The effect of cardiopulmonary bypass on gastric and colonic mucosal perfusion: a tonometric assessment

Abstract

In a study to assess the potential effect of nonpulsatile hypothermic cardiopulmonary bypass (CPB), intramucosal pH (pHi) of the gastric and colonic mucosae was determined by tonometry (n = 8). During the hypothermic phase of CPB, gastric and colonic pHi did not change significantly. Forty minutes after the start of rewarming, despite increases in the cardiac index and mean arterial blood pressure, gastric pHi fell from 7.53 +/- 0.02 to 7.31 +/- 0.03 (p = 0.017) and colonic pHi fell from 7.50 +/- 0.02 to 7.32 +/- 0.03 (p = 0.028). Forty minutes after the end of CPB both the colonic (p = 0.017) and gastric (p = 0.046) pHi remained depressed below pre-CPB values. The difference in the arterial (pHa) and the gastric mucosal pH changed from -0.097 before CPB to 0.016, 40 minutes after the end of CPB (p = 0.027). This alteration in the pHa-pHi underlines the importance of measuring intramucosal pH by tonometry, since the pHa and pHi may move in opposite directions during episodes of haemodynamic stress. Both the gastric and colonic pHi were found to have a linear correlation with the pHa, although changes in the gastric pHi (r = 0.41, p = 0.018) were more strongly correlated with the pHa than the colonic pHi (r = 0.23, p = 0.19) in the rewarming phase of CPB and the immediate post-CPB period when there was a tendency towards intramucosal acidosis. The development of intramucosal acidosis in the rewarming and immediate post-CPB phases following hypothermic nonpulsatile CPB may impair the gut barrier and predispose patients to the absorption of luminal toxins.

Vasopressin Aggravates Cardiopulmonary Bypass-Induced Gastric Mucosal Ischemia

“…Gastric microcirculation determined by laser Doppler fluxmetry in our study showed a pathologic response in line with previous studies [5,6]. Interestingly, increased ET-1 and ET A expressions were observed in the CPB group.…”

“…Several studies have documented alterations in gastric microcirculation during extracorporeal circulation [5,6]. This mechanism provides a plausible explanation for the occurrence of postoperative UGIB.…”

“…Treatment with nonsteroidal anti-inflammatory drugs has been shown to cause gastric ischemia through their inhibitory action on vasodilating prostaglandin production [2]. Gastric ischemia has also been observed during and after CPB [5,6]; thus, a common pathogenetic mechanism can be hypothesized. Impairment of the microcirculation during CPB has been found in different organs, such as the pancreas, kidney and small bowel [5,7].…”

Extracorporeal Circulation and Intestinal Microcirculation: Pathophysiology and Therapeutical Options

“…Although these differences in dosage are slight, the measurement and the comparison of gray values determined with densitometry within the vessel and on the area adjacent to the outer vessel wall would not be correct. This increase in perme-ability is also detectable in patients undergoing cardiac operations with CPB [16]. However, the observed perfusion failure of the microcirculation is not predictable from the measured hemodynamic parameters.…”

Perioperative Endotoxemia and Bacterial Translocation during Major Surgery

“…Hence, the reduction in splanchnic blood volume is disproportionately greater than that observed in other vascular beds. Therefore, it is not suprising that the reported incidence of gut mucosal hypoperfusion detected by a low intramucosal pH at the end of major surgery is in the range of 24-62% [3], In addition, intramucosal acidosis [41], and increased intes tinal permeability [6] have been demonstrated as a conse quence of gut hypoperfusion after cardiopulmonary by pass operations. Mythen and Webb [5] recently reported increased postoperative complications and costs associat ed with intraoperative mucosal hypoperfusion after car diovascular surgery.…”