Effects of Respiratory Rate, Plateau Pressure, and Positive End-Expiratory Pressure on PaO2 Oscillations after Saline Lavage

• Published in: American journal of respiratory and critical care medicine Vol. 166; no. 12; pp. 1556 - 1562
• Main Authors: Baumgardner, James E, Markstaller, Klaus, Pfeiffer, Birgit, Doebrich, Marcus, Otto, Cynthia M
• Format: Journal Article
• Language: English
• Published: New York, NY Am Thoracic Soc 15.12.2002; American Lung Association
• Subjects: Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Animals; Biological and medical sciences; Bronchoalveolar Lavage; Disease Models, Animal; Emergency and intensive respiratory care; Hemodynamics - drug effects; Intensive care medicine; Logistic Models; Medical sciences; Positive-Pressure Respiration; Pulmonary Atelectasis - etiology; Rabbits; Respiration - drug effects; Respiration, Artificial - adverse effects; Respiratory Distress Syndrome, Adult - etiology; Sodium Chloride - pharmacology; Human; Lung disease; Assisted ventilation; Lung function; Treatment; Atelectasis; Adult respiratory distress syndrome; Respiratory disease; Respiratory intensive care; Exploration
• ISSN: 1073-449X; 1535-4970
• DOI: 10.1164/rccm.200207-717OC

One of the proposed mechanisms of ventilator-associated lung injury is cyclic recruitment of atelectasis. Collapse of dependent lung regions with every breath should lead to large oscillations in PaO2 as shunt varies throughout the respiratory cycle. We placed a fluorescence-quenching PO2 probe in the brachiocephalic artery of six anesthetized rabbits after saline lavage. Using pressure-controlled ventilation with oxygen, ventilator settings were varied in random order over three levels of positive end-expiratory pressure (PEEP), respiratory rate (RR), and plateau pressure minus PEEP (Delta). Dependence of the amplitude of PaO2 oscillations on PEEP, RR, and Delta was modeled by multiple linear regression. Before lavage, arterial PO2 oscillations varied from 3 to 22 mm Hg. After lavage, arterial PO2 oscillations varied from 5 to 439 mm Hg. Response surfaces showed markedly nonlinear dependence of amplitude on PEEP, RR, and Delta. The large PaO2 oscillations observed provide evidence for cyclic recruitment in this model of lung injury. The important effect of RR on the magnitude of PaO2 oscillations suggests that the static behavior of atelectasis cannot be accurately extrapolated to predict dynamic behavior at realistic breathing frequencies.