A practical approach to the theoretical models to calculate NO parameters of the respiratory system.

Expired nitric oxide (NO) is used as a biomarker in different respiratory diseases. The recommended flow rate of 50 mL s⁻¹ (F(E)NO0.05) does not reveal from where in the lung NO production originated. Theoretical models of NO transfer from the respiratory system, linear or nonlinear approaches, have therefore been developed and applied. These models can estimate NO from distal lung (alveolar NO) and airways (bronchial flux). The aim of this study was to show the limitation in exhaled flow rate for the theoretical models of NO production in the respiratory system, linear and nonlinear models. Subjects (n = 32) exhaled at eight different flow rates between 10-350 mL s⁻¹ for the theoretical protocols. Additional subjects (n = 32) exhaled at tree flow rates (20, 100 and 350 mL s⁻¹) for the clinical protocol. When alveolar NO is calculated using high flow rates with the linear model, correction for axial back diffusion becomes negligible, -0.04 ppb and bronchial flux enhanced by 1.27. With Högman and Meriläinen algorithm (nonlinear model) the corrections factors can be understood to be embedded, and the flow rates to be used are ≤20, 100 and ≥350 mL s⁻¹. Applying these flow rates in a clinical setting any F(E)NO can be calculated necessitating fewer exhalations. Hence, measured F(E)NO0.05 12.9 (7.2-18.7) ppb and calculated 12.9 (6.8-18.7) ppb. In conclusion, the only possibility to avoid inconsistencies between research groups is to use the measured NO values as such in modelling, and apply tight quality control to accuracies in both NO concentration and exhaled flow measurements.

Methods of NO detection in exhaled breath.

There is still an unexplored potential for exhaled nitric oxide (NO) in many clinical applications. This study presents an overview of the currently available methods for monitoring NO in exhaled breath and the use of the modelling of NO production and transport in the lung in clinical practice. Three technologies are described, namely chemiluminescence, electrochemical sensing and laser-based detection with their advantages and limitations. Comparisons are made in terms of sensitivity, time response, size, costs and suitability for clinical purposes. The importance of the flow rate for NO sampling is discussed from the perspective of the recent recommendations for standardized procedures for online and offline NO measurement. The measurement of NO at one flow rate, such as 50 ml s(-1), can neither determine the alveolar site/peripheral contribution nor quantify the difference in NO diffusion from the airways walls. The use of NO modelling (linear or non-linear approach) can solve this problem and provide useful information about the source of NO. This is of great value in diagnostic procedures of respiratory diseases and in treatment with anti-inflammatory drugs.

Effects of improper source coupling in frequency-domain near-infrared spectroscopy.

Currently, there is no widely used method to assess the reliability of contact between optodes and tissue in near-infrared spectroscopy (NIRS). In this study we observe a high linear dependence (R(2) approximately 0.99) of the logarithmic modulation amplitude (ln(I(AC))), average intensity (ln(I(DC))) and phase (phi) on the source-detector distance (SDD) ranging from approximately 20 to 50 mm on human forehead measurements. The regression of phi is clearly reduced in measurements where light leakage occurs, mainly due to insufficient contact between the source optode and tissue. Utilizing this observation, a novel criterion to detect light leakage is developed. The criterion is applied to study the reliability of hemodynamic responses measured on the human forehead when breathing carbon dioxide-enriched air and during hyperventilation. The contrast of the signals is significantly lower in measurements which were adversely affected by light leakage. Furthermore, such unreliable signals at SDDs >or= 50 mm correlate significantly (for [HbO2] p < 0.01 and for [HbR] p < 0.001) better with the signals measured at SDDs < 20 mm. Using this method, poor contact between the source optode and tissue can be detected and corrected before the actual measurement, which enables us to avoid the acquisition of low contrast cortical signals.

Electroencephalogram spindle activity during dexmedetomidine sedation and physiological sleep.

