Orthostatic Hypotension

Orthostatic hypotension (OH) is, unlike the broader symptom of "dizziness," a specific and measurable diagnosis: a sustained fall in blood pressure on standing, defined by international consensus as a drop in systolic blood pressure of at least 20 mmHg, or in diastolic blood pressure of at least 10 mmHg, within 3 minutes of standing (or of head-up tilt to at least 60°).^[1][2] When supine blood pressure is itself elevated (systolic above roughly 140-160 mmHg), a larger drop — at least 30 mmHg systolic or 15 mmHg diastolic — is used instead, since a fixed 20/10 mmHg threshold under-detects clinically meaningful orthostatic intolerance in a patient who starts from a higher baseline.^[3]

OH is genuinely common, particularly in older adults, and genuinely consequential: it is an independent, well-established risk factor for falls, fall-related injury, syncope, and — through both mechanisms — a meaningful driver of the fracture and loss-of-independence burden documented in Canadian falls surveillance data.^[4] It is also, in a large share of cases, correctable: a first-ever Canadian Cardiovascular Society clinical practice document on syncope and orthostatic hypotension frames the treatment goal explicitly as improving symptoms and functional status, not chasing a specific blood pressure number, and places identifying and addressing a reversible — very often medication-related — cause ahead of any drug started specifically to treat OH.^[5][2]

This chapter is deliberately scoped to OH as its own defined diagnosis: the measurement technique and staging that confirm it, the neurogenic-versus-non-neurogenic distinction that shapes the workup, a genuine centerpiece medication-culprit table with practical deprescribing guidance, and the non-pharmacologic-then-pharmacologic treatment ladder. For the broader "patient says they feel dizzy" differential — vertigo, disequilibrium, vestibulotoxic and sedating medications, hypoglycemia — see the separate Dizziness chapter, which this chapter does not repeat.

Typical symptoms

• Lightheadedness or a feeling of impending faint specifically on standing or after prolonged standing, classically relieved within seconds to minutes of sitting or lying back down.
• Presyncope or frank syncope — a witnessed fall or loss of consciousness on standing is a red flag (see Red Flags & Refer).
• Visual disturbance on standing — blurring, graying out, or tunnel vision.
• "Coat-hanger" pain — an ache or stiffness across the back of the neck, shoulders, and upper back in a coat-hanger distribution, appearing specifically on standing and resolving on sitting. This is a genuinely useful, comparatively specific clue for a neurogenic cause, thought to reflect ischemia of postural neck and shoulder muscles when cerebral and regional perfusion drop with standing.^[3]
• Generalized weakness, fatigue, or a "foggy," slowed cognition specifically brought on or worsened by standing or prolonged upright posture.
• Falls without a clearly recalled preceding lightheaded sensation — common in older adults and in autonomic failure, where impaired baroreflex signalling can blunt the warning symptom itself even as the blood pressure drop is just as severe.
• Many patients, especially older adults and those with autonomic failure, are entirely asymptomatic despite meeting the diagnostic blood-pressure criteria — this is exactly why orthostatic vital signs need to be checked proactively in anyone with a fall, a relevant medication, or a relevant comorbidity, not only in someone who volunteers dizziness.

Neurogenic vs. non-neurogenic orthostatic hypotension — the central diagnostic distinction

The bedside discriminator: heart-rate response to the blood-pressure drop

A validated bedside test distinguishes the two: calculate the ratio of the heart-rate rise to the systolic-BP fall between supine and the point of maximal orthostatic drop (ΔHR ÷ ΔSBP, both in absolute terms). A ratio below 0.5 beats per minute per mmHg — i.e., the heart rate does not rise appropriately given how far the pressure fell — points to a neurogenic cause and warrants referral for formal autonomic assessment; a ratio at or above 0.5 points to a non-neurogenic cause such as volume depletion or a medication effect.^[6] This is directly actionable at a routine orthostatic-vitals check: a manual pulse count taken alongside each standing blood pressure reading is enough to apply it. A genuine caveat — a beta-blocker or another rate-limiting drug will itself blunt the heart-rate response and can produce a falsely "neurogenic-looking" ratio, so interpret this test in the context of the full medication list, not in isolation.

