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Biomedical subjects

A Braghiroli

Publications and source records attributed to A Braghiroli.

At least 19 recordsLinked to original sources
PubMed2000

Blood pressure and heart rate during periodic breathing while asleep at high altitude.

The ventilatory and arterial blood pressure (ABP) responses to isocapnic hypoxia during wakefulness progressively increased in normal subjects staying 4 wk at 5,050 m (Insalaco G, Romano S, Salvaggio A, Braghiroli A, Lanfranchi P, Patruno V, Donner CF, and Bonsignore G; J Appl Physiol 80: 1724-1730, 1996). In the same subjects (n = 5, age 28-34 yr) and expedition, nocturnal polysomnography with ABP and heart rate (HR) recordings were obtained during the 1st and 4th week to study the cardiovascular effects of phasic (i.e., periodic breathing-dependent) vs. tonic (i. e., acclimatization-dependent) hypoxia during sleep. Both ABP and HR fluctuated during non-rapid eye movement sleep periodic breathing. None of the subjects exhibited an ABP increase during the ventilatory phases that correlated with the lowest arterial oxygen saturation of the preceding pauses. Despite attenuation of hypoxemia, ABP and HR behaviors during sleep in the 4th wk were similar to those in the 1st wk. Because ABP during periodic breathing in the ventilatory phase increased similarly to the ABP response to progressive hypoxia during wakefulness, ABP variations during ventilatory phases may reflect ABP responsiveness to peripheral chemoreflex sensitivity rather than the absolute value of hypoxemia, suggesting a major tonic effect of hypoxia on cardiorespiratory control at high altitude.

Acclimatization↗
PubMed2000

[The assessment of breathing during sleep: a curiosity or clinical necessity?].

The study of sleep, which initially focused on the neurophysiological mechanisms and cardiorespiratory function during the night, has shown the presence of sleep-related breathing disorders that epidemiological, pathophysiological and clinical data have indicated to be associated with increased cardiovascular morbidity and mortality: the obstructive sleep apnea syndrome (OSAS) and the central sleep apnea syndrome (CSAS). OSAS is a condition characterized by repetitive respiratory pauses due to the pharynx wall collapse, with a subsequent obstruction to the airflow. The hemodynamic consequences due to the markedly increased negative intrathoracic pressure (induced by the respiratory muscle effort towards the closed upper airways), the progressive hypercapnic hypoxemia and the arousal terminating the apneas, are the pathophysiological keys of the cardiovascular effects of OSAS and may explain the association between OSAS and the documented increase of cardiovascular morbidity and mortality. CSAS is a breathing disorder characterized by recurrent episodes of central hypopneas or apneas and hyperventilation which, is the classical form described by Cheyne and Stokes, show a crescendo-decrescendo pattern of respiration. Pathophysiological and epidemiological data clearly indicate the link between CSAS and heart failure, also showing a correlation between respiratory disorders and the severity of hemodynamic impairment. However, other mechanisms are involved in the genesis of CSAS in explaining the variable presence of CSAS independent of cardiac function and, more importantly, the impact of CSAS on poor prognosis in heart failure. In conclusion, the data available indicate the need to include screening for sleep-related breathing disorders in the evaluation of cardiac patients who are at risk for OSAS and, particularly, in patients with heart failure, who could really benefit from treatment of the respiratory disorder.

Cardiovascular Physiological Phenomena↗
PubMed1999

Prognostic value of nocturnal Cheyne-Stokes respiration in chronic heart failure.

