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    Orthostatic Hypotension


    Last Updated Jan 19, 2022
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    By Joseph Chong, Tracy Huynh


    Orthostatic Hypotension is the second most common etiology of syncope, occurring in approximately 15% of syncope presentations. Often unrecognized or overlooked factor associated with increased cardiovascular morbidity and all-cause mortality.


      • Orthostatic hypotension: decrease in systolic blood pressure of 20 mmHg or decrease in diastolic blood pressure of 10 mmHg within 3 minutes of standing compared with blood pressure from the sitting or supine position.
        • In hypertensive subjects, a cut-off of 30 mmHg fall in sBP may be more appropriate.
      • Initial orthostatic hypotension: decrease in systolic blood pressure of at least 40 mmHg or diastolic blood pressure of at least 20 mmHg within 15 seconds of standing.
      • Delayed orthostatic hypotension: gradual impairment of adaptive mechanisms during orthostasis, resulting in slow decrease in sBP ≥20 mmHg or diastolic ≥10 mmHg, between 3 and 45 minutes.

    Underlying cause

      • Drug-induced:
        • Alpha- and beta-blockers, diuretics, antiparkinsonian agents, antidepressants, anticholinergics, neuroleptics, sedatives.
      • Decreased intravascular volume:
        • Bleeding, dehydration, diarrhea, vomiting, heart failure.
      • Neurogenic:
        • lower heart rate increase when standing upright (usually <10-15 bpm) compared with nonneurogenic causes (usually >15 bpm).
        • Primary: Parkinson’s disease, Dementia with Lewy bodies, Multiple system atrophy, Pure autonomic failure, Guillain-Barre syndrome.
        • Secondary: DM, CKD, autoimmune diseases (Sjogren syndrome, sarcoidosis), endocrine disturbances, paraneoplastic syndromes, alcoholism, amyloidosis, infections (syphilis, HIV, Lyme), B12 deficiency.

    Diagnostic Process


      • Lightheadedness.
      • Dizziness.
      • Presyncope, syncope.
      • Head and neck pain.
      • Hearing and visual disturbances.
      • Weakness, leg buckling.
      • Fatigue.
      • Cognitive slowing.
      • Orthostatic dyspnea or chest pain.

    Physical exam

      • Neurological assessment looking for Parkinsonian features.
      • Volume assessment: mental status, mucous membranes.
      • Evaluation of suspected OH begins with consecutive BP measurements in a supine and upright positions.
        • Patient should be supine for at least 5 minutes.
        • After standing, measure vitals at 1 and 3 minutes to detect fall in BP and blunted (<10-15 bpm) or higher (>15 bpm) HR increase.
          • In the ER, OH may be detected in most cases after 1 and 3 min of standing.
        • Identify reversible causes and underlying medical conditions:
          • Look for clues on HPI:
            • Vomiting, diarrhea, burns: depleted intravascular volume.
            • Fever/chills: infectious.
            • Pill-rolling tremor, rigidity, bradykinesia, shuffling gait: Parkinson’s.
            • Progressive motor weakness: Guillain-Barre syndrome, MSA.
            • Chest pain, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, extremity swelling: heart failure.
          • Medical history: hypertension, diabetes, neurodegenerative disease, cardiovascular disease, renal failure, autoimmune diseases, alcohol use.
          • Medication list: alpha- and beta-blockers, diuretics, tricyclic antidepressants, antiparkinsonian agents, antipsychotics.
        • Once diagnosis of OH is established, basic tests should be performed:
          • CBC.
          • Electrolytes.
          • BUN, Cr.
          • Glucose.
          • TSH.
          • B12.
          • 12-lead ECG.

    Further investigations based on history as needed



    The goal of treatment is to alleviate symptom burden and not to achieve target blood pressure.


      • Discontinue offending medications.
        • If not possible, reduce dose or take at bedtime when possible.
        • Antihypertensives should generally not be discontinued due to established benefits of BP lowering; uncontrolled BP can aggravate OH.
      • Avoid triggers:
        • Avoid large carbohydrate-rich meals to limit postprandial hypotension.
        • Avoid hot environments.
        • Avoid Valsalva maneuvers.
      • Ensure adequate fluid and salt intake:
        • Fluid intake: 2-3 L per day, rapid ingestion of water (500 mL) serves as a rescue measure.
        • Salt intake: 6-10 g/day or target urinary sodium 150-200 mEq.



        • Physical maneuvers to reduce venous pooling such as rising gradually, squatting, bending over at waist.
        • While actively standing, cross legs, perform thigh, abdominal, and buttock contractions.
        • Exercise program focused on improving conditioning.
        • Abdominal and lower extremity compression.
        • In patients with supine hypertension, elevate the head of the bed to reduce nocturnal pressure natriuresis and morning volume depletion.
      • Pharmacologic: should be administered in combination with lifestyle measures.
        • Fludrocortisone: synthetic mineralocorticoid, considered 1st line therapy.
          • Dose: start with 0.1 mg per day, titrate in increments of 0.1 mg per week, maximum 1 mg per day. Dosing should be titrated until symptoms are relieved, or until patient develops peripheral edema.
          • Adverse effects: hypokalemia, headache, supine hypertension, CHF, edema.
          • Patients should be advised to eat potassium-rich foods, wear compression stockings if dependent edema occurs.
        • Other pharmacological therapy used: midodrine, atomoxetine, and pyridostigmine, but consider internal medicine input.

    Quality Of Evidence?


    • Low-Moderate: consensus statements, review from AFP.

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