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Biomedical subjects

R Rodriguez-Roisin

Publications and source records attributed to R Rodriguez-Roisin.

At least 55 records · Page 3Linked to original sources
PubMed1997

Effects of noninvasive ventilation on pulmonary gas exchange and hemodynamics during acute hypercapnic exacerbations of chronic obstructive pulmonary disease.

Noninvasive positive pressure ventilation (NIPPV) can replace tracheal intubation in acute exacerbations of chronic obstructive pulmonary disease (COPD) with severe hypercapnic respiratory failure. However, the underlying mechanisms by which NIPPV improves pulmonary gas exchange are not known. We studied 10 male COPD patients (68 +/- 8 [SD] yr) with acute severe hypercapnic respiratory failure within 36 h after hospital admission. Measurements of pulmonary gas exchange, hemodynamics, and respiratory mechanics were done: (I) breathing spontaneously (baseline); (2) after 15 and 30 min of NIPPV with pressure support (inspiratory pressure = 12 +/- 2 cm H20, PEEP = 3 +/- 2 cm H20); and (3) 15 min after NIPPV withdrawal. Patients were ventilated using a full face mask, keeping FIO2 constant (0.23 +/- 0.02) in all conditions. Compared with baseline, during NIPPV (15 min) we observed a moderate increase in Pa02 (from 50 +/- 6 to 57 +/- 9 mm Hg; p < 0.05), and a fall in PaCO2 (from 66 +/- 10 to 59 +/- 10 mm Hg; p < 0.0001), but AaPO2 increased (from 39 +/- 13 to 48 +/- 13 mm Hg; p < 0.001). Breathing frequency decreased (from 26 +/- 5 to 19 +/- 3 breaths/min; p < 0.0001), tidal volume increased (from 311 +/- 42 to 520 +/- 133 ml; p < 0.0001), and minute ventilation increased (from 8.0 to 1.7 to 9.6 +/- 2.0 L/min; p < 0.05). Cardiac output fell during NIPPV in all patients (from 6.7 +/- 1.6 to 5.8 +/- 1.3 L/min; p < 0.0025) with no impact on mixed venous PO2. No substantial changes in VA/Q mismatching (multiple inert gas elimination technique) were observed. While oxygen uptake showed a trend to decrease, the respiratory exchange ratio (R) increased (from 0.78 +/- 0.17 to 0.90 +/- 0.22; p < 0.001). The effects of NIPPV were unchanged at 30 min compared with 15 min and were reversed after 15 min of NIPPV withdrawal. We conclude that improvement in respiratory blood gases during NIPPV is essentially due to higher alveolar ventilation (p < 0.001) and not to improvement in VA/Q relationships. The increase in AaPO2 was explained by the rise in R due to an increased clearance of body stores of C02 during NIPPV. Our results indicate that attainment of an efficient breathing pattern rather than high inspiratory pressures should be the primary goal to improve arterial blood gases during NlPPV in this type of patient.

Acute Disease↗
PubMed1997

Mechanisms of worsening gas exchange during acute exacerbations of chronic obstructive pulmonary disease.

