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Orthostatic hypertension. Pathogenetic studies
Insights
Orthostatic hypertension, characterized by elevated standing diastolic blood pressure, is common. It stems from excessive blood pooling in the legs upon standing, leading to reduced cardiac output and increased sympathetic activity.
Area of Science:
- Cardiovascular Physiology
- Hypertension Research
- Autonomic Nervous System Function
Background:
- Orthostatic hypotension is a recognized condition, but orthostatic hypertension is less understood.
- Identifying mechanisms of orthostatic hypertension is crucial for managing hypertensive patients.
Purpose of the Study:
- To investigate the prevalence and underlying mechanisms of orthostatic hypertension.
- To compare physiological responses between orthostatic hypertensive and normotensive individuals.
Main Methods:
- Recumbent and standing blood pressure measurements in 1800 hypertensive patients.
- Cardiac output, blood pooling (using gamma counting), and plasma norepinephrine levels were assessed.
- Intervention with an inflatable pressure suit to evaluate its effect on orthostatic responses.
Main Results:
- 181 patients (10%) exhibited orthostatic hypertension (recumbent DBP <90 mmHg, standing DBP >90 mmHg).
- Orthostatic hypertensive patients showed a greater fall in cardiac output and significantly more lower-body blood pooling compared to normotensive subjects.
- Plasma norepinephrine levels increased significantly after standing in orthostatic hypertensive patients.
Conclusions:
- Orthostatic hypertension is a prevalent condition in referred hypertensive patients.
- The mechanism involves excessive gravitational pooling of blood in the lower extremities upon standing.
- This pooling leads to decreased venous return, reduced cardiac output, and compensatory sympathetic activation causing arteriolar constriction.
Abstract:
Among 1800 referred hypertensive patients, 181 had recumbent diastolic blood pressures (DBP) below 90 mm Hg and standing DBP above 90 mm Hg. Orthostatic increments in DBP were greater in these orthostatic hypertensive patients than in 181 persistently hypertensive patients and 134 normotensive subjects. In 12 patients with orthostatic hypertension, the orthostatic fall in cardiac output (27.3 +/- 2.9%, measured by a respiratory method) was double that in 8 normotensive subjects (13.3 +/- 3.7%, p less than 0.01). An inflated pressure suit over the pelvis and lower limbs prevented the excessive fall in cardiac output and significantly reduced (p less than 0.02) the excessive rise in standing DBP in orthostatic hypertensive patients. Gravitational pooling of blood in the legs and reduction of blood in the head was measured by external gamma counting of autologous erythrocytes labeled with sodium pertechnetate Tc 99m through ports in fixed positions over the leg and the temple. Orthostatic intravascular pooling was significantly greater (p less than 0.01) in orthostatic hypertensive subjects than in normotensive subjects, and the magnitudes of orthostatic pooling and orthostatic increases in DBP were closely correlated (r = +0.85). Plasma norepinephrine concentrations were similar in recumbency and after sustained handgrip exercise, but significantly greater (p less than 0.01) after 5 to 60 mins of standing in orthostatic hypertensive subjects than in normotensive subjects. Our results indicate that orthostatic hypertension is common and that its mechanism in representative patients involves excessive orthostatic blood pooling, which results in decreased venous return, decreased cardiac output, increased sympathetic stimulation (presumably through low-pressure cardiopulmonary receptors), and excessive arteriolar, but not venular, constriction.