Introduction: Hypertension is linked to endothelial dysfunction, but causality and direction is not entirely known. The aim was to study the cross-sectional associations between home, office, and central BP and microcirculatory peak oxygen saturation (OxyP). Methods: In the observational Swedish CArdioPulmonary bioImage Study (SCAPIS) Linköping subsample, office and home BP were measured using an oscillometric device and OxyP was measured in forearm skin after a 5-min occlusion of the brachial artery. A linear regression was fitted to evaluate the mean change in OxyP per SD increase in BP. A logistic regression was fitted to evaluate the associations between BP above the median and OxyP below the median. Results: Of participants, 3,291 were included in the analyses. Per SD increase in systolic home BP, the adjusted mean (95% CI) difference in OxyP was −0.4 (−0.6 to −0.1%). In subgroup analyses, the association remained for women but not men, although the interaction by sex was not statistically significant. Also, in women but not in men, OxyP was lower in those with white coat hypertension vs. sustained normotension, i.e., mean (95% CI) 88.8 (88.2–89.4%) vs. 89.6 (89.3–90.0%), and in those with masked hypertension vs. sustained normotension, i.e., 87.5 (85.9–89.1%) vs. 89.6 (89.3–90.0%). Conclusion: Home BP, which better predicts cardiovascular disease than office BP, was inversely associated with OxyP. This correlation remained in subgroup analyses of women but not men, suggesting possible sex-dependent microcirculatory dysfunction or that masked hypertension could be a more important cardiovascular risk marker in women, despite its higher prevalence in men.

Aims The aim was to investigate the relationship between microvascular function, cardiovascular risk profile, and subclinical atherosclerotic burden. Methods and results The study enrolled 3809 individuals, 50-65 years old, participating in the population-based observational cross-sectional Swedish CArdioPulmonary bioImage Study. Microvascular function was assessed in forearm skin using an arterial occlusion and release protocol determining peak blood oxygen saturation (OxyP). Cardiovascular risk was calculated using the updated Systematic Coronary Risk Evaluation [SCORE2; 10-year risk of fatal and non-fatal cardiovascular disease (CVD) events]. The OxyP was compared with coronary artery calcification score (CACS) and to plaques in the carotid arteries. Individuals with OxyP values in the lowest quartile (Q1; impaired microvascular function) had a mean SCORE2 of 5.8% compared with 3.8% in those with the highest values of OxyP (Q4), a relative risk increase of 53%. The risk of having a SCORE2 > 10% was five times higher for those in Q1 (odds ratio: 4.96, 95% confidence interval: 2.76-8.93) vs. Q4 when adjusting for body mass index and high-sensitivity C-reactive protein. The OxyP was lower in individuals with CACS > 0 and in those with both carotid plaques and CACS > 0, compared with individuals without subclinical atherosclerotic burdens (87.5 +/- 5.6% and 86.9 +/- 6.0%, vs. 88.6 +/- 5.8%, P < 0.01). Conclusion In a population without CVD or diabetes mellitus, impaired microvascular function is associated with cardiovascular risk profiles such as higher SCORE2 risk and CACS. We suggest that OxyP may serve as a microcirculatory functional marker of subclinical atherosclerosis and CVD risk that is not detected by structural assessments.

Medical devices, such as non-invasive ventilation masks, save lives in health care settings but can be a cause of tissue injuries due to the pressure and shear loads on skin and soft tissue. These pressure injuries could be painful for the individual and cause a significant economic impact on healthcare providers. In the etiology of device related pressure ulcers, inflammation plays an important role. However, the exact nature and timing of inflammatory biomarker upregulation is still unknown in the early stages of skin damage. This study aimed to explore the inflammatory profile of vulnerable skin sites following non-invasive mask application on a convenience sample of eleven hospital patients. Seventy-one inflammatory proteins were explored from sebum sampled at the skin surface after oronasal mask application. A multivariate analysis to investigate differences between loaded and control site was conducted, with a protein network analysis used to explore interactions in the early inflammation. The study revealed that 21 cytokines and chemokines were important for the separation between loaded and control site. These proteins were associated with remodeling of tissue, vascular wound healing and/or cell death.

