Interplay of intrapulmonary and extrapulmonary factors on pulmonary gas exchange during weaning.
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Humans↗
Biomedical subjects
R Rodriguez-Roisin
Publications and source records attributed to R Rodriguez-Roisin.
Mechanisms of abnormal gas exchange in patients with pneumonia.
The mechanisms of abnormal gas exchange in patients with pneumonia and the gas exchange response while breathing high inspired O2 concentrations have not been clearly elucidated. To this end, we studied 23 inpatients with pneumonia and mild to severe arterial hypoxemia and/or increased alveolar - arterial O2 difference. Ventilation-perfusion (VA/Q) distributions were obtained upon breathing room air (or maintenance inspired oxygen fraction) and 100% O2 in random order. Subjects were divided in two groups according to whether they were spontaneously breathing (SB, n = 13) or their lungs were mechanically ventilated (MV) because of acute severe respiratory failure (n = 10). The SB patients showed only small amounts of shunt (7 +/- 2%) (mean +/- standard error) and moderate VA/Q mismatching, characterized by the presence of a small percentage of blood flow to low VA/Q units (VA/Q less than 0.1) (4 +/- 1%). In contrast, patients whose lungs were MV had larger shunts (22 +/- 5%) and greater percent of perfusion to low VA/Q units (11 +/- 5%). While breathing 100% O2, shunt remained unchanged but the dispersion of the pulmonary blood flow distribution (log SDQ) (normal range, 0.3-0.6) increased in each group (from 1.04 +/- 0.10 to 1.29 +/- 0.13 in SB and from 1.40 +/- 0.11 to 1.64 +/- 0.14 in MV; P less than 0.05 each), suggesting release of hypoxic pulmonary vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Mechanisms of gas-exchange impairment in idiopathic pulmonary fibrosis.
To investigate the mechanisms of pulmonary gas-exchange impairment in idiopathic pulmonary fibrosis (IPF) and to evaluate their potential relationship to the CO diffusing capacity (DLCO), we studied 15 patients with IPF (mean DLCO, 52% of predicted) at rest (breathing room air and pure O2) and during exercise. We measured pulmonary hemodynamics and respiratory gas-exchange variables, and we separated the ventilation-perfusion (VAQ) mismatching and O2 diffusion limitation components of arterial hypoxemia using the multiple inert gas elimination technique. At rest VA/Q mismatching was moderate (2 to 4% of cardiac output perfusing poorly or unventilated lung units), and 19% of AaPO2 was due to O2 diffusion limitation. During exercise VA/Q mismatch did not worsen but the diffusion component of arterial hypoxemia increased markedly (40% AaPO2, p less than 0.005). We observed that those patients with higher pulmonary vascular tone (more release of hypoxic pulmonary vasoconstriction) showed less pulmonary hypertension during exercise (p less than 0.05), less VA/Q mismatching [at rest (p less than 0.005) and during exercise (p less than 0.0025)], and higher arterial PO2 during exercise (p = 0.01). We also found that DLCO corrected for alveolar volume (KCO) correlated with the mechanisms of hypoxemia during exercise [VA/Q mismatching (p less than 0.025) and O2 diffusion limitation (p less than 0.05)] and with the increase in pulmonary vascular resistance elicited by exercise (p less than 0.005). In conclusion, we showed that the abnormalities of the pulmonary vasculature are key to modulate gas exchange in IPF, especially during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Clinical advances in pulmonary gas exchange.
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Anesthesia↗
Ventilation-perfusion mismatch after methacholine challenge in patients with mild bronchial asthma.
