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PubMed1983

Respiratory failure, mechanisms of abnormal gas exchange, and oxygen delivery.

Patients with respiratory failure may have abnormal gas exchange based on a number of mechanisms. Each of these mechanisms may indicate a different underlying pathology and thus suggest different therapeutic interventions. In addition, the ability to monitor changes in physiologic function can be complicated but is achievable when proper protocols are followed. It should be clear that an adequate understanding of the underlying physiology is crucial to the successful management of these very difficult patients.

Humans↗
PubMed1998

Morphometric estimate of gas-exchange tissue in the new-born tammar wallaby, Macropus eugenii.

The lung of the new-born marsupial is at the terminal air sac stage of development. The maturational status of the lung of new-born tammar wallaby was assessed using established morphometric techniques and the results were compared with data from a morphometric study of the lung of the rat. Volume densities of the parenchyma and non-parenchyma, conducting airways and blood vessels, the relative volumes of airspace and tissue, the thickness and the composition of the septa differed between the two species. In addition the volume of capillaries and the surface area of the effective gas-exchange tissue was greater in the new-born rat than in the new-born tammar pouch young. The lung of the new-born tammar appears to be at an earlier phase of the terminal air sac stage than that of the new-born rat. Lung development up to birth appears to be commensurate to the metabolic needs of the organism at birth.

Animals↗
PubMed1998

Effect of cardiac output on pulmonary gas exchange: role of diffusion limitation with VA/Q mismatch.

We studied the effect of the interaction between diffusion limitation and alveolar ventilation to perfusion ratio (VA/Q) mismatch in the relation between blood gas partial pressures and cardiac output (Q). The analysis was based on a mathematical model of gas exchange involving two exchanging compartments and a right to left shunt. A system of equations describing alveolar-arterial mass conservation for O2, CO2 and N2 and Bohr integration for O2 and CO2 was interactively solved to find sets of alveolar and blood gas partial pressures fitting input data. Simulations used values compatible with patients in respiratory failure and neonate piglets. Association of (VA/Q) mismatch and diffusion impairment limited the increase of PaO2 with Q. A maximum in the PaO2 vs. Q curve can be attained, further Q increases lead to reductions in PaO2. The effect was accentuated by increasing (VA/Q) and diffusion to perfusion heterogeneity. Combination of (VA/Q) mismatch and diffusion limitation was synergistic leading to greater reductions in PaO2 than expected from simple addition of their independent influences. The findings are compatible with experimental data.

Cardiac Output↗
PubMed1993

Outcome measurement in scleroderma clinical trials.

Clinical trials in scleroderma were reviewed to assess the clinimetric properties of frequently used outcome measures. Twenty-seven controlled intervention studies were found in the English literature; nine demonstrated effective therapy. The outcome measures used included skin involvement, functional status, physical performance (grip strength, oral aperture), and internal organ involvement (pulmonary, gastrointestinal, renal, and cardiac). Very few outcome measures detected between- or within-group differences even when an active drug was compared with a placebo. Skin measures were found to yield statistical differences in seven studies, patient global assessment in three, and physician global assessments in four. Internal organ measures detected differences between groups only rarely; the pulmonary diffusing capacity was statistically different twice. Physical performance measures (eg, grip strength and oral aperture) never yielded statistical differences, and in only one of five trials did a functional assessment detect statistical differences. To show drug efficacy in future trials in scleroderma, better outcome measures need to be developed and a consensus obtained on which outcomes to use so that potentially effective therapies can be tested in a standardized fashion against a placebo or current therapy. Currently, because of a lack of clinimetric data on outcome measures, therapeutic inefficacy cannot be differentiated from a lack of sensitivity in the outcome measures used. In the future, outcome measures should be chosen on the basis of the adequacy of their reliability, construct, and content validity and be sensitive to change. Ideally, outcome measures also should have criterion validity, ie, show a strong association between the measure (such as a skin score) and an irrefutable gold standard (such as skin pathology).

Clinical Trials as Topic↗
PubMed1998

Optimization of the mammalian respiratory system: symmorphosis versus single species adaptation.

