SAS CARE 1: Sleep architecture changes in a cohort of patients with Ischemic Stroke/TIA.

OBJECTIVE: Changes in sleep architecture following ischemic stroke have been poorly investigated. Our objective was to explore changes of sleep structure in patients with ischemic stroke or transient ischemic attack in order to verify a possible predictive value of sleep with respect to clinical outcome. METHODS: Patients recruited in the prospective SAS-CARE study received two polysomnographies (PSG) in the acute and chronic phases after stroke/TIA. Sleep parameters were compared between the two time-points and matched with a non-stroke population randomly selected from the HypnoLaus cohort. RESULTS: Of the 169 patients investigated with PSG in the acute phase, 104 were again studied 3 months after stroke symptom onset and compared with 162 controls. The acute phase of stroke/TIA was associated with sleep disruption, which significantly improved in the chronic phase, but remained worse than controls (total sleep time improve from 318.8 ± 90.8 to 348.4 ± 81.5 min, compared to 388.2 ± 71.3 in controls, sleep latency from 49.9 ± 58.4 to 27.9 min, compared to 20.2 ± 22 in controls, sleep efficiency from 58.2 ± 18.1% to 27.9 ± 36.4 min, compared to 83.4 ± 10.3% in controls, wakefulness after sleep onset percentage from 36.5 ± 17.3 to 29.3 ± 15.6, compared to 13.2 ± 9.2 in controls). The percentage of REM sleep was negatively associated with stroke severity, whereas stroke topography did not correlate with sleep parameters. CONCLUSIONS: This study confirmed a severe sleep disruption in the acute phase of stroke. Although a significant improvement of sleep quality was observed during the three months after stroke, sleep architecture did not normalize. In particular, sleep efficiency and REM sleep seem to be particularly affected by stroke in the acute phase, with a relative preservation of NREM sleep. We suggest that these sleep architecture changes represent a persistent marker of brain damage due to stroke. Further studies are needed to assess the relationship with stroke topographic and outcome.

Reliability of automatic detection of AHI during positive airway pressure treatment in obstructive sleep apnea patients: A "real-life study".

INTRODUCTION: Automatic event detection (AED) of residual apnea-hypopnea index (AHI) by ventilators is a current practice in sleep and mechanical ventilation Units but this methodology has not been validated in an unselected population of OSA patients. Aim of the present study was to assess in a "real-life" condition the reliability of AED during PAP therapy by the in-built software compared to full polysomnography during follow-up. METHODS: We enrolled 300 OSA patients (105 F; AHI 45.3 ± 27.8) already on Positive airway pressure (PAP) therapy: 53% of the patients were on CPAP while other modalities were used in the rest of the sample. RESULTS: Overall, the built-in software identified residual obstructive AHI (AHIPAP) > 5, 10 or 15 in 18.7, 8.6 or 4.6% of patients, respectively. By using AHIPAP, 28.4% of patients were wrongly classified as "well controlled" despite a residual AHIPSG>5 (6% considering a residual AHIVENT >15); 7% of patients were classified as not controlled while AHIPSG was <5 (1.4% considering a residual AHIVENT >15). Type of ventilation, ventilator parameters, adherence to treatment and level of baseline or follow-up Epworth Sleepiness Scale score were similar between groups. The sensitivity and positive predicted values were very low. Positive likelihood ratio appears adequate only for residual AHIPAP ≥10, but negative likelihood ratio was inconclusive for all the cut-off considered. DISCUSSION: The results of the present study suggest a more cautious approach in the follow-up of OSA patients, since a protocol based only on AED detection and symptoms assessment may not be accurate especially for AHIPAP<15.

SAS CARE 2 - a randomized study of CPAP in patients with obstructive sleep disordered breathing following ischemic stroke or transient ischemic attack.