This study was undertaken to investigate the mechanisms that determine abnormal gas exchange during acute exacerbations of chronic obstructive pulmonary disease (COPD). Thirteen COPD patients, hospitalized because of an exacerbation, were studied after admission and 38+/-10 (+/-SD) days after discharge, once they were clinically stable. Measurements included forced spirometry, arterial blood gas values, minute ventilation (V'E), cardiac output (Q'), oxygen consumption (V'O2), and ventilation/perfusion (V'A/Q') relationships, assessed by the inert gas technique. Exacerbations were characterized by very severe airflow obstruction (forced expiratory volume in one second (FEV1) 0.74+/-0.17 vs 0.91+/-0.19 L, during exacerbation and stable conditions, respectively; p=0.01), severe hypoxaemia (ratio between arterial oxygen tension and inspired oxygen fraction (Pa,O2/FI,O2) 32.7+/-7.7 vs 37.6+/-6.9 kPa (245+/-58 vs 282+/-52 mmHg); p=0.01) and hypercapnia (arterial carbon dioxide tension (Pa,CO2) 6.8+/-1.6 vs 5.9+/-0.8 kPa (51+/-12 vs 44+/-6 mmHg); p=0.04). V'A/Q' inequality increased during exacerbation (log SD Q', 1.10+/-0.29 vs 0.96+/-0.27; normal < or = 0.6; p=0.04) as a result of greater perfusion in poorly-ventilated alveoli. Shunt was almost negligible on both measurements. V'E remained essentially unchanged during exacerbation (10.5+/-2.2 vs 9.2+/-1.8 L x min(-1); p=0.1), whereas both Q' (6.1+/-2.4 vs 5.1+/-1.7 L x min(-1); p=0.05) and V'O2 (300+/-49 vs 248+/-59 mL x min(-1); p=0.03) increased significantly. Worsening of hypoxaemia was explained mainly by the increase both in V'A/Q' inequality and V'O2, whereas the increase in Q' partially counterbalanced the effect of greater V'O2 on mixed venous oxygen tension (PV,O2). We conclude that worsening of gas exchange during exacerbations of chronic obstructive pulmonary disease is primarily produced by increased ventilation/perfusion inequality, and that this effect is amplified by the decrease of mixed venous oxygen tension that results from greater oxygen consumption, presumably because of increased work of the respiratory muscles.

Acute Disease↗
PubMed1997

Acute severe asthma: pathophysiology and pathobiology of gas exchange abnormalities.

Acute severe asthma, or "status asthmaticus", is a devastating clinical condition ultimately resulting in life-threatening hypoxaemia. The pivotal intrapulmonary mechanism of this condition is profound ventilation/perfusion (V'A/Q') mismatch, characterized by a predominant bimodal blood flow pattern reflecting a marked deterioration (increase) of the dispersion of pulmonary blood flow. This V'A/Q' profile is consistent with the presence of numerous alveolar units with low V'A/Q' ratios, in which ventilation is markedly reduced, although never abolished, but perfusion is maintained. Further V'A/Q' worsening whilst breathing 100% O2 suggests the presence of an underlying vigorous hypoxic vascular response. Of equal importance, gas exchange disturbances are poorly related to the severity of reduced maximal airflow rates. Inhaled platelet-activating factor (PAF), both in normal individuals and asthmatic patients, results in moderate-to-severe disturbance of V'A/Q' status, a finding that is probably related to altered microvascular permeability within the airway wall. Salbutamol, but not ipratropium bromide, prevented all PAF-induced systemic and lung function abnormalities, possibly because venoconstriction in the bronchial circulation was antagonized. Taken together, these findings support the hypothesis that platelet-activating factor may play a critical role in the pathobiology of severe acute exacerbations of asthma.

Acute Disease↗
PubMed1997

Effect of acetylsalicylic acid on pulmonary gas exchange in patients with severe pneumonia: a pilot study.

BACKGROUND: It has been hypothesized that local release of prostacyclin in acute pneumonia may ablate hypoxic pulmonary vasoconstriction, thus contributing to the impairment of pulmonary gas exchange in these patients. Inhibition of cyclooxygenase pathway could prevent this phenomenon by reducing the release of these metabolites. METHODS: A study was designed to assess the effect of I.V. acetylsalicylic acid (ASA) (2 g) on pulmonary gas exchange in seven patients (age, 64+/-11 [mean+/-SD] years) with unilateral severe pneumonia (PaO2/fraction of inspired oxygen, 168+/-67) needing mechanical ventilation. Respiratory gases, pulmonary and systemic hemodynamics, and ventilation-perfusion (VA/Q) distributions were studied before and 15 and 60 min after the infusion of ASA. RESULTS: At baseline, the amount of shunt (VA/Q ratios <0.005) was 28+/-17% of cardiac output, blood flow to areas with low VA/Q ratios (<0.1, excluding shunt) was 8+/-7%, and the dispersion of pulmonary blood flow distribution (second moment, log SD Q) was 1.45+/-0.49 (normal range, 0.3 to 0.6). Sixty minutes after the infusion of ASA, we observed a mild reduction of the amount of shunt, from 28+/-17% to 23.5+/-13% (p<0.05) without changes in arterial oxygenation. This was associated with a significant increase in mean pulmonary artery pressure (from 21.9+/-3.6 to 24.4+/-5.1 and 23.9+/-5.3 mm Hg, p<0.025 and p=0.1) and pulmonary vascular resistance (from 1.4+/-0.9 to 1.8+/-0.8 and 1.8+/-1.3 mm Hg x min x L(-1) , p<0.002 and p=0.11) 15 and 60 min after ASA, respectively. The ASA plasma levels were within the normal therapeutic range (120+/-7 microg/mL, 15 min, and 113+/-11 microg/mL, 60 min after ASA infusion). CONCLUSIONS: Although there was a modest improvement in intrapulmonary shunt, our results suggest that perfusion of ASA in this small sample of patients with severe pneumonia appears to be of little benefit as complementary treatment for severe hypoxemia.

