Continuing Education Activity

Orthostatic hypotension is characterized by a sudden drop in blood pressure that occurs upon standing from a sitting or supine position. The condition can be broadly classified as neurogenic or non-neurogenic. This condition is clinically diagnosed when systolic blood pressure decreases by at least 20 mm Hg or diastolic pressure by 10 mm Hg within 3 minutes of standing or being positioned at a 60-degree angle on a tilt table. This sudden drop in blood pressure is usually caused by autonomic reflex failure, central or peripheral nervous system lesions, cardiac dysfunction, volume depletion, or adverse medication effects. 

The condition is associated with a high risk of morbidity and mortality, primarily due to frequent falls that often result in hospital admissions. Symptoms are often related to cerebral hypoperfusion, although some patients may remain asymptomatic. Treatment focuses on identifying the underlying cause of orthostatic hypotension and implementing tailored behavioral modifications. In addition, pharmacological options may be considered based on the underlying pathology if these interventions prove ineffective. This activity explores the etiology, clinical presentation, evaluation, and management of orthostatic hypotension. This activity also highlights the critical role of the interprofessional team in accurately diagnosing, effectively treating, and optimizing outcomes for patients with this condition.

Objectives:

• Identify the clinical signs and symptoms of orthostatic hypotension, including cerebral hypoperfusion and postural blood pressure changes.
• Implement evidence-based lifestyle modifications to prevent falls and manage orthostatic hypotension in symptomatic patients.
• Select appropriate diagnostic tools, such as tilt-table testing or blood pressure monitors, to confirm orthostatic hypotension and guide treatment.
• Collaborate with an interprofessional healthcare team, including neurologists, cardiologists, and primary care providers, to develop a comprehensive management plan.

Introduction

Orthostatic hypotension, also known as postural hypotension, is defined as a sudden drop in blood pressure that occurs upon standing from a sitting or supine position. This condition significantly impacts quality of life and increases the risk of falls, cardiovascular disease, dementia, depression, and mortality.[1][2][3] Clinically, orthostatic hypotension is defined as a sustained drop in systolic blood pressure (SBP) of at least 20 mm Hg or diastolic blood pressure of 10 mm Hg within 3 minutes of standing after being supine for at least 5 minutes or positioned at a 60° angle on a tilt table.[4] This sudden drop in blood pressure is typically caused by autonomic reflex failure, volume depletion, cardiovascular disease, neuropathy, or adverse medication effects.[5][6]

Symptoms on presentation are often related to cerebral hypoperfusion, although some patients may remain asymptomatic. Orthostatic hypotension is associated with a high rate of morbidity and mortality, primarily due to frequent falls and multiple hospital admissions.[7][8][9] Additionally, the condition is closely linked to other causes of morbidity, such as cardiovascular and neurodegenerative diseases.[10][11] 

Orthostatic hypotension occurs due to an inadequate physiological response to postural changes. This condition can be either symptomatic or asymptomatic and may present as acute or chronic. In younger patients, neurogenic causes are typically responsible for orthostatic hypotension unless volume depletion is present. In older patients, age-related orthostatic hypotension, cardiovascular causes, and neuropathy are more commonly observed. Orthostatic hypotension becomes more prevalent with age, affecting about 1 in 5 individuals aged 60 or older. Postprandial hypotension is also common in older patients and those with autonomic failure, where SBP drops by at least 20 mm Hg within 2 hours after having a meal.[10][12]

Etiology

Upon standing from a supine position, approximately 300 to 800 mL of blood pools in the lower extremities due to gravitational forces, as venous capacitance in the lower extremities is significant. This pooling leads to decreased venous return to the heart and a subsequent reduction in cardiac output, as described by the Frank-Starling Curve. The human body normally compensates through increased sympathetic tone, which constricts arterioles and venous splanchnic vessels, and decreased vagal tone, a response known as the baroreceptor reflex. This increase in sympathetic outflow raises peripheral vascular resistance, helping maintain blood pressure despite reduced cardiac output, as:

Mean arterial pressure = Cardiac output × Systemic vascular resistance.