Three timing-based subtypes

Postprandial hypotension — a related but distinct entity

A separate blood-pressure drop of at least 20 mmHg systolic occurring within 2 hours after eating, most pronounced after a large, refined-carbohydrate-rich meal, and common in the same populations prone to OH — older adults, patients with diabetes or Parkinson disease. It is thought to reflect splanchnic blood pooling during digestion outpacing the compensatory reflex. Postprandial hypotension and OH frequently coexist in the same patient and share much of the same non-pharmacologic management (smaller, more frequent, lower-carbohydrate meals; avoiding standing quickly after eating) — ask specifically about post-meal symptoms as part of a complete history, since a patient may not volunteer this as related to their "standing dizziness."

• Age 65 years or older — both prevalence and the consequences of a fall rise sharply with age.
• Polypharmacy, and specifically any of the medication classes in the drug-tables below — the single most correctable risk factor in most patients.
• Volume depletion from any cause — inadequate fluid intake, vomiting/diarrhea, heat exposure, blood loss, or diuretic effect.
• Diabetes with longstanding or poorly controlled disease — autonomic neuropathy blunts the compensatory reflex independent of any medication effect.
• Parkinson disease, multiple system atrophy, pure autonomic failure, or dementia with Lewy bodies — see Special Populations.
• Prolonged bed rest, recent hospitalization, or general deconditioning — reduces both blood volume and the venous/muscular tone that normally assists venous return on standing.
• Anemia — reduces the circulating volume available to maintain cerebral perfusion pressure.
• Adrenal insufficiency — mineralocorticoid deficiency causes volume depletion; a genuinely dangerous, under-recognized cause of new or worsening OH (see Red Flags & Refer).
• Heart failure with reduced ejection fraction — both the disease itself and its diuretic therapy contribute.
• Chronic venous insufficiency or varicose veins — increases lower-extremity venous pooling on standing.
• Spinal cord injury, particularly at or above the mid-thoracic level — disrupts the sympathetic outflow needed for the compensatory vasoconstrictive response.
• Hot environments, hot showers or baths, and alcohol — all promote peripheral vasodilation that compounds any other contributor.
• Large meals, especially refined-carbohydrate-heavy ones — see postprandial hypotension above.
• A prior fall or near-fall, and frailty generally — both a marker of risk and a reason a further fall carries disproportionate consequences; this is the population Canadian falls surveillance data identifies as bearing the greatest burden of fall-related injury, hospitalization, and loss of independence.^[4]

Measuring orthostatic vital signs correctly

Technique genuinely matters — a single supine-to-standing check without correct timing can both miss a real drop and produce a false positive from measurement artifact.^[7]

1. Have the patient rest supine for at least 5 minutes before the first measurement — a shorter rest period is a common source of a falsely elevated baseline.
2. Measure blood pressure and heart rate supine.
3. Have the patient stand (or, if standing is unsafe, sit upright with legs dependent), and measure blood pressure and heart rate at 1 minute and again at 3 minutes after the position change.^[2][7]
4. Record the heart rate at each standing measurement, not only the blood pressure — this is what allows the ΔHR/ΔSBP ratio to be calculated (see Recognize the Condition).
5. Ask specifically about symptoms at each standing measurement, not only at the end, and note whether symptoms reproduce with the measured drop.
6. A drop of at least 20 mmHg systolic or 10 mmHg diastolic (or 30/15 mmHg if supine systolic BP exceeds roughly 140-160 mmHg) confirms the diagnosis.^[1][3]
7. If bedside testing is repeatedly normal but the history is strongly suggestive of a standing-triggered symptom (particularly a brief symptom within the first 15 seconds of standing), consider referral for continuous beat-to-beat monitoring to capture initial OH, which routine intermittent-cuff measurement can miss entirely.

Distinguishing neurogenic from non-neurogenic OH at the bedside

Apply the ΔHR/ΔSBP ratio described in Recognize the Condition using the supine and maximal-drop readings already collected above — a ratio below 0.5 bpm/mmHg suggests a neurogenic cause and warrants referral for formal autonomic testing; a ratio at or above 0.5 suggests a non-neurogenic cause and should prompt the medication review and volume-status assessment below.^[6] Remember that a beta-blocker or other rate-limiting drug blunts this test independent of any true neurogenic contribution — interpret it alongside the full medication list.

