From woozy to well: a primary care approach to orthostatic hypotension

Opening Vignette Madam Ho, a 70-year-old woman, presents to your clinic for regular follow-up of hypertension and diabetes mellitus. Her chronic conditions were well controlled with hydralazine and metformin. During the consultation, she complains of frequent lightheadedness when getting up from bed in the morning, with a near-fall incident a few days ago. You perform a postural blood pressure measurement and note a drop from 120/78 mmHg (supine) to 95/64 mmHg (standing), while heart rate increased from 72 to 88 beats per minute. Based on the findings, you diagnose her with orthostatic hypotension.WHAT IS ORTHOSTATIC HYPOTENSION? Orthostatic hypotension (OH) is defined as a drop in systolic blood pressure ≥20 mmHg and/or diastolic blood pressure ≥10 mmHg within 3 min of standing.[1] It may lead to multiple symptoms, including dizziness and fainting due to reduced blood flow to the brain and other organs. HOW RELEVANT IS THIS TO MY PRACTICE? While OH can be asymptomatic, it may also cause significant disruption to daily activities. It is associated with an increased risk of falls, cardiovascular events, cognitive impairment and mortality, particularly in frail elderly patients.[2] Early recognition and management are crucial to improve patient safety and quality of life. HOW COMMON IS THIS IN MY PRACTICE? In Singapore, the prevalence of OH among elderly patients aged >60 years is estimated to be 7.8%–11%, with the risk increasing with age. Patients with comorbidities such as hypertension, diabetes mellitus, congestive heart failure and kidney disease are particularly vulnerable.[3,4] WHAT CAN I DO IN MY PRACTICE? Unlike in specialist settings, primary care providers often manage OH without access to advanced autonomic testing. Thus, emphasis is placed on clinical bedside assessment, medication reconciliation and lifestyle interventions. Most mild cases of OH can be managed effectively at the primary care level through simple, low-cost interventions. Early recognition and screening Patients with OH may experience a range of symptoms due to hypoperfusion of different organs. Neurological symptoms include dizziness, headache, fatigue, confusion, cognitive slowing, presyncope and syncope; cardiovascular symptoms include chest pain and palpitations; respiratory symptoms, due to ventilation–perfusion mismatch in the lung apices, include shortness of breath; visual symptoms, resulting from retinal or occipital lobe ischaemia, include blurred or dimmed vision; and musculoskeletal symptoms, due to hypoperfusion of the trapezius and shoulder girdle muscles, include neck and shoulder pain (coat hanger syndrome).[5] Symptoms are often exacerbated by warm environments due to peripheral vasodilation. Patients with OH may not voluntarily report their symptoms due to mild severity, gradual onset or cognitive impairment. Some patients may also fear losing their autonomy if family members insist on additional safety measures. Therefore, regular screening is essential for those at high risk of OH. Patients who meet the following conditions should be screened for OH: neurodegenerative disorders associated with autonomic dysfunction (e.g. Parkinson’s disease, multiple system atrophy, dementia with Lewy bodies); peripheral neuropathies linked to autonomic dysfunction (e.g. diabetes mellitus, vitamin B12 deficiency, amyloidosis, HIV infection); a history of unexplained falls or syncope; frailty in older age (≥70 years) or polypharmacy; and hypertension (both at the initial visit and after starting antihypertensive therapy). A simple screening question may help elicit relevant information: ‘Do you experience symptoms when standing up that improve when you sit or lie down?’[6,7] If time permits, detailed symptoms should be assessed, followed by measurement of postural vital signs. The recommended gold standard for postural blood pressure measurement involves measuring blood pressure after resting in the supine position for at least 5 min and at both 1 min and 3 min after standing. If this is impractical, a seated-to-standing blood pressure measurement may be an acceptable alternative.[6] When measuring standing blood pressure, the patient’s calves should not be pressed against the edge of the bed. Understand the physiology and aetiology Upon standing, 500–1000 mL of blood shifts to the lower extremities and splanchnic circulation, reducing venous return and cardiac output. This triggers baroreceptors in the carotid arteries and right atrium, activating a compensatory baroreflex that increases sympathetic tone, heart rate and vasoconstriction. The renin–angiotensin–aldosterone system also helps maintain blood pressure by promoting sodium retention.