A comparison of pulmonary artery occlusion pressure (PaOP) measurements using pressure controlled ventilation (PCV) versus airway pressure release ventilation (APRV)

cc727 CCJ Meeting abstract A comparison of pulmonary artery occlusion pressure (PaOP) measurements using pressure controlled ventilation (PCV) versus airway pressure release ventilation (APRV) Kaplan LJ Bailey H

Medical College of PA Hospital, Departments of Surgery and Emergency Medicine, Division of Trauma and Critical Care, 3300 Henry Avenue, Philadelphia, PA 19129, USA

Critical Care 20th International Symposium on Intensive Care and Emergency Medicine Meeting abstracts 20th International Symposium on Intensive Care and Emergency Medicine Brussels, Belgium

21–24 March 2000

1364-8535 2000 4 Suppl 1 P7 10.1186/cc727 21 3 2000 2000 Current Science Ltd cc-4-s1-p007

Full text

Purpose

To determine the optimal time within the APRV phase cycle to accurately measure PaOP.

Methods

Ten consecutive patients with acute lung injury (ALI) managed with PCV and a pulmonary artery catheter (PAC) were studied. Demographic data was recorded. Patients served as their own controls and were ventilated by a Drager Evita 4 Pulmonary Workstation. No patients received paralytics. PCV settings (AC mode) achieved a pCO₂ of 35–45 (torr) and a pO₂ > 60 (torr) on 60% O₂; PEEP was not controlled. Hemodynamic profiles were recorded 30 min after achieving the above pCO₂ and pO₂values. Patients were then changed to APRV to achieve the same pCO₂ and pO₂ values and hemodynamic measurements were repeated at 30 min. All medications were held constant. PaOP tracings (mmHg) were recorded and compared to the downloaded flow-time trace from the ventilator (Evitaview software). The PCV PaOP was recorded at the end of exhalation and served as the standard for comparisons. PaOP was recorded during the APRV phase cycle (positive pressure and release) and compared to the PCV value. Data are shown as means ± standard deviation and were compared using a two-tailed paired t-test; significance assumed for P < 0.05.

Results

Principal diagnoses were trauma (66%), abdominal sepsis (32%), and other (2%). Mean age was 54 ± 6.2years. PCV blood gas values were pH 7.34 ± 0.04, pCO₂39.3 ± 3.8, pO₂ 77.4 ± 9.5. APRV blood gas values were pH 7.37 ± 0.03, pCO₂ 35.5 ± 2.8, pO₂ 98 ± 11, (P< 0.05 vs PCV). The PCV PaOP was 16.3 ± 3 on a PEEP of 13.6 ± 2.2 cmH₂O with a CI of 3.2 ± 0.5 L/min/m² and an SvO₂ of 76.8 ± 4.5% at a hemoglobin of 9.6 ± 1.04 gm%.The APRV PaOP during the positive pressure phase was 21.2 ± 3.3 (initial), 19 ± 2.5 (mid), and 20.5 ± 2.8 (end); P<0.01 for all versus PCV. The APRV PaOP during the release phase was 19 ± 2.7 (initial, P < 0.05), 17.7 ± 2.3 (mid, P = 0.09), and 16.4 ± 2.6 (end, P = 0.9). CI was significantly increased at 3.6 ± 0.4 (P<0.01 vs PCV) while SvO₂ was unchanged at 79.1 ± 4.1 (P> 0.05 vs PCV).

Conclusions

APRV increases the measured PaOP during the positive pressure phase. PaOP may be reliably measured at the midpoint or end of the release phase of APRV. APRV increases oxygenation and cardiac index compared to PCV in patients with acute lung injury.