Individuals without orthostatic hypotension experience a slight decrease in SBP and a slight increase in diastolic blood pressure upon standing. When this compensatory mechanism is absent, patients present with symptoms of orthostatic hypotension. Activation of the renin-angiotensin-aldosterone system (RAAS) helps sustain upright posture for longer periods. In patients without orthostatic hypotension, transient changes in blood pressure return to the values before postural change within 15 seconds.[10]

Orthostatic hypotension occurs when there is an abnormal or delayed response to shifts in the body's fluid balance upon standing, resulting in an exaggerated drop in SBP (≥20 mm Hg) or diastolic blood pressure (≥10 mm Hg). Responses can be of several types, as mentioned below.

• "Classic" orthostatic hypotension occurs within 3 minutes of standing.
• "Delayed" orthostatic hypotension occurs after 3 minutes.
• "Initial" orthostatic hypotension lasts less than 15 seconds after postural changes.
• "Delayed blood pressure recovery" refers to a blood pressure drop that returns to its original values at a time longer than 15 seconds.

Most studies have focused on classic orthostatic hypotension, with limited data available on other types.[13] Over 95% of patients can be diagnosed based on systolic hypotension alone, making it the most commonly reported metric for this condition.[14] In addition, orthostatic hypotension can also be classified based on the timing of SBP decrease and recovery. Recurrent and transient symptoms are characteristic of initial orthostatic hypotension, whereas classic orthostatic hypotension typically presents with more prolonged symptoms, such as blurred vision, light-headedness, or syncope, occurring over a period of up to 180 seconds.[10][15]

Epidemiology

The prevalence of orthostatic hypotension increases with age, particularly in individuals aged 65 or older, due to impaired baroreceptor sensitivity. A systematic review and meta-analysis found that 1 in 5 adults aged 60 or older living in the community experience orthostatic hypotension, with rates being even higher among those residing in long-term care facilities.[16] Two large population-based studies conducted in the United States suggest that orthostatic hypotension is present in less than 5% of individuals aged 45 to 49, approximately 15% of those aged 65 to 69, and over 25% of individuals aged 85 and older.[17]

Orthostatic hypotension is more likely to be prevalent among geriatric inpatients.[18][19] Factors such as clinical settings, frequency of testing, and encouragement to mobilize can influence its prevalence in hospitals.[20][21] A study reported that 25% of patients presenting to the emergency department with syncope were diagnosed with orthostatic hypotension.[22]

Pathophysiology

Several classification systems exist for the etiology of orthostatic hypotension, commonly distinguishing between neurogenic and non-neurogenic causes. Neurogenic orthostatic hypotension results from autonomic instability due to neuropathic or neurodegenerative disease, or aging conditions. Neuropathic conditions include diabetes, cholinergic receptor autoantibodies, and familial dysautonomia.

Neurodegenerative diseases such as Parkinson disease, multiple system atrophy, and pure autonomic failure can cause neurogenic orthostatic hypotension. Non-neurogenic orthostatic hypotension is typically associated with volume depletion or cardiac dysfunction. Medication-induced orthostatic hypotension, especially in the context of polypharmacy in older patients, should also be carefully considered.[23][24]

Neurogenic Causes

• Neurodegenerative diseases: Parkinson disease, Lewy body dementia, and multiple system atrophy.[25]
• Peripheral neuropathy: Diabetes, vitamin B12 deficiency, amyloidosis, renal failure, autoimmune, rheumatological, and paraneoplastic conditions.[26]

Neurogenic orthostatic hypotension can result from central (CNS) or peripheral nervous system (PNS) lesions. CNS lesions, such as multiple system atrophy, brainstem lesions, or high spinal cord lesions, affect the sympathetic nervous system, causing preganglionic sympathetic degeneration while post-ganglionic nerves remain intact. Plasma norepinephrine levels are typically normal or elevated. CNS synucleinopathies, including Parkinson disease, pure autonomic failure, and peripheral neuropathies, often present with autonomic dysfunction. PNS lesions, such as diabetes, amyloidosis, and multiple sclerosis, are associated with reduced sympathetic tone, upregulated alpha-adrenergic receptors in vascular smooth muscle, low plasma epinephrine levels, and a significant pressure response to norepinephrine.[22][27]