Taylor and Weibel's principle of symmorphosis hypothesized optimal design of the mammalian respiratory system, with no excess structure relative to its maximal O2 flux, VO2max. Although they found symmorphosis not to be a general principle of design, it might apply to a highly adapted aerobic athlete, e.g. the Thoroughbred racehorse. Using a mathematical model based on empirical data of the equine O2 transport system at normoxic VO2max, the fraction of the total limitation to O2 flux contributed by each of the respiratory transport steps is calculated as either the fractional change (F) in VO2max for a 1% change in each component, or as the fraction of total O2 pressure drop (R(int)) across each component at VO2max. When calculated as F, alveolar ventilation (VA) and pulmonary diffusing capacity (DLO2) are major limiting factors, circulatory convection (Q) is nearly as limiting, and peripheral tissue diffusing capacity (DTO2) is only one-third as important. When calculated as R(int), DLO2 is the major factor, VA and DTO2 contribute significantly, and Q is smallest. These patterns contrast with analogous studies in humans, in which Q is the single major limiting factor. The results suggest that strong selection for aerobic power in horses has maximized the malleable components of their respiratory systems until the least malleable structure, the lungs, has become a major limitation to O2 flux. Symmorphosis cannot determine if such a design is or is not optimized, as every system falls on a continuous distribution of relative optimization among species. However, the concept of symmorphosis is useful for establishing a framework within which a single species can be compared with a quantitatively defined hypothesis of optimal animal design, and compared with other species according to those criteria.

Adaptation, Biological↗
PubMed1978

The pulmonary air-blood barrier of human shock lungs (a clinical, ultrastructural and morphometric study).

Interstitial edema in the alveolar septa is the first morphologically recognisable change to be observed in cases of shock. It is brought about by the altered function of the membranes of the damaged epithelium and endothelium in the alveolar wall. At the same time there is an impairment of gaseous exchange, which is rendered more difficult by the exudative process in the interstitium. Pari passu with these events there is injury to the cells of both the alveolar epithelium and the alveolar capillary endothelium. Both these processes are still reversible. The point of irreversibility appears to be reached--so far as time is concerned--at the end of the first week, after which the injurious effects on the cell are established, since the thin alveolar wall necessary for the exchange of gases becomes overgrown with bulky alveocytes (Tpye II), and the fibroblasts in thealveolar interstitium push the capillaries away from the surface of the alveolus. In most of the advanced cases of shock this process of thickening of the alveolar wall exceeds the critical value, and respiratory exchange is so impaired that satisfactory functioning of the lungs is no longer possible.

Adult↗
PubMed2001

Modulation of alveolar-capillary sodium handling as a mechanism of protection of gas transfer by enalapril, and not by losartan, in chronic heart failure.

OBJECTIVES: We sought to compare the protective efficacy of enalapril and losartan on lung diffusion in chronic heart failure (CHF). BACKGROUND: In CHF, hydrostatic overload causes disruption of the alveolar-capillary membrane and depression of carbon monoxide diffusion (DCO); enalapril improves DCO through mechanisms still undefined; and saline infusion in the pulmonary circulation worsens DCO, putatively because of an upregulated sodium transport to the alveolar interstitium. We investigated whether enalapril modulates sodium handling and whether losartan shares the same properties. METHODS: In 29 patients with CHF, DCO, its membrane diffusion subcomponent (DM) and right atrial and pulmonary wedge pressures were monitored during saline infusion, in the control condition, during enalapril therapy (20 mg/day) for two weeks and after crossover to losartan (50 mg/day) for two weeks (first 20 patients), or after the combination of enalapril with aspirin (325 mg/day) for one week (last 9 patients). RESULTS: Saline, 150 ml, lowered DCO (-7.9%; p < 0.01) and DM (-9.9%; p < 0.01) without hydrostatic variations. Responses to 750 ml of saline were qualitatively similar. After treatment with enalapril, baseline DCO (p < 0.01) and DM (p < 0.01) were augmented; after sodium loading, the percent reductions of DCO (p < 0.01) and DM (p < 0.01) were comparable to those before it, resulting in higher absolute values. This suggests that the greater the gas conductance improvement with enalapril, the lower the impedance with saline. Losartan was ineffective on gas transfer at rest and under salt challenge. Aspirin counteracted the benefits of enalapril. CONCLUSIONS: In CHF, enalapril protects lung diffusion, possibly through a prostaglandin-mediated modulation of sodium overfiltration to the alveolar interstitium; losartan does not share this ability.

Adult↗
PubMed2004

[Pulmonary gas exchange during exercise in healthy subjects].