Adult↗
PubMed1996

Worsening of pulmonary gas exchange with nitric oxide inhalation in chronic obstructive pulmonary disease.

BACKGROUND: Inhalation of nitric oxide (NO) causes selective pulmonary vasodilation and improves arterial oxygenation in acute respiratory distress syndrome. But some patients do not respond or gas exchange worsens when inhaling NO. We hypothesised that this detrimental effect might be related to the reversion of hypoxic vasoconstriction in those patients where this mechanism contributes to ventilation-perfusion (V(A)/Q) matching. METHODS: We studied 13 patients with advanced chronic obstructive pulmonary disease (COPD). We compared their responses to breathing room air, NO at 40 parts per million in air, and 100% O2. Changes in pulmonary haemodynamics, blood gases, and V(A)/Q distributions were assessed. FINDINGS: NO inhalation decreased the mean (SE) pulmonary artery pressure from 25.9 (2.0) to 21.5 (1.7) mm Hg (p = 0.001) and PaO2 from 56 (2) 53 (2) mm Hg (p = 0.014). The decrease in PaO2 resulted from worsening of V(A)/Q distributions, as shown by a greater dispersion of the blood-flow distribution (logSD Q) from 1.11 (0.1) to 1.22 (0.1) (p = 0.018). O2 breathing reduced the mean pulmonary arterial pressure to 23.4 (2.1) mm Hg and caused greater V(A)/Q mismatch (logSD Q, 1.49 [0.1]). The intrapulmonary shunt on room air was small (2.7 [0.9]%) and did not change when breathing NO or O2. INTERPRETATION: We conclude that in patients with COPD, in whom hypoxaemia is caused essentially by V(A)/Q imbalance rather than by shunt, inhaled NO can worsen gas exchange because of impaired hypoxic regulation of the matching between ventilation and perfusion.

Administration, Inhalation↗
PubMed1996

Mechanisms of gas exchange impairment in patients with liver cirrhosis.

This article reviews the basic pathophysiologic mechanisms underlying the abnormal pulmonary gas exchange often seen in patients with cirrhosis. To summarize, the following keypoints seem appropriate: (1) Patients with cirrhosis have a low pulmonary vascular tone characterized by a poor or absent hypoxic pressor response. This results in a marked dilation of the pulmonary vasculature. (2) This abnormal pulmonary vascular tone, independently of airway disease, causes VA/Q mismatch and mild to moderate hypoxemia. Yet, as liver disease progresses and hepatocellular function deteriorates, more severe degrees of intrapulmonary shunt emerge and, probably, O2 diffusion limitation ensues, causing severe respiratory failure (see Table 1). (3) At rest, the high cardiac output and minute ventilation of cirrhosis minimize the degree of arterial hypoxemia that otherwise would be expected from the observed degree of both VA/Q inequality and intrapulmonary shunt. During exercise, the relative "normalization' (with respect to metabolic demands) of the hemodynamic and ventilatory status of the patient explains the fall in PaO2. (4) A clear pathogenic mechanism of these pathophysiologic abnormalities is still lacking, although available evidence suggests that both the liver and the endothelial cells may play a pivotal role in the regulation of the pulmonary vascular tone in these patients. (5) To date, no pharmacologic intervention has been effective in treating hypoxemia in these patients. Yet liver transplantation helps in most of them. This observation reinforces the functional nature of the gas exchange abnormalities of cirrhosis.

