Hemodynamic monitoring.
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Breathing near to residual volume produces arterial desaturation demonstrable by ear oximetry. This paper describes the effect on arterial saturation measured by an ear oximeter of expiring to residual volume, taking a normal inspired volume of air from ambient pressure, and then expiring to residual volume against a pressure of 10-15 cm of water. This breathing pattern was continued for several minutes. Carbon dioxide output and oxygen consumption were measured during the study and the closing volume at ambient pressure was compared with that at increased expiratory pressure. Arterial desaturation was actually increased by the increased airways pressure, the increase being modified both by minute volume and tidal volume. Closing volume was only slightly increased, but residual volume was considerably increased, by the raised pressure. The desaturation is only partially explicable on a ventilatory basis, and there is probably a component concerned with perfusion, and the absence of perfusion adaptation from hypoxic areas does not appear to accord with current hypotheses.
It was previously shown that gas exchange could contribute to the rising slope of phase III of the single-breath nitrogen (SB-N2) test. This study was done to quantify this role. We studied eight normal volunteers with a series of SB-N2 derived tests where the RV gas was progressively changed from room air to 90% O2 and 10% N2, by 10% increments in O2 and 10% decreases in N2 concentrations (i.e. room air, 70% N2 30% O2, 60% N2 40% O2, etc.). A similar series of SB-R (single-breath reversed gradients test) derived tests was done. Here the RV contained 100% O2 by previous washout, while the inspired gas was changed by 105 steps from room air to 10% N2 90% O2. We therefore have a situation where dilutional N2 gradients change with the % N2, in either the RV or the inspired gas. However, the alveolar volume loss remains the same for all tests. The mean +/- SD slope of phase III in the SB-N2 series for our eight subjects decreased from 0.87 +/- 0.25 with room air to 0.14 +/- 0.07 with 10% N2 90% O2, while its steepness in the SB-R series decreased from 0.62 +/- 0.23 with the inspired room air to 0.11 +/- 0.06 with the final inspiration being 10% N2 90% O2. From these data, we could calculate that the mean % contribution of gas exchange to the slope of phase III was 10.2%.
In the present study an attempt was made to evaluate the regional pulmonary function tests using positron gases and comparative studies of pulmonary functions were made using these positron gases and the conventional radioisotopes. In this study, 11CO2, 11CO, and 13N2 were used as positron study and then both 133Xe and 99mTc-MAA were used as conventional study. As fundamental tests, we measured the full width at half maximum (FWHM) of the line source of these nuclides and then measured the depth response of energy of these nuclides using the source in water. The subjects comprised normal control subjects, chronic obstructive pulmonary diseases (COPD), pulmonary fibrosis etc. as clinical tests. A single image or sequence of dynamic images were photographed by scintillation camera (Searle Pho-Gamma LFOV) equipped with a high energy collimator for positron and simultaneously the data were collected by computer. The detector of the scintillation camera was positioned in the posterior projection of the chest in a sitting position. A single breath method was used and after a short period of breath holding (10-20 min.), the inspired gas washed out for rebreathing room air. From the dynamic images, wash out curve and clearance rate were extracted with the aid of computer. The right lung field was divided into two zones, the upper and lower zones and upper/lower ratio (U/L ratio) of pulmonary distribution or clearance rate (C.R.) were calculated. As fundamental evaluation, resolving distance between positron and 133Xe were similar. But positron was best depth response of gamma-ray energy of the used nuclides. Clinically, 13N2 study and 133Xe study were similar.(ABSTRACT TRUNCATED AT 250 WORDS)
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This is a review of models built to explain the inefficiency of intrapulmonary gas mixing observed during multibreath tests, or to explain the slope of the alveolar plateau of the expiratory concentration-volume curve during single breath tests. The question, raised in 1917, whether diffusion was the limiting factor, received a negative answer in 1946. It then became necessary to postulate parallel unequal ventilation in combination with asynchronism. After 1966 diffusion was held responsible for stratification, a form of series inequality. However, a quantitative agreement with experimental data could only be achieved after the introduction of asymmetrical branching into the models.
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Male rats weighing 235-350 g were subjected to cooling for 4-6 hours at -20 degrees C. The lungs of the supercooled animals developed interstitial and intraalveolar edema, focal atelectases and local hemorrhages. It was shown that under overall acute hypothermia the following processes occur in the lungs: 1/local impairment of the air-blood barrier integrity due to hydropic dystrophy and degeneration of type I alveolocytes and endotheliocytes; 2/disintegration, aggregation and membrane lysis of the alveolar surfactant which underlie atelectases; 3/accumulation of the surface active material in the interstice of the interalveolar septa both because of elimination of disintegrated surfactant by type I alveolocytes and as a result of phospholipid secretion from the basal side of type II alveolocytes; 4/an increase in functional activity of type II alveolocytes and alveolar macrophages.
UNLABELLED: Twenty three cases with impairment of greater than 40% of DLCO were studied in a search of frequency, severity and pathophysiological mechanisms of PAH. Hemodinamic studies, pulmonary angiography (PA), lung scan (LS), lung biopsies (LB) were performed. The venous admixture was estimated and expressed as percentage ratio of the cardiac output (Qva/Qt x 100). Anatomical pulmonary artery to vein shunt (Qs/Qt) was estimated breathing pure O2. Ninety one percent of cases had PAH; mild to moderate in 76% of cases. Cardiac index (CI) was less than 2.8 in 26% and greater than 4.2 in 39%. The right ventricular work index (RVWI) was greater than 1.25 in 86%. The alveolar arterial oxygen tension gradient (A-aDO2) was abnormal in all cases (greater than 18 mmHg) with a Qva/Qt of greater than 30% in 78% of these cases. The Qs/Qt was found 6% in 39% of cases. IN CONCLUSION: PAH was mild to moderate in DL impairment. The RVWI was usually increased with a normal or high CI. Increase in Qva/Qt that result from V/Q abnormalities and extreme impairment of DL is to be considered as the major factor functional features in the genesis of PAH. Reduction of the cross sectional area of the pulmonary vascular bed and lung function abnormalities are equally important relevants features in the genesis of PAH.
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This paper introduces a series of reports on the structure and function of the respiratory system of mammals. We propose and justify the hypothesis that structural design is a limiting factor for O2 flow at each level of the respiratory system. The background, the reasons, and the plan for the studies are described. The main approach is to compare the size of respiratory structures with maximal O2 consumption in a series of mammals spanning several orders of magnitude in body size. The papers that follow present the methods and results for maximal O2 consumption, pulmonary diffusing capacity, mitochondrial volume, and capillary density in muscles.
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