Assessment Of Blood Pressure Regulatory Controls To Detect Hypovolemia And Orthostatic Intolerance

Regulation of blood pressure is vital for maintaining organ perfusion and homeostasis. A significant decline in arterial blood pressure could lead to fainting and hypovolemic shock. In contrast to young and healthy, people with impaired autonomic control due to aging or disease find regulating blood pressure rather demanding during orthostatic challenge. This thesis performed an assessment of blood pressure regulatory controls during orthostatic challenge via traditional as well as novel approaches with two distinct applications 1) to design a robust automated system for early identification of hypovolemia and 2) to assess orthostatic tolerance in humans. In chapter 3, moderate intensity hemorrhage was simulated via lower-body negative pressure (LBNP) with an aim to identify moderate intensity hemorrhage (-30 and -40 mmHg LBNP) from resting baseline. Utilizing features extracted from common vital sign monitors, a classification accuracy of 82% and 91% was achieved for differentiating -30 and -40 mmHg LBNP, respectively from baseline. In chapter 4, cause-and-effect relationship between the representative signals of the cardiovascular and postural systems to ascertain blood pressure homeostasis during standing was performed. The degree of causal interaction between the two systems, studied via convergent cross mapping (CCM), showcased the existence of a significant bi-directional interaction between the representative signals of two systems to regulate blood pressure. Therefore, the two systems should be accounted for jointly when addressing physiology behind fall. Further, in chapter 5, the potential of artificial gravity (2-g) induced via short-arm human centrifuge at feet towards evoking blood pressure regulatory controls analogous to standing was investigated. The observation of no difference in the blood pressure regulatory controls, during 2-g centrifugation compared to standing, strongly supported the hypothesis of artificial hypergravity for mitigating cardiovascular deconditioning, hence minimizing post-flight orthostatic intolerance

Significant Role of the Cardiopostural Interaction in Blood Pressure Regulation During Standing

Cardiovascular and postural control systems have been studied independently despite the increasing evidence showing the importance of cardio-postural interaction in blood pressure regulation. In this study, we aimed to assess the role of cardio-postural interaction in relation to cardiac baroreflex in blood pressure regulation under orthostatic stress before and after mild exercise. Physiological variables representing cardiovascular control (heart rate and systolic blood pressure), lower limb muscle activation (electromyography), and postural sway (center of pressure derived from force and moment data during sway) were measured from 17 healthy participants (25±2 years; 8 females) during a sit-to stand test before and after sub-maximal exercise. The cardio-postural control (characterized by baroreflex-mediated muscle-pump effect in response to blood pressure changes, i.e., muscle-pump baroreflex) was assessed using wavelet transform coherence and causality analyses in relation to the baroreflex control of heart rate. Significant cardio-postural blood pressure control was evident counting for almost half of the interaction time with blood pressure changes that observed in the cardiac baroreflex (36.6-72.5% pre-exercise and 34.7-53.9% post-exercise). Thus, cardio-postural input to blood pressure regulation should be considered when investigating orthostatic intolerance. A reduction of both cardiac and muscle-pump baroreflexes in blood pressure regulation was observed post-exercise and was likely due to the absence of excessive venous pooling and a less stressed system after mild exercise. With further studies using more effective protocols evoking venous pooling and muscle-pump activity, the cardio-postural interaction could improve our understanding of the autonomic control system and ultimately lead to a more accurate diagnosis of cardio-postural dysfunctions

Skeletal Muscle Pump Drives Control of Cardiovascular and Postural Systems

The causal interaction between cardio-postural-musculoskeletal systems is critical in maintaining postural stability under orthostatic challenge. The absence or reduction of such interactions could lead to fainting and falls often experienced by elderly individuals. The causal relationship between systolic blood pressure (SBP), calf electromyography (EMG), and resultant center of pressure (COPr) can quantify the behavior of cardio-postural control loop. Convergent cross mapping (CCM) is a non-linear approach to establish causality, thus, expected to decipher nonlinear causal cardio-postural-musculoskeletal interactions. Data were acquired simultaneously from young participants (25 ± 2 years, n = 18) during a 10-minute sit-to-stand test. In the young population, skeletal muscle pump was found to drive blood pressure control (EMG → SBP) as well as control the postural sway (EMG → COPr) through the significantly higher causal drive in the direction towards SBP and COPr. Furthermore, the effect of aging on muscle pump activation associated with blood pressure regulation was explored. Simultaneous EMG and SBP were acquired from elderly group (69 ± 4 years, n = 14). A significant (p = 0.002) decline in EMG → SBP causality was observed in the elderly group, compared to the young group. The results highlight the potential of causality to detect alteration in blood pressure regulation with age, thus, a potential clinical utility towards detection of fall proneness