Animals↗
PubMed1996

Physical exercise increases portal pressure in patients with cirrhosis and portal hypertension.

BACKGROUND & AIMS: In healthy subjects, exercise promotes marked hemodynamic and humoral changes characterized by an increase in cardiac output, a redistribution of blood flow to muscular territories under activity, and an increase in sympathoadrenergic activity. The aim of this study was to investigate the extent to which hemodynamic and humoral changes caused by exercise may influence portal and systemic hemodynamics in patients with cirrhosis. METHODS: In 8 patients with liver cirrhosis and portal hypertension, arterial pressure, cardiac output, portal pressure (as hepatic venous pressure gradient [HVPG]), and hepatic blood flow were measured before and at two steps of cycling exercise equivalent to 30% and 50% of their peak workload. RESULTS: Exercise (at 30% of peak work-load) significantly increased arterial pressure and cardiac output and decreased systemic vascular resistance. This was associated with a significant increase in HVPG (from 16.7 +/- 1.5 to 19.2 +/- 1.6 mm Hg; P < 0.01) and a significant reduction in hepatic blood flow (from 1291 +/- 216 to 1034 +/- 152 mL-min-1; P < 0.05). All of these changes were intensified at 50% of target workload. CONCLUSIONS: The present study shows that moderate exercise increases portal pressure and may therefore increase the risk of variceal bleeding in patients with esophageal varices. These findings suggest that cirrhotic patients with portal hypertension should be advised of potential risks during exercise.

Exercise↗
PubMed1996

Histopathologic and microbiologic aspects of ventilator-associated pneumonia.

BACKGROUND: The relationship between microbiology and histology in patients with ventilator-associated pneumonia has been sparsely described. METHODS: Twenty-five patients who died in the intensive care unit after their lungs had been mechanically ventilated for 72 h were studied. Twenty of the 25 died with clinical suspicion of pulmonary infection. A total of 375 immediate postmortem pulmonary biopsies were obtained after death and processed for quantitative microbiology and histology. Four evolutionary stages of pneumonia were defined: early, intermediate, advanced, and resolution. RESULTS: At least one specimen with histologic evidence of pneumonia was found in all but two patients (92%). Histologic pneumonia was a widespread and frequent process (46%) of biopsies examined) involving predominantly the lower lobes (55% of all biopsies with pneumonia) and showing different histopathologic stages of progression coexisting in the same lung lobes. Lung cultures were frequently polymicrobial (149 of 375, 40% of the pulmonary biopsy cultures, and 20 of 25, 80% of the cases) and not always yielding the same pathogen (19 microorganisms) when comparing one lung to the other. Histopathology and microbiologic biopsy cultures showed a weak relationship (28% and 49% of species had counts > or = 10(3) cfu/g in samples without pneumonia from patients with and without prior antibiotic treatment, respectively). Histopathologic evolutionary stages were not associated with any differences in quantitative culture results of pulmonary biopsies, independently of prior administration of antibiotics. Higher bacterial concentrations of biopsy cultures were associated with the absence of prior antibiotic treatment. CONCLUSIONS: Ventilator-associated pneumonia is a frequent diffuse and polymicrobial process showing different coexisting degrees of evolution and involving preferentially the lower lobes. Microbiology and histology can be dissociated even in the absence of prior antibiotic treatment. Lung histology appears more reliable than bacteriology as a diagnostic reference test.

Adult↗
PubMed1996

Comparison of partially attended night time respiratory recordings and full polysomnography in patients with suspected sleep apnoea/hypopnoea syndrome.

