Gastric Intramucosal pH is Stable During Titration of Positive End-Expiratory Pressure to Improve Oxygenation In Acute Respiratory Distress Syndrome

Ibrahim Ozkan Akinci, Nahit Çakar, Gökhan Mehmet Mutlu, Simru Tugrul, Perihan Ergin Ozcan, Musa Gitmez, Figen Esen Lutfi Telci


Crit Care. 2003;7(3) 

In This Article


The results of the present study indicate that incremental increases in PEEP do not impact on splanchnic perfusion, as assessed by gastric tonometry, when cardiac output (and consequently DO2) are maintained.

In animals, PEEP decreases hepatosplanchnic perfusion in a dose-dependent manner, with a limited effect at PEEP levels of less than 10 cmH2O.[2,4,5] Alterations in splanchnic blood flow attributed to PEEP occur in parallel to those in cardiac output and consequently can be reversed with restoration of blood pressure.[4,13] Despite experimental evidence, concerns regarding the effects of PEEP on splanchnic perfusion remain theoretical because large studies in humans are lacking. Similarly, in humans without ALI or ARDS, PEEP reduces splanchnic oxygenation and this is accompanied by decreases in cardiac output, albeit with no change in lactate levels.[14] Recently, Kiefer and colleagues[9] reported no change in splanchnic perfusion when PEEP was titrated on the linear portion of the pressure-volume curve in patients with ALI.[9]

The results presented here, which demonstrate a lack of impact on splanchnic blood flow when PEEP is not accompanied by decreased cardiac output, corroborate those from animal studies[4,13] and from the recent human study conducted by Kiefer and coworkers.[9] The lack of change in pHi at PEEPopt (11 cmH2O) is in agreement with our current understanding that PEEP at 10 cmH2O has a limited effect on splanchnic blood flow. Furthermore, the presence of ARDS limited the relative impact of increased thoracic pressure on the cardiovascular system.

Perhaps more important, these observations were valid for a wide range of PEEP levels, from 5 cmH2O to as high as 17 cmH2O. We ascribed the lack of significant changes in cardiac output and DO2 in the patients to adequate volume status and preload. Relative hypovolaemia appears to be the most likely explanation for the reductions in cardiac output and splanchnic blood flow observed in animal studies. Gastric pHi, and consequently splanchnic blood flow, remained stable at PEEPopt and PEEPmax when cardiac output and DO2 remained relatively unchanged. Preservation of splanchnic blood flow at PEEPopt and PEEPmax was attributed to an increase in oxygen extraction ratio that was sufficient to compensate for the small, insignificant drop in cardiac output and DO2 that occurred during PEEP titration.[15]

It is also noteworthy that there may be individual variations in pHi in response to PEEP. Although differences in pHi response among individuals cannot explained on the basis of changes in DO2, they may be attributed to differences in the relative impact of underlying critical illness on splanchnic perfusion and variations in splanchnic vascular response (i.e. severity and/or duration of vasoconstriction, extraction ratio) to small changes in DO2 among individuals.

Because of concerns about the reliability of pHi for assessing mucosal perfusion, we also calculated the P(t-a)CO2 because it has been proposed to be a better parameter than pHi .[16] The pHi level can sometimes be misleading, particularly in situations in which gastric tissue and arterial bicarbonate levels are not equal. In addition, unlike pHi, which can change with the degree of alveolar ventilation, P(t-a)CO2 remains a reliable parameter because both components (i.e. partial arterial and tissue carbon dioxide tension) are similarly influenced by changes in alveolar ventilation, unless they are associated with alterations in cardiac output.[17] In the present study, changes in P(t-a)CO2 were not statistically significant and correlated with changes in pHi. Consequently, we used pHi values in our discussion because we believe that pHi reliably reflects the accurate tissue pH in patients.

Our results corroborate those from the only other study that evaluated the impact of PEEP on splanchnic perfusion in patients with ALI. Similar to Kiefer and colleagues,[9] we found no change either in pHi or P(t-a)CO2 during PEEP titration. However, there were several differences between two studies. Whereas Kiefer and colleagues used pressure-volume curves for PEEP titration, we titrated PEEP on the basis of improvement in oxygenation, which is a commonly used method in clinical practice because determination of pressure-volume curves can sometimes be cumbersome. Furthermore, the present study was larger and we included patients with more severe disease (ratio of fractional inspired oxygen to PaO2: 139 in the present study versus 168 in that conducted by Kiefer and coworkers).

However, the present study has several limitations. The first and perhaps most important limitation of the study is the liberal titration of PEEP in order to determine its impact on pHi, as described under Method (see above). We acknowledge that in day-to-day clinical practice, some of the patients would not have been managed with such aggressive titration of PEEP and therefore would not have received the levels of PEEP achieved in the study, rendering the clinical implications of these observations quite limited. Second, we did not directly measure splanchnic perfusion but assessed it indirectly by monitoring pHi using gastric tonometry. Although the diagnostic value of gastric tonometry has been questioned because some methodological problems, we believe that we minimized most of these limitations and improved the reproducibility of our measurements by immediate analysis of samples, use of H2 blockers[18] and lack of enteral nutrition,[19] rendering it possible to use gastric pHi to evaluate splanchnic perfusion. Third, PEEPopt in the study (approximately 11 cmH2O) was lower than levels reported in other ARDS studies.[20] Higher tidal volume (10 ml/kg) leading to higher mean airway pressure, the termination criteria used in our study, and the differences in titration technique (based on oxygenation versus pressure-volume curve) may account for this difference. Finally, pHi was measured after patients had been exposed to different levels of PEEP for a short duration. Although short-term application of high PEEP did not significantly change pHi, it is conceivable that longer durations or higher numbers of patients would have led to more prominent reductions and statistically significant differences.

Collectively, the present findings indicate that determination of PEEPopt by titration of PEEP based on improvement in oxygenation is a safe strategy, with no impairment in gastric mucosal perfusion, when cardiac output is preserved. Maintenance of cardiac output during mechanical ventilation with high PEEP may be adequate to prevent its unwanted effects on organs in the splanchnic vasculature. Nonetheless, the possibility that PEEP can alter splanchnic perfusion when it is applied at high levels and for longer durations cannot be completely excluded.


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