Management of Orthostatic Hypotension
Begin by discontinuing medications that worsen orthostatic hypotension—particularly diuretics, alpha-blockers, and vasodilators—as drug-induced autonomic failure is the most frequent cause of orthostatic hypotension. 1
Step 1: Identify and Eliminate Reversible Causes
Medication review is the absolute first priority. Stop or switch (not just reduce the dose) the following culprits: 1
- Alpha-1 blockers (doxazosin, prazosin, terazosin, tamsulosin)
- Diuretics (especially thiazides in elderly patients)
- Vasodilators (hydralazine, minoxidil)
- Centrally-acting antihypertensives (clonidine, methyldopa)
- Psychotropic medications
If the patient requires continued antihypertensive therapy, switch to long-acting dihydropyridine calcium channel blockers (amlodipine) or RAS inhibitors (ACE inhibitors/ARBs), which have minimal impact on orthostatic blood pressure. 2
Assess for volume depletion, anemia, and endocrine disorders (adrenal insufficiency, hypothyroidism). 1
Eliminate alcohol consumption, as it causes both autonomic neuropathy and central volume depletion. 1
Step 2: Implement Non-Pharmacologic Measures (For All Patients)
Volume Expansion
- Increase fluid intake to 2-3 liters daily (unless contraindicated by heart failure). 1
- Increase salt consumption to 6-9 grams daily (unless contraindicated by heart failure or renal disease). 1
- Administer 1-2 liters of saline 24 hours prior to any surgical procedure in patients with catecholamine-producing tumors. 3
Postural Strategies
- Elevate the head of the bed by 10 degrees during sleep to prevent nocturnal polyuria, maintain favorable fluid distribution, and reduce supine hypertension. 1
- Teach gradual staged movements with postural changes—avoid rapid standing from supine or sitting positions. 1
- Acute water ingestion of ≥480 mL provides temporary relief, with peak effect at 30 minutes after consumption. 1
Physical Countermeasures
- Teach leg crossing, squatting, stooping, and muscle tensing during symptomatic episodes—these are particularly effective in patients under 60 years with prodromal symptoms. 1
- Use waist-high compression stockings (30-40 mmHg) and abdominal binders to reduce venous pooling. 1
Dietary Modifications
- Eat smaller, more frequent meals to reduce postprandial hypotension. 1
- Avoid large carbohydrate-rich meals. 4
Exercise
- Encourage physical activity and exercise to avoid deconditioning, which worsens orthostatic intolerance. 1
Step 3: Initiate Pharmacologic Therapy (When Non-Pharmacologic Measures Fail)
The therapeutic goal is minimizing postural symptoms and improving functional capacity, NOT restoring normotension. 1
First-Line Pharmacologic Options
Midodrine is the first-line agent with the strongest evidence base (three randomized placebo-controlled trials, FDA-approved). 1, 5
- Dosing: Start at 2.5-5 mg three times daily, with the first dose taken before arising. 1
- Timing: The last dose must be taken at least 3-4 hours before bedtime (not after 6 PM) to prevent supine hypertension during sleep. 1, 5
- Mechanism: Alpha-1 agonist that increases vascular tone through arteriolar and venous constriction. 5
- Effect: Increases standing systolic BP by 15-30 mmHg for 2-3 hours after a 10 mg dose. 5
- Titration: Can increase up to 10 mg three times daily based on response. 1
Fludrocortisone is an alternative or complementary first-line agent. 1
- Dosing: Start at 0.05-0.1 mg once daily, titrate to 0.1-0.3 mg daily (maximum 1.0 mg daily). 1
- Mechanism: Mineralocorticoid that acts through sodium retention and vessel wall effects. 1
- Monitoring: Check for supine hypertension, hypokalemia, congestive heart failure, and peripheral edema. 1
- Contraindications: Avoid in patients with active heart failure, severe renal disease, or pre-existing supine hypertension. 1
Droxidopa is FDA-approved and particularly effective for neurogenic orthostatic hypotension in Parkinson's disease, pure autonomic failure, and multiple system atrophy. 1
Combination Therapy
- For non-responders to monotherapy, combine midodrine and fludrocortisone, as they work through complementary mechanisms (alpha-1 adrenergic stimulation vs. sodium retention). 1
Alternative Agents for Refractory Cases
Pyridostigmine may be beneficial in refractory neurogenic orthostatic hypotension with a favorable side effect profile (fewer issues than fludrocortisone). 1
- Common side effects include nausea, vomiting, abdominal cramping, sweating, salivation, and urinary incontinence. 1
Step 4: Critical Monitoring and Safety Considerations
Blood Pressure Monitoring
- Measure blood pressure after 5 minutes of lying/sitting, then at 1 and 3 minutes after standing to document orthostatic changes. 1
- Monitor supine blood pressure at every follow-up visit to detect treatment-induced supine hypertension, which is the most important limiting factor and can cause end-organ damage. 1
Follow-Up Timing
- Reassess the patient within 1-2 weeks after medication changes. 1
Special Considerations in Specific Contexts
For patients with catecholamine-producing tumors (pheochromocytoma/paraganglioma):
- Use alpha-adrenoceptor blockers (phenoxybenzamine or doxazosin) for at least 7-14 days preoperatively with gradually increasing dosages. 3
- To reduce the risk of preoperative orthostatic hypotension and postoperative hypotension, employ a high-sodium diet, administer 1-2 liters of saline 24 hours prior to surgery, and use compressive stockings. 3
- Calcium channel blockers may be used as monotherapy in cases of severe orthostatic hypotension when an alpha-adrenoceptor blocker is contraindicated. 3
Common Pitfalls to Avoid
- Do NOT simply reduce the dose of offending medications—switch to alternatives instead. 1
- Do NOT administer midodrine after 6 PM, as this causes supine hypertension during sleep. 1
- Do NOT use fludrocortisone in patients with heart failure or supine hypertension. 1
- Do NOT combine multiple vasodilating agents (ACE inhibitors + calcium channel blockers + diuretics) without careful monitoring. 1
- Do NOT overlook volume depletion as a contributing factor. 1
- Do NOT use beta-blockers in patients with orthostatic hypotension unless there are compelling indications, as they are not effective and may aggravate bradycardia. 1