BACKGROUND: Dexmedetomidine, a selective alpha(2)-adrenoceptor agonist, induces a unique, sleep-like state of sedation. The objective of the present work was to study human electroencephalogram (EEG) sleep spindles during dexmedetomidine sedation and compare them with spindles during normal physiological sleep, to test the hypothesis that dexmedetomidine exerts its effects via normal sleep-promoting pathways. METHODS: EEG was continuously recorded from a bipolar frontopolar-laterofrontal derivation with Entropy Module (GE Healthcare) during light and deep dexmedetomidine sedation (target-controlled infusions set at 0.5 and 3.2 ng/ml) in 11 healthy subjects, and during physiological sleep in 10 healthy control subjects. Sleep spindles were visually scored and quantitatively analyzed for density, duration, amplitude (band-pass filtering) and frequency content (matching pursuit approach), and compared between the two groups. RESULTS: In visual analysis, EEG activity during dexmedetomidine sedation was similar to physiological stage 2 (S2) sleep with slight to moderate amount of slow-wave activity and abundant sleep spindle activity. In quantitative EEG analyses, sleep spindles were similar during dexmedetomidine sedation and normal sleep. No statistically significant differences were found in spindle density, amplitude or frequency content, but the spindles during dexmedetomidine sedation had longer duration (mean 1.11 s, SD 0.14 s) than spindles in normal sleep (mean 0.88 s, SD 0.14 s; P=0.0014). CONCLUSIONS: Analysis of sleep spindles shows that dexmedetomidine produces a state closely resembling physiological S2 sleep in humans, which gives further support to earlier experimental evidence for activation of normal non-rapid eye movement sleep-promoting pathways by this sedative agent.

Assessment of surgical stress during general anaesthesia.

BACKGROUND: Inadequate analgesia during general anaesthesia may present as undesirable haemodynamic responses. No objective measures of the adequacy of analgesia exist. We aimed at developing a simple numerical measure of the level of surgical stress in an anaesthetized patient. METHODS: Sixty and 12 female patients were included in the development and validation data sets, respectively. All patients had elective surgery with propofol-remifentanil target controlled anaesthesia. Finger photoplethysmography and electrocardiography waveforms were recorded throughout anaesthesia and various waveform parameters were extracted off-line. Total surgical stress (TSS) for a patient was estimated based on stimulus intensity and remifentanil concentration. The surgical stress index (SSI) was developed to correlate with the TSS estimate in the development data set. The performance of SSI was validated within the validation data set during and before surgery, especially at skin incision and during changes of the predicted remifentanil effect-site concentration. RESULTS: SSI was computed as a combination of normalized heart beat interval (HBI(norm)) and plethysmographic pulse wave amplitude (PPGA(norm)): SSI = 100-(0.7*PPGA(norm)+0.3*HBI(norm)). SSI increased at skin incision and stayed higher during surgery than before surgery; SSI responded to remifentanil concentration changes and was higher at the lower concentrations of remifentanil. CONCLUSIONS: SSI reacts to surgical nociceptive stimuli and analgesic drug concentration changes during propofol-remifentanil anaesthesia. Further validation studies of SSI are needed to elucidate its usefulness during other anaesthetic and surgical conditions.

Extended NO analysis in asthma.

The discovery of the flow dependence of exhaled NO made it possible to model NO production in the lung. The linear model provides information about the maximal flux of NO from the airways and the alveolar concentrations of NO. Nonlinear models give additional flow-independent parameters such as airway diffusing capacity and airway wall concentrations of NO. When these models are applied to patients with asthma, a clear-cut increase in NO flux is found, and this is caused by an increase in both airway diffusing capacity and airway wall concentrations of NO. There is no difference in alveolar concentrations of NO compared to healthy subjects, except in severe asthma where an increase has been found. Inhaled corticosteroids are able to reduce the airway wall concentrations but not diffusing capacity or alveolar concentrations. Oral prednisone affects the alveolar concentration, suggesting that in severe asthma there is a systemic component. Steroids distributed by any route do not affect the airway diffusing capacity. Therefore, the airway diffusing capacity should be in focus in testing new drugs or in combination treatment for asthma. Exhaled NO analysis is a promising tool in characterizing asthma in both adults and children. However, there is a strong need to agree on the models and to standardize the flow rates to be used for the modelling in order to perform a systematic and robust analysis of NO production in the lung.

Effect of smoking on exhaled nitric oxide and flow-independent nitric oxide exchange parameters.