OBJECTIVE/BACKGROUND: The benefit of Continuous Positive Airway Pressure (CPAP) treatment following ischemic stroke in patients with obstructive sleep-disordered breathing (SDB) is unclear. We set out to investigate this open question in a randomized controlled trial as part of the SAS-CARE study. PATIENTS/METHODS: Non-sleepy patients (ESS < 10) with ischemic stroke or transient ischemic attack (TIA) and obstructive SDB (AHI ≥ 20) 3 months post-stroke were randomized 1:1 to CPAP treatment (CPAP+) or standard care. Primary outcome was the occurrence of vascular events (TIA/stroke, myocardial infarction/revascularization, hospitalization for heart failure or unstable angina) or death within 24 months post-stroke. Secondary outcomes included Modified Rankin Scale (mRS) and Barthel Index. RESULTS: Among 238 SAS-CARE patients 41 (17%) non-sleepy obstructive SDB patients were randomized to CPAP (n = 19) or standard care (n = 22). Most patients (80%) had stroke and were males (78%), mean age was 64 ± 7 years and mean NIHSS score 0.6 ± 1.0 (range: 0-5). The primary endpoint was met by one patient in the standard care arm (a new stroke). In an intent-to treat analysis disregarding adherence, this corresponds to an absolute risk difference of 4.5% or an NNT = 22. mRS and Barthel Index were stable and similar between arms. CPAP adherence was sufficient in 60% of evaluable patients at month 24. CONCLUSION: No benefit of CPAP started three months post-stroke was found in terms of new cardio- and cerebrovascular events over 2 years. This may be related to the small size of this study, the mild stoke severity, the exclusion of sleepy patients, the delayed start of treatment, and the overall low event rate.

Comparison of two humidification systems for long-term noninvasive mechanical ventilation.

There is no consensus concerning the best system of humidification during long-term noninvasive mechanical ventilation (NIMV). In a technical pilot randomised crossover 12-month study, 16 patients with stable chronic hypercapnic respiratory failure received either heated humidification or heat and moisture exchanger. Compliance with long-term NIMV, airway symptoms, side-effects and number of severe acute pulmonary exacerbations requiring hospitalisation were recorded. Two patients died. Intention-to-treat statistical analysis was performed on 14 patients. No significant differences were observed in compliance with long-term NIMV, but 10 out of 14 patients decided to continue long-term NIMV with heated humidification at the end of the trial. The incidence of side-effects, except for dry throat (significantly more often present using heat and moisture exchanger), hospitalisations and pneumonia were not significantly different. In the present pilot study, the use heated humidification and heat and moisture exchanger showed similar tolerance and side-effects, but a higher number of patients decided to continue long-term noninvasive mechanical ventilation with heated humidification. Further larger studies are required in order to confirm these findings.

Medico-legal implications of sleep apnoea syndrome: driving license regulations in Europe.

BACKGROUND: Sleep apnoea syndrome (SAS), one of the main medical causes of excessive daytime sleepiness, has been shown to be a risk factor for traffic accidents. Treating SAS results in a normalized rate of traffic accidents. As part of the COST Action B-26, we looked at driving license regulations, and especially at its medical aspects in the European region. METHODS: We obtained data from Transport Authorities in 25 countries (Austria, AT; Belgium, BE; Czech Republic, CZ; Denmark, DK; Estonia, EE; Finland, FI; France, FR; Germany, DE; Greece, GR; Hungary, HU; Ireland, IE; Italy, IT; Lithuania, LT; Luxembourg, LU; Malta, MT; Netherlands, NL; Norway, EC; Poland, PL; Portugal, PT; Slovakia, SK; Slovenia, SI; Spain, ES; Sweden, SE; Switzerland, CH; United Kingdom, UK). RESULTS: Driving license regulations date from 1997 onwards. Excessive daytime sleepiness is mentioned in nine, whereas sleep apnoea syndrome is mentioned in 10 countries. A patient with untreated sleep apnoea is always considered unfit to drive. To recover the driving capacity, seven countries rely on a physician's medical certificate based on symptom control and compliance with therapy, whereas in two countries it is up to the patient to decide (on his doctor's advice) to drive again. Only FR requires a normalized electroencephalography (EEG)-based Maintenance of Wakefulness Test for professional drivers. Rare conditions (e.g., narcolepsy) are considered a driving safety risk more frequently than sleep apnoea syndrome. CONCLUSION: Despite the available scientific evidence, most countries in Europe do not include sleep apnoea syndrome or excessive daytime sleepiness among the specific medical conditions to be considered when judging whether or not a person is fit to drive. A unified European Directive seems desirable.

Nutritional status and airflow obstruction: two independent contributors to CO diffusing capacity impairment in COPD.