Non-Neurogenic Causes

• Volume depletion: Anemia, dehydration, hemorrhage, and hyperglycemia.
• Cardiovascular diseases: Aortic stenosis, hypertension, atherosclerosis, heart failure, vascular stiffening, and arrhythmias.
• Other: Adrenal insufficiency, physical deconditioning, and aging.

Anemia warrants special attention due to its multiple mechanisms in causing orthostatic hypotension. This also reduces blood viscosity and carrying capacity. Hemoglobin is also a scavenger for nitrous oxide, which is a vasodilator; thus, decreased hemoglobin levels lead to increased venodilation. Erythropoietin has been shown to decrease orthostatic hypotension.[22][28]

Contributing Factors

• Medications: Alpha-blockers, antihypertensives, diuretics, nitrates, tricyclic antidepressants, selective serotonin reuptake inhibitors, antipsychotics, beta-blockers.
• Alcohol consumption

  • Short term: Diuretic effect, peripheral vasodilation, impairment of vasoconstriction.[29] 
  • Long-term or chronic: Neurotoxic effects.
• Idiopathic

Medications can cause orthostatic hypotension as an adverse effect. Individual factors such as susceptibility, comorbidities, age, and polypharmacy determine whether patients develop this condition.[30] The total number of antihypertensive medications prescribed may be a better predictor of orthostatic hypotension than any single drug class.[1][18]

Vasovagal syncope and postural tachycardia syndrome (POTS) are the 2 key conditions that must be differentiated from orthostatic hypotension. Both conditions are often accompanied by additional signs of autonomic dysfunction, such as sweating or palpitations. POTS predominantly affects premenopausal females (5:1) aged 15 to 50, with symptoms including fatigue, headache, palpitations, sleep disturbances, nausea, and bloating. The etiology of POTS is complex, involving multiple pathophysiological mechanisms, including disproportionate sympathoexcitation, volume depletion, autoimmune dysfunction, and cardiac or physical deconditioning.

Vasovagal syncope is a type of reflex syncope caused by a failure in blood pressure autoregulation, leading to reduced cerebral perfusion and transient loss of consciousness. The mechanisms behind this include both decreased cardiac output and reduced vascular tone. Please see StatPearls' companion resources, "Postural Tachycardia Syndrome" and "Vasovagal Episode," for further information.

History and Physical

The diagnosis of orthostatic hypotension relies on a thorough history and physical examination, including orthostatic vital signs. Screening with orthostatic vitals is essential, especially in patients aged 60 or older. Despite being simple and cost-effective, this critical diagnostic step is often overlooked in clinical practice.

Symptoms of orthostatic hypotension are triggered by postural changes and typically resolve when sitting or lying down. Symptoms may occur in the morning upon rising from bed or during the day with postural changes such as sitting to standing, lying to standing, or lying to sitting. Symptoms associated with orthostatic changes should prompt evaluation for orthostatic hypotension.

Some patients remain asymptomatic, with orthostatic hypotension identified incidentally during clinical examination. Observational studies indicate that approximately one-third of patients with orthostatic hypotension are asymptomatic.[31][32] However, the clinical significance of asymptomatic orthostatic hypotension remains unclear.

Symptomatic patients commonly report lightheadedness, dizziness, or syncope. Less frequent symptoms include weakness in the limbs, gait disturbances, cognitive impairment, fatigue, chest pain, or recurrent falls. Symptom presentation can vary in the same patient across different episodes of orthostatic hypotension.[10] 

Identifying preceding or precipitating events and reviewing the medication list are essential. A thorough cardiovascular and neurological examination is needed to rule out these etiologies. Abnormal findings, such as tremors or muscle rigidity, should prompt a comprehensive neurological evaluation.[33] Ruling out hypovolemia caused by diuretics, blood loss, vomiting, or polypharmacy is essential. Symptoms of orthostatic hypotension are often more pronounced upon awakening, after exercise, in hot weather, or with physical deconditioning.

