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At least 1,063 records · Page 59Linked to original sources
PubMed1992

Hypoxaemia and liver cirrhosis: a new argument in favour of a "diffusion-perfusion defect".

Liver cirrhosis is sometimes associated with very severe hypoxaemia, which is thought to be the result of intrapulmonary vascular dilatations (IPVDs). These vascular abnormalities, although close to the gas exchange units, are so dilated that diffusion of oxygen molecules to their centre is impaired, causing an increase in alveolar-arterial oxygen tension difference (P(A-a)O2). On the other hand, administration of 100% oxygen provides enough driving pressure to overcome this relative diffusion defect and rules out a true intrapulmonary shunt. We report a case in which, in spite of a normal increase in arterial oxygen tension (PaO2) under 100% oxygen, exercising results in a marked impairment of oxygen exchange and a large intrapulmonary shunt. This is probably due to the increased cardiac output and preferential blood flow through these low resistance IPVDs.

Cardiac Output↗
PubMed2006

Clinical use of evidence-based medicine--clinical questions: Acetylcysteine, a new treatment for an old foe?

This is a small, good quality, randomized controlled trial that shows a modest slowing in the deterioration of VC and DLco with the addition of high dose N-acetylcysteine to standard therapy in IPF. Overall the study should be interpreted with caution given its high drop out rate, which may have biased the results towards a more dramatic slowing of the disease progression. There were no differences in dyspnea score or functional status. There was no increase in the adverse events in the N-acetylcysteine group and the medication is inexpensive. Given only modest effects of N-acetylcysteine on VC and DLco, no change in functional scores, and the flaws of the study we would hesitate to use N-acetylcysteine as standard therapy in all patients with IPF.

Acetylcysteine↗
PubMedDate not supplied

[Significance of the alveolo-arterial PO2 gradient in the diagnosis of pulmonary thromboembolism].

The diagnostic value of alveolar-arterial PO2 gradient P(A-a)O2 in pulmonary thromboembolism is tested. The significance of alveolar-arterial PO2 gradient in acute pulmonary thromboembolism was determined in prospective study. The study group consisted of 7 patients with pulmonary thromboembolism documented by digital-subtraction angiography (DSA) and lung scans and ten healthy subjects with normal alveolar-arterial PO2 gradient. Hypoxemia was present in 3 patients, hypocapnia in 4 patients and an increased P(A-a)O2 gradient in all 7 patients. The results suggest that a normal P(A-a)O2 gradient in patients during room air breathing can be used as evidence against the presence of pulmonary emboli. P(A-a)O2 gradient is a very sensitive diagnostic parameter in acute pulmonary embolism but procedure is fast.

Humans↗
PubMed1991

Red blood cell pulmonary capillary transit time during exercise in athletes.

The purpose of this study was to test the hypothesis that the exercise-induced hypoxemia observed in endurance athletes is due to a reduction in the mean red blood cell pulmonary capillary transit time consequent to a plateau in pulmonary capillary blood volume (Vc) as exercise intensity progresses from moderate to heavy levels. Measurements of Vc, mean transit time, arterial O2 tension (PaO2), and end tidal-arterial O2 tension difference (AaDO2) were made in 16 subjects (mean maximal oxygen uptake (VO2max) = 4.90 l.min-1) at rest and during five cycle exercise bouts designed to elicit 55, 65, 75, 85, and 95% VO2max. Mean PaO2 fell from 101 mm Hg at rest to 85 mm Hg during heavy exercise. Mean AaDO2 increased linearly from one stage to the next and at the highest work rate equaled 22.3 mm Hg. Mean Vc failed to plateau with increasing exercise intensity and increased on average by 16 ml from one stage to the next. Mean transit time, on average, dropped from 1.05 s at rest to 0.46 s at the lowest work rate. Mean transit time did not decrease further with increasing exercise intensity (range, 0.42-0.46 s). We conclude that, under the conditions of this study, the AaDO2 increases and PaO2 decreases observed in endurance athletes during exercise of increasing intensity is not caused by a plateau in Vc and a consequent reduction in mean transit time.

Adult↗
PubMed1991

[Quantimetry and lung heterogeneity in hamsters (Mesocricetus auratus) treated with endotracheal or intrapleural infusion of elastase. Individual and contralateral variations].

