Blood Pressure Management in POTS
In POTS, blood pressure typically remains normal or even elevated during orthostatic stress—the defining feature is inappropriate tachycardia (≥30 bpm increase within 10 minutes of standing) WITHOUT orthostatic hypotension, so BP management focuses on preventing supine hypertension from treatments rather than raising BP. 1
Understanding BP Behavior in POTS
POTS is explicitly diagnosed only when orthostatic hypotension is absent—defined as systolic BP drop <20 mmHg and diastolic BP drop <10 mmHg within 3 minutes of standing 1, 2
The pathophysiology involves excessive venous pooling with compensatory peripheral vasoconstriction that maintains BP, but at the cost of excessive tachycardia 3, 4
Patients with POTS demonstrate normal to excessive total peripheral resistance increase during standing, unlike autonomic failure patients who cannot vasoconstrict 4
Syncope in POTS is rare and typically occurs only when vasovagal reflex activation is superimposed, not from the POTS mechanism itself 1, 5
When BP Does Drop: Distinguishing POTS from Other Conditions
If orthostatic hypotension is present (BP drop ≥20/10 mmHg), the patient does NOT have POTS—consider delayed orthostatic hypotension, classical orthostatic hypotension, or orthostatic vasovagal syncope instead 1
Delayed orthostatic hypotension occurs beyond 3 minutes of standing with progressive BP fall and may trigger secondary reflex syncope 1
Some patients may have overlapping conditions where POTS coexists with vasovagal syncope, but these are distinct mechanisms 1
BP Considerations in POTS Treatment
Neuropathic POTS Phenotype
Midodrine (alpha-adrenergic agonist) is used to enhance vascular tone and venous return, not to raise BP per se, but to reduce venous pooling 6, 3
When using midodrine, monitor carefully for supine hypertension—patients should avoid taking doses if they will be supine for extended periods and take the last daily dose 3-4 hours before bedtime 7
Midodrine can enhance or precipitate bradycardia when combined with cardiac glycosides, and increases hypertension risk when combined with other vasopressors (phenylephrine, pseudoephedrine, ephedrine) 7
Hypovolemic POTS Phenotype
Volume expansion with increased fluid (2-3 liters daily) and salt intake (10-12 grams daily) is first-line treatment, which may modestly increase BP but primarily improves venous return 6, 3
Fludrocortisone (mineralocorticoid) increases blood volume but carries risk of supine hypertension, requiring careful BP monitoring 8
Hyperadrenergic POTS Phenotype
Beta-blockers are used to blunt excessive tachycardia, not to lower BP—the goal is heart rate control while maintaining adequate perfusion 6, 3, 8
Avoid norepinephrine reuptake inhibitors in hyperadrenergic POTS as they worsen the hyperadrenergic state 3
Critical Monitoring Parameters
Measure BP both supine and standing during initial evaluation—supine hypertension may develop or worsen with vasoconstrictor therapy 7
The 10-minute active stand test should document BP at baseline (after 5 minutes supine), immediately upon standing, and at 2,5, and 10 minutes to confirm absence of orthostatic hypotension 2, 9
Avoid testing after large carbohydrate-rich meals, which cause splanchnic vasodilation and can precipitate orthostatic symptoms even without true hypotension 5
Common Pitfalls in BP Management
Do not confuse postprandial hypotension (which occurs in autonomic failure) with POTS—POTS is defined by tachycardia without hypotension 5
Failing to check supine BP when initiating vasoconstrictors or volume expansion can lead to dangerous supine hypertension 7
Using vasopressors aggressively as if treating orthostatic hypotension will cause supine hypertension without addressing the core POTS mechanism of venous pooling 6, 3
Droxidopa showed minimal impact on BP or quality of life in POTS patients despite some symptom improvement, and 40.5% discontinued due to side effects or ineffectiveness 10