a patient has underlying conditions such as hypertension. The presence of even mild hypotension upon arrival at the emergency department has been associated with a doubled risk of in-hospital mortality.
In the most severe presentations, hypotension can progress to septic shock, a life-threatening condition where blood pressure drops so low that organs begin to fail. Low blood pressure in any hospitalized patient requires close monitoring. It can precede or coincide with organ damage, including a four to nine-fold increased risk of acute kidney injury.
How COVID-19 Affects Blood Pressure Regulation
The SARS-CoV-2 virus triggers a complex systemic response that disrupts the body’s mechanisms for controlling blood pressure. One primary mechanism involves widespread inflammation, sometimes referred to as a cytokine storm. Inflammatory molecules, or cytokines, cause the blood vessels to relax and widen (vasodilation), which subsequently lowers systemic blood pressure.
The virus also interacts with the renin-angiotensin-aldosterone system (RAAS), a hormonal pathway that regulates blood pressure and fluid balance. SARS-CoV-2 uses the Angiotensin-Converting Enzyme 2 (ACE2) receptor to enter cells, which downregulates the receptor’s protective function. Since ACE2 normally inactivates substances that cause vasodilation, its reduced activity can lead to an accumulation of molecules like bradykinin, a potent vasodilator that drives increased vascular permeability, edema, and hypotension.
The inflammatory environment and viral interaction also affect the lining of the blood vessels, known as the endothelium. Endothelial dysfunction contributes to the loss of vascular tone and an inability to properly constrict vessels to maintain blood pressure.
A reduction in effective circulating blood volume due to fluid shifts from damaged vessels or dehydration from fever and decreased intake can also contribute to low blood pressure. Damage to the heart muscle, such as myocarditis or stress-induced cardiomyopathy, can also lower blood pressure by reducing the heart’s ability to pump blood efficiently.
Clinical Management of COVID-Related Hypotension
Managing acute hypotension in a patient with COVID-19 focuses on stabilizing circulation to prevent organ failure. Initial treatment often involves fluid resuscitation, administering intravenous (IV) fluids to increase circulating blood volume. However, in patients with severe acute respiratory illness, fluid administration must be conservative, as excessive fluid can worsen lung function and oxygenation.
If low blood pressure persists despite fluid administration, healthcare providers use vasopressors, such as norepinephrine or dopamine, to constrict blood vessels and increase blood pressure. These potent medications are typically given through a central or large peripheral IV line and require close monitoring in an intensive care setting. Timely use of vasopressors is important, especially in septic shock, to ensure adequate blood flow to vital organs.
In patients previously taking blood pressure-lowering medications, such as ACE inhibitors or Angiotensin Receptor Blockers (ARBs), these drugs may be temporarily reduced or stopped. Adjusting the treatment plan prevents further blood pressure drops and associated complications. This individualized approach is part of the broader supportive care needed for critically ill patients during the acute phase of the illness.
Persistent Low Blood Pressure and Long COVID
Low blood pressure symptoms can persist or develop long after the initial COVID-19 infection has resolved, a condition associated with Post-Acute Sequelae of COVID-19 (PASC), or Long COVID. This lingering issue is rooted in a disorder of the autonomic nervous system (ANS), which regulates heart rate and blood pressure. This condition is broadly known as dysautonomia.
A common manifestation of this post-viral dysautonomia is orthostatic hypotension, a significant drop in blood pressure upon standing up. Another related syndrome is Postural Orthostatic Tachycardia Syndrome (POTS), where standing causes an excessive increase in heart rate. These conditions are often accompanied by symptoms like dizziness, lightheadedness, and fatigue, and are thought to be caused by a virus- or immune-mediated disruption to the ANS.
Management for this persistent form of low blood pressure differs from acute care, often focusing on non-pharmacological methods first. Patients are frequently advised to increase their fluid and salt intake to boost blood volume, use compression stockings, and change positions slowly. Pharmacological interventions, such as the medication midodrine, may be used in some cases to promote vasoconstriction and help maintain blood pressure.