The aim of this study was to investigate nursing staff induced repositionings and the patients' spontaneous movements during the day and night among older immobile patients in nursing care. Furthermore, the aim was to identify factors associated with the nursing staff induced repositionings and the patients' spontaneous movement frequency. An observational cross-sectional design was used. Spontaneous movements among patients (n = 52) were registered continuously using the MovinSense monitoring system. The nursing staff documented each time they repositioned the patient. Patients spontaneous movements were compared with nursing staff induced repositionings. There were large variations in the patients' spontaneous repositioning frequency during both days and nights, which shows that, although immobilised, some patients frequently reposition themselves. Analgesics were positively related to the movement frequency and psycholeptics were negatively related. The nursing staff more often repositioned the patients who were assessed as high risk than those assessed as low risk, but the patients' spontaneous movement frequency was not correlated to the risk score. This may be important when planning repositioning schedules. A monitoring system may be useful in decision making with regard to planning repositioning and positions used in the prevention of pressure ulcers among elderly immobile patients.

Objective: The aim of this study was to explore the interaction between interface pressure and pressure-induced vasodilation and reactive hyperemia with different pressureredistribution mattresses.

Method: A cross-sectional study was performed with a convenience sample of 42 healthy individuals between 18 and 64 years of age, 38 healthy individuals 65 years or older, and 35 inpatients 65 years or older at a university hospital in Sweden. Blood flow was measured at depths of 1 mm, 2 mm, and 10 mm using a combined system of laser Doppler flowmetry and photoplethysmography. The blood flow, interface pressure and skin temperature were measured in the sacral tissue before, during, and after load while lying on one standard hospital mattress and three different pressure-redistribution mattresses.

Results: There were significant differences between the three foam mattresses with regard to average sacral pressure, peak sacral pressure, and local probe pressure with the lowest values at the visco-elastic foam/air mattress (23.5 ± 2.5 mmHg, 49.3 ± 11.1 mmHg, 29.2 ± 14.0 mmHg respectively). A greater proportion of subjects had affected blood flow in terms of lack of pressure-induced vasodilation on the visco-elastic foam/air mattress compared to the alternating pressure mattress at tissue depths of 2 mm (39.0% vs. 20.0%, respectively) and 10 mm (56.9 % vs. 35.1%, respectively). Eleven individuals, including subjects in all three subject groups were identified with no pressure-induced vasodilation or reactive hyperemia in any mattress, and this was considered a high-risk blood flow response.

Conclusion: Interface pressure magnitudes considered not harmful during pressure-exposure lying on different pressure-redistribution mattresses can affect the microcirculation in different tissue structures. Despite having the lowest pressure values compared to the other mattresses, the visco-elastic foam/air mattress had the highest proportion of subjects with decreased blood flow indicating a more affected blood flow. Three young healthy individuals were identified with the high-risk blood flow response, indicating an innate vulnerability to pressure exposure and may not benefit from pressure-redistribution mattresses. Finally it was shown that the evaluation of pressure-redistribution support surfaces in terms of mean blood flow during and after tissue exposure is not feasible but assessment of pressure-induced vasodilation and reactive hyperemia could be a new possibility to assess individualized physiological measurements of mechanisms known to be related to pressure ulcer development.

Background. Pressure induced vasodilation (PIV) protects the skin from pressure induced ischemia. PIV responses at individual level during a long-term measurement period have not previously been described in an elderly population in a clinically relevant situation.

Aim. To describe individual PIV responses in a nursing home resident population for 1-hour periods of bed rest.

Method. From May 2011 to August 2012, blood flow at three tissue depths was measured for one hour over the sacrum in 0° supine position and 30° supine tilt position in 25 individuals aged 65 years or older while lying on a pressure redistributing mattress. Measurements were made using the non-invasive optical techniques Laser Doppler Flowmetry (LDF) and photoplethysmography. The individuals were divided into a PIV group and a non-PIV group based upon the LDF data.

Results. In the PIV group, the blood flow in almost all cases increased immediately and remained over baseline for the entire 60 minutes of loading in both positions, while the blood flow decreased immediately and remained below baseline in the non-PIV group. These blood flow patterns were also seen in deeper tissue layers although a PIV response was most common in the underlying tissue in both groups.

Conclusion. The cutaneous blood flow response among the nursing home residents was distinct, appeared early and remained during the one hour of loading in both the PIV and non-PIV group. The non-PIV group may be more vulnerable to pressure and thus may be at risk for pressure ulcer development. More research is needed in order to verify the results.

Background: Although repositioning is considered an important intervention to prevent pressure ulcers, tissue response during loading in different lying positions has not been adequately explored.

Aim: To compare the effects of different lying positions on interface pressure, skin temperature, and tissue blood flow in nursing home residents.