A key differential to exclude: postural tachycardia (POTS)

A patient whose heart rate rises more than 30 beats per minute (or exceeds 120 bpm) within 10 minutes of standing, without meeting the OH blood-pressure criteria, may have postural orthostatic tachycardia syndrome (POTS) rather than OH — a distinct diagnosis with its own separate workup, not covered in this chapter. Consider this specifically when a patient's symptoms are clearly standing-triggered but the blood pressure drop is absent or minimal.

History

Establish the timing (immediate vs. delayed), any postprandial pattern, and a full medication history including OTC products and recent dose changes, correlating the timeline against the pharmacy fill/refill record where available. Ask specifically about fluid intake, recent illness with vomiting/diarrhea, weight loss, and — in a patient with Parkinsonian or other neurologic features — bladder, bowel, and sweating symptoms suggestive of broader autonomic involvement. Apply the medication list against the AGS Beers Criteria and STOPP/START version 3, the same structured screening tools used across this platform's geriatric-relevant chapters, rather than relying on memory or the single most "obvious" suspect.^[8][9]

Physical examination and investigations

Beyond orthostatic vital signs: a cardiac exam (rate, rhythm, murmurs suggesting a structural cause of syncope), a screening neurologic exam for Parkinsonian signs, and a look for the coat-hanger pain pattern on prolonged standing if time allows. Basic bloodwork — CBC (anemia), electrolytes and renal function, and morning cortisol/ACTH if adrenal insufficiency is genuinely suspected — helps identify a reversible non-neurogenic cause. An ECG is reasonable when a cardiac contributor to syncope is suspected. Formal autonomic function testing (Valsalva maneuver response, deep-breathing heart-rate variability, quantitative sudomotor axon reflex testing) and tilt-table testing are reserved for cases where the bedside evaluation is equivocal, where initial or delayed OH is suspected but not confirmed, or where a neurogenic cause needs formal characterization before specialist pharmacotherapy — refer to neurology or a dedicated autonomic/syncope clinic rather than attempting these in a routine visit.

Differential diagnosis

• Confirm the diagnosis with correctly performed orthostatic vital signs before committing to a treatment plan.
• Distinguish neurogenic from non-neurogenic OH using the ΔHR/ΔSBP ratio, since this materially changes both urgency and the specialist referral decision.
• Identify and correct every plausible reversible, non-neurogenic contributor — volume depletion, anemia, adrenal insufficiency — before or alongside any medication change.
• Treat symptoms and functional status as the goal, not a specific target blood pressure number — a patient can have a measured drop that meets diagnostic criteria and still be adequately managed if they are asymptomatic and functioning well.
• Apply a structured medication review against the whole drug list, using the culprit table below and the Beers Criteria/STOPP-START screen, in collaboration with the prescriber.
• Exhaust non-pharmacologic measures and medication optimization before starting a drug specifically to treat OH.
• When pharmacotherapy is genuinely needed, avoid overcorrecting into supine hypertension — this is a real, separate harm, not merely a theoretical concern.
• Confirm the original indication for any adjusted or deprescribed medication remains adequately treated after the change.
• Reduce fall risk through both the medical correction and non-pharmacologic falls-prevention counselling, given the genuinely serious fracture and independence-loss consequences of a fall in an older adult.

Step 1 — Correct reversible non-neurogenic causes

Preferred approach address volume depletion with adequate fluid intake, treat any identified anemia or adrenal insufficiency, and where a diuretic is being used for an indication that no longer requires it, discuss stopping rather than merely adjusting it with the prescriber.

Step 2 — Structured medication review

Preferred approach apply the drug-tables below systematically against the full medication list, following a structured deprescribing process rather than an ad hoc single-drug reduction: identify the patient's overall risk (falls, frailty, functional decline), measure blood pressure, identify the specific candidate drug(s) for adjustment, make one change at a time with an appropriate interval before the next (commonly 2-4 weeks) to isolate its effect, and monitor blood pressure and symptoms after each change.^[10] Situational where a flagged drug is genuinely needed for its primary indication (e.g., heart failure, resistant hypertension, a needed antipsychotic), a dose reduction, timing adjustment, or within-class substitution to a lower-OH-risk agent is often possible without abandoning the indication entirely — see the specific guidance in each drug-table row.

