The Implications of Arterial Po2 Oscillations for Conventional Arterial Blood Gas Analysis

Abstract

In a surfactant-depletion model of lung injury, tidal recruitment of atelectasis and changes in shunt fraction lead to large Pao2 oscillations. We investigated the effect of these oscillations on conventional arterial blood gas (ABG) results using different sampling techniques in ventilated rabbits. In each rabbit, 5 different ventilator settings were studied, 2 before saline lavage injury and 3 after lavage injury. Ventilator settings were altered according to 5 different goals for the amplitude and mean value of brachiocephalic Pao2 oscillations, as guided by a fast responding intraarterial probe. ABG collection was timed to obtain the sample at the peak or trough of the Pao2 oscillations, or over several respiratory cycles. Before lung injury, oscillations were small and sample timing did not influence Pao2. After saline lavage, when Po2 fluctuations measured by the indwelling arterial Po2 probe confirmed tidal recruitment, Pao2 by ABG was significantly higher at peak (295 +/- 130 mm Hg) compared with trough (74 +/- 15 mm Hg) or mean (125 +/- 75 mm Hg). In early, mild lung injury after saline lavage, Pao2 can vary markedly during the respiratory cycle. When atelectasis is recruited with each breath, interpretation of changes in shunt fraction, based on conventional ABG analysis, should account for potentially large respiratory variations in arterial Po2.

Maintenance of end-expiratory recruitment with increased respiratory rate after saline-lavage lung injury

“…The saline lavage model replicates the surfactant dysfunction of ARDS (34,70), but other features such as epithelial and endothelial damage and alveolar inflammation take several hours to develop after lavage (41,59). Our model of mild injury with surfactant depletion in mature lungs is most likely relevant to early stages of injury in patients at risk for development of ARDS and ALI (52,57,70).…”

“…Whether collapse occurs at a particular end-expiratory pressure depends not just on that pressure and the volume history, but also on how long the airway has remained at that pressure (5). Several methods that have the potential to directly assess cyclical recruitment have been applied in recent research studies, including electrical impedance tomography (15,32,71), dynamic CT (39,40,46,47,71), subpleural vital microscopy (24, 65), rapid continuous Pa O 2 monitoring (5), timed blood gas collection (52), and fast pulse oximetry (66). None of these methods have been used, however, to study the dynamics of end-expiratory collapse in ARDS.…”

Relation between Shunt, Aeration, and Perfusion in Experimental Acute Lung Injury

“…To prevent alveolar derecruitment throughout the apnea (10,35) and to match lung volume during the 13 N 2 scan, at which regional shunt was measured, with mean lung volume during the transmission scan, at which aeration was measured, apnea was performed at an airway pressure equal to mean airway pressure during breathing. Blood gas samples were drawn over two respiratory cycles to minimize variability due to sample timing (11). Accordingly, measurements of shunt and aeration should reflect the physiologic condition of the lung at approximately mean lung volume and be comparable to measurements of lung density obtained by averaging dynamic CT frames over consecutive respiratory cycles (42,43).…”

“…Because Pa O 2 varies during the respiratory cycle in the acutely injured lung (10,11), lack of synchrony between the phases of the cycle at which lung density and blood gases are measured is expected to introduce spurious variability in the relation between shunt fraction and lung aeration. Another possible explanation is that measurements of regional density do not take into account the effect of the regional distribution of perfusion on gas exchange.…”

Assessing gas exchange in acute lung injury/acute respiratory distress syndrome: diagnostic techniques and prognostic relevance

“…In fact, at the moment, a routine method to assess cyclical recruitment at bedside is not available. It has been suggested that the monitoring of time-dependent intra-arterial oxygen tension oscillations may reflect this phenomenon, as shown in surfactant-depleted ventilated rabbits [22,23]. This method, however, requires the use of a probe inserted in the distal aorta.…”