The American review of respiratory disease
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Am. Rev. Respir. Dis. · Aug 1990
Comparative StudyAdverse effects of large tidal volume and low PEEP in canine acid aspiration.
When normal lungs are ventilated with large tidal volumes (VT) and end-inspired pressures (Pei), surfactant is depleted and pulmonary edema develops. Both effects are diminished by positive end-expiratory pressure (PEEP). We reasoned that ventilatory with large VT-low PEEP would similarly increase edema following acute lung injury. ⋯ Venous admixture (Qva/Qt) was similarly greater in the large VT-low PEEP group (49.8 versus 23.5%) (p less than 0.05). We conclude that small VT-high PEEP is a better mode of ventilating acute lung injury than large VT-low PEEP because edema accumulation is less and venous admixture is less. These advantages did not result from differences in Pei, end-inspiratory lung volume, or preload (Ppwtm).(ABSTRACT TRUNCATED AT 250 WORDS)
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Am. Rev. Respir. Dis. · Aug 1990
Lung edema caused by high peak inspiratory pressures in dogs. Role of increased microvascular filtration pressure and permeability.
Mechanical ventilation with high peak airway pressures (Paw) has been shown to induce pulmonary edema in animal experiments, but the relative contributions of transvascular filtration pressure and microvascular permeability are unclear. Therefore, we examined the effects of positive-pressure ventilation on two groups of open-chest dogs ventilated for 30 min with a peak Paw of 21.8 +/- 2.3 cm H2O (Low Paw) or 64.3 +/- 3.5 cm H2O (High Paw). ⋯ Lung lymph protein clearances and minimal lymph/plasma ratios of total protein were significantly higher (p less than 0.05) after 2 h of increased left atrial pressure (PLA) in the High Paw group versus the Low Paw group, which indicates a significant increase in microvascular permeability. Lymph prostacyclin concentration in pulmonary lymph, measured as the stable metabolite 6-0-PGF1 alpha, was increased significantly by 70 to 150% from baseline (p less than 0.05) in both groups during the periods of increased Paw and increased PLA, but it was not significantly different between the groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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Am. Rev. Respir. Dis. · Jun 1990
Comparative StudyEmphysema in silicosis. A comparison of smokers with nonsmokers using pulmonary function testing and computed tomography.
The presence of emphysema in silicosis is believed to be secondary to the development of progressive massive fibrosis (PMF). However, it is difficult to separate out other causative factors, particularly cigarette smoking. In order to attempt to distinguish these factors, we examined 30 patients with silicosis by means of pulmonary function testing and computed tomography (CT) scans of the chest. ⋯ In the group without PMF (silicosis Grade 0, 1, or 2), smokers had worse emphysema than nonsmokers (p less than 0.01); there was no such difference among the patients with PMF (silicosis Grade 3 or 4). Only one of the nonsmoking subjects with silicosis but without PMF had any emphysema detected on CT. Our data suggest that silicosis, in the absence of PMF, does not cause significant emphysema, and that it is primarily the degree of emphysema rather than the degree of silicosis that determines the level of pulmonary function.
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Am. Rev. Respir. Dis. · May 1990
Hyperdynamic sepsis modifies a PEEP-mediated redistribution in organ blood flows.
Changes in organ blood flow (Q) produced by 20 cm H2O positive end-expiratory pressure (PEEP) were measured before and after the induction of hyperdynamic sepsis in nine unanesthetized sheep. During the baseline nonseptic study, PEEP was associated with a 9% fall in thermodilution-measured systemic Q, although arterial perfusing pressures were unaffected. Concurrently, microsphere-derived Q was maintained to the brain and heart, but fell to liver, spleen, pancreas, kidney, large intestine, and gastrocnemius. ⋯ We postulate that differences noted in the distribution of organ Q between the nonseptic and hyperdynamic septic studies after the application of PEEP were secondary to the vasculopathy of sepsis and/or an alteration in the function of specific organ microcirculations. However, these data do not address whether the changes in organ Q distribution after a PEEP-mediated depression in systemic Q during sepsis significantly restricted tissue DO2. The inability to acutely reverse the PEEP-mediated changes in organ Q after restoring systemic Q by a fluid infusion also suggests the need to evaluate alternative methods of support to organ Q in acute respiratory failure secondary to sepsis when the addition of PEEP acutely depresses systemic DO2.
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In order to investigate whether the changes in PaO2 reported during acid-base disturbances are due to modifications of ventilation/perfusion relationships or only to extrapulmonary factors, we studied the hemodynamics and blood gases of eight critically ill patients maintained in constant mechanical ventilation, before and after selective correction of metabolic alkalosis by infusion of 1 N hydrochloric acid (HCl). HCl infusion decreased arterial pH from 7.55 to 7.40 (p less than 0.001) and increased PaO2 from 76 to 98 mm Hg (p less than 0.05) at the end of the study. ⋯ In patients with QS/QT greater than 20% (n = 4), QS/QT decreased from 27 to 22% (p less than 0.05), hemoglobin saturation increased from 93 to 96% (p less than 0.05), and PaO2 increased from 65 to 100 mm Hg (p less than 0.05), which reflects an improvement in ventilation/perfusion relationships, probably because of enhanced hypoxic pulmonary vasoconstriction. These data indicate that metabolic alkalosis deteriorates pulmonary ventilation/perfusion relationships in patients with marked respiratory failure (QS/QT greater than 20%), and that reversing this effect with HCl infusion can improve PaO2 significantly.