It is a well-known fact that smoking is associated with a reduction in exhaled nitric oxide (NO) levels. There is, however, limited knowledge relating to the smoking-induced changes in production or exchange of NO in different compartments of the airways. This study comprised 221 adult subjects from the European Community Respiratory Health Survey II, who were investigated in terms of their exhaled NO, lung function, immunoglobulin E sensitisation and smoking habits. The following parameters were determined using extended NO analysis: airway tissue nitric oxide concentration (Caw,NO), airway transfer factor (or diffusing capacity) for nitric oxide (Daw,NO), alveolar nitric oxide concentration (CA,NO) and fractional exhaled nitric oxide concentration at a flow rate of 50 mL x s(-1) (FeNO,0.05). Maximum total airway nitric oxide flux (J'aw,NO) was calculated from Daw,NO(Caw,NO-CA,NO). Current smokers (n = 35) exhibited lower (geometric mean) FeNO,0.05 (14.0 versus 22.8 ppb), Caw,NO (79.0 ;versus 126 ppb) and J'aw,NO (688 versus 1,153 pL x s(-1)) than never-smokers (n = 111). Ex-smokers (n = 75) were characterised by lower FeNO,0.05 (17.7 versus 22.8 ppb) and Jaw,NO (858 versus 1,153 pL x s(-1)) than never-smokers. These relationships were maintained after adjusting for potential confounders (sex, age, height, immunoglobulin E sensitisation and forced expiratory volume in one second), and, in this analysis, a negative association was found between current smoking and CA,NO. Snus (oral moist snuff) consumption (n = 21) in ex-smokers was associated with an increase in Daw,NO and a reduction in Caw,NO, after adjusting for potential confounders. Passive smoking was associated with a higher CA,NO. Using extended nitric oxide analysis, it was possible to attribute the reduction in exhaled nitric oxide levels seen in ex- and current smokers to a lower total airway nitric oxide flux in ex-smokers and reduced airway and alveolar nitric oxide concentrations in current smokers. The association between snus (oral tobacco) use and reduced nitric oxide concentrations in the airways and increased nitric oxide transfer from the airways warrants further studies.

Administration of nitric oxide into open lung regions: delivery and monitoring.

BACKGROUND: Pulsed administration of nitric oxide has proven effective in relieving pulmonary hypertension and in improving oxygenation. With this delivery method the nitric oxide administration to low ventilated lung regions is avoided with subsequent enhancement in oxygenation. This study presents (i) pulsed administration technique for nitric oxide during artificial ventilation, (ii) evaluation of the delivery in an animal model, and (iii) validation of the delivery device in a laboratory setting. METHODS: Nitric oxide was delivered in four different pulse volumes synchronously with inspiration. The delivery was monitored with a fast responding high sensitivity nitric oxide monitor and nitric oxide uptake was calculated. Pulse delivery dose range, accuracy of the delivered dose, and stability of successive doses were analysed in a laboratory setting. RESULTS: Uptake of the delivered nitric oxide was 87-92%. Measured nitric oxide pulse concentration was 1.6-fold the delivery concentration, calculated as the ratio of nitric oxide flow to inspiration flow. Dose accuracy and stability were both 5% or 3 nmol in the validated range of 3-1000 nmol. CONCLUSION: With pulsed administration nitric oxide therapy can be directed to well-ventilated lung regions. Avoiding administration to the anatomic dead space eliminates nitric oxide exhalation effectively, which makes the method optimal for nitric oxide therapy in a rebreathing circuit. The required dose range from paediatric to adult is covered by the delivery device with a single nitric oxide gas supply.

Increased nitric oxide elimination from the airways after smoking cessation.

Smokers have been found to have low exhaled nitric oxide (NO) levels. The aim of the present study was to investigate where in the respiratory system the decrease in NO occurs, and whether this decrease was affected by smoking cessation. Measurements of exhaled NO were carried out in smokers (n=20) and non-smoking control subjects (n=30). In nine of the smokers, exhaled NO was analysed 1, 2 and 4 weeks after smoking cessation. The level of exhaled NO at a flow rate of 0.1 litre/s was significantly lower in smokers (4+/-2 p.p.b.) than in non-smokers (7+/-5 p.p.b.; P=0.007). A calculation of the contributions from different areas of the lung showed that the NO flux from the airways was significantly lower (14+/-10 compared with 36+/-26 nl/min; P=0.0001) and the alveolar fraction was significantly higher (2.1+/-0.8 compared with 1.5+/-0.9 p.p.b.; P=0.006) in smokers than in non-smokers. Nine smoking subjects refrained from smoking for 4 weeks, and this resulted in increased NO flux from the airways of 28+/-17 nl/min, which was no longer significantly different from controls. In conclusion, endogenous production of NO in the airways is decreased in smokers, but can be restored to normal values by 4 weeks after cessation of smoking. Smokers have an increased alveolar fraction of NO, and this might be a diagnostic sign of lung damage. Thus NO monitoring can be used to indicate improvements when a smoker decides to stop smoking.

