The American review of respiratory disease
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Am. Rev. Respir. Dis. · May 1985
Measurement of static compliance of the total respiratory system in patients with acute respiratory failure during mechanical ventilation. The effect of intrinsic positive end-expiratory pressure.
In mechanically ventilated patients with acute respiratory failure, the static compliance of the total respiratory system is conventionally obtained by dividing the tidal volume by the difference between the "plateau" pressure measured at the airway opening (PaO) during an occlusion at end-inspiration and positive end-expiratory pressure (PEEP) set by the ventilator. This analysis is valid only if the elastic recoil pressure of the respiratory system is zero at the end of expiration, indicating that the system has reached its elastic equilibrium point. To test if this is always the case, in 14 mechanically ventilated patients with acute respiratory failure, measurements were made of PaO and of flow and volume changes. ⋯ By contrast, in the remaining 10 subjects, expiratory flow was still present when the ventilator had already begun to increase PaO, indicating that the end-expiratory elastic recoil pressure was not zero. Indeed, in all these 10 patients, a positive delta PaO (as much as 7.5 cm H2O) had to be applied by the ventilator before the actual onset of inspiratory flow. This delta PaO represents the pressure required to counterbalance the end-expiratory elastic recoil before inspiratory flow will begin, and can be termed intrinsic PEEP.(ABSTRACT TRUNCATED AT 250 WORDS)
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Am. Rev. Respir. Dis. · May 1985
Case ReportsAcute respiratory failure caused by primary pulmonary coccidioidomycosis. Two case reports and a review of the literature.
Acute respiratory failure caused by infection with Coccidioides immitis is a rare, usually fatal, event. We report 2 patients who survived acute respiratory failure caused by primary pulmonary coccidioidomycosis. ⋯ Their treatment included antifungal therapy with amphotericin B and diuresis to decrease noncardiogenic pulmonary edema. Coccidioidomycosis causing respiratory failure may be more frequent than currently clinically appreciated and may result from primary pulmonary coccidioidomycosis, miliary pulmonary disease, or as part of the multisystem organ failure seen in fungemic patients.
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Am. Rev. Respir. Dis. · Jan 1985
Distribution of ventilation and perfusion during positive end-expiratory pressure in the adult respiratory distress syndrome.
The response of respiratory gas exchange to incremental increases in positive end-expiratory pressure (PEEP) was studied in patients with the adult respiratory distress syndrome (ARDS). Fifty total changes in PEEP were studied in 19 PEEP trials performed in 16 patients. The initial patterns of ventilation-perfusion distribution as measured by the multiple inert gas elimination technique showed a large shunt flow (32 +/- 14% of total cardiac output), which was accompanied in half of the patients by perfusion to a region of low ventilation-perfusion ratio (VA/Q ratio less than 0.1). ⋯ In the increments where no increase was observed in PaO2, this reduction in blood flow to shunt or low VA/Q regions did not occur. In some instances, there was an increase in ventilation to unperfused alveoli and evidence of high ventilation-perfusion ratio (VA/Q greater than 10) as the level of PEEP increased. Because patients had an adequate pulmonary artery wedge pressure at the start of the PEEP trial (mean wedge pressure, 12.8 +/- 1.5 mmHg) improvements in oxygenation could usually be attained with only mild decreases in cardiac output.
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A variety of central nervous system (CNS) insults may be complicated by the acute development of pulmonary edema. This occurrence has been termed neurogenic pulmonary edema (NPE), and experimental models have clearly shown that CNS insults may cause pulmonary edema. Unfortunately, the pathophysiologic aspects of this response are not clearly understood. ⋯ The mediating factor for a permeability defect is not clear. The implications of these findings are that NPE may be caused by either permeability abnormalities or hydrostatic insults, may present clinically in a variety of ways, and may require different approaches to treatment. Our understanding of the CNS sites that might mediate NPE is not sophisticated enough, at present, to define the neural mechanisms involved in the pathogenesis of NPE.