Orthostatic hypotension (HO) of neurogenic origin is a prevalent and disabling manifestation of autonomic dysfunction, due to neurodegenerative diseases.
The presentation of HO is very variable, and may not be recognized until an advanced stage. Epidemiological studies have shown a high morbidity and mortality in association with HO.
The physiopathogenesis of HO indicates as a main component the alteration in the skeletal muscle and in the splanchnic territory of the vasoconstriction mechanism mediated by the baroreflex, caused by damage or by dysfunction in the efferent path of the baroreflex, both at the central level and at the level peripheral.
3 variants of the HO are described:
1. The first is defined by the sustained reduction of blood pressure (BP) by at least 20 mm Hg of systolic BP, or at least 10 mm Hg of diastolic BP, within 3 minutes of incorporation from the supine position. or to raise the head in the test of the tilting table. HO can be associated with hypertension in the supine position.
2. Delayed HO is defined by a sustained decrease in BP after 3 minutes of standing or upright position on the tilting table. It is estimated that 15% of patients with classic OH have a fall in BP between 3 minutes and 10 minutes, and 39% have it beyond 10 minutes. Patients with delayed HO tend to have fewer adrenergic symptoms with hypotension, suggesting a milder form of the disorder.
3. Initial HO is a transient reduction in BP (≥ 40 mm Hg systolic BP or ≥ 20 mm Hg diastolic BP), within 15 seconds of being incorporated from the supine decubitus position. It occurs more frequently among young people, it is not associated with significant morbidity and mortality and its pathophysiology has not been completely elucidated.
What are your symptoms?
The symptoms can be described by patients in different ways, such as “dizziness”, “feeling of instability”, “vertigo”, “dizziness” or “fading”, and they change according to body posture. Patients may also report dyspnea, precordial pain, headache, fatigue, confusion, difficulty concentrating, cognitive changes, cervical contractures and blurred vision.
The prevalence of HO depends on age, concurrent diseases and drugs used by patients.The prevalence of HO increases with age, in association with the natural decline in baroreceptor sensitivity and the higher prevalence of autonomic neurodegenerative diseases.
HO is uncommon in patients younger than 65 years. Epidemiological studies in populations between 45 and 65 years indicate a global prevalence of 5%, between 25% and 30% in individuals with diabetes and 64% in hospitalized patients.
The natural history of HO depends, to a large extent, on the associated diseases. Individuals with diabetes or neurodegenerative diseases tend to have a progressive worsening over time. The progression is:
– Slow in isolated autonomic insufficiency.
– Faster in Parkinson’s disease and in dementia with Lewy bodies.
– Very fast in multisystem atrophy.
– Diabetic patients with good glycemic control show delay in HO progression.
The HO can be divided into 2 physiopathological types: the neurogenic HO and the non-neurogenic HO. Neurogenic HO is due to the loss of reflex vasoconstriction in the splanchnic and visceral territories, due to the dysfunction of the baroreflex efferent pathways.
The common causes of non-neurogenic HO include volume depletion (vomiting, diarrhea, other intestinal losses, hemorrhage and inadequate fluid intake, among others) and the use of drugs that alter the effective volume (vasodilators, diuretics). Visit our catalog HERE