Cardio-postural Interactions and Muscle-pump Baroreflex Are Severely Impacted by 60-day Bedrest Immobilization

To understand fundamental mechanisms associated with post-flight orthostatic intolerance we investigated the interaction between the cardiovascular and postural functions before and after 60 days of head down bedrest (HDBR). Twenty healthy young males (35.0 ± 1.7 years) were subjected to 60-day HDBR at 6˚ to simulate spaceflight-induced fluid shifts. A supine-to-stand (STS) test was conducted to evaluate cardio-postural control before and after (R) HDBR while an assessment of cardiovascular function was performed during HDBR. Beat-to-beat heart period, systolic blood pressure, and electromyography impulses were derived for wavelet transform coherence and causality analyses of the cardio-postural control and used to assess changes in the muscle-pump baroreflex. During quiet stand of the STS test, compared to baseline, heart rate was 50% higher on the day of exit from bedrest (R0) and 20% higher eight days later (R8). There was a 50% increase in deoxygenated hemoglobin on R0 and R8. Leg muscle activity reduced, and postural sway increased after HDBR. Causality of the muscle-pump baroreflex was reduced on R0 (0.73 ± 0.2) compared to baseline (0.87 ± 0.2) with complete recovery by R8. The muscle-pump baroreflex also had decreased gain and fraction time active following HDBR. Overall, our data show a significantly impaired muscle-pump baroreflex following bedrest

Effect of Aging on Muscle-Pump Baroreflex of Individual Leg Muscles During Standing

Activation of leg muscles is an important component in the regulation of blood pressure during standing, failure of which could result in syncope and falls. Our previous work demonstrated baroreflex mediated activation of leg muscles (muscle-pump baroreflex) as an important factor in the regulation of blood pressure during standing; however, the effect of aging on the muscle-pump baroreflex of individual leg muscles during standing remains to be understood. Here, the interaction between systolic blood pressure (SBP) and the activation of lateral gastrocnemius (LG), medial gastrocnemius (MG), tibialis anterior (TA), and soleus (SOL) muscles during standing was quantified. Beat-to-beat heart period (RR interval), SBP, electromyography impulse (EMGimp) were derived from continuously acquired electrocardiography, finger blood pressure, and calf-electromyography, respectively. The cardiac baroreflex (SBP→RR) causality (0.88 ± 0.08 vs. 0.94 ± 0.03, p = 0.01), percent time with significant coherence (%SC: 50.95 ± 23.31 vs. 76.75 ± 16.91, p = 0.001), and gain (4.39 ± 4.38 vs. 13.05 ± 8.11, p < 0.001) was lower in older (69 ± 4 years) compared to young (26 ± 2 years) persons. Muscle-pump baroreflex (SBP→EMGimp) causality of LG (0.81 ± 0.08 vs. 0.88 ± 0.05, p = 0.01) and SOL (0.79 ± 0.11 vs. 0.88 ± 0.04, p = 0.01) muscles was lower in older compared to young persons. %SC was lower for all muscles in the older group (LG, p < 0.001; MG, p = 0.01; TA, p = 0.01; and SOL, p < 0.001) compared to young. The study outcomes highlighted impairment in muscle-pump baroreflex with age in addition to cardiac baroreflex. The findings of the study can assist in the development of an effective system for monitoring orthostatic tolerance via cardiac and muscle-pump baroreflexes to mitigate syncope and falls