BACKGROUND: The association between weight loss and Chronic Obstructive Pulmonary Disease (COPD) has been recognised from many years. Based on the evidence that nutritional status reflects metabolic disturbances in COPD, the relationship between body mass index (BMI), severity of airflow obstruction and CO diffusing capacity (DL(CO)), that is the functional hallmark of emphysema, is relevant to the management of COPD phenotypes. METHODS: We reviewed 104 patients with COPD (82 males), aged 66 +/- 9 years (mean +/- SD). Height averaged 165 +/- 8 cm, weight 71 +/- 16 Kg, FEV1 50 +/- 18 (% of predicted), RV 169 +/- 49%, and DL(CO) 56 +/- 26%. Multiple linear regression was performed using BMI, FEV1 and RV, as explanatory variables for DL(CO). Patients were also classified into four groups according to BMI < or = 18.5 (low), > 18.5 and < or = 25 (ideal), > 25 and < or = 30 (overweight), > 30 (obese), and post-bronchodilator FEV1 < 50%. Using this categorisation, a two-factor analysis of variance, testing for interaction and main effects (BMI and FEV1) was performed as confirmatory analysis for the association between BMI (kg/m2), FEV1% and DL(CO)%. RESULTS: FEV1 and BMI were significantly and independently associated to DL(CO) according to the equation: DL(CO) = -18.32 + 0.65 x FEV1 + 1.59 x BMI (R2 = 0.40, p < 0.0001). The contribution of RV % to DL(CO) % was largely non-significant (p = 0.16). A close relationship was found between BMI (kg/m2) and DL(CO) %, for all of the four BMI groups segregated by post-bronchodilator FEV1 %, (p < .0001). No interaction was found between these two factors (p = 0.30). CONCLUSION: Nutritional status as assessed by BMI contributes substantially to impairment of DL(CO) independently of the severity of airflow obstruction. This data confirms the association between emphysematous process and weight loss in advanced COPD, independent of the airflow obstruction severity.

Erectile dysfunction in men with obstructive sleep apnea: an early sign of nerve involvement.

Erectile dysfunction (ED) is common in men with obstructive sleep apnea (OSAS) but no completely convincing hypotheses about the underlying pathogenic mechanisms have been published in the literature. The aims of the present study were to assess the presence of ED in a group of OSAS patients without daytime respiratory failure and to determine whether this dysfunction was related to peripheral nerve involvement. Evaluation of the bulbocavernosus reflex (BCR) and the somato-sensory evoked potentials of pudendal nerve (PSEPs), the most widely established method of documenting pudendal neuropathies as being the cause of impotence, was performed in 25 patients. Data on BCR were compared with those of 25 healthy males volunteers matched for age. BCR was altered in 17 patients: in 6 it was elicited while in 11 it had a prolonged latency and reduced amplitude. Patients with altered BCR presented an higher AHI, an higher percentage of sleep time spent with SaO2 <90% (TST90) and a lower daytime PaO2. Six patient had clinically silent neurophysiological signs of mild polyneuropathy. The degree of OSAS and gas exchange alteration was more severe in patients with polyneuropathy than in those with isolated BCR alteration. ED is a common finding in OSAS patients and this alteration seems to be related to a nerve dysfunction. The development of nerve dysfunction is associated with a more severe degree of OSAS and nocturnal hypoxia.

Is it safe for patients with chronic hypercapnic respiratory failure undergoing home noninvasive ventilation to discontinue ventilation briefly?

