• A Nahum, W C Burke, S A Ravenscraft, T W Marcy, A B Adams, P S Crooke, and J J Marini.
• University of Minnesota, Section of Pulmonary and Critical Care Medicine, St. Paul-Ramsey Medical Center, Minnesota 55101-2595.
• Am. Rev. Respir. Dis. 1992 Oct 1;146(4):965-73.

AbstractIncreased awareness of pressure-related injury to the alveolar-capillary interface has renewed interest in modes of ventilation that limit alveolar distention such as pressure-controlled ventilation (PCV). We examined respiratory system mechanics and gas exchange during PCV in six dogs. Our data conformed to the predictions of our single-compartment mathematical model of respiratory dynamics during PCV (J Appl Physiol 1989; 67:1081-92). For a fixed pressure (Pset) and inspiratory time fraction (Tl/Ttot) (15 cm H2O and 0.3, respectively), minute ventilation (VE) reached a well-defined plateau as frequency (f) increased from 10 to 50 breaths/min and tidal volume (VT) fell progressively. Concomitantly, the physiologic dead-space fraction (VD/VT) increased from 0.50 +/- 0.04 to 0.85 +/- 0.04, and arterial PCO2 (PaCO2) rose from 39 +/- 4 to 76 +/- 12 mm Hg. At a fixed combination of frequency, applied pressure, and Tl/Ttot (40 breaths/min, 15 cm H2O, and 0.3), VE did not change when we introduced fresh gas continuously from an intratracheal catheter. However, PaCO2 and VD/VT fell progressively as catheter flow increased from zero to 14 L/min (60 +/- 12 to 40 +/- 12 mm Hg and 0.83 +/- 0.03 to 0.25 +/- 0.14 mm Hg, respectively). We conclude that during PCV at a fixed Pset and Tl/Ttot increasing frequency caused VT to fall and VE to reach a plateau. Declining VT was associated with a rise in PaCO2 because of a subsequent fall in alveolar ventilation. Insufflating fresh gas by an intratracheal catheter increased alveolar ventilation and improved CO2 elimination by washing out the anatomic dead space.(ABSTRACT TRUNCATED AT 250 WORDS)

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