Step 3 — Non-pharmacologic measures

Preferred approach apply the full non-pharmacologic measures described in the next section in parallel with the medication review, not only after it — most patients benefit from starting physical counter-maneuvers and, where appropriate, compression and fluid/salt measures immediately rather than waiting for the medication review to finish.

Step 4 — Pharmacotherapy, when steps 1-3 are insufficient

Escalate after a genuine trial of medication optimization and non-pharmacologic measures (typically several weeks) leaves symptoms significant enough to affect function or safety, move to pharmacotherapy: midodrine is generally the first pharmacologic choice for non-neurogenic or mixed OH without a contraindication (uncontrolled supine hypertension, significant urinary retention, severe organic heart disease); fludrocortisone is a reasonable alternative or adjunct, particularly when a volume-expansion component is prominent, used cautiously in heart failure. See Pharmacologic Treatment Options for full dosing and monitoring detail.^[3][2]

Confirmed neurogenic OH

Situational once a neurogenic cause is confirmed or strongly suspected (ΔHR/ΔSBP ratio <0.5, or a known neurodegenerative or neuropathic cause), involve neurology for formal autonomic assessment and to help navigate the genuinely difficult concurrent-supine-hypertension problem before or alongside starting pharmacotherapy — this population needs closer titration and monitoring than a straightforward non-neurogenic case.^[3]

Physical counter-maneuvers

Simple, immediate, and genuinely effective when taught properly — these can be used the moment a patient feels an OH symptom coming on, or proactively before a known trigger (standing after a meal, a hot shower):

• Leg crossing while contracting the leg, buttock, and abdominal muscles.
• Squatting, or crouching down, if the setting allows.
• Calf raises, marching in place, or tensing the leg muscles for 30 seconds before and during standing.
• Rising in stages: sit at the edge of the bed for a moment before standing, rather than going straight from lying to standing — particularly important first thing in the morning, when nocturnal fluid shifts make OH characteristically worse.

The water bolus technique

Rapid ingestion of approximately 500 mL of cold water over a few minutes produces a measurable pressor effect within 5-15 minutes, lasting roughly an hour, through an osmopressor reflex distinct from simple volume expansion. This is a genuinely useful, low-risk, and underused technique — teach patients to use it proactively before a predictable trigger, such as first thing in the morning or before a shower, rather than only reactively once symptomatic.

Graduated compression garments

Knee-high (left) versus thigh-high (right) graduated compression stockings. Because most of the venous pooling relevant to orthostatic hypotension occurs in the splanchnic and abdominal circulation as well as the legs, waist-high garments or an abdominal binder are generally more effective than knee-high stockings alone, though adherence and ease of donning are real practical limits, especially in frail patients. (Lentpjuve, CC BY-SA 4.0, Wikimedia Commons)

Discuss realistically with the patient (or caregiver) how the garment will actually be put on each morning — a knee-high stocking a frail patient can manage independently is more useful in practice than a waist-high garment that goes unused because it cannot be donned without help. Compression should be applied before rising, while still supine, for full effect.

Head-of-bed elevation

Elevating the head of the bed by roughly 10-20 cm (4-8 inches) — using bed blocks or a wedge, not just extra pillows, which mainly flex the neck without changing the whole-body angle — reduces nocturnal pressure natriuresis and improves morning OH. This is also a key part of managing coexisting nocturnal supine hypertension in neurogenic OH (see Special Populations), so it is worth implementing even before pharmacotherapy is considered.

Salt and fluid intake

Where not contraindicated by heart failure, significant renal disease, or uncontrolled hypertension — confirm this individually with the prescriber — increased dietary salt and a fluid intake in the range of roughly 2-3 litres daily can meaningfully reduce OH symptoms by expanding circulating volume.^[3] This is a genuine point of caution: default "healthy eating" advice to reduce salt intake can actively worsen OH in a patient for whom it is not otherwise contraindicated, so this needs to be addressed explicitly rather than left to generic dietary counselling.