STUDY OBJECTIVES: A brief discontinuation (< 1 week) of long-term ventilation may be necessary in patients who are not totally ventilator-dependent in cases of technical problems, intolerable nasal irritation, upper airway congestion, or travel. We examined the incidence, timing, and causes of possible clinical deterioration after a brief withdrawal of ventilation in patients with chronic respiratory failure (CRF) who were well-established on long-term noninvasive mechanical ventilation (NIMV). STUDY DESIGN: Prospective clinical study. PATIENTS: Eleven inpatients in clinically stable condition (COPD, 6 patients; and restrictive thoracic disease [RTD], 5 patients) who had severe CRF (PaCO(2), > 50 mm Hg) and had been receiving NIMV for (mean +/- SD) 19.3 +/- 5.3 months were enrolled. INTERVENTIONS AND MEASUREMENTS: Arterial blood gas (ABG) levels, maximal inspiratory pressure (PImax), breathing pattern, dyspnea rating, and life symptoms (measured by a questionnaire) were recorded daily after NIMV withdrawal for 6 days or until the patients showed clinical and/or ABG level deterioration. Pulmonary function tests were performed and neuromuscular drive was measured at the beginning and the end of the study. RESULTS: Five of the 11 patients (45.4%) [COPD, 3 patients; and RTD, 2 patients] were reconnected to a ventilator before the scheduled time because of ABG level deterioration. Despite these changes, none of the patients reported severe worsening of symptoms or other medical complications. The patients whose ABG levels worsened had statistically significant decreases in tidal volume and PImax, suggesting that the development of alveolar hypoventilation was related to respiratory muscle weakness. CONCLUSIONS: A brief discontinuation of NIMV in patients who were affected by chronic hypercapnic respiratory failure and were well-established on NIMV is associated with a relatively high incidence of ABG level worsening due to the development of alveolar hypoventilation. If NIMV must be briefly interrupted for clinical reasons, the patient should be monitored closely for abrupt worsening, and prompt technical intervention should be provided if a ventilator fails.

The development of hyperventilation in patients with chronic heart failure and Cheyne-Strokes respiration: a possible role of chronic hypoxia.

AIM: To analyze the relationship between daytime respiratory and cardiac function in patients with compensated chronic heart failure (CHF) with and without periodic breathing (PB) or Cheyne-Stokes respiration (CSR). PATIENTS: We studied 132 patients (female, 13%; mean age, 53+/-8 years; body mass index, 25.9+/-3.5 kg/m2; left ventricular ejection fraction <40%; 23% in New York Heart Association class I, 43% in class II, and 34% in class III-IV). METHODS: Measurement of pulmonary function and blood gases, hemodynamic evaluation, analysis of breathing profile, echocardiography, recording of ECG, beat-to-beat arterial oxygen saturation, and respiration during spontaneous breathing. RESULTS: Fifty-eight percent of patients showed PB or CSR. Patients with PB or CSR have greater cardiac function impairment. Mean values of lung volumes and PaO2 were similar in the three groups of patients considered. In contrast, patients with PB or CSR had an increased minute ventilation and reduced PaCO2 values. Interestingly, patients with PB or CSR had lower values of arterial content of O2 and systemic oxygen transport (SOT) than patients with a normal breathing pattern (SOT, 394+/-9.8, 347+/-9.6, 438+/-11 mL of O2/min/m2, respectively; analysis of variance p<0.001). Weak correlations were found among lung volumes, blood gases, and cardiac function parameters: ie, vital capacity was correlated inversely with pulmonary capillary wedge pressure (PCWP) (-0.25; p<0.05); PaCO2 with PCWP (r=0.26; p<0.05), lung-to-ear circulation time (LECT) (r=-0.4; p<0.05), SOT (r=-0.33; p<0.0001), and cardiac index (CI) (r=0.27; p=0.003). Multiple regression analyses showed that arterial PCO2 was significantly correlated with SOT, LECT, and CI (r=0.51; r2=0.26; p<0.000001); the correlation became stronger considering only CSR patients (r=0.64; r2=0.4; p<0.001). CONCLUSIONS: Our study shows that patients with daytime breathing disorders have chronic hypocapnia. A reduced SOT may be one of the stimuli determining increased minute ventilation in these patients.

Salbutamol delivery during non-invasive mechanical ventilation in patients with chronic obstructive pulmonary disease: a randomized, controlled study.