Effect of different pulses of nitric oxide on venous admixture in the anaesthetized horse.

BACKGROUND: Dependent atelectatic lung areas open towards the end of inspiration when the lung opening pressure increases, and recollapse during expiration. We hypothesized that inhaled nitric oxide (NO) counteracts hypoxic vasoconstriction in these collapsing lung areas, resulting in increased pulmonary shunt perfusion. METHODS: We administered NO as a pulse and varied the pulse timing during inspiration in equine anaesthesia, where atelectasis develops regularly. Six spontaneously breathing standard breed trotters were studied under isoflurane anaesthesia in lateral recumbency. NO pulsed into the first 30% of inspiration (group NOp1) was assumed to affect open lung areas. To cover more open lung areas NO was then pulsed into the first 60% of inspiration (group NOp2). In a third group, administration between 50 and 80% of inspiration was aimed at the intermittently opening lung areas (group NOp3). RESULTS: With NOp1, venous admixture decreased by 8 (2)% (mean (SEM), P=0.045) and with NOp2 by 10 (1)% (P=0.01). With NOp3, venous admixture reduction was insignificant. CONCLUSIONS: Pulsed administration of NO in early inspiration is optimal in reducing right to left vascular shunt in atelectatic equine lung. This reduction is positively correlated with the magnitude of the initial shunt. With administration in early inspiration, NO is mostly taken up by the lung. This prevents NO accumulation and NO2 formation in rebreathing circuits. These findings may be important in humans when atelectasis occurs increasingly with overweight and age during anaesthesia, but also in postoperative intensive care and in ARDS.

Extended NO analysis applied to patients with COPD, allergic asthma and allergic rhinitis.

The recommended method to measure exhaled nitric oxide (NO) cannot reveal the source of NO production. We applied a model based on the classical Fick's first law of diffusion to partition NO in the lungs. The aim was to develop a simple and robust solution algorithm with a data quality control feature, and apply it to patients with known alterations in exhaled NO. Subjects with allergic rhinitis, allergic asthma, chronic obstructive pulmonary disease (COPD) smokers and controls were investigated. NO was measured at three expiratory flow rates. An iteration method was developed to partition NO. The airway tissue content of NO was increased in asthma, 144 +/- 80 ppb (P = 0.04) and decreased in smokers, 56 +/- 36 ppb (P = 0.02). There was no difference between subjects with rhinitis, 98 +/- 40 ppb and controls, 98 +/- 44 ppb. The airway transfer rate was increased in allergic asthma and allergic rhinitis, 12 +/- 4 vs. 12 +/- 5 ml sec(-1), compared to controls, 8 +/- 2 ml sec(-1) (P < 0.001). The alveolar levels were no different from controls, 2 +/- 1 ppb. In COPD the alveolar levels were increased, 4 +/- 2 ppb (P < 0.001). Extended NO analysis reveals from where in the respiratory system NO is generated. Hence, this new test can be added to the tools the physician has for the diagnosis and treatment of patients with respiratory disorders.

Inhaled mannitol shifts exhaled nitric oxide in opposite directions in asthmatics and healthy subjects.

We investigated if healthy subjects could release NO upon hyperosmolar challenge as a defence mechanism, and whether asthmatics with atopy showed an altered response. A plot of NO output versus flow rate was used to calculate the alveolar level and the NO-flux from the airways. The asthmatics had a higher NO output and this was due to an increased NO-flux from the airways, 86+/-30 nl min(-1) compared with control 21+/-2 nl min(-1) (P<0.05). The alveolar NO levels showed no difference. In response to a dry powder of mannitol the exhaled NO concentration decreased in asthmatics by 37+/-7%, but increased in the control by 9+/-4% (P<0.001). The FEV(1.0) decreased 13+/-2% and airway conductance 42+/-7% in asthmatics and in the controls 2+/-1% and 0+/-7%, respectively (P<0.001). We conclude that asthmatics have an altered response to mannitol challenge in regards to exhaled NO. This may result from down regulation of constitutive NO production as a result of high levels of NO flux from the airways.

