The Science Journal of the American Association for Respiratory Care

2001 OPEN FORUM Abstracts

Tracheal Gas Insufflation (TGI) During Pressure Control Ventilation (PCV): Effect of Exhalation Valve Control

Robert S. CampbellRRT, FAARC, Paul N. Austin PhD CRNA (Lt Col USAF), Richard D. Branson RRTFAARC, Jay A. Johannigman MD, Fred A. Luchette MD, Sandra L. Miller MD, KennethDavis Jr. Md. University of Cincinnati, Cincinnati, OH 45267-0558

BACKGROUND:TGI may be useful in patients with elevated PaCO2. TGI lowers PaCO2 and reducesdeadspace ventilation by flushing CO2 from the upper and artificial airwaysduring exhalation and by augmenting Vt delivery at the tracheal level. We designeda lung model study to evaluate the effect of TGI on Vt and airway pressure deliveryduing PCV with four acute care vents.

Methods: Fourvents with PCV were evaluated: 300 (Siemens), and 840 (Puritan-Bennett), Evita4 (Drager), Galileo (Hamilton Medical). Each vent was set to ventilate one sideof a two chamber test lung (TTL, Michigan Instruments at compliance (C)/resistance(R) combinations of: 20/5, 20/20, and 50/20. An 8-mm ET tube was inserted intoan artificial trachea and TGI was produced via a 2.9 mm ID catheter positionedwith the tip 2 cm beyond the end of the ET tube. TGI continuous flows of 0,4, 8, and 12 LPM were used. Each vent was set to a CMV rate of 15, PCV (ÆP)of 20 cmH2O, PEEP of 10 cmH2O. Inspiratory time (T1) was set to 1.0 and 2.0seconds. A pneomotach and pressure transducer were placed between the tracheaand test lung to measure flow, volume, and pressure delivered to the lung. Peakinspiratory pressure and Vt were measured by each vent were also recorded. Fivebreaths at each condition were recorded.

Results: Table1 shows the Vt delivered to the lung and measured Vt by each vent at baselineand with 12lpm TGI flow at each T1 (C20, R20).

TGI Flow
T1 = 1sec
T1 = 2sec
Vt (vent)Vt (lung)Vt (vent)Vt (lung)
Evita 40443383443389
Galileo 0449397438398

Vents (840, Evita4) with “active”exhalation valves, limit delivery of additional Vt to the lung during TGI by“bleeding off” TGI flow once vent flow output reaches zero. Alveolarpressure is maintained at the preset level throughout T1. Vents (300, Galileo)without “active” exhalation valves force TGI flow into the lung durigTi. This results in increased alveolar pressure and Vt whe Crs is low and Tiis long.

CONCLUSION: Active exhalation valves limit alveolar pressure during TGI and thus limit Vt as compared to exhalation valves that are not active. Clinical investigations are necessary to elicit the effects of exhalation valve control on ABGs and pulmonary variables during TGI with PCV.


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