BACKGROUND: Laboratory full polysomnography (PSG) is considered to be the gold standard for the diagnosis of the sleep apnoea/hypopnoea syndrome (SAHS), but it is expensive and time consuming. A study was undertaken to evaluate the diagnostic usefulness of a partially attended night time respiratory recording (NTRR) and a clinical questionnaire in patients with suspected SAHS in comparison with full PSG. METHODS: Seventy six patients (54 men) of mean (SD) age 51 (11.5) years with a body mass index of 31 (5.7) kg/m2 were studied at random on two different nights with full PSG at the sleep laboratory and with NTRR on a respiratory ward. NTRR records oximetry, airflow, chest and abdominal motion. All signals were continuously displayed on a computer screen throughout the night and respiratory events were scored automatically the following morning. All patients completed a clinical questionnaire. RESULTS: Mean values of the apnoea/hypopnoea index (AHI) using NTRR were lower than those obtained with full PSG (22.7 (2.4) versus 32.2 (3) events/hour) which was mainly due to underrecognition of hypopnoeas. Sensitivity and specificity of NTRR for the diagnosis of SAHS were 82% and 90%, respectively, taking as reference AHI > 10 on full PSG (AHI-PSG > 10). The mean (+/-2SD) difference in AHI between the two methods was 9.6 (range -5.4-24.6) (95% confidence interval 6.2 to 13). Symptoms of witnessed apnoeas, impotence, the overall clinical impression of a trained physician, and a neck size over 40 cm were significantly more prevalent in patients with AHI-PSG of > 10, but impotence was the only clinical feature significantly more prevalent in patients with false negative compared with true negative NTRR results that helped to distinguish patients with NTRR < 10 but AHI-PSG > 10. CONCLUSIONS: NTRR is a helpful and easy complementary diagnostic tool in clinical practice because it detects patients with moderate to severe SAHS reasonably well and therefore can be useful for confirming a diagnosis of SAHS and also for treatment decisions. It is suggested that patients with suspicion of SAHS should be initially studied by NTRR. When NTRR is negative, a full PSG should be performed if witnessed apnoeas, impotence, systemic hypertension, ischaemic heart disease, and a trained physician's clinical impression of SAHS are present.

Adult↗
PubMed1996

Value of intracellular bacteria detection in the diagnosis of ventilator associated pneumonia.

BACKGROUND: Markers of ventilator associated pneumonia are of interest for confirming the diagnosis and for guiding the initial management of this frequent complication of mechanical ventilation. The detection of intracellular organisms in the polymorphonuclear leucocytes (PMNLs) and/or macrophages of bronchoalveolar lavage (BAL) fluid has been suggested as a specific test for the early indication of an infectious pulmonary process. METHODS: The diagnostic value of detecting intracellular organisms in two types of BAL fluid--protected (P-BAL) and conventional (C-BAL)--in 25 patients who died in one unit was prospectively studied. Immediately after death both P-BAL and C-BAL were performed bilaterally. Through a minithoracotomy on both sides of the chest bilateral bronchoscopically guided open lung biopsy samples were obtained from the same area, and an average of eight open lung blind biopsy samples (not bronchoscopically guided) were taken from each lung for histological examination. BAL fluid was examined for quantitative cultures (threshold 10(4) cfu/ml) and for the presence of intracellular organisms and extracellular organisms, and differential cell counts were also performed. RESULTS: Using the histopathology of the bronchoscopically guided open lung biopsies as the gold standard, detection of intracellular organisms in P-BAL (> or = 5%) and C-BAL (> or = 5%) fluids yielded 75% and 57% positive predictive values, and 83% negative predictive values, respectively. Prior treatment with antibiotics decreased the positive and negative predictive values of intracellular organism detection for both types of BAL fluid. The presence of intracellular organisms was correlated with the quantitative cultures of P-BAL and C-BAL samples. Quantitative cultures from P-BAL fluid were less sensitive (22% versus 45%) and more specific (100% versus 55%) than those from C-BAL samples. The percentage of extracellular organisms and the differential cell count in P-BAL and C-BAL samples could not discriminate between the presence or absence of pneumonia. CONCLUSIONS: The presence of > or = 5% intracellular organisms infecting PMNLs or macrophages in P-BAL or C-BAL fluids is a specific marker of ventilator associated pneumonia.

Bronchoalveolar Lavage Fluid↗
PubMed1996

Computed tomography-guided bronchoalveolar lavage in idiopathic pulmonary fibrosis.