Avoiding known triggers

• Hot showers, baths, saunas, and hot weather — all promote peripheral vasodilation; a lukewarm rather than hot shower, and a shower chair, are simple practical measures.
• Alcohol, which independently promotes vasodilation and volume loss.
• Large, refined-carbohydrate-heavy meals — smaller, more frequent meals reduce postprandial hypotension; avoid standing quickly after eating.
• Prolonged standing without movement — encourage periodic muscle tensing or weight-shifting rather than standing still.
• Straining (Valsalva maneuver) — manage constipation proactively, since straining at stool can itself provoke a significant drop.

Exercise, reframed rather than avoided

Prolonged inactivity worsens deconditioning-related OH, so exercise should be encouraged, not avoided — but in a form that does not itself provoke symptoms. Recumbent or seated exercise (recumbent cycling, rowing, swimming) is generally better tolerated than prolonged upright exercise for a patient whose OH is significant, and is a reasonable way to maintain conditioning while the underlying cause is being addressed.

Older adults and frailty

This is the population with both the highest OH prevalence and the highest stakes from an unaddressed fall — Canadian falls surveillance data identifies older, frailer adults as bearing the greatest share of fall-related injury, hospitalization, and loss of independence.^[4] Preferred approach apply the Beers Criteria and STOPP/START to every medication list in this group, not only when OH is the presenting complaint, and treat even asymptomatic OH found incidentally as worth addressing given the fall-risk stakes.^[8][9]

Parkinson disease, multiple system atrophy, pure autonomic failure, and dementia with Lewy bodies

Neurogenic OH is genuinely common in this group, reflecting both the disease's intrinsic autonomic involvement and, often, a direct effect of dopaminergic therapy itself. Avoid reflexively reducing dopaminergic therapy without neurology involvement — under-treating the motor symptoms carries its own real cost, and the right balance is a specialist-guided decision, not a unilateral primary-care change.^[3] Coexisting supine hypertension is a genuinely difficult, common combination in this population: head-of-bed elevation and avoiding pharmacotherapy timing that peaks overnight (see Pharmacologic Treatment Options) are first-line management before adding a separate antihypertensive at bedtime, which itself needs specialist coordination.^[3]

Diabetes with autonomic neuropathy

Longstanding or poorly controlled diabetes blunts the normal compensatory heart-rate and vasoconstrictive response independent of any medication, compounding any antihypertensive's own OH risk. Hypoglycemia can present similarly to OH-related presyncope — check a point-of-care glucose alongside orthostatic vitals rather than assuming one or the other. SGLT2 inhibitors add a real, if modest, osmotic-diuresis-driven OH risk in this population and are easy to overlook as a contributor since they are not prescribed as antihypertensives (see drug-tables).^[11]

Chronic kidney disease and dialysis

Intradialytic hypotension is a related but distinct phenomenon from OH and needs its own dialysis-specific management. Fludrocortisone should be used with particular caution given its renal sodium-retention mechanism and this population's already-narrow fluid margins; potassium and volume status need closer monitoring than in a patient with normal renal function.

Heart failure with reduced ejection fraction

A genuinely difficult population to manage: diuretic therapy needed for the heart failure itself is a common OH contributor, but reducing it risks decompensation, and fludrocortisone's fluid-retaining mechanism is a poor fit for a patient with reduced ejection fraction. Midodrine's vasoconstrictive mechanism warrants caution given the risk of worsening afterload and supine hypertension. This balance needs individualized cardiology input rather than a standard OH treatment ladder applied unmodified.

Pregnancy

Some degree of orthostatic intolerance is physiologic in pregnancy given normal hemodynamic changes and is not itself pathologic in most cases — avoid unnecessary medication changes for mild, non-red-flag orthostatic symptoms. Severe or persistent OH in pregnancy is not physiologic and warrants the same red-flag evaluation as in any other patient (see Red Flags & Refer), plus confirmation that any medication adjustment considered is appropriate in pregnancy.