BACKGROUND: Nocturnal Cheyne-Stokes respiration (CSR) occurs frequently in patients with chronic heart failure (CHF), and it may be associated with sympathetic activation. The aim of the present study was to evaluate whether CSR could affect prognosis in patients with CHF. METHODS AND RESULTS: Sixty-two CHF patients with left ventricular ejection fraction </=35%, in NYHA class II to III, underwent clinical evaluation, Doppler echocardiography, ergospirometry, phenylephrine test, Holter recording, and a sleep study to evaluate the occurrence of CSR, expressed as percentage of periodic breathing, and apnea/hypopnea index (AHI) (ie, the number of apneas and hypopneas per hour of recording). During a mean follow-up of 28+/-13 months, 15 patients died of cardiac causes. Nonsurvivors were in a higher NYHA functional class than survivors (P<0.001) and had a more depressed left ventricular ejection fraction (P<0.03), a shorter deceleration time of early filling (P<0. 05), larger left and right atria (P<0.05 and P<0.02, respectively) and a lower peak V(O2) (P<0.05). Nonsurvivors also spent a greater percentage of the night in periodic breathing (P<0.01) with a greater AHI (P<0.03) and showed lower values of diurnal baroreflex sensitivity (P<0.05) and of heart rate variability (sdNN: P<0.01). Multivariate analysis revealed the AHI (chi2, 10.4; P<0.01), followed by left atrial area (chi2, 5.7; P<0.01), as the only independent and additional predictors of subsequent cardiac death. Patients at very high risk for fatal outcome could be identified by an AHI >/=30/h and left atria >/=25 cm2. CONCLUSIONS: The AHI is a powerful independent predictor of poor prognosis in clinically stable patients with CHF. The presence of an AHI >/=30/h adds prognostic information compared with other clinical, echocardiographic, and autonomic data and identifies patients at very high risk for subsequent cardiac death.

Aged↗
PubMed1999

Periodic breathing during sleep in patients affected by fibromyalgia syndrome.

Seventeen patients affected by fibromyalgia syndrome (FMS) (16 females and one male) and 17 matched healthy subjects underwent formal polysomnography, a sleep questionnaire and lung function tests. FMS patients slept significantly less efficiently than the healthy controls (p<0.01), had a higher proportion of stage 1 sleep (mean+/-SD, 21+/-6% versus 11+/-4%; p<0.001), less slow wave sleep (p<0.01) and twice as many arousals per hour of sleep (p<0.001). The respiratory pattern of FMS patients showed a high occurrence of periodic breathing (PB) (15+/-8% of total sleep time) in 15/17 patients, versus 2/17 control subjects. The short length of apnoeas and hypopnoeas did not affect the apnoea/hypopnoea index (5.1+/-3.5 versus 3.2+/-1.6; NS), but FMS patients had a greater number of desaturations per hour of sleep (8+/-5 versus 3+/-3; p<0.01). Pulmonary volumes did not differ between the two groups, but FMS patients had a lower transfer factor of the lung for carbon monoxide (TL,CO (5.8+1 versus 7.7+1 mmol x min(-1) x kPa(-1); p=0.001). PB occurrence correlated with TL,CO (r=-0.62; p=0.01), number of desaturations (r=0.76, p=0.001) and carbon dioxide tension in arterial blood (Pa,CO2) (r=-0.50; p=0.05). Stepwise multiple linear regression analysis showed desaturation frequency (p=0.0001) and TL,CO (p=0.029) to be the best predictors of PB percentage (R2 0.73; p=0.0001). Patients complaining of daytime hypersomnolence had a higher number of tender points, about twice as many arousals per hour and a lower sleep efficiency than patients who did not report this symptom. TL,CO was more impaired and the occurrence of PB was higher. The occurrence of periodic breathing in fibromyalgia syndrome patients, which was previously unreported, and is shown to be linked to a reduction of transfer factor of the lung for carbon monoxide could play a major role in the symptoms of poor sleep of these patients.

Disorders of Excessive Somnolence↗
PubMed1998

Effects of high-altitude periodic breathing on sleep and arterial oxyhaemoglobin saturation.

This study aimed to investigate the effect of periodic breathing (PB) at high altitude on sleep structure and arterial oxygen saturation (Sa,O2). Five healthy subjects underwent polysomnographic studies at sea level, and during the first and the fourth week of sojourn at 5,050 m. Their breathing pattern, sleep architecture and Sa,O2 were analysed. PB was detected in the high-altitude studies during nonrapid eye movement (NREM) sleep and tended to increase from the first to the fourth week. Stages 3-4 were absent in four subjects at the first week, but only in one at the fourth week, irrespective of the amount of PB. The arousal index was 11.6+/-3.8 at sea level, 30.1+/-15.5 at the first week at altitude and 33.0+/-18.2 at the fourth week. At altitude, arousal index in NREM sleep was higher during PB than during regular breathing. In NREM sleep, the mean highest Sa,O2 levels in NREM epochs with PB were higher than in those with regular breathing by 2.8+/-1.7% at the first week and 2.9+/-1.5% at the fourth week (p<0.025). From the first to the fourth week, mean Sa,O2 increased significantly during wakefulness (5.6%), NREM (5.2% with regular breathing and 5.3% with PB) and rapid eye movement sleep (7.6%). The data demonstrate a slight role of periodic breathing in altering sleep architecture at high altitude and also show that periodic breathing induces only a minor improvement in arterial oxygen saturation during nonrapid eye movement sleep.