The initial evaluation of patients with orthostatic hypotension requires a thorough medication reconciliation, as medications such as vasodilators, diuretics, antidepressants, antipsychotics, and dopaminergic drugs are common precipitants. The symptoms of orthostatic hypotension can be summarized below.

Common Symptoms

• Lightheadedness or presyncope [24]
• Dizziness or vertigo
• Transient loss of consciousness
• Falls [34]

Less Common or Nonspecific Symptoms

• Blurry vision
• Visual field deficits
• Difficulty in concentration
• Cognitive slowing
• Weakness
• Fatigue
• Shortness of breath (due to hypoperfusion of lung apices)
• Chest pain (especially in the setting of coronary artery disease)
• Backache
• Lower extremity pain
• "Coathanger" pain (neck and shoulder pain in the posterior cervical and shoulder areas)
• Dream enactment behavior (suggesting disturbed rapid eye movement [REM] sleep) [10]

Neurogenic Orthostatic Hypotension

Neurogenic causes may lead to hypotensive unawareness, where patients experience low blood pressure but are unaware of it. Observers might notice cognitive slowing that the patient does not perceive. This condition increases the risk of falls and serious injury. Neurogenic orthostatic hypotension is often accompanied by other autonomic signs, such as bladder dysfunction, constipation, and erectile dysfunction.[10] Another indicator of a neurogenic cause is dream enactment behavior, where the normal atonia of REM sleep is disturbed, resulting in motor movements accompanying dreams. This symptom can precede overt neurodegenerative disease by years and is considered a poor prognostic indicator.[35] Postprandial hypotension (occurring within 2 hours of a large meal) is another common manifestation of sympathetic nervous system dysfunction. Neurogenic orthostatic hypotension is also aggravated by exercise and prolonged bed rest.[22]

Neurogenic orthostatic hypotension is often associated with supine hypertension, occurring in about half of cases. This is defined as a SBP greater than 140 mm Hg or diastolic blood pressure DBP greater than 90 mm Hg while supine after 5 minutes.[10][22] This condition can lead to end-organ damage and is a common complication of orthostatic hypotension and its treatment. Evidence suggests that consuming a high-calorie snack or drinking a glass of wine before sleep may help counteract this condition. Additionally, insulin, a known vasodilator, and drugs that decrease insulin secretion, like alpha-glucosidase inhibitors, may be beneficial.[22][36]

Evaluation

Accurate blood pressure measurement is crucial for detecting orthostatic hypotension. Manual oscillometry should be performed at 1, 2, and 3 minutes after transitioning from sitting to standing. Additional diagnostic methods may be necessary for detecting variations in classic presentations. For example, initial orthostatic hypotension may occur too early to be detected by oscillometry and requires a thorough history, while delayed orthostatic hypotension typically presents after 3 minutes. In addition, blood pressure should also be measured after certain activities, such as eating or exercising. Ambulatory blood pressure monitors can also provide additional insights.[37][38][39] The optimal thresholds for diagnosing orthostatic hypotension based on these measurements remain unclear.[40][41] The oscillometry method is the most commonly used for blood pressure measurement; however, beat-to-beat blood pressure machines, which use noninvasive finger cuffs for immediate readings, offer greater accuracy but are less readily available than oscillometry machines.[10][42]

Fluctuations in heart rate should be monitored when measuring lying and standing blood pressure. A useful metric is the ratio of the change in heart rate (HR) to the change in blood pressure, ie, ΔHR/ΔBP (using SBP change). A ratio of less than 0.5 beats per minute/mm Hg indicates an inappropriately low heart rate change, which suggests a neurogenic etiology of orthostatic hypotension.[10] Another recommendation for evaluating heart rate and orthostatic hypotension is that a rise of fewer than 15 beats per minute in heart rate may suggest a neurogenic cause, while a rise of more than 15 beats per minute may indicate a non-neurogenic cause. However, heart rate alone is not a specific indicator of the underlying cause and can be inaccurate if the patient is on a beta-blocker or other chronotropic medications, or has an arrhythmia.[43]

