Elaine M. Fisher

A Comparison of Gastric and Rectal CO? in Cardiac Surgery Patients

Critical care nurses assess and treat clinical conditions associated with inadequate oxygenation. Changes in regional organ (gut) blood flow are believed to occur in response to a decrease in oxygenation. Although the stomach is a widely accepted monitoring site, there are multiple methodological and measurement issues associated with the gastric environment that limit the accuracy of P CO2 detection. The rectum may provide nurses with an alternative site for monitoring changes in PCO2 without the limitations associated with gastric monitoring. This pilot study used a repeated measures design to examine changes in gastric and rectal PCO2 during elective coronary artery bypass grafting with cardiopulmonary bypass (CPB) and in the immediate 4-hr postoperative period in 26 subjects. The systemic indicators explained little variation in the regional indicators during protocol. A comparison of rectal and gastric PCO2 revealed no statistically significant differences in the direction or magnitude of change over any phase of cardiac surgery (baseline, CPB, post-CPB). A reduction in both rectal and gastric PCO2 occurred during CPB, and both values trended upward during the post-CPB phase. However, poor correlation and agreement was found between the measures of PCO2 at the two sites. Although clinically important, the cause is unclear. Possible explanations include variation in CO2 production between the gastric and rectal site, differences in sensitivity of the two monitoring instruments, or the absence of hemodynamic complications, which limited the extent of change in PCO2. Further investigation using patients with more profound changes in oxygenation are needed to identify response patterns and possible mechanisms.

Gut dysoxia: Comparison of sites to detect regional gut dysoxia

Dysoxia, a state in which O2 supply is inadequate to meet tissue metabolic needs, is often first detected in regional organs such as the gut. An increase in PCO2 is believed to reflect the development of gut dysoxia. The stomach is a well-documented clinical site for detecting gut PCO2; however, measurement issues make this a less than ideal monitoring site. Other sites along the GI tract may be equally sensitive to detect changes in PCO2. Rectal CO2 measurement may have the advantage of being less invasive, low risk, and continuous without the limitations associated with gastric monitoring. In this study, we compared PCO2 at two sites (gastric, rectum) at baseline and during a dysoxic challenge, cardiac arrest. We obtained similar values of PCO2 at both sites. Ten male Wistar rats were anesthetized with 1%-2% Isoflurane/50% nitrous oxide/balanced O2 and the tail artery and right atrium were cannulated. Severinghaus-type active tip PCO2 electrodes (Microelectrode Inc, Bedford, NH) were calibrated and one electrode was surgically inserted into the stomach (G-PCO2) and a second electrode was placed in the rectum (R-PCO2). Animals were stabilized following surgery. Cardiac arrest was induced by administering a rapid injection of norcuron (0.1-0.2 mg/kg) and potassium chloride solution (0.5 M/L; 0.12 mL/100 gm of body weight). Animals were monitored for 15 minutes post-arrest. Data were collected at one minute intervals using the software Data Collect. All data are reported as mean +/- SD. Baseline G-PCO2 was 64 +/- 17 torr, not significantly different from R-PCO2, 58 +/- 7 torr. After 15 minutes of cardiac arrest, G-PCO2 rose to 114 +/- 42 torr, again not significantly different from R-PCO2, which reached 112 +/- 35 torr. Monitoring PCO2 in the rectum is less invasive and might provide similar information when compared with gastric monitoring at baseline and during a dysoxic challenge.

Changes in Gastric Mucosa, Submucosa, and Muscularis IC pH May Herald Irreversible Tissue Injury

Previously we noted an abrupt rise in gastric intracellular pH (IC pH) and bicarbonate buffering between 15 and 30 min of cardiac arrest which we termed agonal alkalinization, failure of pH regulation. Agonal alkalinization may represent the transition point between reversible and irreversible injury. We asked the question, what is the sequence of change in IC pH within the gastric layers, mucosa, submucosa, and muscularis, and which layer is most sensitive? This research explored changes in IC pH within the stomach layers, mucosa, submucosa, and muscularis, at 0, 5, 15, 30, and 40 min, under three conditions, normoxia (control), ischemia (cardiac arrest), and eucapnic hypoxia (12 % oxygen). The mucosa was the most alkalotic gastric layer at baseline. Ischemia and hypoxia at 40″ produced different layer responses with the mucosa and submucosa the most sensitive layers during ischemia and the muscularis during hypoxia. Further study to examine the mechanism of changes between gastric layers using spatial-temporal techniques may assist in understanding the transition to irreversible injury.