BACKGROUND: High resolution computed tomography (HRCT) is now recognised as a sensitive tool for predicting the histological characteristics of the lung parenchymal abnormalities in patients with idiopathic pulmonary fibrosis (IPF). A reticular pattern on HRCT scanning is indicative of fibrotic histology while a ground glass pattern has been associated with inflammatory disease. The purpose of the present study was to investigate whether the cell population in the bronchoalveolar lavage (BAL) fluid from different lobes differs according to HRCT characteristics in patients with IPF. METHODS: Twenty six patients with IPF (18 men) of mean (SE) age 67 (2) years were included in the study. A semiquantitative analysis of the extent of the abnormalities on the HRCT scan was applied by summing the proportion of both reticular and ground glass patterns in each lobe (expressed as percentage of total area evaluated) and 100 ml double BAL was then randomly performed in the lobe with the most extensive involvement (lobe A) and that with the least extensive involvement (lobe B). RESULTS: Twenty three of the 26 patients (88%) had an abnormal cell count in the BAL fluid from lobe A compared with 18 patients (69%) with abnormalities in the BAL fluid from lobe B. The median (range) percentage of 8.5% (0-34%) and the absolute numbers of neutrophils (1.3 x 10(4)/ml, 0-14.6 x 10(4)/ml) in lobe A were significantly higher than those in lobe B (5% (0-26%) and 1.2 x 10(4)/ml (0-5 x 10(4)/ml), respectively). The percentage (3%, 0-19%) and absolute numbers (0.65 x 10(4)/ml, 0-4 x 10(4)/ml (0-4.8 x 10(4)/ml), respectively). For the group as a whole a correlation was found between the percentage and absolute numbers of neutrophils in the BAL fluid and the total score of abnormalities on the HRCT scan in the most involved lobe (lobe A). Multiple regression analysis indicated that both the percentage and absolute numbers of neutrophils were significantly and independently related to the extent of ground glass pattern. CONCLUSIONS: In patients with IPF the cell population in the BAL fluid is not homogeneous and seems to be related to the characteristics of the abnormalities on the HRCT scan present in the lavaged lobe.

Aged↗
PubMed1996

Salbutamol reduces pulmonary neutrophil sequestration of platelet-activating factor in humans.

To investigate whether salbutamol inhibits platelet-activating factor (PAF)-induced neutrophil sequestration in the lungs, we studied eight nonatopic, nonsmoking, healthy subjects (six men; aged 27.0 +/- 1.5 (SE) yr) with PAF-induced bronchial response. Prior to PAF challenge (24 micrograms), they inhaled either salbutamol (300 micrograms) or placebo in a randomized, double-blind, crossover manner two weeks apart. Respiratory system resistance (Rrs), arterial blood gases, and neutrophil counts were measured 4, 8, 12 and 30 min after PAF. Neutrophil kinetics in the lungs were assessed by tracking autologous 99mTc-erythrocytes and 111in-neutrophils. Compared with salbutamol, arterial blood neutrophil counts fell (p < 0.04) maximally at 4 min after PAF, followed by a mild rebound neutrophilia, whereas Rrs increased (p < 0.01) and Pao2 decreased (p < 0.05) at 4 min only. The intrapulmonary activity of 111in-neutrophils after pretreatment with placebo was higher compared with salbutamol (1.98 +/- 0.15 versus 1.33 +/- 0.23 cps/mCi/pixel) (p < 0.01) although both their initial sequestration (first-pass) and subsequent washout were not significantly different. Inhaled salbutamol blocks pulmonary neutrophil sequestration and lung function abnormalities following PAF challenge in humans.

Administration, Inhalation↗
PubMed1996

Community-acquired pneumonia in the elderly: A multivariate analysis of risk and prognostic factors.