Patients at risk for cardiac disease should undergo a comprehensive cardiac evaluation, starting with an electrocardiography (ECG). Further testing, such as a Holter monitor, echocardiogram, or additional diagnostics, should be considered if the history suggests a cardiogenic origin. Laboratory tests should assess for anemia, dehydration, diabetes, alcohol use disorder, or heart failure.

Tilt table testing has become a useful adjunct to history and physical examination for identifying the causes of syncope, particularly orthostatic conditions such as orthostatic hypotension or reflex syncope. Several protocols are used, most of which involve positioning patients in a near-upright position. Tilt table testing aims to provoke the same symptoms and signs that prompted the initial evaluation. Additional maneuvers, such as the Valsalva maneuver and hyperventilation, can provide further insight. Tilt table testing is especially useful in diagnosing all 4 forms of orthostatic hypotension (classic, delayed, initial, and delayed blood pressure recovery), orthostatic vasovagal syncope, and POTS.[44] Please see StatPearls' companion resource, "Tilt Table," for more information. 

Treatment / Management

The management of orthostatic hypotension is determined by its underlying cause. The primary goal of the treatment is to alleviate symptoms and prevent associated morbidity rather than to normalize blood pressure. Asymptomatic patients typically do not require treatment, and some causes, such as hypovolemia or cardiac failure, may be reversible with correction of the underlying issue. Non-pharmacological interventions form the cornerstone of treatment, as pharmacological approaches raise blood pressure indiscriminately and can exacerbate supine or sitting hypertension. Non-pharmacological strategies are tailored to each patient's triggers and lifestyle, with a combination approach often proving the most effective.[22]

Non-Pharmacological Treatments

Non-pharmacological treatments focus on restoring a patient's functional status and improving their ability to perform daily activities rather than targeting a specific blood pressure level. Education is crucial in helping patients create a personalized treatment plan based on their daily routines. Key aspects of education should include recognizing the warning signs of orthostatic hypotension episodes and identifying triggers such as prolonged standing, large meals, dehydration, alcohol consumption, hot environments, and hot baths or showers.[20] Recent systematic reviews highlight the lack of robust evidence supporting these measures.[45][46] However, efforts should be made to minimize orthostatic stress, such as sitting rather than standing, changing positions slowly, and sleeping with the head of the bed elevated.

Physical measures: Physical counter-pressure maneuvers can also be used to help increase blood pressure. Some of these maneuvers include crossing the legs, placing a foot on a chair, squatting when standing, and crossing the legs while seated. These maneuvers are most effective for patients with a prodrome of orthostatic hypotension and those without balance impairments. Physical conditioning and strengthening of lower body muscles further enhance the effectiveness of these measures. Patients at risk of falling can benefit from supervised exercises, such as using reclining bicycles. Elevating the head of the bed by at least 20 cm can help reduce supine hypertension and alleviate daytime orthostatic hypotension symptoms.[10][47] Abdominal compression is more effective than lower extremity compression in reducing splanchnic pooling. However, compression devices can be uncomfortable and difficult to apply, which may lead to reduced patient compliance.[48][49]

Dietary measures: Bolus water drinking has been used to activate the osmopressor reflex to counteract orthostatic hypotension. In this approach, water is rapidly ingested (eg, 500 mL in 2-3 minutes), which decreases osmolarity and triggers sympathetic nervous system activation. This reflex is believed to be mediated by hepatoreceptors and renal sympathetic nerves. Importantly, this effect is not reproduced by hypo-osmolar or iso-osmolar fluids, so plain water should be consumed.[36][50]

A high-salt diet of up to 10 grams of salt daily, combined with a liberal water intake of 2 to 3 L/d, has been recommended to promote intravascular expansion. However, this should be carefully balanced with cardiac function parameters and the potential for end-organ damage.[51] 

Summary of Non-Pharmacological Treatments for Postural Hypotension

• Gradually changing position in phases (from lying to sitting to standing) rather than abruptly.
• Maintaining adequate hydration.
• Avoiding alcohol, warm environments, large meals, and hot showers or baths.
• Sleeping with the head of the bed elevated.
• Crossing the legs while standing.
• Tensing the muscles in the legs and hips after standing.
• Using binders or stockings to compress the abdomen and lower limbs.
• Engaging in recumbent exercises or swimming.

