Orthostatic syncope

Source: Wikipedia, the free encyclopedia.

Orthostatic syncope refers to syncope resulting from a postural decrease in blood pressure, termed orthostatic hypotension.[1]

Orthostatic hypotension occurs when there is a persistent reduction in

upright position.[3][2][1]

Signs and symptoms

Orthostatic syncope may occur suddenly with no warning or may be preceded by symptoms.

diaphoresis, a sense of warmth or blurred vision.[1] Other general symptoms regardless of the position include a feeling of generalized weakness, headache, fatigue, cognitive slowing and shortness of breath.[2][3][4]

Symptoms may be sudden or gradual, getting progressively worse until the patient

loses consciousness.[1] Patients may have a single episode with an identifiable precipitating factor or recurrent episodes without an overt, identifiable, precipitating factor.[1]

Blood pressure and

standing positions. As described above, orthostatic hypotension diagnosis is when there is a drop of greater than or equal to 20 mmHg or greater or equal to 10 mmHg in systolic and diastolic blood pressures, respectively within 3 minutes of standing.[1] In the case of hypovolemia, there is also a compensatory rise in heart rate of greater than 15 beats/minute.[1]

Complications

Complications of orthostatic syncope include:[1]

  1. Trauma or injury from falls during an episode of orthostatic syncope.
  2. Stroke
    from changes in blood pressure due to decrease blood flow to the brain.
  3. Cardiovascular complications including heart failure, chest pain, and arrhythmias
    .

Etiology

There are multiple causes of orthostatic hypotension which could lead to syncope including neurally mediated (

neurogenic) and non-neurally mediated causes.[3]

Neurally mediated causes include conditions that cause either primary or secondary failure of the autonomic system:[3]

Non-neurally mediated causes include:[3]

Pathophysiology

The

autonomic dysfunction, there is an inadequate engagement of the autonomic nervous system in response to a decrease in blood pressure leading to persistent hypotension. [1]

Diagnosis

Orthostatic vitals including blood pressure and heart rate in response to upright posture for at least 3 minutes is essential for the diagnosis of orthostatic syncope. A resting 12-lead

metabolic or renal derangements. In selected patients with suspected neurodegenerative disease and syncope, referral for autonomic evaluation is reasonable to improve diagnostic and prognostic accuracy.[5]

Differential Diagnosis

Differential diagnosis includes other causes of

Management

The history and physical examination are essential components in the evaluation of a patient with orthostatic syncope. The history may reveal a cause for

hospitalization, may have reduced muscle tone. [1]

Review of the patients' medication list may show

antihypertensives) and steroids (a clue to steroid-induced adrenal insufficiency). [1]

Review of the past medical history will reveal associated predisposing medical conditions (diabetes, Parkinsonism, dementia). [1] Patient compliance with both pharmacological and nonpharmacological therapy is recommended for successful treatment. [1]

Treatment of orthostatic syncope depends on the underlying cause and includes both nonpharmacological and pharmacological measures. [3][4]

Nonpharmacological treatment measures aim at either increasing venous return to the heart while decreasing venous pooling in the lower extremities or increasing blood volume to maintain blood pressure in the supine position and include[3][4]:

  1. Avoiding physical deconditioning in the elderly which helps maintain muscle tone in lower extremities
  2. abdominal binders
  3. leg crossing
  4. Review of home medications and discontinue diuretics and vasodilators if possible
  5. Increase water and fluid intake to about 2-3 liters per day, avoid dehydration, bolus water ingestion of 500mls of water in 2 to 3 minutes especially in the morning
  6. Dietary measures including liberal salt diet 6-10g/day, eating small frequent low carbohydrate meals a day in case of postprandial orthostatic hypotension, avoid alcohol intake
  7. In patients with
    autonomic dysfunction and supine hypertension, raising the head of the bed to 10 degrees at night reduces nocturnal diuresis
  8. Life style modification by avoiding activities that increase

The goal of pharmacological treatment is to increase blood volume or peripheral vascular resistance and includes[3][4]:

  1. Midodrine 2.5 to 15 mg orally once to thrice daily
  2. Fludrocortisone 0.1 to 0.2 mg daily in the morning titrated up to 1 mg daily if needed
  3. Pyridostigmine 30 to 60 mg orally trice daily
  4. Yohimbine 5.4 to 10.8 mg orally trice daily
  5. Octreotide 12.5 to 50 ug subcutaneously twice daily
  6. Cafergot such as caffeine 100 mg and ergotamine
    100 mg

Prognosis

Prognosis for orthostatic syncope depends on the underlying cause of orthostatic hypotension. The prognosis is good in non-neurally mediated orthostatic syncope once the cause of postural hypotension is identified and treated -

volume depletion, transfusion for blood loss, discontinuation of offending antihypertensive medications. In neurally mediated syncope, prognosis depends on the course of the underlying medical condition. However, in the Framingham heart study, patients with syncope of unknown cause or neurologic syncope had an increased risk of death from any cause in multivariable-adjusted hazard ratios of 1.32 and 1.54 respectively. [6]

Orthostatic hypotension is one of the most frequently identified causes of

Epidemiology

Orthostatic hypotension is more frequent in elderly patients because of multiple factors such as

vasoconstrictor responses and a decrease in muscle tone, cardiac and vascular compliance. Neurogenic orthostatic hypotension showed a prevalence of 18% in patients older than 65 years and resulted in syncope in 9.4% of patients in the NIH funded Framingham cohort. [3][6]

References