How should I evaluate and manage orthostatic hypotension in an older adult, including diagnosis, reversible causes, non‑pharmacologic measures, and pharmacologic options?

Evaluation and Management of Orthostatic Hypotension in Older Adults

Diagnosis

Measure blood pressure after 5 minutes of supine or seated rest, then at 1 minute and 3 minutes after standing, with the arm maintained at heart level throughout all measurements. 1, 2 Orthostatic hypotension is defined as a drop of ≥20 mmHg systolic or ≥10 mmHg diastolic within 3 minutes of standing. 1, 2

Measurement Technique

• Have the patient rest supine or seated for 5 minutes in a quiet, temperature-controlled environment (21-23°C). 2
• Patients should avoid caffeine, exercise, and smoking for at least 30 minutes before testing and empty their bladder beforehand. 2
• Use a validated blood pressure device with appropriate cuff size (bladder encircling 80% of arm circumference). 2
• Record blood pressure and heart rate at baseline, then at 1 and 3 minutes after standing. 1, 2
• Measure blood pressure in both arms at the first visit; if systolic BP differs by >10 mmHg between arms, use the arm with higher readings for subsequent measurements. 2

High-Risk Populations Requiring Screening

• All patients ≥65 years, especially those ≥80 years 2
• Diabetic patients before starting or intensifying antihypertensive therapy 2
• Patients with Parkinson's disease 2
• Anyone with symptoms of dizziness, lightheadedness, blurred vision, weakness, fatigue, syncope, or falls 1, 3

Identify and Address Reversible Causes

Immediately discontinue or switch medications that worsen orthostatic hypotension rather than simply reducing doses. 1

Medication Review (Most Common Cause)

Drug-induced autonomic failure is the most frequent cause of orthostatic hypotension. 1 Discontinue or switch:

• Alpha-1 blockers (doxazosin, prazosin, terazosin, tamsulosin) – most problematic in older adults 1
• Diuretics – especially in combination with other vasodilators 1
• Vasodilators (hydralazine, minoxidil, nitrates) 1
• Beta-blockers – unless compelling indication exists (heart failure, recent MI) 1
• Centrally acting agents (clonidine, methyldopa) 1

Other Reversible Causes to Evaluate

• Volume depletion: dehydration, blood loss, hypovolemia 1, 3
• Alcohol consumption: causes both autonomic neuropathy and central volume depletion 1
• Endocrine disorders: adrenal insufficiency, hypothyroidism 1, 3
• Cardiac causes: heart failure, arrhythmias 3, 4

Special Consideration for Diabetic Patients

In diabetic patients >50 years with orthostatic hypotension, assess for cardiovascular autonomic neuropathy (CAN) using cardiac autonomic reflex tests (CARTs). 1 CAN is a Level A evidence risk marker for all-cause mortality and confers additional mortality risk beyond heart rate variability abnormalities. 1 Measure resting heart rate and obtain a 12-lead ECG; QTc ≥460 ms in women or ≥450 ms in men is linked to increased mortality. 1

Non-Pharmacologic Measures (First-Line for All Patients)

Implement non-pharmacologic interventions before or alongside pharmacologic treatment, as these form the cornerstone of management. 1, 3

Volume Expansion

• Increase fluid intake to 2-3 liters daily (unless contraindicated by heart failure) 1
• Increase salt intake to 6-9 grams daily (unless contraindicated by heart failure) 1
• Acute water bolus: drink ≥480 mL of water for temporary relief, with peak effect at 30 minutes 1

Physical Countermaneuvers

• Leg crossing, squatting, stooping, and muscle tensing during symptomatic episodes – particularly effective in patients <60 years with prodromal symptoms 1
• These maneuvers increase venous return and can be implemented at symptom onset 1

Compression Garments

• Waist-high compression stockings (30-40 mmHg) and abdominal binders reduce venous pooling 1
• Thigh-high and abdominal compression are recommended 1

Postural and Dietary Modifications

• Elevate head of bed by 10 degrees during sleep to prevent nocturnal polyuria, maintain favorable fluid distribution, and ameliorate nocturnal hypertension 1
• Eat smaller, more frequent meals to reduce postprandial hypotension 1
• Gradual staged movements with postural changes 1
• Encourage physical activity and exercise to avoid deconditioning, which worsens orthostatic intolerance 1

Pharmacologic Options (When Non-Pharmacologic Measures Fail)