Sensorimotor postural control in healthy and pathological stance and gait

Postural control during standing and walking is an inherently unstable task requiring the interaction of various biomechanical, sensory, and neurophysiological mechanisms to shape stable patterns of whole-body coordination that are able to counteract postural disequilibrium. This thesis focused on the examination of central aspects of the functional roles of these mechanisms and the modes of interaction between them. A further aim was to determine the conditions of dynamic stability for healthy standing and walking performance as well as for certain balance and gait disorders. By studying movement fluctuations in the walking pattern it could be demonstrated that dynamic stability during walking depends on gait speed and is differentially regulated for the medio-lateral and the fore-aft walking planes. Stability control in the fore-aft walking plane exhibits attractor dynamics typical for a dynamical system. Accordingly, the most stable pattern of movement coordination in terms of minimal fluctuations in the order parameter (i.e., the relative phase between the two oscillating legs) can be observed at the attractor of self-paced walking. Critical fluctuations occur at increasingly non-preferred speeds, indicating a loss of dynamic gait stability close to the speed boundaries of the walking mode. Moreover, stability control during slow walking is critically dependent on sensory feedback control, whereas dynamic stability during fast walking relies mainly on the smooth operation of cerebellar pacemaker regions. Disturbances of sensory and cerebellar locomotor control in certain gait disorders could be further linked to a loss of dynamic gait stability, in particular an increased risk of falls. Furthermore, this thesis examined alterations in the sensorimotor postural control scheme that may trigger the experience of subjective imbalance and vertigo in the conditions of phobic postural vertigo and visual height intolerance. Both conditions are characterized by an inadequate mode of balance regulation featuring increased levels of open-loop balance control and a precipitate integration of closed-loop sensory feedback into the postural control scheme. This inadequate balance control strategy is accompanied by a stiffening of the anti-gravity musculature and is elicited by specific influences of attention and sensory feedback control. The findings of this thesis contribute to the understanding of central sensorimotor mechanisms involved in the control of dynamic postural stability during standing and walking. They further provide relevant information for the differential diagnosis and fall risk estimation of certain balance and gait disorders

Sensorimotor postural control in healthy and pathological stance and gait

Postural control during standing and walking is an inherently unstable task requiring the interaction of various biomechanical, sensory, and neurophysiological mechanisms to shape stable patterns of whole-body coordination that are able to counteract postural disequilibrium. This thesis focused on the examination of central aspects of the functional roles of these mechanisms and the modes of interaction between them. A further aim was to determine the conditions of dynamic stability for healthy standing and walking performance as well as for certain balance and gait disorders. By studying movement fluctuations in the walking pattern it could be demonstrated that dynamic stability during walking depends on gait speed and is differentially regulated for the medio-lateral and the fore-aft walking planes. Stability control in the fore-aft walking plane exhibits attractor dynamics typical for a dynamical system. Accordingly, the most stable pattern of movement coordination in terms of minimal fluctuations in the order parameter (i.e., the relative phase between the two oscillating legs) can be observed at the attractor of self-paced walking. Critical fluctuations occur at increasingly non-preferred speeds, indicating a loss of dynamic gait stability close to the speed boundaries of the walking mode. Moreover, stability control during slow walking is critically dependent on sensory feedback control, whereas dynamic stability during fast walking relies mainly on the smooth operation of cerebellar pacemaker regions. Disturbances of sensory and cerebellar locomotor control in certain gait disorders could be further linked to a loss of dynamic gait stability, in particular an increased risk of falls. Furthermore, this thesis examined alterations in the sensorimotor postural control scheme that may trigger the experience of subjective imbalance and vertigo in the conditions of phobic postural vertigo and visual height intolerance. Both conditions are characterized by an inadequate mode of balance regulation featuring increased levels of open-loop balance control and a precipitate integration of closed-loop sensory feedback into the postural control scheme. This inadequate balance control strategy is accompanied by a stiffening of the anti-gravity musculature and is elicited by specific influences of attention and sensory feedback control. The findings of this thesis contribute to the understanding of central sensorimotor mechanisms involved in the control of dynamic postural stability during standing and walking. They further provide relevant information for the differential diagnosis and fall risk estimation of certain balance and gait disorders

Vestibular symptoms and relations with postural balance, inner ear function, and long term survival

