Autonomics and Orthostatic Hypotension

Gary Salomon


Background

  • Orthostatic hypotension (OH): sustained ↓SBP ≥20 mmHg (or ≥30 mmHg in patients with supine hypertension) or↓ DBP ≥10 mmHg after at least 2 minutes of standing or head-up tilt to 60 degree.
  • Pathophysiology: Standing causes 500-1000 mL venous pooling; normally compensated by baroreceptor-triggered sympathetic vasoconstriction and increased heart rate, but this fails in OH due to autonomic dysfunction (neurogenic OH) or inadequate intravascular volume (non- neurogenic OH).
ClassificationMechanismKey FeaturesCauses
Neurogenic OH (nOH)Autonomic dysfunction → impaired baroreflex-vasoconstrictionBlunted heart rate response (ΔHR/ΔSBP 0.5 beats/min per mmHg has 91% sensitivity and 88% specificity)

Parkinson, MSA, LBD, Pure autonomic failure

Diabetic neuropathy, Amyloidosis, Spinal cord disorders, Autoimmune neuropathy

Non-neurogenic OHReversible factors impairing hemodynamic compensation

Preserved/exaggerated heart rate response (ΔHR/ΔSBP >0.5)

Note: ΔHR/ΔSBP ratio is invalid in patients with atrial fibrillation or on beta-blockers

Hypovolemia (dehydration, blood loss), medications (diuretics, vasodilators, alpha-blockers), cardiac disease, anemia

Evaluation

  • Evaluate for orthostatic symptoms (dizziness, lightheadedness, vision changes, syncope, falls), timing (worse in morning, after meals, in heat), medication review.
  • Obtain orthostatic Vital Signs - Active Stand Test (AST). 
    • Measure BP/HR after 5 minutes supine. 
    • Measure BP/HR immediately upon standing, then at 1, 2, and 3 minutes. 
    • Assess for symptoms during testing.
  • Optimal timing: Morning testing (when symptoms most prominent) - Alternative: Sit-to-stand test (lower sensitivity but useful when supine position not feasible).

Labs

  • CBC, CMP, EKG, TSH, B12, LFTs. 
  • Consider SPEP/UPEP, paraneoplastic panel, autonomic function testing depending on clinical context.

Special Considerations

  • Delayed OH: BP drop occurring >3 minutes after standing; associated with progression to autonomic failure. 
  • Postprandial hypotension: Screen in all nOH patients; common comorbidity. 
  • Supine hypertension: Present in ~50% of nOH patients; critical to identify as it affects treatment selection.

Management

  • Medication Review: Discontinue or reduce causative medications when possible. 
  • Avoid alpha-blockers, diuretics, and long-acting vasodilators in nOH. 
  • Hydration and Salt: Fluid intake: 2-2.5 L/day. Salt intake: increase to 2.3-4.6g/day. 
  • Acute intervention: Drink 500 mL (16 oz) water 15-30 minutes before standing (can raise SBP by ~30 mmHg). 
  • Compression Garments: Waist-high compression stockings (30-40 mmHg) or abdominal binder (most effective). 
  • HOB 30-45 degrees always for supine HTN.
  • Small, frequent meals to minimize postprandial hypotension.

Pharmacologic therapies ideally should be used only after conservative measures fail and patient has undergone formal autonomic testing:

DrugDoseMechSide effects
Fludrocortisone
(Florinef)
0.1mg QD
↑ by 0.1 mg
Max: 0.3 mg QD
Mineralocorticoid → increase blood volume.
Enhances sensitivity to catecholamines
Edema, HTN, ↓K
Contraindications:
- CHF
Midodrine
(genera)
2.5mg TID
↑ by 2.5mg
Up to 10mg TID
Peripheral-selective α1 agonist → constricts both aa & vvSupine HTN, Pilomotor reactions, Pruritus, GI sx

Contraindications:
- uncontrolled HTN
- urinary retention
- Heart disease
Droxidopa100mg
↑ by 100mg
Max: 600mg TID
NE precursor that crosses BBBSupine HTN
less than midodrine
Atomoxetine10mg or 18mgSNRIContraindications:
- glaucoma
- MAOI

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