Intrapleural administration of elastase was found to induce pulmonary emphysema identical to that seen after an endotracheal instillation of elastase in 33% of cats and 14% of rats given the treatment [15]. This experiment was repeated using hamsters, a species extremely sensitive to elastolytic factors reaching the lung via the airways. Linear intercept measurements (Lm) demonstrated no evidence of emphysema or alveolar dilatation four weeks after an intrapleural infusion of elastase, whereas quantified lung heterogeneity reached 40%, i.e., twice the control value; 17% of treated hamsters exhibited a statistically significant increase in heterogeneity of the right or left lung. These findings suggest that occurrence of alveolar dilatation after administration of a protease is dependent on access of the enzyme to the lung; if the enzyme fails to access the lung, abnormal lung heterogeneity may develop: this anomaly reflects a strong statistical likelihood of a disease state with or without concomitant emphysema, as was found in other species under identical conditions.

Administration, Inhalation↗
PubMed1991

Carbon dioxide-oxygen relationships in gas exchange of animals. In memory of Hermann Rahn.

In external gas exchange of vertebrates, behavior of the respiratory gases CO2 and O2 can in many cases adequately be explained by the different physico-chemical properties of the gases, including solubility, chemical combination in blood and tissue, and diffusivity. In particular, the differences in behavior between CO2 and O2 are often of particular relevance. This is demonstrated on a number of examples of gas exchange mechanisms in vertebrates, including (1) exchange ratio after changes in ventilation, (2) local variations of pulmonary ventilation/perfusion ratio, (3) absorption of gas from gas pockets, (4) water vs. air breathing, (5) multimodal breathing, (6) skin breathing, (7) gas exchange of avian eggs, (8) anomalous gas/blood CO2 equilibration, (9) blood/gas CO2 equilibration in avian lungs, (10) pulmonary diffusing capacity, (11) blood/water CO2 equilibration in fish gills, (12) deposition of gas into fish swim bladder.

Air↗
PubMed1991

Ventilation-perfusion inequality in patients with non-alcoholic liver cirrhosis.

Ventilation-perfusion relationships were studied in patients with non-alcoholic liver cirrhosis. Spirometry was essentially normal but the transfer factor of the lung (DLCO) was reduced by an average 34% of predicted. Arterial oxygen tension (PaO2) ranged from normal down to 6.9 kPa. Varying degrees of ventilation-perfusion (VA/Q) abnormalities (multiple inert gas elimination technique) were observed with increased dispersion of the perfusion distribution (log SDQ, 0.90; range 0.32-1.71; upper normal limit, 0.60) and the presence of both regions of low VA/Q ratios (between 0.1 and 0.005) (mean 4.1%; range 0-18.8%) and shunt (VA/Q ratios below 0.005) (mean 3.9%; range 0.19.8%). There was a close similarity between measured and calculated PaO2 in normoxaemic patients, but calculated values exceeded measured PaO2 in hypoxaemic patients. The difference between calculated and measured PaO2 correlated inversely to DLCO (r = 0.65, p less than 0.05). An inverse correlation was also noted between DLCO and the sum of shunt and low VA/Q regions (r = 0.87, p less than 0.001). It is concluded that hypoxaemia in non-alcoholic liver cirrhosis patients can be accounted for by intrapulmonary shunting and VA/Q mismatch, and possibly a "diffusion-perfusion" defect in patients with more severe gas exchange impairment.

Adult↗
PubMed1991

[Prognosis following extubation in severe ARDS].

The heterogeneity of patient characteristics and the impossibility of ever including all ARDS survivors in follow-up pulmonary function studies over an extended period of time makes statements on the outcome in ARDS patients rather questionable and difficult to compare. Our conclusions are drawn from our own experience in eleven patients who survived a very serious ARDS and from recently published data. In the immediate course of ARDS all patients show restrictive ventilatory impairment and gas exchange abnormalities on exercise, often even at rest. Rarely, hypercapnic hypoxemia is seen. In the months following extubation lung function gradually improves, though sometimes this is delayed and often involves some degree of residual impairment. Pulmonary function may continue to recover for several years. A disproportionate improvement in lung volumes and gas exchanging function is not uncommon, as is the absence of clinical symptoms in the presence of residual pulmonary dysfunction. The very acute first days of ARDS onset are of little prognostic value as to incomplete repair, in contrast to the good correlation between time of mechanical ventilation or amount of oxygen needed and remaining functional deficit. There is good evidence that the recovery pattern is not influenced by the illness underlying ARDS. At present the repair mechanisms are scarcely influenced by therapeutic measures.

Adult↗