To investigate the effects of methacholine (MTH) challenge on spirometry, lung mechanics, respiratory gases, and ventilation-perfusion (VA/Q) distributions, 16 subjects 16 to 58 yr of age with stable mild asthma (FEV1, 92 +/- 5% [SEM] predicted; FEF25-75, 71 +/- 7% predicted; respiratory system resistance (Rrs) at 4 Hz, 4.6 +/- 0.4 cm H2O/L-1 s; PaO2, 88 +/- 3 mm Hg; AaPO2, 23 +/- 3 mm Hg) were recruited. Baseline VA/Q distributions were unimodal and relatively narrow in 12 patients and modestly bimodal in the other four. The dispersion of pulmonary blood flow (log SD Q) was slightly enlarged (0.71 +/- 0.09) and that of ventilation (log SD V) was normal (0.57 +/- 0.04) (normal range, 0.3 to 0.6); an index of overall VA/Q heterogeneity (DISP R-E*) was also mildly abnormal (5.3 +/- 0.8) (normal values less than 3.0). After MTH challenge, FEV1, FEF25-75, and PaO2 fell (to 62 +/- 3 and 35 +/- 3% predicted, and to 71 +/- 1 mm Hg, respectively), whereas Rrs (p less than 0.001 each), minute ventilation (p less than 0.02), heart rate (p less than 0.01), and AaPO2 increased (p less than 0.001). VA/Q relationships mildly to moderately worsened (log SD Q increased to 0.98 +/- 0.04 [p less than 0.01], log SD V to 0.79 +/- 0.04, and DISP R-E* to 9.8 +/- 0.6 [p less than 0.001 each]). Qualitatively, the pattern of blood flow distribution was broadly unimodal in 13 patients and modestly bimodal in three, of whom only one had a bimodal baseline distribution.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Severe community-acquired pneumonia. Epidemiology and prognostic factors.
Over a period of 4 consecutive yr, 92 nonimmunosuppressed patients (21 women and 71 men aged 53 +/- 16 yr, means = SD) with critical acute respiratory failure (PaO2/FiO2, 209 +/- 9 mm Hg) caused by severe community-acquired pneumonia were admitted to the respiratory intensive care unit (RICU) of a general hospital. The most frequent underlying clinical condition was chronic obstructive pulmonary disease (44 patients, 48%). A total of 56 patients (61%) required mechanical ventilation for a mean period of 10.7 +/- 12.5 days, 29 of them (52%) needing PEEP (9.9 +/- 3.8 cm H2O). A group of 23 (25%) patients had criteria of adult respiratory distress syndrome (ARDS). A causal microorganism was identified in 48 patients (52%), the two most frequent etiologies being Streptococcus pneumoniae (14, 15%) and Legionella pneumophila (13, 14%). Pseudomonas aeruginosa (5, 5%) was always associated with bronchiectasis. Mortality due to severe community-acquired pneumonia was 22% (20 patients). According to univariate analysis, mortality was associated with anticipated death within 4 to 5 yr, inadequate antibiotic treatment before RICU admission, mechanical ventilation requirements, use of PEEP, FIO2 greater than 0.6, coexistence of ARDS, radiographic spread of the pneumonia during RICU admission, septic shock, bacteremia, and P. aeruginosa as the cause of the pneumonia. Further, recursive partitioning analysis selected two factors significantly related to the prognosis: the radiographic spread of the pneumonia during RICU admission and the presence of septic shock.(ABSTRACT TRUNCATED AT 250 WORDS)
Female↗
Gas exchange during exercise in mild chronic obstructive pulmonary disease. Correlation with lung structure.
To investigate whether or not the pathologic features in the lungs of patients with chronic obstructive pulmonary disease (COPD) are related to the gas exchange response during exercise, we studied 17 patients (15 men, two women) with mild-to-moderate airflow obstruction (FEV1/FVC ratio, 59 +/- 3%), undergoing resective lung surgery, at rest and during submaximal exercise (71 +/- 5% predicted VO2max). During exercise, arterial PO2 increased (from 81 +/- 3 to 86 +/- 3 mm Hg, p less than 0.05) as a result of an overall improvement in VA/Q relationships. This improvement included an increase in the mean VA/Q ratios of both ventilation and blood flow distributions, and a more homogeneous ventilation distribution (logSD V, from 0.66 +/- 0.06 to 0.50 +/- 0.03; p less than 0.01; normal value, less than or equal to 0.6). The morphologic evaluation of the resected specimens disclosed a moderate degree of emphysema (emphysema score, 16 +/- 4) and mild abnormalities in membranous bronchioles (total pathology score, 107 +/- 8). At rest, significant correlations were found between the severity of the pathologic findings and both the degree of hypoxemia and the extent of VA/Q mismatching. During exercise, no relationship between bronchiolar abnormalities and gas exchange measurements was observed, whereas the severity of emphysema was correlated with PaO2 (r = -0.54, p less than 0.05). Both the overall increase in and the more efficient distribution of ventilation accounted for the improvement in VA/Q distributions during exercise. These changes were more pronounced in patients with a greater degree of bronchiolar abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Gas exchange abnormalities in asthma.