Pharmacological Treatments

Pharmacological treatment is considered when non-pharmacological interventions fail to alleviate symptoms. Fludrocortisone and midodrine are first-line options, though several other therapies may be utilized. Fludrocortisone works by expanding intravascular volume and is commonly prescribed for orthostatic hypotension. Long-term use, however, carries risks, including heart failure, renal fibrosis, and increased all-cause hospitalization; therefore, doses should not exceed 0.2 mg/d.[22][52]

Pressor agents, such as midodrine (an alpha-1 agonist) and droxidopa (a norepinephrine precursor), are options for managing orthostatic hypotension. Droxidopa has a shorter duration of action than midodrine and may be safer for long-term use. Midodrine is specifically indicated for orthostatic hypotension caused by autonomic dysfunction, although its use for other types of orthostatic hypotension is considered off-label.[53] Droxidopa is particularly effective in patients with peripheral sympathetic denervation, as evidenced by low norepinephrine levels (see Pathophysiology section for further explanation). Atomoxetine, approved for the treatment of attention deficit hyperactivity disorder, acts as a norepinephrine transporter inhibitor, increasing synaptic norepinephrine concentrations. The effectiveness of the drug depends on the presence of endogenous norepinephrine secretion. Pyridostigmine, an acetylcholinesterase inhibitor, is rarely as effective as monotherapy, but it can be used in combination with midodrine or atomoxetine to enhance treatment outcomes.[10][27][54]

All of these medications increase vascular tone through different mechanisms.[55][56][57]

Summary of Pharmacological Treatments 

• Fludrocortisone is recommended for patients with volume depletion.

• Droxidopa or midodrine is likely effective for patients with low norepinephrine levels (eg, <220 pg/mL).

• If norepinephrine levels are within normal limits, a norepinephrine reuptake inhibitor, such as atomoxetine, may be initiated.

Patients with Orthostatic Hypotension and Cardiac Disease 

The prevalence of cardiac disease and orthostatic hypotension rises with age, highlighting the importance of effective management of the condition in patients. Evidence strongly associates orthostatic hypotension with cardiovascular disease, independent of other cardiac risk factors, and with increased cardiovascular mortality.[58][59] In addition, cardiovascular disease is a common underlying cause of orthostatic hypotension. The Systolic Blood Pressure Intervention Trial (SPRINT) trial counterintuitively found that intensive blood pressure treatment was associated with a reduced risk of orthostatic hypotension. However, as most participants in the SPRINT study were asymptomatic, its generalizability is limited.[60] This evidence indicates that orthostatic hypotension should not automatically preclude intensive blood pressure management in patients with cardiac disease risk factors.

Differential Diagnosis

Vasovagal syncope, reflex tachycardia, and POTS share similar presentations and underlying mechanisms involving autonomic dysfunction, as noted above. Refer to the Etiology section for a detailed description.

Carotid sinus syndrome is a rare condition characterized by carotid sinus hypersensitivity, which can lead to syncope, near-syncope, or unexplained falls. Similar to orthostatic hypotension, it is more prevalent in older adults and can be challenging to differentiate clinically. The 2 conditions may also coexist. Tilt-table testing, typically performed in a cardiology setting for patients with syncope of uncertain origin, can aid in distinguishing between them.