Hypobaric Hypoxia Reduces GLUT2 Transporter Content in Rat Jejunum more than in Ileum

To define some of the specific cellular effects of chronic hypoxia on the small intestine, we measured the concentration of glucose transporter 2 (GLUT2) at two sites, the jejunum and ileum. Wister rats were subjected to 21-day normoxia (n = 6) or to continuous 21-day hypobaric hypoxia approximately 0.5 ATM (n = 5). Western blot analysis was performed and the abundance of GLUT2 protein was quantified as relative densitometric units and normalized to actin. GLUT2 content was similar in the jejunum and ileum under normoxic (jejunum = 0.65 +/- 0.13 mean +/- SD; ileum = 0.56 +/- 0.22 OD; mean difference 0.09, p = 0.09) and hypoxic conditions (jejunum = 0.56 +/- 0.14 OD mean +/- SD; ileum = 0.58 +/- 0.16; mean difference -0.01, p = 0.42). GLUT2 decreased by 14% of the mean normoxic jejunal levels whereas ileal GLUT2 was slightly increased. A maximum decline in weight of 15% occurred at day 4 followed by a blunted rate of weight gain for rats in the hypoxic group. Thus, sustained exposure to hypobaric hypoxia reduced the availability of GLUT2 for glucose transport in the jejunum. Regulating small intestinal content of glucose transporters may be an important mechanism for tissue adaptation to chronic hypoxia. This finding provides initial insight into hypoxic tolerance of the gut to chronic hypobaric hypoxic exposure.

Intracellular pH in gastric and rectal tissue post cardiac arrest.

We directly measured pHi using the pH sensitive dye, neutral red. We defined pHi for rectal and gastric tissue in whole tissue and by layer under control and arrest conditions. Fifteen minutes of arrest was not sufficient time to alter the pHi at the rectal or gastric site. On initial inspection, the stomach may be more sensitive to ischemic changes than the rectum. Understanding the mechanism by which PCO2 generation is used to track clinical changes is vital to the early detection of tissue dysoxia in order to effectively treat and manage critically ill patients.

Challenges to Intestinal pO2 Measurement Using EPR

Acute and chronic intestinal ischemia has been linked to the development of gastrointestinal symptoms such as abdominal pain, nausea and vomiting, bowel dysfunction and more seriously, the complications of sepsis, shock and death. Advances in electron paramagnetic resonance (EPR) oximetry have resulted in accurate and reliable in vivo measurement of the partial pressure of oxygen (pO(2)) in solid organs (e.g., muscle, heart) [1], but has yet to be tested in thin walled organs such as intestine. Our ultimate goal is to noninvasively monitor intestinal pO(2) during acute and chronic intestinal ischemia in a rat model. A series of experiments to deliver oxygen-sensitive indicator probes to the small/large intestine by intravenous, luminal and wall injection, as well as direct placement of a solid probe against the outer intestinal wall were attempted. Only the LiNc:BuO:PDMS chip sutured to the peritoneal wall and in direct contact with the intestine allowed for noninvasive pO(2) measurement by EPR. However, the validity of site-specific intestinal pO(2) measurement could not be confirmed and the obtained pO(2) value likely reflected peritoneal cavity oxygenation. Developing methods for probe placement on or inside the intestinal wall are needed for noninvasive, site-specific intestinal pO(2) measurement by EPR to track changes during acute and chronic intestinal ischemia.

Conceptualizing Compensatory Responses: Implications for Treatment and Research

Many scientists approach the discovery and application of knowledge of physiological processes from a reductionistic paradigm. A reductionistic approach focuses on treating one or a few key disease-related variables but overlooks the interaction of systems and their dependency on one another to produce homeostasis. The purposes of this article are to examine the current paradigm underlying treatment and its effect on patient outcome and to present an alternative perspective for understanding the bodys compensatory responses and their implications for treatment and research. Chaos theory and nonlinear methods are presented as possible ways to conceptualize and explore the complex integration of physiological patterns in response to disease, aging, and treatment.