Informal caregivers' participation in elderly-patient care: an interrupted time-series study.

This study is an evaluation of a project in Finland that aimed to promote the participation of informal caregivers in the hospital care of elderly patients. The staff who worked in the wards that were studied built up activation programmes for informal caregivers, and changed ward policies to encourage caregivers' participation. To explore changes in caregivers' participation in the study and the control wards, non-equivalent control groups were used. During periods of two months in 1991, 1992 and 1993, the data were collected from informal caregivers (N = 369) using a structured questionnaire. The results indicated that total participation of informal caregivers in daily activities increased in long-term care settings, but not in the university hospital. However, a small increase in informal caregivers' participation in some daily activities of elderly patients took place in the study wards of each setting. The findings and implications for nursing are discussed.

Exhaled nitric oxide partitioned into alveolar, lower airways and nasal contributions.

During the last year exhaled nitric oxide (NO) has been proposed as a marker of airway inflammation. More knowledge of the production and transfer of this molecule are needed in order for NO analysis to become a clinical tool. This was the aim of the study. Exhaled NO values from multiple flow rates were used to model alveolar NO, transfer rate and tissue concentration of NO in the airways. Three flows rates, 0.005, 0.1 and 0.51 sec(-1) were found to be optimal. The NO transfer rate of the airways was 9 +/- 2 ml sec(-1), the tissue source was 75 +/- 28 ppb and the alveolar fraction of NO was 2 +/- 1 ppb in 10 healthy subjects (mean +/- CI95%). In conclusion, we have shown that it is possible to get more information about the distribution of NO in the lungs and the airways than only a single value from one expiratory flow rate can give. Further studies will reveal if this airway modelling can be useful in disease of the respiratory system.

Theoretical and experimental comparison of constant inspired concentration and pulsed delivery in NO therapy.

OBJECTIVE: Inhaled NO therapy of artificially ventilated patients has been established as being based on constant inspired concentration of NO. In this study a new volumetrically controlled pulsed NO delivery mode is compared with the established concentration-based concept. DESIGN: To evaluate the relationship between NO delivery parameters, alveolar NO fraction, and patient uptake, a mathematical lung model was created where NO delivery can be simulated in varying ventilator settings, delivery modes, and lung properties. This model and the efficacy of pulsed delivery in inducing pulmonary capillary vasodilatation were examined experimentally. SETTING: Animal laboratory, Department of Medical Sciences, Clinical Physiology. SUBJECTS: The experimental study was performed with nine pigs of mixed breed weighing 25-35 kg. INTERVENTIONS: The pigs were anaesthetised and artificially ventilated. Pulmonary vasoconstriction was induced by hypoxia. NO was delivered periodically in the various delivery modes. MEASUREMENTS AND RESULTS: In simulation, in all delivery modes the NO uptake was found to be dependent on the ventilator settings and the volume of the dead space. Measured from pulmonary artery pressure, the pulsed delivery was as effective in reducing the induced pulmonary vasoconstriction as the constant inspired concentration delivery. The amount of NO that could reduce the vasoconstriction back to baseline was 105 nmol x min(-1). By delivering in the early part of the inspiration, ambient contamination by the exhaust gas is avoided. The expired NO values obtained in the simulation and the experiments were equal. Based on the simulation, the alveolar NO fraction and the NO uptake depend on the ventilator settings and the dead space in both volumetric- and concentration-based delivery. CONCLUSIONS: With pulsed delivery, a therapeutic effect comparable to constant inspired concentration delivery is achieved, NO gas is used more effectively, and environmental exhausts are reduced. The theoretical model shows that the NO delivery does not predict alveolar NO fraction and the NO uptake. However, it still remains an open question if the online measurement of these parameters would provide useful information, having added value in predicting and controlling the efficacy of the NO treatment.

Accuracy of an indirect calorimeter for mechanically ventilated infants and children: the influence of low rates of gas exchange and varying FIO2.