The following is a concise list of differential diagnoses to consider when evaluating a patient for orthostatic hypotension. Many of these conditions can also contribute to the development of orthostatic hypotension, including:

• Anemia
• Adrenal insufficiency
• Cardiac arrhythmia
• Congestive heart failure
• Diabetes insipidus
• Hyperglycemia
• Hypokalemia
• Myocardial infarction
• Myocarditis
• Pheochromocytoma

Prognosis

Although orthostatic hypotension is often asymptomatic or associated with minimal symptoms, it is linked to increased mortality and a higher risk of myocardial infarction, heart failure, stroke, and atrial fibrillation. The elevated vascular mortality associated with orthostatic hypotension may be attributed to its association with cardiac and cerebrovascular diseases, such as myocardial infarctions, transient ischemic attacks, ECG abnormalities, and carotid stenosis.[61] Blood flow through the coronary arteries occurs during diastole; therefore, diastolic hypotension can impair coronary blood flow, placing patients at a particularly elevated risk for cardiovascular events.[62]

Complications

Orthostatic hypotension contributes to declining physical function, impaired balance, and reduced ability to perform activities of daily living independently.[63] Large meta-analyses have reported an increased risk of the following in patients with orthostatic hypotension:

• Falls [1]
• Cardiovascular disease [64]
• All-cause mortality [2]

Small studies have reported an increased risk of cognitive impairment, depression, and dementia.[65][66] Whether the risk varies between symptomatic and asymptomatic patients or across different age groups remains unclear.

Deterrence and Patient Education

Screening the general population for orthostatic hypotension is not recommended but may be considered selectively for individuals with specific risk factors. For example, the National Institute for Health and Care Excellence (NICE) guidelines suggest evaluating orthostatic hypotension in patients with hypertension who also have type 2 diabetes or are aged 80 or older. Similarly, the American Diabetes Association (ADA) advises assessing orthostatic hypotension during the initial evaluation of hypertension in all patients with diabetes mellitus and periodically during follow-up, even in the absence of symptoms.[67] 

Patients and the general population should be informed about the symptoms of orthostatic hypotension and its association with changes in posture. Education should emphasize that primary care providers can diagnose the condition and recommend appropriate lifestyle modifications. The primary goal of treatment is to prevent falls in the community. Lifestyle changes are the first-line treatment, although pharmacological options are also available when necessary.

Enhancing Healthcare Team Outcomes

The management of orthostatic hypotension is most effective when performed by an interprofessional healthcare team that may include endocrinologists, internists, primary care providers, neurologists, advanced practitioners, nurses, pharmacists, social workers, and other healthcare professionals. Treatment strategies are guided by the underlying etiology, with the primary goals being symptom relief and the prevention of associated morbidity. For patients whose condition is medication-related, optimizing their medication regimen is essential. An interprofessional approach is often necessary to manage comorbidities such as diabetes, hypertension, and Parkinson disease. Patients experiencing dehydration require prompt volume resuscitation. While the prognosis for asymptomatic patients is generally excellent, those with symptomatic orthostatic hypotension often experience a reduced quality of life. Effective interprofessional collaboration and communication are key to improving patient outcomes.

A strategic approach is essential, incorporating evidence-based strategies to optimize treatment plans while minimizing adverse effects. Ethical considerations should guide all decision-making, ensuring informed consent and respecting patient autonomy in treatment choices. Each healthcare professional must understand their responsibilities and contribute their unique expertise to the care plan, thereby fostering a definite multidisciplinary approach. Effective interprofessional communication is vital, facilitating seamless information exchange and collaborative decision-making among healthcare team members. Care coordination is equally critical, ensuring the patient’s journey from diagnosis to treatment and follow-up is well-organized, minimizing errors and enhancing safety. By prioritizing skill, strategy, ethics, accountability, communication, and coordination, healthcare professionals can provide patient-centered care, improving outcomes and enhancing team performance in the management of orthostatic hypotension.

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Disclosure: Matthew Ringer declares no relevant financial relationships with ineligible companies.

Disclosure: Muhammad Hashmi declares no relevant financial relationships with ineligible companies.

Disclosure: Sarah Lappin declares no relevant financial relationships with ineligible companies.