To assess the risk and prognostic factors of community-acquired pneumonia occurring in the elderly (over age 65 yr) requiring hospitalization, two studies, case-control and cohort, were performed over an 8-mo period in a 1,000-bed university teaching hospital. We studied 101 patients with pneumonia (cases), age 78.5 +/- 7.9 yr (mean +/- SD). Each case was matched for sex, age (+/- 5 yr), and date of admission (+/- 2 d) with a control subject, without pneumonia during the preceding 3 yr, arriving at the emergency room. Etiologic diagnosis was obtained in 43 of 101 (42%) cases. The main microbial agents causing pneumonia were: Streptococcus pneumoniae (19 of 43, 44%), and Chlamydia pneumoniae (9 of 43, 21%). Gram-negative bacilli were uncommon (2 of 43, 5%). The multivariate analysis demonstrated that large-volume aspiration, and low serum albumin (< 30 mg/dl) were independent risk factors associated with the development of pneumonia. Crude mortality rate was 26% (26 of 101), while pneumonia-related mortality was 20% (20 of 101). The attributable mortality was 23% (odds ratio [OR]: 11.3; 95% confidence interval [CI]: 3.25 to 60.23; p < 0.0001). The multivariate analysis showed that patients had a worse prognosis if they were previously bedridden, had prior swallowing disorders, body temperature on admission was less than 37 degrees C, respiratory frequency was greater than 30/min or had three or more affected lobes on chest radiograph. Age by itself was not a significant factor related to prognosis. Among the significant risk factors, only nutritional status is probably amenable to medical intervention. The prognostic factors found in this study may help to identify, upon admission, those subjects at higher risk and who may require special observation.

Aged↗
PubMed1996

Comparison of manual and automatic CPAP titration in patients with sleep apnea/hypopnea syndrome.

Automatic CPAP (auto-CPAP) is engineered to automatically provide a positive pressure to the upper airway in response to apnea, hypopnea, airflow limitation, or snoring in patients with the sleep apnea/ hypopnea syndrome (SAHS). Self-adjusted CPAP has theoretical advantages over traditional fixed CPAP. We investigated the value of auto-CPAP regulation in 20 patients with SAHS in order to predict future fixed-level CPAP needs, as an alternative method to conventional polysomnographically (PSG)-controlled CPAP titration. This was accomplished through comparison of the optimal CPAP level obtained with PSG with that obtained with auto-CPAP. There were no significant differences between the optimal CPAP level achieved with full PSG or with auto-CPAP. As a secondary analysis, we analyzed auto-CPAP performance with regard to sleep-stage distribution and arousals in a group of nine male patients, and compared it with the previous group of 20 patients in which manually CPAP titration was guided by PSG. After adequate CPAP was reached, upward and downward fluctuations in the CPAP level had no significant effect on sleep architecture or fragmentation. We conclude that auto-CPAP permits the prediction of future fixed-level CPAP needs, and does so without sleep disruption.

Adult↗
PubMed1996

Visual and different automatic scoring profiles of respiratory variables in the diagnosis of sleep apnoea-hypopnoea syndrome.

The purpose of our study was to explore the diagnostic accuracy of different methods of scoring night time recording of respiratory variables (NTRRV) for the diagnosis of the sleep apnoea-hypopnoea syndrome (SAHS). Within a 2 week period, we performed a partially attended night time recording of respiratory variables and a full polysomnography (PSG) for reference in patients with suspected SAHS. Night time recording of respiratory variables was carried out using equipment which records, and continuously displays on a monitor, oximetry, airflow, chest and abdominal motion and body position. Night time recording of respiratory variables was scored manually and automatically, according to different combinations of the parameters described previously. Full polysomnography was performed in the Sleep Laboratory following conventional standards. Thirty six patients were studied. Visual analysis and different automatic scoring profiles of night time recording of respiratory variables were compared to full polysomnography in terms of agreement, sensitivity and specificity. Visual scoring of night time recording of respiratory variables gave the finest agreement-sensitivity-specificity relationship. Automatic scoring of nighttime recording of respiratory variables showed a trend to underestimate the apnoea-hypopnoea index (AHI) with respect to full polysomnography due mainly to underrecognition of hypopnoeas. Agreement-sensitivity-specificity relationships of automatic night time recording of respiratory variables with respect to full polysomnography varied depending on the automatic profile used. Some had a good agreement and sensitivity whilst others had a good specificity. These findings show that visual scoring of night time recording of respiratory variables is the most accurate method of analysis when compared to full polysomnography. The usefulness of the automatic methods of scoring of respiratory variables depends on the end-point chosen and is not reliable enough to be used in all situations. Night time recording of respiratory variables represents a real complement to conventional full polysomnography in clinical practice.