The therapeutic goal is minimizing postural symptoms and improving functional capacity, NOT restoring normotension. 1, 5 Balance the benefits of increasing standing blood pressure against the risk of worsening supine hypertension. 1

First-Line Pharmacologic Agents

Midodrine (Strongest Evidence Base)

Midodrine has the strongest evidence among pressor agents, with three randomized placebo-controlled trials demonstrating efficacy. 1

• Dosing: Start 2.5-5 mg three times daily, titrate up to 10 mg three times daily based on response 1
• Mechanism: Alpha-1 adrenergic agonist causing arteriolar and venous constriction 1
• Effect: Increases standing systolic BP by 15-30 mmHg for 2-3 hours 1
• Critical timing: Last dose must be taken at least 3-4 hours before bedtime (not after 6 PM) to prevent supine hypertension during sleep 1
• Monitoring: Check for supine hypertension development 1

Fludrocortisone

• Dosing: Start 0.05-0.1 mg once daily, titrate to 0.1-0.3 mg daily (maximum 1.0 mg daily) 1
• Mechanism: Mineralocorticoid that increases plasma volume through sodium retention and vessel wall effects 1
• Monitoring: Check for supine hypertension, hypokalemia, congestive heart failure, and peripheral edema 1
• Contraindications: Active heart failure, significant cardiac dysfunction, severe renal disease, pre-existing supine hypertension 1
• Electrolyte monitoring: Check potassium, BUN, and creatinine periodically due to mineralocorticoid effects 1

Droxidopa

• FDA-approved for neurogenic orthostatic hypotension 1
• Particularly effective for Parkinson's disease, pure autonomic failure, and multiple system atrophy 1
• May reduce falls in these populations 1

Combination Therapy for Inadequate Response to Monotherapy

For patients who do not achieve adequate symptom control with a single agent, combine midodrine with fludrocortisone, as they act via complementary mechanisms (vascular constriction plus sodium retention). 1

Second-Line Agent for Refractory Cases

Pyridostigmine (Preferred When Supine Hypertension is a Concern)

Pyridostigmine is beneficial for refractory orthostatic hypotension in elderly patients who have not responded to other treatments, with fewer side effects than alternatives and no worsening of supine blood pressure. 1, 6

• Dosing: 60 mg orally three times daily (maximum 600 mg daily) 1
• Mechanism: Acetylcholinesterase inhibitor that enhances ganglionic sympathetic transmission 1
• Advantage: Does not worsen supine hypertension, making it ideal for patients with concurrent supine hypertension and orthostatic hypotension 1, 6
• Side effects: Nausea, vomiting, abdominal cramping, sweating, salivation, urinary incontinence (generally manageable) 1
• Evidence: Class IIa recommendation from ACC/AHA/HRS guidelines for neurogenic orthostatic hypotension refractory to other treatments 1

Special Considerations for Concurrent Hypertension and Orthostatic Hypotension

For patients ≥85 years with both hypertension and orthostatic hypotension, use long-acting dihydropyridine calcium channel blockers (e.g., amlodipine) or RAS inhibitors as first-line antihypertensive agents. 1

• Avoid alpha-1 blockers, which are explicitly contraindicated in this scenario 1
• Switch BP-lowering medications that worsen orthostatic hypotension to alternative therapy rather than simply reducing doses 1
• Defer antihypertensive treatment in patients ≥85 years with pre-treatment symptomatic orthostatic hypotension, moderate-to-severe frailty, or limited life expectancy until office BP ≥140/90 mmHg 1
• Target "as low as reasonably achievable" (ALARA) rather than strict 130/80 mmHg in frail elderly 1
• Asymptomatic orthostatic hypotension during treatment should not trigger automatic down-titration of therapy, as intensive BP lowering may actually reduce orthostatic hypotension risk by improving baroreflex function 1

Monitoring and Follow-Up

• Measure both supine and standing BP at each visit to detect treatment-induced supine hypertension 1
• Reassess within 1-2 weeks after medication changes 1
• Monitor orthostatic vital signs at each follow-up visit 1
• Check electrolytes, BUN, and creatinine if using fludrocortisone 1

Common Pitfalls to Avoid

• Do not simply reduce the dose of offending medications – switch to alternative therapy instead 1
• Do not administer midodrine after 6 PM – risk of nocturnal supine hypertension 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 target normotension – focus on symptom relief and functional improvement 1, 5