Recovery of mobility function and life-space mobility after ischemic stroke: the MOBITEC-Stroke study protocol.

BACKGROUND: Stroke is a major cause of disability and stroke incidence increases with age. Stroke frequently results in permanent limitations of mobility, and, consequently, the need for the help of others in activities of daily living. In order to optimize rehabilitative efforts and their functional outcomes, detailed knowledge of the functional recovery process, regarding mobility, is needed. Objectives of the MOBITEC-Stroke study are: 1.) To characterize mobility, including lower extremity physical function (LEPF) and life space (the geospatial extent of all of a person's movements), and changes in mobility within the first year after stroke. 2.) To identify and characterize subgroups with different mobility trajectories. 3.) To evaluate whether changes in LEPF are associated with changes in life-space. 4.) To evaluate participants' reasons for going outdoors, transportation use, and assistance needed for outdoor movement. METHODS: Patients with incident first stroke who live in their own homes (target N = 59, based on sample size calculation) will be included in this cohort study. At 3, 6, 9, and 12 months after stroke a battery of mobility tests will be performed at the study centre, including laboratory-based tests of balance and strength, and quantitative gait analysis. Life-space assessment (including 1-week GPS measurements) will be performed in participants' real life. Semantic information on visited locations (reasons for going outdoors, transportation use, assistance needed) will be collected by using interactive digital maps. Linear mixed effects models will be used to model the trajectories of mobility measures for the total sample and for predefined subgroups. As an exploratory analysis, growth mixture models (GMMs) will be used to identify relevant subgroups with different trajectories. Linear mixed effect models will be used to test whether changes in LEPF parameters are associated with changes in life-space. Participants' motivation for going outdoors, transportation use, and assistance needed for outdoor mobility will be analysed descriptively. DISCUSSION: A comprehensive and detailed knowledge of recovery patterns will enable the planning of targeted and adaptively tailored rehabilitation measures. Information about patients' reasons for outdoor mobility will provide the opportunity to define individualized and patient-oriented rehabilitation goals. TRIAL REGISTRATION: ISRCTN85999967 (on 13 August 2020; retrospectively).

[Security rules in acute inpatient wards in psychiatric hospitals in the greater area of Athens].

This research concerns the recording of safety measures in acute mental health wards of psychiatric hospitals in the greater area of Athens. The practices of control and testing on patients performed by nurses are also reported. The total sample consists of 14 acute inpatient psychiatric wards. The results indicated that important differences were noticed in the controls and prohibitions. Moreover, the main characteristic was the lack of protocols and measures of safety, a situation that burdened nursing practice. The lack of rules and strategies that would promote the safety of patient, professionals and therapeutic milieu, were brought into light by nurses' quotes.

Response of ventilator-dependent patients to different levels of pressure support and proportional assist.

The ventilator's response to the patient's effort is quite different in proportional assist ventilation (PAV) and pressure support ventilation (PSV). We wished to determine whether this results in different ventilatory and breathing pattern responses to alterations in level of support and, if so, whether there are any gas exchange consequences. Fourteen patients were studied. Average elastance (E) was 22.8 (range, 14 -36) cm H2O/L and average resistance (R) was 15. 7 (range, 9-21) cm H2O/L/s. The highest PSV support (PSVmax) was that associated with a tidal volume (VT) of 10 ml/kg (20.4 +/- 3.2 cm H2O), and the highest level of PAV assist (PAVmax) was 78 +/- 7% of E and 76 +/- 7% of R. Level of assist was decreased in steps to the lowest tolerable level (PSVmin, PAVmin). Minute ventilation, VT, ventilator rate (RRvent), and arterial gas tensions were measured at each level. We also determined the patient's respiratory rate (RRpat) by adding the number of ineffective efforts (DeltaRR) to RRvent. There was no difference between PSVmin and PAVmin in any of the variables. At PSVmax, VT was significantly higher (0.90 +/- 0.30 versus 0.51 +/- 0.16 L) and RRvent was significantly lower (13.2 +/- 3.9 versus 27.6 +/- 10.5 min-1) than at PAVmax. The difference in RRvent was largely related to a progressive increase in ineffective efforts on PSV as level increased (DeltaRR 12.1 +/- 10.1 vs 1.4 +/- 2.1 with PAVmax); there was no significant difference in RRpat. The differences in breathing pattern had no consequence on arterial blood gas tensions. We conclude that substantial differences in breathing pattern may occur between PSV and PAV and that these are largely artifactual and related to different patient-ventilator interactions.

Control of breathing during sleep assessed by proportional assist ventilation.