Bakgrunn: Svimmelhet og balanseproblemer er vanlige symptomer som i befolkningsstudier har vært assosiert med økt dødelighet, men det er ikke kjent om det er sykdommer i balanseapparatet som forårsaker denne økte dødeligheten. Kunnskapsgrunnlaget for å vurdere og behandle pasienter med svimmelhet har vært vurdert som dårlig og ofte er det kun pasientens beskrivelse av symptomer som danner grunnlaget for å diagnostikken. Mål: Å evaluere hvilke symptomer som gir nyttig informasjon, og undersøke sammenhenger mellom balanse, funksjonen av det indre øre og langtidsoverlevelse. Materialer og metode: En gruppe pasienter henvist for vurdering med tanke på vestibulær sykdom i perioden mellom 1992 og 2004. Resultater: De fleste pasienter (72,1%) valgte kun en tids-kategori for å beskrive sine symptomer, mens mindre enn halvparten (47,1%) valgte kun en type svimmelhet. Oppkast var assosiert med økt risiko for asymmetri på kalorisk prøve (odds ratio 1,50. 95% konfidensintervall 1,24-2,06). 10-dB økning i hørselstap på det best hørende øret var assosiert med 6,0% økning i kurvelengde. Standardisert mortalitetsrate var 1,03 (0,94-1,12). Periodiske eller korte anfall av svimmelhet var assosiert med redusert dødelighet med hasard rate på henholdsvis 0,62 (0,50-0,77) og 0,76 (0,63-0,93). Pasient-rapportert ustøhet og ustøhet målt ved posturografi var assosiert med økt dødelighet med hasard rate på 1,30 (1,08-1,47) og 1,44 (1,14 – 1,82). Konklusjon: Det bør fokuseres på tidsaspektet av vestibulære symptomer og det bør skilles mellom oppkast og kvalme. Hvilken type svimmelhet pasienten opplever gir noe tilleggsinformasjon, men virker ikke å være nyttig for å kunne gruppere pasienter. Vestibulær sykdom kunne ikke forklare sammenhengen mellom hørsel og balanse i denne studien og vestibulær sykdom ser ikke ut til å være hovedårsaken til den økte dødeligheten blant personer med svimmelhet og balanseplager i den generelle befolkningen. For å finne årsakssammenhenger er det behov for ytterligere studier på dødsårsaker blant pasienter med vestibulære symptomer, vestibulær sykdom, dårlig balanse og nedsatt hørsel.Background: Dizziness and unsteadiness are common symptoms that can be caused by pathologies in various organ-systems. In the general population such symptoms are associated with increased mortality, but it is not known if this increased mortality is caused by vestibular pathology. Today, many of the common vestibular diagnoses depend on patient-reported symptoms alone, and the evidence base for evaluating and treating patients with dizziness has been described as low. Aim: To critically evaluate which symptoms reported by dizzy patients provide useful information, and further to evaluate the interrelations between posturography, inner ear function, and long-term survival. Material and methods: A cohort of patients examined from 1992 to 2004 at an otolaryngology department for suspected vestibular disorder. Results: While most patients (72.1%) chose only one timing category, fewer than half the patients (47.1%) describe their complaints with only one type of dizziness. Vomiting was associated with increased risk for caloric asymmetry (Odds ratio 1.60, 95 % CI 1.24–2.06). A 10-dB increase in hearing loss in the best-hearing ear was associated with a 6.0% increase in path length measured on a balance platform. The standardized mortality ratio was 1.03 (0.94–1.12). Periodic or short attacks of dizziness were associated with reduced mortality with a hazard ratio of 0.62 (0.50–0.77) and 0.76 (0.63–0.93), respectively. Both self-reported and unsteadiness on posturography were associated with increased mortality with a hazard ratio of 1.30 (1.08–1.47) and 1.44 (1.14–1.82). Conclusions: The timing of vestibular symptoms and a differentiation between nausea and vomiting should be targeted when interviewing patients. The type of dizziness provides additional information but does not appear useful for categorization. The association between hearing and postural balance was not explained by unilateral vestibular disorders. Vestibular pathology is probably not the main cause of the increased mortality seen among patients with vestibular symptoms and balance problems in the general population. Further studies exploring cause of death related to vestibular symptoms, hearing, and postural balance are advocated.Doktorgradsavhandlin

The relationships of prolonged standing induced low back pain development with lumbopelvic posture and movement patterns

