What are the diagnostic and treatment approaches for Vasovagal (Vasovagal Syncope) syncope, Postural Orthostatic Tachycardia Syndrome (POTS), and Orthostatic Hypotension?

Distinguishing Vasovagal Syncope, POTS, and Orthostatic Hypotension

Diagnostic Criteria

Orthostatic Hypotension (OH)

Orthostatic hypotension is diagnosed when there is a sustained decrease in systolic BP ≥20 mmHg, diastolic BP ≥10 mmHg, or systolic BP falling to <90 mmHg within 3 minutes of standing or 60-degree head-up tilt. 1, 2 In patients with supine hypertension, use a threshold of ≥30 mmHg systolic drop. 1, 2

Key diagnostic features:

• Measure BP after 5 minutes supine, then at 1 and 3 minutes of standing 2
• Neurogenic OH shows blunted heart rate increase (usually <10 bpm) 1
• Non-neurogenic OH (hypovolemia) shows preserved or enhanced HR increase 1
• Symptoms correlate more with absolute BP level than magnitude of drop 1, 2
• OH is associated with increased mortality and cardiovascular disease 1, 2

Postural Orthostatic Tachycardia Syndrome (POTS)

POTS is characterized by excessive HR increase (≥30 bpm or HR >120 bpm) within 10 minutes of standing WITHOUT a concomitant BP fall meeting OH criteria. 1, 2 For patients aged 12-19 years, use a threshold of ≥40 bpm increase. 2

Key diagnostic features:

• Chronic daily symptoms of orthostatic intolerance (light-headedness, palpitations, tremor, weakness, blurred vision, fatigue) 1
• Syncope is rare in pure POTS; when present, usually due to superimposed vasovagal reflex 1
• More common in young women, often following infection or trauma 1
• Associated with joint hypermobility syndrome 1

Vasovagal Syncope (VVS)

Vasovagal syncope is diagnosed clinically when precipitating events (fear, pain, emotional distress, instrumentation, prolonged standing) are associated with typical prodromal symptoms of autonomic activation. 1

Key diagnostic features:

• Prodrome: nausea, sweating, pallor, visual changes (dark spots, loss of color vision), sounds from distance 1, 3
• Preceded by relative tachycardia, then sudden hypotension and bradycardia 4, 3
• Loss of consciousness typically brief (<30 seconds if measured) 1
• Situational variants: micturition, defecation, cough, swallowing 1

Critical Distinctions

Timing and Hemodynamic Pattern

• Initial OH: BP drop within 0-15 seconds of standing, transient 1
• Classical OH: BP drop within 3 minutes, sustained 1, 2
• Delayed OH: BP drop after >3 minutes, may progress to reflex syncope 1
• POTS: HR increase within 10 minutes without BP drop 1, 2
• VVS: Variable timing, preceded by autonomic activation and tachycardia before sudden bradycardia/hypotension 1, 4

The Tachycardia Confounder

Do not conflate excessive tachycardia during tilt testing in VVS patients with POTS. 4 In young patients with recurrent VVS, 44% showed HR increases ≥40 bpm before fainting during tilt testing, but this represents the vasovagal response, not POTS. 4 The key distinction: POTS patients have chronic daily orthostatic symptoms without syncope, while VVS patients have episodic syncope with clear triggers. 1, 4

Treatment Approaches

Orthostatic Hypotension Management

Begin with non-pharmacologic measures; reserve pharmacologic treatment for patients with persistent symptoms despite lifestyle modifications. 5

Non-pharmacologic (first-line):

• Discontinue or reduce blood pressure-lowering medications 6, 5
• Increase salt and fluid intake 6
• Compression stockings 7
• Counterpressure maneuvers 5
• Avoid prolonged standing and rapid postural changes 6

Pharmacologic (for symptomatic patients):

• Midodrine is FDA-approved for symptomatic OH, causing marked elevation of supine BP (>200 mmHg systolic possible); use only when lives are considerably impaired despite standard care 7
• Fludrocortisone for volume expansion 6
• Selective serotonin reuptake inhibitors show promise 6

Critical pitfall: Neurogenic OH often coexists with supine hypertension, requiring careful medication timing and dose adjustment. 1, 5

Vasovagal Syncope Management

Treatment focuses on trigger avoidance, patient education, and increased salt/water intake; pharmacologic therapy remains investigational. 6

Non-pharmacologic:

• Recognize and avoid triggers (prolonged standing, heat, dehydration) 1
• Increase salt and water intake 6
• Physical counterpressure maneuvers when prodrome recognized 6

Pharmacologic (under investigation):

• Beta-blockers 3
• Scopolamine 3
• Disopyramide 3

POTS Management

Treatment addresses the underlying mechanism: deconditioning, immune-mediated processes, or hyperadrenergic state. 1

Approach:

• Gradual exercise reconditioning program 1
• Increased salt and fluid intake 1
• Compression garments 1
• Address recent infection or trauma if present 1

Diagnostic Algorithm

1. Measure orthostatic vitals properly: 5 minutes supine, then 1 and 3 minutes standing 2
2. If BP drops ≥20/10 mmHg within 3 minutes: Diagnose OH; assess HR response to distinguish neurogenic (blunted HR) from non-neurogenic (preserved HR) 1, 2
3. If HR increases ≥30 bpm without BP drop: Consider POTS if chronic daily symptoms present 1, 2
4. If clear triggers with prodrome and brief LOC: Diagnose VVS clinically 1
5. If excessive tachycardia precedes syncope during tilt test in patient with episodic syncope: This is VVS, not POTS 4

Common pitfall: Delayed OH may progress to reflex syncope, creating overlap between OH and VVS. 1 The prolonged prodrome (dizziness, fatigue, visual disturbances) distinguishes this from pure VVS. 1