OBJECTIVE: We investigated the clinical response to equivalent doses of salbutamol delivered, via metered dose inhaler (MDI) during non-invasive mechanical ventilation (NIMV-MDI), during spontaneous breathing using a spacer (MDI-Spacer), and also during intermittent positive pressure breathing (IPPB). SETTING: A respiratory intensive care unit. DESIGN: Prospective, randomized, and placebo-controlled study. PATIENTS: Eighteen stable patients with chronic obstructive pulmonary disease (mean FEV1=38.5+/-8.8% predicted). RESULTS: Overall salbutamol administration induced, compared to placebo, a significant improvement in FEV1, irrespective of the mode of administration (+7.9+/-7.1% or +108+/-91 ml for IPPB, +9.6+/-8.8% or 112+/-67 ml for MDI-NIMV (inspiratory pressure=14.3+/-1.8 cmH2O; expiratory pressure=none), and +10.8+/-11.4% or 119+/-114 ml for MDI-Spacer, respectively). DeltaFVC significantly increased from placebo only in MDI-NIMV (+214+/-182 ml P=0.02). A second set of experiments performed in eight patients to ascertain the possible effect of NIMV on pulmonary function tests, showed a significant improvement from baseline values in FVC both after the delivering of placebo or salbutamol via NIMV-MDI (+206+/-147 ml and 208+/-145, respectively). FEV1 significantly increased only after salbutamol. No changes in gas exchange were observed after bronchodilator delivery. CONCLUSIONS: We show that delivery of bronchodilators via MDI with a spacer chamber during NIMV is feasible and induces a significant bronchodilator effect compared to placebo, even though it may be slightly less effective than the classical delivery system (MDI-Spacer).

Periodic breathing in heart failure patients: testing the hypothesis of instability of the chemoreflex loop.

In this study, we applied time- and frequency-domain signal processing techniques to the analysis of respiratory and arterial O(2) saturation (Sa(O(2))) oscillations during nonapneic periodic breathing (PB) in 37 supine awake chronic heart failure patients. O(2) was administered to eight of them at 3 l/min. Instantaneous tidal volume and instantaneous minute ventilation (IMV) signals were obtained from the lung volume signal. The main objectives were to verify 1) whether the timing relationship between IMV and Sa(O(2)) was consistent with modeling predictions derived from the instability hypothesis of PB and 2) whether O(2) administration, by decreasing loop gain and increasing O(2) stores, would have increased system stability reducing or abolishing the ventilatory oscillation. PB was centered around 0.021 Hz, whereas respiratory rate was centered around 0.33 Hz and was almost stable between hyperventilation and hypopnea. The average phase shift between IMV and Sa(O(2)) at the PB frequency was 205 degrees (95% confidence interval 198-212 degrees). In 12 of 37 patients in whom we measured the pure circulatory delay, the predicted lung-to-ear delay was 28.8 +/- 5.2 s and the corresponding observed delay was 30.9 +/- 8.8 s (P = 0.13). In seven of eight patients, O(2) administration abolished PB (in the eighth patient, Sa(O(2)) did not increase). These results show a remarkable consistency between theoretical expectations derived from the instability hypothesis and experimental observations and clearly indicate that a condition of loss of stability in the chemical feedback control of ventilation might play a determinant role in the genesis of PB in awake chronic heart failure patients.

Orthopnea and inspiratory effort in chronic heart failure patients.

STUDY OBJECTIVE: Orthopnea is a typical feature of patients with chronic heart failure (CHF), the factors contributing to it are not completely understood. We investigated changes in dyspnea and other respiratory variables, induced by altering posture (from sitting to supine) in 11 CHF patients (NYHA classes II-IV) and 10 control subjects. METHODS AND RESULTS: We measured dyspnea (Borg scale) the diaphragm pressure time product per minute (PTPdi/m, index of metabolic consumption), and mechanical properties of the lung (lung compliance (C,L) and resistances (R,L). CHF patients also underwent a trial of non-invasive mechanical ventilation (NIMV) in the supine position in order to ascertain whether unloading the inspiratory muscles could somehow relieve dyspnea. While sitting the PTPdi/min was significantly higher in CHF patients than in controls (181 +/- 54 cm H2O x s/min vs. 96 +/- 32; P<0.05). Assuming a supine position caused no major changes in controls, whereas CHF patients showed a significant worsening in dyspnea, a rise in PTPdi/min (243 +/- 97 p<0.01) and R,L (4.7 +/- 1.2 cm H2O/L x s sitting vs. 7.9 +/- 2.5 supine; P<0.01) and a decrease in C,L (0.08 +/- 0.02 L/cm H2O sitting vs. 0.07 +/- 0.01 supine; P<0.05). Applying NIMV to supine CHF patients significantly reduced the PTPdi/min to 81 +/- 42 (P<0.001). Changes in dyspnea, produced by varying position or applying NIMV, were significantly correlated with PTPdi/min (r=0.80, P<0.005 and r=0.58, P<0.01, respectively). CONCLUSIONS: CHF patients had a higher PTPdi/min than controls when sitting, and assuming a supine position induced severe dyspnea, a large rise in R,L, and a reduction in C,L so that PTPdi/min increased further. Orthopnea was strongly correlated with the increased diaphragmatic effort.

