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.

Definition

• • 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.

Symptoms:

• • 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.

Nonpharmacologic

• • 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.

Lifestyle:

• • • 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 1^st 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.

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6. Pharmacologic treatment of orthostatic hypotension.
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1. • Understanding Neurogenic Orthostatic Hypotension
     Podcast Episode 94: | Parkinson’s Foundation
     -Parkinson’s Foundation Podcast