There has been considerable interest over the last years in gas exchange abnormalities that occur in patients with bronchial asthma, particularly during an acute attack. These are essentially characterized by moderate to severe hypoxemia and hypocapnia caused by considerable ventilation-perfusion (VA/Q) mismatch. Using the multiple inert gas elimination technique, the baseline pattern of VA/Q distribution reveals a bimodal bloodflow distribution of VA/Q ratios but no shunt. Inhaled salbutamol seems to be an efficient and safe therapeutic approach, owing to the lack of deleterious effect on VA/Q inequality. Following intravenous salbutamol there is development of further VA/Q mismatch for the same degree of bronchodilation, the resulting deleterious effect on PaO2 being offset by the improvement in mixed venous PO2 due to increased cardiac output.
Airway Resistance↗
The lung in patients with cirrhosis.
To summarize, nowadays it seems clear that in patients with cirrhosis: (a) the pulmonary circulation is usually markedly dilated. (b) This vasodilation is due to a loss of vascular tone and it is characterized by a poor (or even absent) vascular reactivity in front of the hypoxic stimulus. (c) This abnormal behaviour of the pulmonary circulation results in VA/Q mismatching (basically perfusion of low VA/Q units) independently of airway disease, and may lower arterial PO2. (d) In the most severe cases, shunt (and perhaps O2 diffusion limitation) is becoming progressively more important. (e) The high cardiac output and minute ventilation of these patients minimize or prevent the appearance of arterial hypoxemia at rest. (f) The fall in arterial PO2 during exercise is not due to a deterioration of the degree of VA/Q mismatching seen at rest nor to any limitation in the diffusion of oxygen. It is caused by the relative 'normalization' (with respect to the metabolic demands) of the haemodynamic and ventilatory status of the patient. This may not apply to patients with severe resting arterial hypoxemia in whom the mechanisms modulating pulmonary gas exchange during exercise have not yet been addressed. What remains to be elucidated at the present time? (a) Which is (are) the precise biochemical mediator(s) of this low pulmonary vascular tone and, presumably, failure of hypoxic pulmonary vasoconstriction? It might be either a substance(s) that the failing liver fails to produce or detoxify. Thus, the ultimate biochemical basis of these physiological abnormalities must still necessarily remain speculative while awaiting future studies.(ABSTRACT TRUNCATED AT 250 WORDS)
Humans↗
Pulmonary gas exchange in severe chronic asthma. Response to 100% oxygen and salbutamol.
Ventilation-perfusion (VA/Q) inequality has been evaluated using the multiple inert gas technique in nine nonsmoking patients (mean +/- SD, age 56 +/- 10 yr) with stable, severe, chronic asthma (partially reversible airway obstruction; baseline FEV1, 39 +/- 10% predicted) before and during 100% O2 breathing and then 15 min after three puffs (300 micrograms) of inhaled salbutamol. The aim of this study was to investigate whether this type of asthma was associated with a different pattern of VA/Q inequality from that observed in acute episodes and in particular to determine whether the VA/Q pattern was fixed or could be altered by bronchodilator agents or O2 breathing. The predominant pattern of VA/Q distribution was broad and unimodal but without shunt (VA/Q = 0) or low VA/Q areas (VA/Q less than 0.1 to greater than 0.005). The amount of VA/Q inequality as assessed by the dispersion of the distribution of pulmonary bloodflow (log SDQ) was not great (log SDQ, 0.77 +/- 0.09), and no correlation was found with the degree of airway obstruction, PaO2 or AaPO2. During 100% O2 breathing, VA/Q inequality worsened (from log SDQ of 0.77 +/- 0.09 to 1.11 +/- 0.21, p = 0.01) with an increase in the perfusion of low VA/Q units (from 0.43 +/- 0.66% to 6.3 +/- 6.5%, p = 0.02) but still no development of shunt. This suggests the presence of hypoxic pulmonary vasoconstriction breathing air, possibly contributing to the preservation of VA/Q relationships.(ABSTRACT TRUNCATED AT 250 WORDS)
Administration, Inhalation↗
Single-breath carbon monoxide diffusing capacity prediction equations from a Mediterranean population.