Sleep disordered breathing in patients with chronic obstructive pulmonary disease.

Sleep has effects on breathing, including changes in respiratory control, airways resistance and muscular contractility. These sleep-related modifications in the respiratory system do not induce adverse effects in healthy subjects, but may cause problems in patients with chronic obstructive pulmonary disease (COPD). Hypo-ventilation causes the most important gas-exchange alteration during sleep in COPD patients, leading to hypercapnia and hypoxemia, especially during rapid-eye-movement (REM) sleep. Blood gases alterations lead to increased arousals, sleep disruption, pulmonary hypertension and higher mortality. The presence of other sleep-related breathing disorders, like sleep apnea syndrome, may induce a more pronounced impairment of gas exchange, both during sleep and wakefulness, and development of symptoms like excessive daytime somnolence. Nocturnal oximetry is recommended to evaluate gas exchange during sleep in COPD patients. Sleep studies are usually indicated when there is a possibility of sleep apnea or obesity-hypoventilation syndrome. The role of non-invasive mechanical ventilation in managing COPD patients with nocturnal hypoventilation is discussed.

Sleep disorders in neuromuscular diseases.

This article reports the results of several studies on neuromuscular patients (9 Duchenne's muscular dystrophy, 10 myotonic muscular dystrophy, 8 mitochondrial myopathies, 6 spinal muscular atrophy). An evaluation of respiratory function during wakefulness, a sleep questionnaire and an overnight polysomnography were performed in all patients. Recurrent hypoxaemia of variable degree was observed during sleep. In most cases, night-time hypoxaemia appears not to be predictable during wakefulness. Nocturnal hypoxaemia occurs in relation to apnoeas or hypopnoeas, mainly of central type, especially when these breathing irregularities occur during rapid eye movement (REM) sleep. Moreover, polygraphic sleep-apnoea patterns, as defined by international criteria, seem to be an infrequent condition, except for those neuromuscular diseases, characterized by an involvement of the central nervous system.

Chronic respiratory failure in a patient with type I Arnold-Chiari malformation (ACM1) and syringomyelia.

We present the case of a young adult with type I Arnold-Chiari malformation (AMC1) and syringomyelia who developed central sleep apnoea and chronic respiratory failure, successfully treated with nocturnal noninvasive positive pressure ventilation ventilation (NIPPV). An extensive syringomyelic cavity (from bulbar to L4 segment) with severe impairment of the IX cranial nerve was documented and remains, although reduced, after the neurosurgical treatment. At baseline evaluation, the patient showed a moderate restrictive ventilatory defect, severe hypercapnic respiratory failure, abnormal control of breathing characterized by the absence of response to hypoxia and hypercapnia, and severe nocturnal central apnoeas. Nocturnal NIPPV was then started in the A/C mode with an improvement in blood gas values. Further evaluations were performed 10 and 18 months later. A progressive significant improvement of lung volumes, both in sitting and supine position, associated with a slight improvement of blood-gas values were observed. Nonetheless, the breathing pattern abnormalities persisted. Polysomnographic evaluation during mechanical ventilation showed a normalization of breathing pattern with arterial oxygen saturation (SaO2) > 90% throughout the night.

Respiratory function in precapillary pulmonary hypertension.