[5,8] When one or more of these compensatory mechanisms fail, OH occurs. Orthostatic hypotension is classified into: (a) neurogenic (caused by impaired baroreflex function, often due to neurodegenerative diseases or neuropathies) and (b) non-neurogenic (typically caused by extrinsic factors such as volume depletion or medication use). The causes of OH are summarised in Box 1. The absence of a compensatory heart rate increase is a key clue to the presence of autonomic failure, distinguishing neurogenic OH from non-neurogenic OH. A heart rate increase of ≤0.5 beats per minute per mmHg drop in systolic blood pressure on standing is more indicative of neurogenic OH.[9]Box 1: Causes of orthostatic hypotension.Common medications that cause OH are summarised in Table 1. Among antihypertensive agents, calcium channel blockers (CCBs), angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) are generally associated with a low risk of OH. Some medications may contribute to OH indirectly. For example, the prolonged use of metformin can lead to Vitamin B12 deficiency and subsequent peripheral neuropathy, which in turn may result in OH.Table 1: Common medications causing orthostatic hypotension (OH).Initial assessment in clinic A thorough history and physical examination should be performed to confirm the diagnosis, identify the underlying cause and assess the impact on function and safety. The key areas to assess are shown in Box 2. Investigations are conducted based on findings from the history and physical examination. For example, a full blood count may be performed to assess for anaemia, a haematocrit and renal panel to evaluate for dehydration and an electrocardiogram to check for cardiac arrhythmias.Box 2: Key areas to confirm diagnosis of OH.Stepwise management in primary care The primary goal of OH management is to alleviate symptoms and improve daily function, rather than normalise blood pressure.[6] Asymptomatic patients may benefit from education and non-pharmacological measures. Identifiable extrinsic factors should be corrected first. Underlying conditions such as dehydration, anaemia, adrenal insufficiency and cardiac disease should be treated appropriately. A comprehensive medication review is crucial. Drugs that exacerbate OH, such as opioids, should be reduced or discontinued where possible. Within the same drug class, medications with a lower risk of OH are preferred. For example, tamsulosin can be used instead of terazosin, and atenolol or bisoprolol can replace propranolol. Recent studies indicate that relaxing blood pressure targets do not necessarily mitigate OH, and discontinuing antihypertensive medications may worsen supine hypertension, thereby increasing the risk of OH-related symptoms.[10] Instead of stopping antihypertensives entirely, regimens should be optimised. High-risk medications such as alpha-blockers and central acting sympatholytics should be replaced with safer alternatives such as CCBs or ACEIs/ARBs.[7,10] Non-pharmacological measures Non-pharmacological management involves dietary modifications, lifestyle changes and the use of compression garments. Patients should aim for a fluid intake of 2–3 L per day to maintain adequate hydration.[6] A practical advice for patients is to keep a glass of water by the bedside and drink it before getting out of bed in the morning. Increased salt intake, with an additional one or two teaspoons (2.3–4.6 g) per day, is also recommended unless contraindicated.[6] Patients with other comorbidities such as heart failure or renal disease require individualised adjustments to their fluid and salt intake. Patients should be advised to change positions gradually, particularly when transitioning from lying to standing. Physical counter-manoeuvres, such as leg crossing and tensing the muscles of the buttocks, abdomen, arms and legs while standing, can help reduce venous pooling. Elevating the head of the bed by 30°–45° can reduce supine hypertension, which helps to relieve symptoms of OH. Exercises that are not gravitationally challenging, such as stationary cycling, rowing or swimming, are preferred because they carry a lower risk of falls, while activities that promote vasodilation, such as hot showers or saunas, should be avoided. Valsalva manoeuvres, such as straining during defaecation or forceful coughing, can exacerbate blood pressure fluctuations and should be appropriately managed, e.g., using laxatives for constipation or antitussives for cough.