Because of unanswered questions about prediction equations for the single-breath carbon monoxide diffusing capacity (DLCO) and as part of a larger collaborative project, standardized DLCO measurements were carried out in a selected sample of 361 healthy nonsmoking volunteers (194 men and 167 women) living in the Barcelona metropolitan area (Spain). Except for the test FIO2 (0.18), the study essentially followed the American Thoracic Society (ATS) and European Community for Coal and Steel (ECCS) recommendations for standardizing the methodology of measuring DLCO. Prediction equations for ages 20 through 70 were calculated separately for both sexes. Simple linear equations using age, height, and body weight as independent variables predicted the DLCO indices (DLCO, VA, and DL/VA) as well as more complex equations. In addition, a complete analysis of the residuals (predicted measured values) showed that the assumptions of the multiple regression analysis (independence, homoscedasticity and Gaussian distribution of residuals) were fulfilled using simple linear equations. Correction for the instrumental and anatomic dead spaces decreased the DLCO an average of 4.7%. The standard error of estimates was lower than those reported from other series in the literature. The predicted values from this study were lower than those reported by some investigators and were in reasonable agreement with other studies. A portion but not all of the differences could be explained on the basis of recognized differences in testing methodology. The results of this study may be of value to clinical laboratories seeking predictive equations for DLCO most appropriate for their testing methodology and patient population, and may assist in the resolution of some controversies regarding differences among predictive equations for DLCO.
Adolescent↗
Lung structure and gas exchange in mild chronic obstructive pulmonary disease.
To investigate the influence of pulmonary emphysema and small airways abnormalities on ventilation-perfusion (VA/Q) mismatching in mild chronic obstructive pulmonary disease (COPD), we studied 23 patients (mean predicted FEV1, 76 +/- 15%) before lung resection because of a localized neoplasm. Respiratory gas exchange and VA/Q distributions were measured while the patients breathed room air and 100% O2. Breathing room air, the AaPO2 was moderately increased (25 +/- 12 mm Hg) as was VA/Q mismatching, indicated by the dispersion (log SD) of both blood flow (Q) and ventilation (V) distributions (log SD Q, 0.78 +/- 0.3; and log SD V, 0.66 +/- 0.28, respectively) (normal range, 0.3-0.6). AaPO2, log SD Q, and log SD V all significantly correlated with the emphysema severity assessed morphologically from the resected lung specimens (r = 0.57, r = 0.62, and r = 0.45, respectively). Log SD V also significantly correlated with the severity of the inflammatory infiltrate of membranous bronchioles (r = 0.62). During 100% O2 breathing there was an increase in VA/Q mismatching (log SD Q rose to 1.12 +/- 0.08, p less than 0.001), suggesting release of hypoxic pulmonary vasoconstriction. This increase in VA/Q inequality was not significantly related to the severity of lung pathologic findings. We conclude that, in mild COPD, both pulmonary emphysema and small airways abnormalities contribute to VA/Q mismatch, the severity of emphysema being the major morphologic correlate of the increase in AaPO2.
Adult↗
Effects of propranolol on arterial oxygenation and oxygen transport to tissues in patients with cirrhosis.