Acclimatization↗
PubMed1997

Nocturnal asthma: mechanisms and therapy.

Nocturnal worsening of symptoms affects a large number of patients suffering from asthma. Recent studies show that airway inflammation underlies nocturnal awakenings and increased airway hyperreactivity. These studies, however, yield conflicting results concerning the pathogenesis of the disease, making it difficult to understand the mechanisms involved in sustaining nocturnal asthma. This article reviews the principal pathogenetic mechanisms of nocturnal asthma, showing that worsening of symptoms at night may be the result of a more severe disease as well as of increased inflammation at night and higher susceptibility. We also review the pharmacologic treatment of nocturnal asthma which is mainly based on antiinflammatory treatment with inhaled or oral steroids or combined therapies with theophylline and beta 2 agonists. The activity of antileukotrine compounds in asthma is also summarized.

Anti-Asthmatic Agents↗
PubMed1997

Causes of death in patients with COPD and chronic respiratory failure.

Although the factors associated with mortality, such as forced expiratory volume in one second (FEV1), arterial oxygen tension (Pa,O2) and pulmonary arterial pressure, have been well described, there is limited information on the circumstances of death in patients with chronic obstructive pulmonary disease (COPD). The aim of this study was to investigate the causes and circumstances of death in patients with COPD and chronic respiratory failure (Pa,O2 < 8.0 kPa (60 mmHg) breathing air), treated with long-term oxygen therapy (LTOT). Ten European centres participated in the study and data were collected from patients both during a period of clinical stability and at the time of death. Of the 215 patients evaluated (161 males and 54 females; aged 66 +/- 10 yrs), the major causes of death were: acute on chronic respiratory failure (38%); heart failure (13%); pulmonary infection (11%); pulmonary embolism (10%); cardiac arrhythmia (8%); and lung cancer (7%). Seventy five percent of patients died in hospital. There was no difference in the number of patients who died in the morning, afternoon and night hours. Twenty percent of the total died during sleep and in 26% death was unexpected. A lower arterial carbon dioxide tension (Pa,CO2), less oxygen usage per 24 h, and increased incidence of arrhythmias were seen in those patients who died suddenly. Drug therapy was not related to unexpected death. The majority of patients with chronic obstructive pulmonary disease on long-term oxygen therapy died from chronic or acute on chronic respiratory failure. Prevention and treatment of respiratory failure in patients with chronic obstructive pulmonary disease is likely to have the greatest impact in reducing mortality.

Aged↗
PubMed1997

Pulmonary failure as a cause of death in COPD.

Data on the outcome of patients with chronic obstructive pulmonary disease (COPD) are limited. We know that the prognosis is poor when respiratory insufficiency develops, but we have little information on the actual cause of death. Epidemiological studies are suitable for the assessment of the prevalence of the disease, but give no details on the actual cause of death. Age and forced expiratory volume in one second (FEV1) have been recognized as the best predictors of mortality in studies designed to quantify survival of COPD patients, particularly when the post-brochodilator value is used, as this provides a better estimate of airway and parenchymal damage. Data from Intensive Care Units on acute respiratory failure have several significant limitations. Firstly, it is probable that some patients elect not to undergo intensive treatment for a terminal bout of respiratory failure, particularly if it is not first episode. Secondly, the actual cause of death is often not described in adequate detail. Hypoxaemia and acidaemia are the main risk factors in acute exacerbation of the disease and the presence of pulmonary infiltrates on chest radiographs worsens the prognosis. A single bout of respiratory failure appears to have no effect on the prognosis of COPD patients after recovery, but there is a consistent increase in mortality after the second episode. It seems possible to manage the majority of episodes of acute respiratory failure with mechanical ventilation administered with noninvasive techniques. When endotracheal intubation is necessary, the prognosis is usually poor and the survival after 1 yr is usually lower than 40%. The role of long-term home mechanical ventilation is still unclear. Results from pivotal studies have been encouraging, although survival is far less impressive than in neuromuscular disorders. In patients with end-stage lung disease, lung transplantation can be considered the only possibility of increasing pulmonary functional capacity. However the technique is reserved only for a highly selected group of patients and data on the long-term outcome are awaited.