Over 80% of individuals will suffer from low back pain at least once in their lifetime. The cause within the population is not homogenous, leading to sub-classifications of non-specific low back pain. One such sub-classification is low back pain in response to prolonged standing. Over 50% of people who have never suffered a low back injury will develop transient low back pain when completing a prolonged standing occupational simulation where there is no option to sit. Many service and manufacturing tasks require prolonged standing and the introduction of sit-stand desks into the office workplace means that even more workers will be standing on the job. Many workplace health and safety societies recommend the use of standing aids to prevent the negative effects of prolonged standing; however, very few of these standing aids have been validated. Currently, it is difficult to provide advice for people who perform these jobs and get low back pain, as we still do not know enough about the origins of this pain. As a result, the purpose of this thesis was to investigate the relationships of prolonged standing induced low back pain development with lumbopelvic postures and movement patterns. The four specific questions asked were (1) Are movement patterns different between pain and non-pain developers (2) Do pain and non-pain developers have different lumbopelvic postures? (3) How do different foot positions alter lumbopelvic posture?, and (4) Can a standing aid that alters posture or movement patterns prevent low back pain development in standing? Study #1: Previous research points to the lack of movement during prolonged standing as a pre-disposing factor to low back pain. Such movements could be at the level of the lumbar spine or at the foot-ground interface. The primary purpose of this in vivo study was to determine if there were differences in magnitude, region, and frequency of movement patterns between pain and non-pain developers. Thirty-two participants reported their low back pain development using a visual analogue scale over 2-hrs of prolonged standing. Time-varying lumbar spine kinematics were used to assess the magnitude and frequency of lumbar spine fidgets and shifts. Ground reaction forces were used to assess the magnitude and frequency of whole body weight transfers and anterior-posterior center of pressure movements. Fourteen of 32 participants (43.75%) were categorized as pain developers. The first 15 minutes of standing distinguished the two pain groups, as non-pain developers performed a higher frequency of lumbar spine flexion/extension fidgets and large body weight transfers. Both of these differences may be pre-disposing factors for transient low back pain development, as they both occurred prior to pain developers reaching the 10 mm visual analog scale threshold for low back pain classification. Study #2: The purpose of this study was to investigate differences in lumbar posture between 17 participants categorized as a pain or non-pain developers during level ground standing. A secondary purpose was to evaluate the influence of two standing aids (an elevated surface to act as a foot rest and declined sloped surface) on lumbopelvic posture. Four sagittal plane radiographs were taken– a normal standing position on level ground, when using an elevated foot rest and declined sloped surface, and maximum lumbar spine extension to act as a reference posture. Lumbosacral lordosis, total lumbar lordosis, and individual intervertebral joint angles were measured on each radiograph. On level ground, pain developers stood closer to their maximum lumbosacral lordosis and L5/S1 intervertebral joint maximum extension angles. The elevated surface was most effective at causing lumbosacral lordosis flexion, while the declined surface was more effective at inducing L1/L2 intervertebral joint flexion. The differences between the posture and the influence of standing aids point to postural characteristics as a factor influencing pain development. Study #3: While it is common to assess postural characteristics that may predispose a person to low back pain, these measures do not capture valuable information on the intrinsic properties of the lumbar spine, such as stiffness. The purpose of this study was to assess the relationship between the in vivo lumbar spine lumped passive stiffness and the location of the neutral zone with the self-selected lumbar spine angle of pain and non-pain developers in four standing postures. Twenty-two participants with known pain group status stood in four postures for 5 minutes each: on level ground, while resting a foot on an elevated surface, with their feet staggered, and on a sloped decline. Median lumbar spine angle was calculated for each position. Participants were then placed in a near-frictionless jig and brought through passive lumbar spine extension and flexion to characterize their passive stiffness curve and location of their neutral zone. Overall, pain developers stood with a lumbar spine angle that was further beyond their passive lumbar spine neutral zone than non-pain developers. Not all aids thought to be successful at reducing low back pain worked in a similar manner, as only the elevated surface brought the lumbar spine into flexion and closer to the passive neutral zone. As a result, pain developers may be standing in a position that puts higher mechanical loads on the passive tissues of the lumbar spine. While flexion was induced by the elevated surface, the lack of changes caused by the sloped surface signal that there may be other postural changes other than just altered lumbar spine angle that are important for reducing low back pain. Study #4: While alternating standing position on a declined and inclined surface has proven successful at reducing low back pain during standing, the purpose of this study was to evaluate standing solely on a declining sloped surface to isolate the influence of the postural change alone. Seventeen participants performed two 75-minute prolonged standing occupational simulations in a random order – one on level ground and one a declining surface. Fifty-three percent of participants (9/17) were categorized as pain developers during the level ground standing condition; however, the average maximum pain scores of pain developers were 58% lower during sloped standing. All participants showed hip joint flexion, trunk-to-thigh angle flexion, and posterior translation of the trunk center of gravity towards the ankle joint when standing on the sloped surface compared to level ground. These postural changes could cause the muscles crossing the posterior aspect of the hip joint to increase their passive stiffness and assist with stabilizing the pelvis. This study stresses the importance of hip kinematics, not just lumbar spine posture alone, in reducing low back pain during prolonged standing. General Conclusions: The differences in posture of the lower lumbar arc between pain groups, the influence of standing aids on posture, and lower self-reported low back pain reports with a change in posture point to postural differences between the pain groups as being responsible for prolonged standing induced low back pain development. A working hypothesis for pain development is that when standing on level ground, pain developers stand with their lower lumbar arc closer to its end range of extension, placing additional mechanical load on the posterior elements of the lumbar spine resulting in transient pain. When mild flexion is induced, the mechanical load on these tissues would be decreased – a potential reason that low back pain is decreased as well. Future work should focus on lower lumbar arc and hip posture differences between the pain groups and alternative interventions that do not require a physical standing aid to reduce pain development. These include further assessment of the staggered standing position and the influence of an exercise intervention on posture and movement patterns