Patients with cirrhosis may show ventilation-perfusion (VA/Q) inequality in the absence of any intrinsic heart or lung disease. However, the high cardiac output of cirrhosis generally prevents or minimizes the appearance of a severe degree of arterial hypoxemia. Propranolol has been used to reduce cardiac output and portal pressure in these patients. We wondered whether it might alter arterial oxygenation and reduce O2 transport to tissues. We studied eight patients (three women) 54 +/- 3 (SEM) yr of age before and after intravenous propranolol (0.1 mg/kg followed by 2 mg/h). Cardiac output (QT) fell from 7.8 +/- 0.7 to 6.0 +/- 0.7 L/min (p less than 0.05), and portal pressure was reduced (22 +/- 2 to 19 +/- 2 mm Hg, p less than 0.01). Arterial PO2 did not change (88 +/- 4 to 89 +/- 5 mm Hg) because the fall in mixed venous PO2 (43 +/- 1 to 40 +/- 1 mm Hg, p less than 0.01) that followed the lower QT was counterbalanced by a lower intrapulmonary shunt (multiple inert gas technique) (4 +/- 2 to 2 +/- 1%, p less than 0.05) and a shift of the VA/Q distributions toward a higher VA/Q ratio. Paralleling the fall in QT, oxygen transport to tissues (QO2) was reduced (19 +/- 2 to 14 +/- 1 ml/min/kg, p less than 0.01). However, O2 uptake (VO2) remained constant (3.4 +/- 0.2 to 3.6 +/- 0.2 ml/min/kg) because O2 extraction by the tissues increased appropriately (22 +/- 2 to 28 +/- 1%, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Female↗
Incidence, risk, and prognosis factors of nosocomial pneumonia in mechanically ventilated patients.
Seventy-eight (24%) episodes of nosocomial pneumonia (NP) were detected in 322 consecutive mechanically ventilated patients admitted to a 1,000-bed teaching hospital from April 1987 through May 1988 to assess the incidence, risk, and prognosis factors of NP acquired during mechanical ventilation (MV). The risk and prognosis factors for developing NP during MV were studied using both univariate and multivariate statistical techniques. Multivariate analysis selected the following variables significantly associated with a higher risk for developing ventilator-associated pneumonia: more than one intubation during MV (p = 0.000012), a prior episode of aspiration of gastric content (p = 0.00018), a MV period longer than 3 days (p = 0.015), the presence of chronic obstructive pulmonary disease (COPD) (p = 0.048), and the use of positive end-expiratory pressure (PEEP) during MV (p = 0.092). The presence of an ultimately or rapidly fatal underlying disease (p = 0.0018), worsening of acute respiratory failure caused by pneumonia (p = 0.0096), the presence of septic shock (p = 0.016), an inappropriate antibiotic treatment (p = 0.02), and the type of intensive care unit (ICU) hospitalization (noncardiac surgery and nonsurgical ICU compared with post-cardiac surgery ICU) (p = 0.08) were those factors selected by a stepwise logistic regression analysis as independently worsening the prognosis. The overall fatality rate was 23% (73 of 322). The mortality of patients with NP was higher (33%; 26 of 78; p less than 0.01) when compared with fatality rates of patients without NP (19%; 47 of 244).(ABSTRACT TRUNCATED AT 250 WORDS)
Cross Infection↗
Clinical relevance of ventilation-perfusion inequality determined by inert gas elimination.
The first part of this review deals with the basic mechanisms and factors determining hypoxaemia and hypercapnia and the different approaches used in clinical practice and in clinical research to assess the presence of ventilation-perfusion mismatching, shunt and diffusion limitation for oxygen, and more specifically the multiple inert gas elimination technique (MIGET), in pulmonary medicine. The second part reviews three different respiratory disorders where the complex interplay between intrapulmonary and extrapulmonary factors regulating oxygen are essentially interpreted through the results afforded by the MIGET over the last decade. The gas exchange response to bronchodilators in bronchial asthma, an airway disease, and then the major determinants governing abnormal gas exchange in acute pulmonary embolism, a pulmonary vascular disorder, and during haemodialysis, a respiratory entity of extrapulmonary origin, are successively explored in the light of the inert gas method.
Asthma↗
Bronchial reactivity in patients with chronic renal failure undergoing haemodialysis.
