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Updated: Jan 11, 2026

Tilt Testing with Combined Lower Body Negative Pressure: a "Gold Standard" for Measuring Orthostatic Tolerance
Published on: March 21, 2013
Haemodynamic determinants of supine hypertension in patients with classical orthostatic hypotension
Amber H van der Stam1,2, Boriana S Gagaouzova2,3, Fabian I Kerkhof2
1Radboud University Medical Center, Donders Institute for Brain, Cognition and Behavior, Department of Neurology, Center of Expertise for Parkinson & Movement Disorders, Nijmegen.
Insights
Classical orthostatic hypotension (cOH) patients exhibit high supine blood pressure due to elevated total peripheral resistance (TPR). This high TPR fails to increase upon standing, leading to orthostatic hypotension.
Area of Science:
- Cardiovascular Physiology
- Autonomic Nervous System Function
- Hypertension Research
Background:
- The interplay between supine hypertension and classical orthostatic hypotension (cOH) remains poorly understood.
- Investigating the determinants of blood pressure regulation in individuals with cOH is crucial for understanding cardiovascular pathophysiology.
Purpose of the Study:
- To elucidate the relationship between classical orthostatic hypotension (cOH) and supine hypertension.
- To determine the relative contributions of heart rate (HR), stroke volume (SV), and total peripheral resistance (TPR) to supine and upright blood pressure (BP).
Main Methods:
- Retrospective analysis of tilt tests in normotensive controls, hypertensive controls, and cOH patients with (cOH/SH+) and without (cOH/SH-) supine hypertension.
- Linear regression and logratio analysis were employed to assess the contributions of HR, SV, and TPR to BP regulation.
- Hypertension defined as supine systolic blood pressure (SBP) ≥ 140 mmHg; P < 0.003 considered significant.
Main Results:
- High supine SBP was consistently associated with elevated TPR in both patients and controls.
- Orthostatic SBP decrease was more pronounced in cOH patients with higher supine SBP, primarily due to a failure of TPR to increase upon standing in the cOH/SH+ group.
- Stroke volume (SV) contributed less to orthostatic BP changes in cOH/SH- compared to cOH/SH+, while heart rate (HR) contributions were similar across cOH groups.
Conclusions:
- Elevated supine TPR is a key factor in supine hypertension within cOH patients.
- The inability to adequately increase upright TPR significantly contributes to the orthostatic blood pressure fall in cOH.
- While autonomic failure explains the BP drop, the persistent high supine TPR suggests a role for slow-acting vasoconstrictors in maintaining supine hypertension.
Objective:
The relation between classical orthostatic hypotension (cOH) and supine hypertension is largely unknown. We investigated the relative contributions of heart rate (HR), stroke volume (SV) and total peripheral resistance (TPR) to supine and upright blood pressure (BP).
Methods:
In this retrospective study, tilt tests were divided in four groups: 19 normotensive and 61 hypertensive controls, 50 cOH patients with SH (cOH/SH+) and 30 without (cOH/SH-). Hypertension was defined as supine SBP at least 140 mmHg. We used linear regression to relate cOH severity to supine SBP, and the logratio method to analyse relative contributions of HR, SV and TPR. P values less than 0.003 were considered significant.
Results:
High supine SBP was associated with high TPR in patients and controls. Orthostatic SBP decrease in cOH was larger in those with higher supine SBP. The main parameter explaining this effect was a high supine TPR that did not increase after tilt in cOH/SH+ compared to cOH/SH- (logratio difference, P < 0.002). SV logratio decreased more in cOH/SH- than in cOH/SH+ ( P < 0.003), and HR logratio contributed similarly to orthostatic SBP in both cOH groups ( P = 0.028).
Conclusion:
While high supine TPR explained SH, a failure to further increase upright TPR explained the orthostatic SBP fall in patients. Autonomic failure can explain the SBP fall but not directly the high supine TPR that causes SH. We assume that slow-acting humoral vasoconstrictors are triggered in the upright position and continue to act after tilting back, causing high TPR and SH.
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