Spinal cord injury

Neurogenic OH is near-universal with injury at or above the mid-thoracic level, reflecting loss of the sympathetic outflow needed for compensatory vasoconstriction. This population also carries a real risk of autonomic dysreflexia — a separate, dangerous hypertensive emergency triggered by a noxious stimulus below the level of injury — so blood pressure management here needs specialized spinal-cord-injury rehabilitation input rather than a standard primary-care OH approach.

Amyloidosis

Both cardiac (restrictive cardiomyopathy) and autonomic involvement can coexist, meaning volume-expansion therapy (fludrocortisone, increased salt/fluid intake) that would help a purely neurogenic OH picture can meaningfully worsen a restrictive cardiomyopathy — this combination needs cardiology and neurology input together rather than either specialty's standard approach alone.

Reassess within days to a couple of weeks after any medication adjustment or new pharmacotherapy started for OH — confirm the symptom and functional-status goal has genuinely improved (not simply that a blood-pressure number has changed), and just as importantly, confirm the original indication for any adjusted drug remains adequately controlled.^[2] Repeat orthostatic vital signs at follow-up rather than relying on symptom report alone.

• Screen actively for emergent supine hypertension at every follow-up once midodrine or fludrocortisone is started — check blood pressure after the patient has been lying down for at least 5 minutes, not only while seated in clinic, since this is easy to miss without deliberately checking for it.
• Monitor potassium and weight/edema at each fludrocortisone titration step.
• Reassess fall risk specifically at each visit, not only OH symptoms in isolation — a patient can have "improved" blood pressure numbers and still carry meaningful residual fall risk from deconditioning, polypharmacy, or an unaddressed home-safety hazard.
• For a patient initially classified as non-neurogenic OH whose symptoms progress or whose pattern changes over time, reconsider the neurogenic-vs-non-neurogenic distinction at follow-up rather than assuming the original classification still holds — some autonomic disorders present first as apparently uncomplicated OH.
• Reinforce non-pharmacologic measures at every visit — adherence to physical counter-maneuvers, compression garments, and fluid/salt measures tends to decline over time without active reinforcement.

1. Before concluding a measure has failed, confirm it was actually implemented correctly and given an adequate trial — fludrocortisone needs several weeks of titration to judge fully, and non-pharmacologic techniques (compression garment timing, counter-maneuver technique, water bolus timing) are frequently under-taught rather than genuinely ineffective; retrain and reassess before escalating.
2. Re-screen the full medication list for a second, less obvious culprit — a patient on multiple relevant drug classes commonly has more than one contributor, and correcting only the first one found is a common source of apparent treatment failure.
3. Reassess volume status, hydration, and salt intake adherence directly rather than assuming counselling alone achieved the intended behaviour change.
4. If a neurogenic cause was not previously assessed, apply the ΔHR/ΔSBP ratio (or repeat it if borderline) and consider referral for formal autonomic testing and neurology involvement.
5. Screen specifically for emergent supine hypertension complicating dosing — this can paradoxically limit how far a drug like midodrine or fludrocortisone can be safely titrated, and correcting it (timing adjustment, head-of-bed elevation) may allow the underlying therapy to actually work rather than needing to be abandoned.
6. Reassess for a missed non-neurogenic cause not yet worked up — anemia, adrenal insufficiency, occult gastrointestinal bleeding, or an unrecognized infection.
7. Consider combination pharmacotherapy (midodrine plus fludrocortisone, or adding pyridostigmine) under specialist guidance once single-agent therapy and the steps above have genuinely been exhausted.
8. For refractory, multifactorial OH — particularly in a frail older adult with ongoing polypharmacy or confirmed neurogenic disease — referral to a dedicated syncope/autonomic clinic or geriatric medicine service is a reasonable and often necessary escalation rather than a sign primary care has failed.