We hypothesized that patients with chronic renal failure may present nonspecific bronchial hyperreactivity due to subclinical interstitial lung oedema. To assess lung function disturbances and methacholine (MTH) bronchial responsiveness in this condition, we studied 12 patients (9 men and 3 women; 41.8 +/- 13.3 yrs (SD] with chronic renal failure undergoing regular haemodialysis (HD). Before HD, mean results of conventional lung function tests were within the normal range: forced expiratory volume in one second (FEV1), 89 +/- 12.9% predicted; forced mid-expiratory flow (FEF25-75), 81 +/- 36.7% predicted; total lung capacity (TLC), 94 +/- 14.6% predicted, but 3 subjects presented mild reduction in lung volumes and 5 individuals showed mild obstructive ventilatory impairment. After HD, maximal expiratory flow rates increased significantly (FEV1, + 8.2 +/- 5.1% (p less than 0.005); FEF25-75, +26.2 +/- 25.9% (p less than 0.005]. Interestingly, these increases in FEV1 after HD correlated with body weight loss during HD (r = 0.74, p less than 0.01). In contrast, pre-HD bronchial reactivity was within the normal range (mean % change in FEV1 after MTH, -3.7 +/- 4.5%; range, +1- -14%) without significant changes in methacholine bronchial responsiveness after HD. We speculate that interstitial lung oedema may play a significant role in lung function impairment observed in patients with chronic renal failure. This study shows that nonspecific bronchial hyperreactivity is not present in clinically stable patients with this disorder.
Adult↗
Characteristics of patients with soybean dust-induced acute severe asthma requiring mechanical ventilation.
Patients presenting with acute severe asthma during the Barcelona's outbreaks caused by soybean dust inhalation from August, 1981, through September, 1987, characteristically showed an abrupt severe onset of each attack followed by a rapid relief of symptoms after treatment. To throw further light on clinical findings, pathophysiology and outcome in the most life-threatening episodes, we reviewed records of acute severe asthma patients treated by mechanical ventilation in one of the four main hospitals of the city. Twelve such patients (15 episodes) were compared to 24 non-epidemic asthmatic patients (25 episodes) also treated by mechanical ventilation in the same institution during the same period of time. There was a male predominance during outbreaks (p less than 0.03) and epidemic patients were ventilated fewer hours (12 +/- 8 h) (mean +/- SD), admitted fewer days to intensive care (1.6 +/- 0.7 days), and hospitalized fewer days (7.1 +/- 4.4 days) than non-epidemic patients (65 +/- 84 h, 4.6 +/- 3.8 days (p less than 0.001, each), and 16.0 +/- 13.2 days (p less than 0.004), respectively). These differences together with both the fulminant presentation of the episodes of epidemic asthma and the point-source origin of the asthma outbreaks previously shown are consistent with the unusual nature of the aetiologic agent, soybean dust.
Acute Disease↗
Community outbreaks of asthma associated with inhalation of soybean dust. Toxicoepidemiological Committee.
Since 1981, 26 outbreaks of asthma have been detected in the city of Barcelona. The geographic clustering of cases close to the harbor led us to consider the harbor as the probable source of the outbreaks. We therefore studied the association between the unloading of 26 products from ships in the harbor and outbreaks of asthma in 1985 and 1986. All 13 asthma-epidemic days in these two years coincided with the unloading of soybeans (lower 95 percent confidence limit of the risk ratio, 7.2). Of the remaining 25 products, only the unloading of wheat was related to the epidemics of asthma, although when adjusted for the unloading of soybeans the relation was not statistically significant. High-pressure areas and mild southeasterly to southwesterly winds, which favored the movement of air from the harbor to the city, were registered on all epidemic days. Particles of starch and episperm cells that were recovered from air samplers placed in the city had morphologic characteristics identical to those of soybean particles. Furthermore, the lack of bag filters at the top of one of the harbor silos into which soybeans were unloaded allowed the release of soybean dust into the air. We conclude that these outbreaks of asthma in Barcelona were caused by the inhalation of soybean dust released during the unloading of soybeans at the city harbor.
Asthma↗