Adult↗
PubMed1996

Effect of nitric oxide inhalation on respiratory system resistance in chronic obstructive pulmonary disease.

Nitric oxide (NO) has been identified as a neurotransmitter of nonadrenergic noncholinergic bronchodilator nerves. To investigate whether inhaled NO exerts a bronchodilator effect in patients with chronic obstructive pulmonary disease (COPD), we measured the resistance of the respiratory system, using the forced oscillation technique, while breathing NO. Eight patients with COPD (7 men and 1 woman; aged 66 +/- 7 yrs (mean +/- SD); forced expiratory volume in one second (FEV1) 37 +/- 17% of predicted) and eight healthy subjects (7 men and 1 woman; 33 +/- 4 yrs; FEV1 108 +/- 14% pred) were studied. Nitric oxide, at a concentration of 40 parts per million (ppm) in air, was inhaled for 20 min. Total resistance (Rrs) and reactance (Xrs) of the respiratory system, arterial oxygen saturation, heart rate, tidal volume, and breathing frequency were continuously recorded at baseline, and during and after ceasing NO inhalation. Methaemoglobin levels were additionally measured in healthy subjects. At baseline, patients with COPD showed higher Rrs than healthy subjects (Rrs at 10 Hz (Rrs,10) 4.97 +/- 2.19 vs 2.29 +/- 0.65 hPa.L-1.s). During NO inhalation, no significant change in Rrs or in Xrs was observed. Mean variation in Rrs,10 while breathing NO was negligible and similar in the two groups (-0.10 +/- 0.13 hPa.L-1.s in COPD patients and -0.02 +/- 0.13 hPa.L-1.s in healthy subjects). Moreover, there were no differences in oxygen saturation, heart rate, tidal volume and breathing frequency during NO inhalation. Methaemoglobinaemia increased at the end of NO inhalation (from 0.48 +/- 0.18 to 0.81 +/- 0.16%), and this increment remained 10 min later (0.86 +/- 0.31%). From these results, we conclude that inhaled nitric oxide, at a concentration of 40 ppm, exerts no effect on respiratory system resistance in patients with chronic obstructive pulmonary disease or in healthy subjects.

Administration, Inhalation↗
PubMed1996

Gas exchange, expiratory flow obstruction and the clinical spectrum of asthma.

More than any other chronic respiratory disease, asthma is characterized by functional and clinical variability: expiratory flow obstruction, dyspnoea and wheezing may be absent, mild, or severe. Moreover, pulmonary gas exchange often does not closely relate to measured airway obstruction. Accordingly, the correlation between arterial oxygen tension and airflow (Pa,O2) rate indices of obstruction is poor, both in a single patient over time, and within groups of clinically similar patients. Here, these concepts are extended by examining relationships between airflow obstruction and gas exchange across the clinical spectrum of asthma (from asymptomatic to acute severe). Six individual studies encompassing 86 patients are analysed together, focusing on: 1) airways obstruction; 2) arterial blood gas data; and 3) the distribution of alveolar ventilation/perfusion (V'A/Q') ratios, measured by the multiple inert gas elimination technique. V'A/Q' mismatching was greater than normal even when forced expiratory volume in one second (FEV1) was normal, but with increasing severity of airways obstruction there was essentially no further deterioration in gas exchange until FEV1 reached about 40% of predicted normal values. Then, with little further airways obstruction, gas exchange rapidly worsened, Pa,O2 falling to about 50 torr. This study emphasizes that what has been observed in individual patients and within clinically similar patient groups can be extended across the spectrum of asthma severity: airways obstruction and gas exchange are poorly correlated. Furthermore, these results suggest that spirometric data alone may not adequately define remission, nor clearly identify those patients liable to serious gas exchange deterioration.

Airway Obstruction↗