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.

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 body's 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.

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.

Do I take the job?: Assessing fit with the organization.

PURPOSE: A good 'fit' with an organization is critical to a leader's success yet when searching for a new position assessment an evaluation of many aspects may be overlooked, such as culture. This paper presents key considerations around 'fit' that applicants for leadership positions should consider prior to, during, and after the interview. Suggestions are provided on how to approach an evaluation of 'fit'. CONCLUSION: The importance of assessing individual fit with an organization prior to accepting a leadership position cannot be over-emphasized.

A comparison of gastric and rectal CO2 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 P CO2 without the limitations associated with gastric monitoring. This pilot study used a repeated measures design to examine changes in gastric and rectal P CO2 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 P CO2 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 P CO2 occurred during CPB, and both values trended upward during the post-CPB phase. However, poor correlation and agreement was found between the measures of P CO2 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 P CO2. 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.

Fostering the scholarship of discovery and integration for advanced practice education.

Graduate faculty are challenged to foster the scholarship of discovery and integration in their students. Fostering this scholarship requires that faculty critically analyze their approach to teaching and learning with the ultimate goal of helping students grow exponentially in ways that will continue after completion of their course or class. This article describes a course activity designed to enhance students' abilities to read, critique, and apply literature from multiple scientific disciplines to a clinical realm while maintaining their focus on their health-related scientific discipline. Applied to a course in advanced pathophysiology, the course activity described is amenable for adoption to multiple graduate-level courses and encourages individual, collective, and practice-specific growth.

Noninvasive monitoring of small intestinal oxygen in a rat model of chronic mesenteric ischemia.

We noninvasively monitored the partial pressure of oxygen (pO2) in rat's small intestine using a model of chronic mesenteric ischemia by electron paramagnetic resonance oximetry over a 7-day period. The particulate probe lithium octa-n-butoxynaphthalocyanine (LiNc-BuO) was embedded into the oxygen permeable material polydimethyl siloxane by cast-molding and polymerization (Oxy-Chip). A one-time surgical procedure was performed to place the Oxy-Chip on the outer wall of the small intestine (SI). The superior mesenteric artery (SMA) was banded to ~30% of blood flow for experimental rats. Noninvasive measurement of pO2 was performed at the baseline for control rats or immediate post-banding and on days 1, 3, and 7. The SI pO2 for control rats remained stable over the 7-day period. The pO2 on day-7 was 54.5 ± 0.9 mmHg (mean ± SE). SMA-banded rats were significantly different from controls with a noted reduction in pO2 post banding with a progressive decline to a final pO2 of 20.9 ± 4.5 mmHg (mean ± SE; p = 0.02). All SMA-banded rats developed adhesions around the Oxy-Chip, yet remained asymptomatic. The hypoxia marker Hypoxyprobe™ was used to validate the low tissue pO2. Brown cytoplasmic staining was consistent with hypoxia. Mild brown staining was noted predominantly on the villus tips in control animals. SMA-banded rats had an extended region of hypoxic involvement in the villus with a higher intensity of cytoplasmic staining. Deep brown stainings of the enteric nervous system neurons and connective tissue both within layers and in the mesentery were noted. SMA-banded rats with lower pO2 values had a higher intensity of staining. Thus, monitoring SI pO2 using the probe Oxy-Chip provides a valid measure of tissue oxygenation. Tracking pO2 in conditions that produce chronic mesenteric ischemia will contribute to our understanding of intestinal tissue oxygenation and how changes impact symptom evolution and the trajectory of chronic disease.

Hepatorenal syndrome: beyond liver failure.

Critical care nurses occasionally confront patient conditions that are not common. One such condition is hepatorenal syndrome (HRS). Three primary processes contribute to regional alterations in circulation in the renal and splanchnic beds. These processes include effective hypovolemia from the massive release of vasoactive mediators, thereby underfilling circulation, systemic and splanchnic vasodilation along with renal vasoconstriction, and hyperdynamic circulation. A "second-hit" hypothesis, whereby a triggering event causes intravascular volume depletion, likely initiates the development of HRS. The idea of a second hit focuses the attention of the health care team on surveillance strategies to prevent or limit HRS in patients with advanced cirrhosis and ascites. The treatment goal is to restore systemic and splanchnic vasoconstriction, while promoting renal vasodilation, balance sodium, and achieve euvolemia. The critical care nurse must maintain ongoing education to care for the patient with this complex syndrome in order to prevent complications and death.