Since dyspnoea on exertion is very often the first symptom of precapillary pulmonary hypertension (PPH), either from chronic thromboembolic pulmonary hypertension (CTEPH) or from idiopathic pulmonary hypertension (IPH), these patients are often first examined in a pulmonary function laboratory. We carried out a retrospective study (1987-1992) on pulmonary function in 34 patients diagnosed to have PPH by means of specific diagnostic tools, out of 5,467 patients first attending our laboratory. Nine suffered from IPH, 10 from CTEPH and 15 from Eisenmenger physiology. This last group differed from the others, since its diagnosis had been known for a long time and the stage of the disease was more advanced, when pulmonary function tests were performed in our laboratory (with a view to transplantation). Respiratory function, blood gases and arterial oxyhaemoglobin saturation (HbSaO2) during exercise (Bruce protocol), diffusing capacity of the lungs for carbon monoxide (DLCO), shunt fraction (QS%) (approximation obtained from arterial oxygen tension (PaO2) after 100% oxygen breathing) had been evaluated. In the first two groups, in contrast to other reports, we could observe no obstructive defect. Only 20% of the subjects had restrictive defects, however mild. The typical functional picture of these patients revealed normal lung volumes, normal or slightly reduced DLCO, mild hypoxaemia with hypocapnia, severe HbSaO2 drops during exercise, and pathological QS%. We conclude that every time a patient presents with breathlessness at rest or on exercise, a normal chest X-ray and respiratory function tests, pulmonary hypertension must be suspected and subject to specific and invasive tests. More severe functional impairment was observed in the PPH from the Eisenmenger disorder. This might be due to a more advanced stage of this type of hypertension at the time of our observation and/or to the different mechanisms of the diseases themselves.

Chronic respiratory symptoms, bronchial responsiveness and dietary sodium and potassium: a population-based study.

A possible relationship between Na+ intake and increased prevalence and mortality from asthma and chronic obstructive pulmonary disease (COPD) has been suggested but not clearly proven for several reasons (difficulty in assessing Na+ and K+ both by 24 h excretion and dietary recall, too small an effect of these ions on the pathology, and the role of potential confounders). We wanted to determine the relationship of Na+ and K+ intake, assessed by means of a 7 day recall, with chronic respiratory symptoms and bronchial responsiveness in a sample of the general population. Two hundred and five subjects were studied, with complete dietary and respiratory questionnaires, and baseline respiratory function tests, together with a subsample of 146 subjects who underwent histamine challenge. The 7 day recall consisted of two parts: the first assessed discretionary Na+; and the second assessed Na+ and K+ contained in food. The whole sample was split into two groups based on the levels of consumption, and the statistical analysis was performed contrasting the three lower quartiles vs the highest. Smoking habit, social economic status, age and body mass index (BMI) were not confounders for Na+ and K+ intake. The prevalence of symptomatic subjects and baseline respiratory function values were not significantly different in the two groups of quartiles for Na+ and K+. Baseline respiratory values and dose-response slope of the subsample were also not significantly different. We did not prove a relationship between these dietary factors and either bronchial responsiveness or chronic respiratory symptoms. Although we consider that our questionnaire is more reliable than other methods for Na+ and K+ assessment, several potential biases still remain.(ABSTRACT TRUNCATED AT 250 WORDS)

Identification of chronic heart failure patients at risk of Cheyne-Stokes respiration.

Chronic heart failure (CHF) patients frequently show sleep-disordered breathing consisting of periodic breathing (PB) and Cheyne-Stokes respiration (CSR) with central sleep apnoea (CSA). Since the diagnosis of sleep-disordered breathing, in CHF patients, can be made only by means of full polysomnography, the aim of the present study was to evaluate whether or not daytime respiratory function can identify patients at risk of nocturnal PB and/or CSR/CSA. Twenty-seven patients (mean age 54 +/- 8.5 yrs), eight New York Heart Association Functional Class (NYHAFC) II, 17 NYHAFC III and two NYHAFC IV, with severe cardiac failure (cardiac output 2.0 +/- 0.66 L.min-1, ejection fraction 22.5 +/- 5.77%, pulmonary capillary wedge/pressure 23 +/- 9.05 mmHg). Mouth occlusion pressure (P0.1)/maximal inspiratory pressure (MIP) was significantly higher in patients with nocturnal CSR/CSA (5.04 +/- 1.49 versus 3.24 +/- 2.13%, analysis of variance (ANOVA) 0.03), whereas their arterial carbon dioxide tension (Pa,CO2) was significantly lower (4.15 +/- 0.56 (31.2 +/- 4.23 mmHg) versus 4.67 +/- 0.53 kPa (35.1 +/- 4 mmHg), ANOVA 0.02). Logistic regression analysis demonstrated that CSR/CSA occurrence may be predicted by daytime measurement of P0.1/MIP and Pa,CO2 (p = 0.04 and 0.01 respectively; odds ratio 1.93 and 0.76 respectively). The sensitivity was 70%, specificity 76.5%, false positive rate 36.4%, false negative rate 18.8%, positive predictive value 71.4% and negative predictive value 85%. This model seems useful for predicting respiratory pattern changes in chronic heart failure patients and the authors suggest that polysomnography be performed only in high-risk patients, saving costs and the resources of sleep laboratories.

