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. 1972 Sep;51(9):2315–2323. doi: 10.1172/JCI107042

Ventilation with end-expiratory pressure in acute lung disease

Konrad J Falke 1, Henning Pontoppidan 1, Anil Kumar 1, David E Leith 1, Bennie Geffin 1, Myron B Laver 1
PMCID: PMC292397  PMID: 4565164

Abstract

In 10 patients with severe, acute respiratory failure we studied the effects of positive end-expiratory pressure when intermittent positive pressure ventilation (IPPV) with inspired oxygen (FIO2) up to 0.5 failed to maintain arterial oxygen tension (PaO2) above 70 torr.

Positive end-expiratory pressures (PEEP) of 0, 5, 10, and 15 cm H2O were applied for 30-min periods each and in random order. Blood gas exchange, lung volumes, compliance, and hemodynamics were studied at each level of PEEP. PaO2 (FIO2 = 1.0) rose linearly with elevation of PEEP, the mean increase being from 152 to 347 torr, or 13 torr/cm H2O PEEP. Mean functional residual capacity (FRC) was 1.48±0.78 liters at zero PEEP (i.e., IPPV) and the increase was essentially linear, reaching 2.37 liters at 15 cm H2O PEEP. PaO2 and FRC showed a close correlation. Total and lung static compliance were greater during ventilation with high than with low levels of PEEP. The increase in PaO2 correlated with the specific lung compliance. Dynamic lung compliance decreased progressively with rising levels of PEEP except for an increase with 5 and 10 cm H2O PEEP in patients with initial values of 0.06 liter/cm H2O or higher. Cardiac index fell in some patients and rose in others and there was no correlation of mean cardiac index, systemic blood pressure, or peripheral vascular resistance with level of PEEP. The most probable explanation for the effect of PEEP on PaO2 and compliance is recruitment of gas exchange airspaces and prevention of terminal airway closure.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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