• Measuring "orthostatic vitals" as a single supine-to-standing check without the correct timing (5 minutes supine, then standing at 1 and 3 minutes), which can both miss a real drop and produce a false positive.
• Not recording the heart rate at each standing measurement, making the neurogenic-vs-non-neurogenic ΔHR/ΔSBP discriminator impossible to apply after the fact.
• Starting midodrine or fludrocortisone before completing a structured medication review and a trial of non-pharmacologic measures.
• Prescribing or dispensing midodrine without counselling on the "no dose within 4 hours of lying down" rule, risking supine hypertension.
• Using fludrocortisone in a patient with heart failure without explicit caution and specialist input.
• Not checking potassium after a fludrocortisone dose increase.
• Assuming asymptomatic OH found incidentally does not need to be addressed in a patient with meaningful fall risk.
• Attributing a diabetic patient's standing-related symptoms to "their sugar" without actually checking orthostatic vital signs.
• Assuming a cause is neurogenic based on a blunted heart-rate response without first considering whether a beta-blocker or another rate-limiting drug is the actual explanation.
• Giving generic "reduce your salt intake" dietary advice to a patient with OH for whom salt restriction is not otherwise indicated, unintentionally worsening their symptoms.
• Missing a PDE5 inhibitor on the medication list of a man taking an alpha-blocker or a nitrate — a common, high-consequence interaction patients rarely volunteer without being asked directly.
• Stopping a needed antihypertensive abruptly without a taper or follow-up plan, rather than adjusting dose or timing first.
• Not reassessing after a medication change to confirm both symptom improvement and that the original indication remains adequately treated.

How to use this table: this catalogues medications that cause or worsen orthostatic hypotension, organized by class, to support the structured medication review that is this chapter's central pharmacist intervention — it is not a treatment menu. Doses shown are typical adult doses only and require patient-specific confirmation, including renal/hepatic adjustment. Select any drug name to open its complete Pharmasist Drug Database page.

Diuretics — Thiazide, Thiazide-Like, and Loop Agents

Reduce circulating volume; risk is dose-related and compounds sharply during dehydration, hot weather, or intercurrent illness.

Vasodilating Antihypertensives — ACE Inhibitors/ARBs, Dihydropyridine Calcium Channel Blockers, Direct Vasodilators, and Nitrates

Individually lower risk than the sympathetic-inhibitor classes below in the largest available randomised-trial meta-analysis, but risk rises sharply when combined with each other or with a diuretic, especially at initiation or dose increase.^[11]

Beta-Blockers

Carried the single highest odds ratio for OH of any class in the largest randomised-trial meta-analysis to date (OR 7.76), by blunting the compensatory heart-rate rise that normally offsets a postural BP drop.^[11] This is also why the bedside ΔHR/ΔSBP discriminator (see Recognize the Condition) is unreliable in a patient on a beta-blocker — a blunted heart-rate response may simply reflect the drug, not a neurogenic cause.

Central Alpha-2 Agonists

Combine OH with sedation; never stop abruptly (see Common Errors).

Peripheral Alpha-1 Blockers

Carry a well-documented first-dose and dose-increase OH risk (OR 1.87 in the same meta-analysis), most pronounced within hours of the first dose or any increase.^[11]

Tricyclic Antidepressants

Carried the second-highest odds ratio in the meta-analysis (OR 6.30) — driven by combined alpha-1 blockade, anticholinergic effect, and sedation.^[11]

Antipsychotics

Second-generation agents as a class carried a real, though smaller, odds ratio for OH (OR 2.38); first-generation low-potency agents such as chlorpromazine carry a long-recognized, comparatively higher risk through pronounced alpha-1 blockade.^[11]

Dopaminergic Parkinson Disease Therapy

OH in Parkinson disease reflects both the disease's intrinsic autonomic involvement and a genuine drug effect — dopaminergic therapy itself can cause or worsen OH, on top of the disease's own neurogenic contribution (see Special Populations).

PDE5 Inhibitors — An Interaction Risk, Not a Standalone Cause

PDE5 inhibitors used alone carry limited intrinsic OH risk, but combined with any nitrate, an alpha-blocker, or another antihypertensive, the interaction can produce severe, symptomatic hypotension — this is one of the single most important interaction checks in this entire chapter.

SGLT2 Inhibitors

A newer, genuinely relevant addition to the OH differential: the osmotic diuresis these agents produce carries a small but statistically real OH risk (OR 1.24), distinct from the classic diuretic mechanism.^[11]