Method: From May 2011 to August 2012, interface pressure, skin temperature, and blood flow at three tissue depths were measured for 1 hr over the sacrum in 30 supine tilt and 0 supine positions and over the trochanter major in 30lateral and 90lateral positions in 25 residents aged 65 years or older. Measurement of interface pressure was accomplished using a pneumatic pressure transmitter connected to a digital manometer, skin temperature using a temperature sensor, and blood flow using photoplethysmography and laser Doppler flowmetry.

Results: Interface pressure was significantly higher in the 0supine and 90lateral positions than in 30supine tilt and 30 lateral positions. The mean skin temperature increased from baseline in all positions. Blood flow was significantly higher in the 30 supine tilt position compared to the other positions. A hyperemic response in the post pressure period was seen at almost all tissue depths and positions.

Conclusion: The 30supine tilt position generated less interface pressure and allowed greater tissue perfusion, suggesting that this position is the most beneficial.

OBJECTIVE: To characterize pressure-induced vasodilatation and reactive hyperemia at different sacral tissue depths in different populations under clinically relevant pressure exposure.

METHODS: Forty-two subjects (< 65 years), 38 subjects (≥ 65 years), and 35 patients (≥ 65 years) participated. Interface pressure, skin temperature, and blood flow at tissue depths of 1 mm, 2 mm, and 10 mm (using laser Doppler flowmetry and photoplethysmography) were measured in the sacral tissue before, during, and after load in a supine position.

RESULTS: pressure-induced vasodilatation and reactive hyperemia were observed at three tissue depths. At 10 mm depth, the proportion of subjects with a lack of pressure-induced vasodilatation was higher compared to superficial depths. The patients had higher interface pressure during load than the healthy individuals, but there were no significant differences in blood flow. Twenty-nine subjects in all three study groups were identified with a lack of pressure-induced vasodilatation and reactive hyperemia.

CONCLUSIONS: pressure-induced vasodilatation and reactive hyperemia can be measured at different tissue depths. A lack of these responses was found in healthy individuals as well as in patients indicating an innate susceptibility in some individuals, and are potential important factors to evaluate in order to better understand the etiology of pressure ulcers.

The overall aim of this thesis was to combine optical methods into a system with the ability to simultaneously measure blood flow changes at different tissue depths. The goal of such a system was to reveal vascular mechanisms relevant to pressure ulcer etiology under clinically relevant conditions and in relation to the evaluation of pressure-redistribution support surfaces.

This thesis consists of four quantitative, cross-sectional studies measuring blood flow responses before, during, and after pressure exposure of the sacral tissue. Two optical methods – photoplethysmography and laser Doppler flowmetry – were combined in a newly developed system that has the ability to discriminate blood flows at different tissue depths. Studies I and II explored blood flow responses at different depths in 17 individuals. In Study I the blood flow was related to tissue thickness and tissue compression during pressure exposure of ≥ 220 mmHg. In Study II, the sacral tissue was loaded with 37.5 mmHg and 50.0 mmHg, and the variation in blood flow was measured. Studies III and IV included 42 healthy individuals < 65 years, 38 healthy individuals ≥ 65 years, and 35 patients ≥ 65 years. Study III included between-subject comparisons of blood flow and pressure between individuals in the three study groups lying in supine positions on a standard hospital mattress. Study IV added within-subject comparisons while the individual was lying on four different types of mattress. The studies explored the vascular phenomena pressure-induced vasodilation (PIV) and reactive hyperemia (RH).

The most common blood flow response to tissue exposure in this thesis was PIV, although a decrease in blood flow (a lack of PIV) was observed in some individuals. The patients tended to have higher interface pressure during pressure exposure than the healthy groups but no differences in blood flow responses were seen. Our results showed that pressure levels that are normally considered to be harmless could have a significant effect on the microcirculation in different tissue structures. Differences in individual blood flow responses in terms of PIV and RH were seen, and a larger proportion of individuals lacked these responses in the deeper tissue structures compared to more superficial tissue structures.

This thesis identified PIV and RH that are important vascular mechanisms for pressure ulcer development and revealed for the first time that PIV and RH are present at different depths under clinically relevant conditions. The thesis also identified a population of individuals not previously identified who lack both PIV and RH and seem to be particularly vulnerable to pressure exposure. Further, this thesis has added a new perspective to the microcirculation in pressure ulcer etiology in terms of blood flow regulation and endothelial function that are anchored in clinically relevant studies. Finally, the evaluation of pressureredistribution support surfaces in terms of mean blood flow during and after tissue exposure was shown to be unfeasible, but the assessment of PIV and RH could provide a new possibility for measuring individual physiological responses that are known to be related to pressure ulcer development.