Acute Disease↗
PubMed1996

Cardiovascular and ventilatory response to isocapnic hypoxia at sea level and at 5,050 m.

To assess the effect of chronic hypoxic conditions on ventilatory, heart rate (HR), and blood pressure (BP) responses to acute progressive isocapnic hypoxia, we studied five healthy Caucasian subjects (3 men and 2 women). Each subject performed one rebreathing test at sea level (SL) and two tests at the Pyramid laboratory at Lobuche, Nepal, at the altitude of 5,050 m, 1 day after arrival (HA1) and after 24 days of sojourn (HA2). The effects of progressive isocapnic hypoxia were tested by using a standard rebreathing technique. BP, electrocardiogram, arterial oxygen saturation, airflow and end-tidal CO2 and O2 were recorded. For each subject, the relationships between arterial oxygen saturation and HR, systolic BP and minute ventilation (VE), respectively, were evaluated. At HA1, the majority of subjects showed a significant increase in VE and BP response and a decrease in HR response to progressive isocapnic hypoxia as compared to SL. At HA2, VE and BP responses further increased, whereas the HR response remained similar to that observed at HA1. A significant relationship between hypoxic ventilatory responses and both systolic and diastolic BP responses to progressive hypoxia was found. No significant correlation was found between hypoxic ventilatory and HR responses.

Adult↗
PubMed1996

When is liquid oxygen really needed?

Liquid oxygen is a synonym for portable oxygen, as it combines a big cylinder with an easy-to-fill portable unit, suitable for exercise and use out-doors. The main drawback is its high cost, inherent in a home delivery system, which discouraged many nations from its introduction. The best candidates are patients able to move, who are still active and do not have psychological reticence to its use in public. Transtracheal systems and the advantage of a round the clock treatment and a reduction of flow rate, crucial both to lengthen the autonomy of portable units and to avoid flows higher than 4 L.min-1, which cannot be maintained. Finally, patients on liquid oxygen usually have a better adherence to treatment, mainly compared to those using a concentrator, possibly improving its effectiveness, which is notoriously dependent on total usage per day.

Humans↗
PubMed1995

The effects of doxofylline versus theophylline on sleep architecture in COPD patients.

Theophylline is known to alter sleep architecture because of its affinity to adenosine receptors. One of the consequences of disrupted sleep is impaired cognitive performance. A single-blind, randomized cross-over study of eight male chronic obstructive pulmonary disease (COPD) patients was undertaken to evaluate the effects of theophylline versus doxofylline on sleep architecture. The patients, who were all ex-smokers, had been treated with theophylline. Mean age was 53 +/- 12 yrs, forced expiratory volume in one second (FEV1) 50 +/- 22% predicted and forced vital capacity (FVC) 70 +/- 18% predicted. Following a wash-out period, four patients were given oral slow-release theophylline (T) (300 mg b.i.d.) for one week, followed by a cross-over to doxofylline (D) (400 mg t.i.d.) for a second week. The other four patients were given the drugs in the reverse order. All patients underwent polysomnography at baseline and at the end of each week of treatment. The number of arousals per hour was 5.5 +/- 2.9 at baseline, 9.4 +/- 5.2 during T treatment and 5.4 +/- 4.4 during D treatment. During T treatment, sleep efficiency was 60 +/- 19% vs 75 +/- 13% recorded at baseline trial and 68 +/- 25 recorded during D treatment. Sleep quality, during T treatment, was poorer than at baseline, with a greater increase in the percentage of wakefulness and more stage 2 sleep than at baseline. Slow wave sleep was reduced with both treatments, particularly D. Neither drug affected the arterial oxygen saturation (Sao2) or respiratory rate during sleep.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Long-term oxygen therapy.