[5] Compression therapy using waist-high compression stockings can help reduce peripheral blood pooling by applying graded pressure to the lower extremities and abdomen. However, adherence may be limited due to discomfort, particularly in warm climates.[6] In addition, compression stockings should be avoided in patients with peripheral arterial disease, as they can exacerbate circulation issues. For such cases, abdominal binders offer a more tolerable alternative. Pharmacological measures For patients who have persistent symptoms despite non-pharmacological interventions, pharmacotherapy should be considered. Midodrine, an alpha-1 adrenergic receptor agonist, is the first-line treatment due to its effectiveness in increasing vascular resistance. It is typically initiated at 2.5 mg two to three times daily, with titration up to 10 mg three times daily as needed. Since midodrine can cause supine hypertension, it should be avoided 3–5 h before bedtime. A common regimen comprises 2.5 mg at 7 AM and 2 PM, and occasionally, a short-acting antihypertensive may be added for nighttime use. Other common side effects of midodrine include scalp itching and urinary retention. Another commonly used agent is fludrocortisone, a synthetic mineralocorticoid, which enhances sodium and water retention to expand intravascular volume, but its use requires monitoring for hypertension and hypokalaemia. The approach to OH is summarised in Figure 1.Figure 1: Flowchart for evaluation and management of orthostatic hypotension (OH). DBP: diastolic blood pressure, SBP: systolic blood pressureWHEN SHOULD I REFER TO A SPECIALIST? For patients with a high clinical suspicion of OH but normal bedside postural blood pressure measurement, referral for head-up tilt table testing is recommended. If an underlying neurological cause of autonomic failure is suspected and has not been previously evaluated, referral to a neurologist is warranted. Similarly, if a cardiac or an endocrine cause of OH is suspected, referral to a cardiologist and endocrinologist should be considered. Finally, if symptoms of OH remain poorly controlled despite non-pharmacological interventions in primary care, referral to a specialist for further treatment with medication should be considered. In primary care, the focus should be on identifying reversible causes, such as medications, dehydration or anaemia, while optimising blood pressure management without overtreatment. Most patients respond to lifestyle changes and safer antihypertensive substitutions. Pharmacological treatment is initiated only when non-pharmacological measures fail. Specialist referral is warranted when there is diagnostic uncertainty, suspected neurogenic OH or persistent disabling symptoms despite appropriate primary care management. TAKE-HOME MESSAGES Osteostatic hypotension is a common condition often overlooked in primary care, and is prevalent in the elderly and those with comorbidities. Early recognition and diagnosis are crucial, as OH is associated with an increased risk of falls and mortality. Neurogenic OH results from autonomic dysfunction, while non-neurogenic OH is caused by volume depletion, medications and cardiac conditions. Medication review is essential for patients with OH. Antihypertensives, opioids and certain antidepressants can worsen OH, and adjusting these medications can improve symptoms. Non-pharmacological management should be the first-line approach for managing OH. Increasing fluid and salt intake, slow posture changes, compression garments and physical counter-manoeuvres can help reduce symptoms. Medications are reserved for patients with persistent symptoms. Midodrine is the first-line medication but requires monitoring for side effects such as supine hypertension. Closing Vignette You teach Madam Ho physical counter-manoeuvres and advise her to increase fluid intake, adopt slow posture changes and use compression stockings to manage her condition. After reviewing her medications, you replace hydralazine with losartan. At the next follow-up, she reports no further episodes of postural giddiness and no falls.Financial support and sponsorship Nil. Conflicts of interest How CH is a member of the SMJ Editorial Board and was thus not involved in the peer review and publication decisions of this article. SMC CATEGORY 3B CME PROGRAMME Online Quiz: https://www.sma.org.sg/cme-programme Deadline for submission: 6 pm, 12 January 2026