The efficacy of noninvasive mechanical ventilation on nocturnal hypoxaemia in Duchenne's muscular dystrophy.

The aim of this 2 yr follow-up study was to evaluate the efficacy of nocturnal noninvasive mechanical ventilation in a group of 10 Duchenne's muscular dystrophy (DMD) patients who desaturated during the night but had normal daytime blood gases: mean (range) age 18.3 (15-22) yrs; mean (SD) vital capacity (VC) 752.5 (460-1,308) mL; mean time in bed (TIB) with arterial oxygen saturation (Sa,O2) < 90% 22.8% of total TIB (range: 16.6-32.0); mean arterial oxygen tension (Pa,O2) 10.3 (9.3-11.7) kPa (78 (70.0-87.8) mmHg); mean arterial carbon dioxide tension (Pa,CO2) 5.9 (4.8-6.5) kPa (44.3 (36.3-48.5) mmHg). All the patients were noninvasively ventilated during the night with a bilevel positive pressure ventilation (BiPAP) devise in spontaneous mode in order to correct the episodes of nocturnal desaturation. Nocturnal Sa,O2 values normalized during nocturnal noninvasive mechanical ventilation, and daytime sleep-disordered breathing disappeared, for the entire study period. No statistically significant differences were observed between baseline and follow-up daytime blood gas values, although a slight increase in Pa,O2 was found. During the follow-up, VC declined at a rate of 79.1 +/- 25 mL.yr-1, less than that generally reported in the past in untreated patients in the same age range. In conclusion, our data suggest that patients with advanced Duchenne's muscular dystrophy with pronounced nocturnal desaturation, not fulfilling criteria for imperative ventilation, could be successfully treated with "elective" nocturnal ventilation with immediate benefits consequent to the correction of the nocturnal blood gas anomalies and with long-term benefits related to the preservation of residual respiratory function, delay of development of chronic hypercapnia and thus the requirement for imperative mechanical ventilation.

Daytime PaO2 in OSAS, COPD and the combination of the two (overlap syndrome).

BACKGROUND: OSAS and COPD are often associated with day-time hypoxemia. Overlap Syndrome (OS), the association between both diseases, increases the risk of day-time hypoxemia. The aim of this study was to investigate the mechanisms which could justify the low oxygen level and the effect of CPAP. METHODS: We performed a retrospective analysis in all patients referred to our institutes for suspected OSAS and who also underwent spirometry and blood gas analysis during our evaluation. Thus, 720 patients were selected. According to pulmonary function test parameters they were divided into 3 groups: OSAS (N = 466,65%); OS (N = 168,23%) and COPD (N = 86,12%). In order to evaluate the differences between the three groups, ANOVA analyses were carried out, whereas a multivariate analysis was performed in order to evaluate which factors determine the diurnal PaO(2). In 90 patients we also have the data on blood gas analysis after one year of CPAP treatment, so we evaluate the PaO(2) improvement in accordance with compliance to treatment in these patient subgroups. RESULTS: The OS group showed a lower level of daytime PaO(2) compared with OSAS patients and T90 was higher in OS compared with OSAS. A multivariate analysis showed that in the OS diurnal PaO(2) correlated with age (ß = -0.20) and moreover with FEV(1) (ß = 0.31) and T90 (ß = 0.37), while in the OSAS a correlation was found with FEV(1) (ß = -0.11) and mostly with BMI (ß = 0.25), age and T90. In all patients with good compliance to CPAP day-time PaO(2) improved. CONCLUSIONS: Our data suggest that day-time hypoxemia in OSA patients is largely determined by the increase of body weight and severity of nocturnal hypoxia. However, CPAP therapy has been shown to improve daytime PaO(2) values both in OSAS and in OS.