In clinical practice, sleep-apnea may be accurately monitored by RWPP. RWPP seems to reflect autonomic influences and may be particularly well-suited for the study of vascular reactivity. Thus, further descriptions of disease-specific cardiovascular reactivity patterns may be possible with techniques based on RWPP. Other clinical uses of RWPP are investigational.

No abstract

The clinical syndrome of supine hypertension associated with orthostatic hypotension (OH) in given individuals is recognized by specialists, but is underdiagnosed in the community. The objective of this study was to assess supine hypertension associated with hypotensive reactions on head-up tilt (SH-HRT) among patients evaluated for nonspecific dizziness. Consecutive patients with nonspecific dizziness were studied with a 10-min supine 30-min head-up tilt test. Supine hypertension (SH) was diagnosed when supine systolic blood pressure (SBP) was X140 mmHg and/or supine diastolic blood pressure (DBP) was X90 mmHg. Hypotensive reactions on tilt (HRT) were diagnosed when SBP decreased by X30 mmHg on tilt and/or DBP decreased by X15 mmHg. Of 430 patients tested, 42 (9.8%) had SH-HRT. The median age was 67 years; 37 had a pretest diagnosis of hypertension, with treatment.The median supine BP was 162/90 mmHg; the median nadir BP on tilt was 118/78 mmHg. Four SH-HRT patterns were recognized: (I) SH with typical neurogenic OH (n ¼ 6), (II) SH with vasovagal reaction on tilt (n ¼ 4), (III) SH with sustained HRT (n ¼ 28), and (IV) SH with mixed orthostatic-vasovagal reaction on tilt (n ¼ 4). Dizziness on tilt occurred in 25% of patients category III (SH with sustained HRT), while appearing universally in other SH-HRT patterns. In conclusion, nonspecific dizziness may be the chief complaint in patients with SH-HRT, a disorder often unrecognized by clinicians. Different patterns of SH-HRT on HUTT may reflect different aberrations in cardiovascular homeostasis and may require differentiated management strategies.

Based on prior studies, the hypothesis that hyperventilation (HV) may have a pressor effect and play a causal role in hypertension has been suggested. The objective of this study was to correlate HV with blood pressure (BP)-change during a postural challenge. Consecutive subjects referred for evaluation of syncope, dizziness, chronic fatigue syndrome (CFS), fibromyalgia, or non-CFS fatigue were assessed with a 10-min supine 30-min head-up tilt test combined with capnography. We selected for analysis the records of patients aged 17-70 years, not taking vasoactive medications, having sitting systolic BP (SBP)o140 mmHg, sitting diastolic BP (DBP) o90 mmHg, and who completed 30 min of tilt. HV was diagnosed when end-tidal pressure of CO 2 o30 mmHg was recorded consecutively for X10 min. Postural hypertension (PHT) was diagnosed when DBP on tilt X90 mmHg was recorded consecutively for X10 min. DBP-change was computed as (median DBP on tilt) À(median DBP supine). PHT and DBP-change were correlated with HV. A total of 320 patient charts were reviewed. PHT was present in 30 cases. The mean DBP-change in patients with PHT was þ 9.9 mmHg (s.d. 5.8), with three patients manifesting HV. Of the remaining 290 patients, 56 had HV, their mean DBP-change was -0.3 mmHg (s.d. 7.2). The other 234 patients without HV had a mean DBP-change þ 0.95 mmHg (s.d. 5.7), comparable to the DBP-change in patients with HV. In, conclusion, posturally induced HV was not associated with an increase in BP, nor was PHT associated with HV, except in a small minority of cases.