INTRODUCTION: The modifications of gas exchange on exercise reflect the consequences of the control and limits of adaptation of the respiratory apparatus to the mechanical loads imposed on the muscles and the oxygen requirements of the organism. In the majority of cases, even if the thoraco-pulmonary apparatus is perfectly adapted to the increase in these requirements, the balance between the metabolic demands of the tissues and the pulmonary supply appears difficult to satisfy beyond certain limits without hypoxaemia, particularly in those subjects with a low ventilatory response to exercise. Based on the populations reported in the literature the functional limits of the control of the thoraco-pulmonary system and the possible modifications of the structures of the lung are discussed for each of these mechanisms. STATE OF KNOWLEDGE: At certain levels of duration and intensity of exercise there is an increase in the alveolar-arterial oxygen gradient [P(A-a)O2] associated inconsistently with a fall in PaO2. It is mainly the use of inert gas techniques that has established over many years the respective roles of the different possible patho-physiological mechanisms: shunt, unequal distribution of VA/Q ratios, limitation of alveolar-capillary diffusion and its components. The inequalities of VA/Q increase at low levels of exercise but beyond certain levels of VO2 limitation of oxygen diffusion may develop. In effect, particularly in subjects capable of high levels of exercise, the interaction between diminished transit time of the red cells in the pulmonary capillaries and possible delay in equilibration of partial pressures between the blood and gas phases may create a limitation of diffusion. This added to the inequalities of distribution of VA/Q and reduction in PVO2 leads, in certain subjects, to a transitory exercise induced hypoxaemia. VIEWPOINTS AND CONCLUSIONS: New techniques of investigation seem to be necessary to clarify the sources of the observed changes and the development of modifications of pulmonary structure that establish the functional limits of the lungs on exercise. It remains to demonstrate the true impact of these anomalies on the limitation of human performance.

Exercise↗
PubMed1995

Effects of inhaled prostacyclin as compared with inhaled nitric oxide in a canine model of pulmonary microembolism and oleic acid edema.

OBJECTIVE: Recently, it has been shown that the inhalation of nitric oxide (NO) and of prostacyclin (PGI2) elicits selective pulmonary vasodilation in a canine model of pulmonary hypertension induced by hypoxic pulmonary vasoconstriction. The present study was designed to investigate whether inhaled NO or PGI2-aerosol, respectively, is also effective in decreasing pulmonary artery pressure in a canine model of acute pulmonary microembolism and oleic acid edema. DESIGN: Prospective, randomized, cross-over design. SETTING: University animal research laboratory. PARTICIPANTS: Eight anesthetized, mechanically ventilated dogs (28 +/- 1 kg). INTERVENTIONS: Acute pulmonary microembolization (PME) was induced using glass microbeads (mean diameter: 100 microns) and 0.01 mL/kg of oleic acid. Subsequently, inhaled PGI2 (concentration: 10 micrograms/mL) or NO (50 ppm), respectively, was randomly administered for 15 minutes each and then withdrawn. MEASUREMENTS AND MAIN RESULTS: Central hemodynamics (heart rate [HR], cardiac output [CO], stroke volume [SV], mean arterial pressure [MAP], systemic vascular resistance [SVR], mean pulmonary artery pressure [PAP], pulmonary vascular resistance [PVR]) and gas exchange (PaO2/FIO2 ratio, intrapulmonary shunt [Qs/Qt], alveolar-arterial oxygen difference, [AaDO2]) were assessed. Measurements were performed at control, after PME, and during administration of PGI2 and NO, respectively. PME induced a significant increase (p < 0.001) of MAP (+9%), PAP (+68%), and PVR (+163%), whereas HR, CO, and SV remained unchanged and lung function deteriorated. Inhalation of NO slightly decreased PAP (-10%; p < 0.05) and PVR (-26%; p < 0.01) and improved AaDO2 and PaO2/FIO2. In contrast, inhalation of PGI2 had no consistent effect on pulmonary vascular tone or gas exchange. CONCLUSION: The data demonstrate that inhaled NO may elicit selective pulmonary vasodilation and improve gas exchange in a canine model of pulmonary microembolism and respiratory insufficiency. However, the degree of these effects was relatively small. The aerosolization of PGI2 under conditions of positive-pressure ventilation did not exert a significant vasodilatory effect on pulmonary vessels and did not improve pulmonary gas exchange in this model.

Administration, Inhalation↗
PubMed1997

Liquid ventilation: a mathematical model of gas diffusion in the premature lung.