Controlled studies have demonstrated that the correction of tissue hypoxia increases survival and reduces pulmonary hypertension in patients with chronic obstructive pulmonary disease (COPD) receiving oxygen therapy 15 h/day or longer. Long-term oxygen therapy (LTOT) is recommended to any patient with COPD who has a PaO2 of < or = 7.3 kPa. In most countries, the PaO2 threshold is 8kPa in patients with chronic hypoxemia (PaO2 > or = 55 mm Hg) with associated hematocrit > or = 55%, pulmonary hypertension or cor pulmonale. Desaturations during sleep or exercise should be investigated, although a consensus as to whether and how these episodes should be treated has yet to be reached. The indications for LTOT in restrictive lung diseases, such as interstitial pulmonary fibrosis and pneumoconiosis, remain controversial. In many countries, oxygen is not prescribed if the patient is a current smoker. Breathlessness without hypoxemia should not be considered an indication for LTOT. The oxygen is usually administered through nasal cannula. Venturi type masks, nasopharyngeal and transtracheal catheters are associated with several drawbacks. Oxygen is usually supplied by the relatively cheap oxygen concentrator. Liquid oxygen is favored when a portable source is an important requirement. Many questions remain unanswered concerning the duration of added survival, the effect of LTOT on physiological parameters such as pulmonary artery pressure, respiratory failure in non-COPD patients, exercise and nocturnal desaturations.

Humans↗
PubMed1993

Overnight urinary uric acid: creatinine ratio for detection of sleep hypoxemia. Validation study in chronic obstructive pulmonary disease and obstructive sleep apnea before and after treatment with nasal continuous positive airway pressure.

During hypoxia ATP degradation to uric acid is increased in animal models and humans. To assess the reliability of an overnight increase in uric acid excretion as a marker of nocturnal hypoxemia, we selected 10 normal volunteers (7 males and 3 females), 29 COPD patients (26 males and 3 females), and 49 subjects with obstructive sleep apnea (OSA) (43 males and 6 females). The patients underwent standard polysomnography, which was repeated in 14 subjects with nasal continuous positive airway pressure (CPAP), and were subdivided into two groups: Group D included desaturating subjects who spent at least 1 h at SaO2 < 90% and 15 min below 85%, and Group ND were nondesaturating subjects. The overnight change in the uric acid:creatinine ratio (delta UA:Cr) was negative in normal subjects (-27.5 +/- 9.1 [mean +/- SD]) and ND groups: -19.7 +/- 14.3 in COPD, -16.1 +/- 13.0 in OSA. In both COPD and OSA Group D, the ratio was usually positive: delta UA:Cr was 17.9 +/- 31.4 in Group D COPD (p < 0.001 versus ND) and 10.1 +/- 30.7 in Group D OSA (p < 0.001 versus ND and versus normal subjects) despite 4 of 15 false negative results in COPD and 8 of 20 in OSA. CPAP effective treatment induced a marked reduction ((p = 0.0024) in delta UA:Cr, leading to a negative value. We conclude that delta UA:Cr seems to be a promising index of significant nocturnal tissue hypoxia, with good specificity but poor sensitivity (about 30% false negative), which might be useful for the long-term follow-up of outpatients on nasal CPAP with a positive ratio at baseline.

Adult↗
PubMed1993

Home mechanical ventilation in kyphoscoliosis.

The aim of the study was to determine whether intermittent positive pressure ventilation (IPPV), delivered either by nasal mask or by tracheostomy, is able to improve alveolar gas exchange in kyphoscoliotic patients with respiratory failure. We evaluated 17 patients, 10 females and 7 males, aged 52 +/- 12 (mean +/- SD) yrs. Eight had severe respiratory failure (arterial oxygen tension (PaO2) 53.2 +/- 9.3 mmHg (7.1 +/- 1.2 kPa); arterial carbon dioxide tension (PaCO2) 73.3 +/- 12.5 mmHg (9.7 +/- 1.6 kPa), breathing supplemental oxygen), and were put on IPPV via tracheostomy (TIPPV). The others (PaO2 54.5 +/- 5.5 mmHg (7.3 +/- 0.7 kPa); PaCO2 57.9 +/- 7 mmHg (7.7 +/- 0.9 kPa), breathing air), were put on IPPV via nasal mask (NIPPV). Home mechanical ventilation (HMV) was performed at night (7 +/- 1 h) by means of a volume-cycled pressure respirator in control mode. The frequency was adapted to the patient's spontaneous respiratory rate, and then eventually modified according to blood gases. A silicone mask was moulded onto the patient's nose. Supplemental oxygen (to maintain arterial oxygen saturation (SaO2) > 90%) was used only for tracheostomized patients, whereas NIPPV was performed with fractional inspiratory oxygen (FIO2) 21%. Arterial blood samples were obtained for all patients in steady-state condition, 8 +/- 1 h from the withdrawal, breathing air, after 1 and 6 months of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