Circulatory response to passive and active changes in posture

Abstract

To understand the sequence of hemodynamic events elicited by active (stand-up) and passive (head-up tilt, HUT) changes in posture, we monitored heart rate and arterial blood pressure continuously in ten healthy volunteers at rest, during rapid tilts (7s' HUTover 2 secs), slow tilts (75" HUToverSOsecs), andstand tests. A marked initial transient dmp in mean arterial pressure (MAP) and increase in heart rate (HR) seen during rapid tilt, RZ and stand-up, SU, were absent during slow tilt, SZ While the magnitudes of transient heart rate peak and blood pressure minimum for RT and SU, respectively, were different, their relative timing was well preserved. We attribute the fiming to the response of homeostatic repex mechanisms. No statistically significant difference could be detected when comparing steady-state values of MAP and HR for SU and HUT 140 seconds afer the onset of the respective stress. IntroductionCardiovascular adaptation to the upright posture depends on the proper interplay of the hemodynamic system and the reflex mechanisms that maintain blood pressure homeostasis. Failure of one of the subsystems to adapt to the gravitation-induced shifts in blood volume often results in a collection of clinical symptoms termed orthostatic intolerance (01).Clinically, 01 is diagnosed on the basis of a drop in arterial blood pressure or an excessive increase in heart rate measured a certain time after the assumption of the upright posture. However, little is learned about the mechanisms underlying 0 1 by making a single isolated measurements of MAP and HR at a certain time after onset of gravitational stress. Research done in our laboratory aims at using the information contained in the transient response of hemodynamic variables to gravitational stress to identify mechanisms underlying cardiovascular maladaptation to the upright posture. To achieve this goal, it is necessary to understand better the transient hemodynamic events elicited by an active change in posture and passive changes in posture. Specifically, we are interested in quantifying the degree of similarity between the hemodynamic responses seen during stand up, rapid, and slow head-up tilt. 2. MethodsWe recruited ten healthy volunteers (5 males. 5 females) to participate in this study. The mean age was 28.7f1.2 years, the mean height was 172.8f4.0 cm, and the mean weight was 70.6f4.5 kg'. Participants regularly engaged in light to moderate physical activity and had no sign of cardiovascular disease. Each volunteer gave written, informed consent prior to participation in the study. Each participant was instrumented with a standard clinical ECG monitor and a non-invasive blood pressure monitoring device (FINAPRES). ECG and the arterial pressure waveforms were recorded throughout the duration of the experiment. After instrumentation, subjects rested on a tilt table with foot support and subsequently underwent a series of six changes in posture: two stand-ups, two rapid HUTs (75" HUT over 2 secs), and two slow HUTs (75' HUT over 50 secs) each lasting ...

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“…Our analysis of the heartbeat interval series from the subjects in the tilt-table study showed that the time courses of the mean R-R intervals and the heart rate series follow the well-documented patterns of cardiovascular response to orthostatic stress (7,16,25,26,46,50). Together, the instantaneous heart rate, instantaneous mean R-R interval, R-R standard deviation, and heart rate standard deviation provided a different signature for each of the three types of postural changes ( Fig.…”

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“…4). First, the time courses of the mean R-R intervals and the heart rate series follow the well documented patterns of cardiovascular response to orthostatic stress (Borst et al, 1982;Ewing et al, 1980;Heldt et al, 2002Heldt et al, ,2003Sprangers et al, 2003;Tanaka et al, 1995). In contrast, our heart rate variability series revealed a new pattern of temporal dynamics.…”

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“…The tilt-table test (see Figure 4.top.left) is a simple, noninvasive, and informative test first described in 1986 as a diagnostic tool for patients with syncope of unknown origin [Heldt et al, 2003]. Beyond diagnosing the condition, the test may reveal the cause, neurological disorder, metabolic disorder, mechanical heart disease, cardiac arrhythmias, etc.…”