The liquid ventilation (LV) technique was previously demonstrated to be a valuable alternative to ordinary gas ventilation, particularly for newborn patients with severely distressed lungs. This work describes a mathematical model of gas transfer phenomena occurring within the lungs of a preterm newborn baby ventilated with liquid perfluorocarbon (PFC) RM-101. The model was conceived in order to perform computer simulations of LV treatments. Its input parameters are tidal volume, respiratory frequency, oxygen and carbon dioxide tension in inlet PFC; its output data are the partial pressures of respiratory gases in the alveolar environment. Such values may be evaluated at any instant from the beginning of the treatment, in order to judge whether the therapy is able to meet the necessary conditions to arterialize properly the patient's venous blood. The model also enables optimisation procedures to be defined and performed. Quantitative results and graphs are supplied, with reference to the simulation of LV applied to a preterm newborn of 28 gestational weeks. The main results point out that a relatively short duration of initial transients is attainable (200 to 240 s) and that blood arterialization is possible even with low oxygen tension in inlet PFC (29.7 kPa (223 mmHg)).

Biomedical Engineering↗
PubMed2002

Axial and radial distribution of the bronchial vasculature in sheep.

A morphometric analysis was made on the bronchial vasculature of intrapulmonary airways in sheep lungs. This study provides the parameters to calculate the quantity of soluble gas diffusion between the vasculature and airways for use in a mathematical model describing heat and mass exchange in the lungs. To achieve these results, the lungs of four adult sheep (30-36 kg.) were excised, fixed, dissected and microtomed to obtain airway cross-sections for measurement. Blood vessel size and airway proximity was measured using a microscope interfaced with a computer. Distance from airway lumen to most airway vessels ranged from 30 to 270 microm. It was found that the bronchial vessels surrounding intraparenchymal airways can be described by a right-skewed distribution. Most importantly, a practical description of the bronchial capillary size and airway proximity as a function of airway diameter was found using a weighed average. This analysis facilitates calculation of soluble gas flux from the bronchial vasculature to the airway for use in a mathematical model.

Animals↗
PubMed2003

Morphometry and allometry of the postnatal marsupial lung development: an ultrastructural study.

An utrastructural morphometric study of the postnatally remodelling lungs of the quokka wallaby (Setonix brachyurus) was undertaken. Allometric scaling of the volumes of the parenchymal components against body mass was performed. Most parameters showed a positive correlation with body mass in all the developmental stages, except the volume of type II pneumocytes during the alveolar stage. The interstitial tissue and type II cell volumes increased slightly faster than body mass in the saccular stage, their growth rates declining in the alveolar stage. Conversely, type I pneumocyte volumes increased markedly in both the saccular and alveolar stages. Both capillary and endothelial volumes as well as the capillary and airspace surface areas showed highest rates of increase during the alveolar stage, at which time the rate was notably higher than that of the body mass. The pulmonary diffusion capacity increased gradually, the rate being highest in the alveolar stage and the adult values attained were comparable to those of eutherians.

Aging↗
PubMed1999

IgG antibodies, chronic bronchitis, and pulmonary function values in farmer's lung patients and matched controls.

We measured IgG antibody levels against eight different microbes in farmer's lung (FL) patients an average of 14 years after the first diagnosed episode of FL and in matched controls. The study population consisted of 87 FL patients and 81 control farmers, matched by age, sex, and smoking habits. Clinical studies included the measurement of IgG antibody levels against Absidia corymbifera, Aspergillus umbrosus, A. fumigatus, Humicola grisea, Saccharopolyspora rectivirgula, Penicillium brevicompactum, Rhodotorula glutinis, and Thermoactinomyces vulgaris, in addition to spirometry, pulmonary diffusing capacity (DL(CO)), and the evaluation of chronic bronchitis. Median IgG antibody levels were two or more times higher in FL patients than control farmers against Ab. corymbifera, S. rectivirgula, and T. vulgaris (P<0.001). Against A. fumigatus, H. grisea, and R. glutinis, FL patients also had significantly higher antibody levels. FL patients often had positive antibody titers against several microbes, whereas control farmers usually had a positive titer against one or two microbes. A positive association between IgG antibody levels and chronic bronchitis and DL(CO) was observed in FL patients, but not in control farmers. It is suggested that the high antibody levels noted in FL patients were due not only to high exposure but also to individual sensitivity to environmental microbes.

Adult↗