OBJECTIVE: To test the accuracy and validity of the Deltatrac II MBM-200 metabolic monitor for use in mechanically ventilated infants and children in the pediatric intensive care unit. DESIGN: Laboratory validation of an indirect calorimeter with a ventilated lung model. The influence of low tidal volumes and low levels of oxygen consumption (V(O2)) and carbon dioxide production (V(CO2)) in combination with different levels of inspired oxygen concentrations (F(IO2)) was investigated. SETTING: University research laboratory. SUBJECTS: Low tidal volumes were provided with two intermittent flow types of ventilators, a Servo 300 and a Servo 900C. INTERVENTIONS: A butane flame with a V(O2) approximating 20 mL/min and 40 mL/min was ventilated. To investigate the effect of different levels of F(IO2) on the accuracy of V(O2), V(CO2), and respiratory quotient (RQ), measurements were performed at F(IO2) target values of 0.25, 0.40, and 0.60. MEASUREMENTS AND MAIN RESULTS: No significant differences were found between the ventilators regarding V(O2), V(CO2), and RQ measurements. The mean deviation of V(O2) increased significantly with increasing F(IO2) to -7.98% with a V(O2) of 21.0 mL/min and to -8.46% with a V(O2) of 38.9 mL/min (F(IO2), 0.558) with a variability (2 SD) of +/- 4.86% and +/- 6.82%, respectively. The mean deviation and variability of V(CO2) in all tests remained within 8%. The mean deviation of RQ increased significantly with increasing F(IO2) to 5.5% with a V(O2) of 21.0 mL/min and to 5.69% with a V(O2) of 38.9 mL/min (F(IO2), 0.558) with a variability (2 SD) of +/- 5.62% and +/- 5.76%, respectively. The minute to minute delivered F(IO2) fluctuated significantly when increasing the level of F(IO2). CONCLUSIONS: The Deltatrac II MBM-200 metabolic monitor appears accurate for low levels of V(O2) and V(CO2) during mechanical ventilation with F(IO2) levels up to 0.390. With increasing F(IO2) to 0.558, the increase in deviation of V(O2) for single measurements can be of clinical relevance for mechanically ventilated infants and children. The increased fluctuation of delivered F(IO2) on higher levels of F(IO2) is likely the cause of the inaccuracy.

Error in measurement of oxygen and carbon dioxide concentrations by the DeltatracII metabolic monitor in the presence of desflurane.

In experiments in dogs on the metabolic effects of inhalation anaesthetics, we noticed that in the presence of desflurane, oxygen uptake (VO2) measured with the Deltatracll metabolic monitor seemingly increased whereas it decreased when determined independently by the Fick principle. This difference remained even after correction for changes in gas concentration on addition of an inhalation anaesthetic. Therefore, we suspected that desflurane interferes with the measurement of gas concentrations. Using different precision gases, we found that desflurane disturbed both the paramagnetic oxygen sensor and the infrared carbon dioxide detector so that the measured oxygen (when FIO2 was > 0.21) and carbon dioxide concentrations were greater than expected. These errors multiply in the computing process of oxygen uptake by the DeltatracII. When the DeltatracII is to be used during inhalation anaesthesia, its results should be corrected for the presence of an anaesthetic gas. More importantly, corrections must also be made for measurement errors of the oxygen and carbon dioxide sensors, unless the device has been equipped with a modified (nickel membrane) oxygen sensor insensitive to the presence of volatile agents.

[Sleep disturbances affecting hospital patients]. / Potilaan nukkuminen sisätautien ja kirurgian osastolla.

The purpose of this article is to describe patients' sleep in hospital. The article is based on a study of patients' sleep in a hospital's medical or surgical ward and to clarify the disturbance factors relating to their sleep. The patients of the Central Hospital of Northern Carelia's two medical and two surgical wards took part in the research. The data were collected by a structured questionnaire and a follow-up questionnaire in May-June 1996. Of the replies of 181 patients, the results of 177 were taken to the final analysis. The data were analysed by statistical methods. The data and the results are presented in frequency and percent distributions, and the background variables of those patients sleeping well and those sleeping poorly are analysed and compared. The results indicated that 65% of the researched patients slept badly in the hospital. Environmental factors were found to be related to most of the patients' sleep disturbances: 80% of them regarded those factors as the cause for their disturbed sleep. Other patients, noise, and the nurses' work were regarded as the most disturbing of the environmental factors. The internal factors had disturbed patients' sleep in the hospital less than the environmental factors. Pain was regarded as the most sleep disturbing internal factor: over half of the researched patients felt disturbed by it. During their stay in the hospital the patients experienced more positive (trust, contentment, safety) than negative feelings (fear, anxiety, depression, distrust), and those who experienced negative feelings had more difficulties in sleeping.