Key Points
- To synthesize current understanding of the physiological mechanisms, diverse etiologies, clinical and subclinical comorbidities, and therapeutic targets associated with orthostatic hypotension.
- Narrative synthesis of orthostatic cardiovascular control mechanisms, including neurovascular compensation, skeletal muscle pumping, neurohumoral signaling, and cerebral autoregulation.
- Evaluation of secondary etiologies, autonomic syndromes (such as vasovagal syncope and postural orthostatic tachycardia syndrome), and related chronic comorbidities across pediatric and adult cohorts.
- Orthostatic regulation relies on coordinated autonomic, muscular, and neurohumoral mechanisms to sustain systemic blood pressure and cerebral perfusion during postural transitions.
- Orthostatic hypotension and reduced cerebral blood flow qualitatively associate with impaired cognition, depressive symptoms, anxiety, attention deficits, diabetes mellitus, and Parkinson disease.
- Subclinical blood pressure drops during orthostasis associate with behavioral impairments and intergenerational behavioral sequelae between mother and child.
Structured PICO
PPopulationPatients with clinical or subclinical orthostatic hypotension
This review emphasizes the broad systemic and cognitive impacts of both clinical and subclinical orthostatic hypotension, highlighting the need for better diagnostic and therapeutic strategies.