We used proportional assist ventilation (PAV) to evaluate the sources of respiratory drive during sleep. PAV increases the slope of the relation between tidal volume (VT) and respiratory muscle pressure output (Pmus). We reasoned that if respiratory drive is dominated by chemical factors, progressive increase of PAV gain should result in only a small increase in VT because Pmus would be downregulated substantially as a result of small decreases in PCO2. In the presence of substantial nonchemical sources of drive [believed to be the case in rapid-eye-movement (REM) sleep] PAV should result in a substantial increase in minute ventilation and reduction in PCO2 as the output related to the chemically insensitive drive source is amplified severalfold. Twelve normal subjects underwent polysomnography while connected to a PAV ventilator. Continuous positive air pressure (5.2 +/- 2.0 cmH2O) was administered to stabilize the upper airway. PAV was increased in 2-min steps from 0 to 20, 40, 60, 80, and 90% of the subject's elastance and resistance. VT, respiratory rate, minute ventilation, and end-tidal CO2 pressure were measured at the different levels, and Pmus was calculated. Observations were obtained in stage 2 sleep (n = 12), slow-wave sleep (n = 11), and REM sleep (n = 7). In all cases, Pmus was substantially downregulated with increase in assist so that the increase in VT, although significant (P < 0.05), was small 0.08 liter at the highest assist). There was no difference in response between REM and non-REM sleep. We conclude that respiratory drive during sleep is dominated by chemical control and that there is no fundamental difference between REM and non-REM sleep in this regard. REM sleep appears to simply add bidirectional noise to what is basically a chemically controlled respiratory output.

Effects of extrinsic positive end-expiratory pressure on mechanically ventilated patients with chronic obstructive pulmonary disease and dynamic hyperinflation.

OBJECTIVE: To examine the circulatory and respiratory effects of extrinsic positive end-expiratory pressure (PEEPe) in patients with chronic obstructive pulmonary disease (COPD) and dynamic hyperinflation during controlled mechanical ventilation. DESIGN: Different levels of PEEPe were applied randomly in mechanically ventilated patients with COPD and dynamic hyperinflation. SETTING: Respiratory Intensive Care Unit of a University Hospital. PATIENTS: 9 patients with acute respiratory failure and dynamic hyperinflation due to acute exacerbation of COPD. INTERVENTIONS: PEEPe 35%, 58% and 86% of intrinsic PEEP (PEEPi) were applied. MEASUREMENTS AND RESULTS: Using flow-directed pulmonary artery catheters hemodynamic measurements were obtained, while simultaneously lung volumes, airflows and airway pressures were recorded. In order to estimate alveolar pressures (Palv), rapid airway occlusions during passive expiration were also performed. At no level of PEEPe were significant changes in cardiac output, gas exchange variables, dead space, airways inflation resistances and respiratory system static end-inspiratory compliance observed. At high level of PEEPe central venous, mean pulmonary arterial and pulmonary capillary wedge pressures were increased significantly. All but one patient were flow-limited during passive expiration. PEEPe 86% of PEEPi caused a significant increase in end-expiratory lung volume and total PEEP. Iso-volume pressure-flow curves showed volume-dependence expiratory flow limitation in 2 patients, while in 8 patients volume-dependence of critical driving pressure (Palv-mouth pressure) that decreased flows was also observed. CONCLUSIONS: The effects of PEEPe on iso-volume flow and hence on lung mechanics and hemodynamics, depend on many factors, such as airways resistances, lung volumes and airway characteristics, making the patient response to PEEPe unpredictable.

Respiratory short-term poststimulus potentiation (after-discharge) in patients with obstructive sleep apnea.

In conscious normal humans after a brief hypoxic ventilatory stimulus, ventilation slowly decays to baseline and does not undershoot though the subjects are hyperoxic and hypocapnic. This phenomenon is attributed to short-term poststimulus potentiation (STP), which may be an important factor promoting ventilatory stability by preventing periodic breathing. It has been proposed that obstructive sleep apnea (OSA) is a variant of periodic breathing, with obstruction occurring when ventilatory drive is low. If this were the case, patients with OSA might have reduced STP. To test this, seven normal adults and 12 patients with OSA (mean apnea index, 52.4 +/- 6.9 SE events/h) were studied. Ventilation (VI) was measured in awake seated subjects during 30 to 45 s of exposure to hypoxia (end-tidal O2: 50 mm Hg) followed by hyperoxia. A total of 57 hypoxic-hyperoxic runs were analyzed (36 in the patients and 21 in the normal subjects). During hypoxia VI increased and end-tidal CO2 decreased by similar amounts in both groups. In normal subjects after hypoxia there was a gradual decay in VI to prehypoxic levels without an undershoot. In patients, there was on average a ventilatory undershoot at 35 s of hyperoxia, with a mean VI of 83% of baseline. The undershoot was due mainly to a decrease in tidal volume, which was significantly lower than that of the normal subjects for several seconds. These changes were particularly prominent in seven patients who were not different from the others in terms of baseline characteristics, hypoxic responses, and OSA severity.(ABSTRACT TRUNCATED AT 250 WORDS)