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* From the Departments of Surgery and Critical Care Medicine (Dr. Hameed), University of Calgary, Calgary, Alberta, Canada; and Divisions of Trauma/Surgical Critical Care (Dr. Cohn), Ryder Trauma Center, University of Miami, Miami, FL.
Correspondence to: Stephen M. Cohn, MD, FCCP, Daughtry Family Department of Surgery, Divisions of Trauma and Surgical Critical Care, PO Box 016960 (D-40), Miami, FL 33131; e-mail: stephen.cohn{at}miami.edu
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Abstract |
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 TOP Abstract IntroductionThe Problem of Occult...Gastric TonometryTonometry-Directed Therapy:...Discussion and Future DirectionsReferences |
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Key Words: gastric tonometry • mucosal acidosis • shock
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Introduction |
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TOPAbstractIntroductionThe Problem of Occult...Gastric TonometryTonometry-Directed Therapy:...Discussion and Future DirectionsReferences |
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Shock is broadly classified as hemorrhagic or nonhemorrhagic—the former being by far more common in trauma situations, and the latter being further subclassified as cardiogenic, obstructive, neurogenic, or resulting from sepsis. Most initiatives in the acute phase of trauma care are based on the premise that the prevention or limitation of impairment of perfusion and oxygenation resulting from hemorrhage is critical to favorable patient outcome. Minimization of transport times from the field to definitive-care centers through the creation of streamlined trauma systems has been emphasized as an important method to reduce the duration of shock. Once patients arrive at the hospital, protocols (which include aggressive oxygenation and hemodynamic interventions), along with expeditious surgery, and ICU support are aimed at restoring adequate metabolic support, as reflected by oxygen delivery (
O2) to both injured tissues, and secondarily affected organ systems. Ideally, these interventions should be titrated against objective measures of tissue perfusion to ensure adequacy of resuscitation, and to prevent complications associated with overresuscitation.
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The Problem of Occult Hypoperfusion - Compensated Shock |
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TOPAbstractIntroductionThe Problem of Occult...Gastric TonometryTonometry-Directed Therapy:...Discussion and Future DirectionsReferences |
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Resuscitation of shock patients has relied on more direct global indexes of hypoperfusion such as serum pH, base deficit, and lactate levels. These indexes attempt to measure the magnitude of tissue hypoperfusion as reflected by oxygen debt and ensuing acidosis, and all of them have been found to be predictive of surgical complications, multiple organ failure, and even mortality. Unfortunately, although easily measured, the above indexes are global measures, and may not be sensitive indicators of regional or occult hypoperfusion. Global measures of tissue oxygenation can be normal in the presence of significant splanchnic ischemia; in fact, many, if not most patients with uncompensated shock are found to have normal global indexes of ischemia.6 Oxygen deprivation in one tissue bed may not be appreciated by the systemically diluted global measures. Furthermore, a profound compromise of tissue perfusion may be required to cause a measurable abnormality in these indexes. Unrecognized hypoperfusion can advance ischemic insult to irreversible levels, and can even potentially touch off secondary effects that may be difficult to rectify unless recognized early, or prevented.
Regional Hypoperfusion in Shock - Pathologic and Diagnostic Implications
The basic circulatory response to hypovolemic shock is redistribution of blood flow to "vital" tissue beds, and away from capillaries supplying less critical organs. Accordingly, blood flow to the splanchnic organs may be disproportionately reduced in response to hypovolemia. Splanchnic ischemia that leads to a reduction in gut barrier function and the subsequent translocation of endotoxin, inflammatory mediators, and microorganisms through an ischemic and leaky GI mucosa may ultimately result in the development of multiple organ failure.7
Although uniquely susceptible to hypoperfusion, the gut is unable to tolerate dysoxia for long periods of time. Its microvascular arrangement of a single capillary surrounded by several venules promotes nutrient absorption by creating a countercurrent flow pattern, but is unable to significantly increase blood flow in response to underperfusion. As perfusion is the most important determinant of dysoxia tolerance, organs with a capacity of recruiting numerous capillaries have great control over local blood flow and survive dysoxic conditions longer than organs with fewer capillaries which are more predisposed to anoxic injury.8
Furthermore, a significant increase in splanchnic oxygen consumption (
O2) occurs in sepsis and may contribute to the risk of visceral hypoxia even if blood flow is greater than normal. This is particularly relevant if splanchnic oxygen extraction is impaired through some disturbance of microcirculatory autoregulation.9
Gastric tonometry, which provides an index of oxygen debt in the GI tract, has been promoted both as a sentinel for impending global hypoperfusion and as a marker for a potentially correctable element in the pathogenesis of multiple organ failure. Therapies aimed at restoration of splanchnic flow have been postulated to be beneficial in shock management outcomes. This hypothesis rests both on the benefits of early identification of occult shock, as well as on the theoretical benefits of maintaining gut perfusion and thereby avoiding phenomena such as mucosal ischemia,10 which can range from increased capillary permeability to increased gut permeability to gross transmural infarction, bacterial translocation or endotoxin release, and resultant multiple organ dysfunction.11
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Gastric Tonometry |
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TOPAbstractIntroductionThe Problem of Occult...Gastric TonometryTonometry-Directed Therapy:...Discussion and Future DirectionsReferences |
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The concept that fluid in a hollow viscus could be used to approximate gas tensions in surrounding tissues was first forwarded by Dawson and colleagues.13 In the late 1950s, Boda and Muryani14 were able to measure gastric intramucosal PCO2 indirectly by measuring carbon dioxide levels in samples of air from latex balloons that were allowed to equilibrate with gastric mucosa. This measurement was intended to be a reflection of arterial PCO2, and was indeed found to correlate closely with arterial PCO2 in healthy subjects. The investigators recognized that balloon-measured carbon dioxide levels reflected contributions from both regular oxidative phosphorylation, and from buffering of the acidic products of local anaerobic metabolism, and could therefore make the gastric PCO2 estimates of arterial PCO2 "misleadingly high." Interestingly, it is actually this discrepancy which is exploited in the calculation of the intramucosal-arterial PCO2 gap, an index of mucosal acidosis and oxygen debt.8 15
Fiddian-Green and colleagues16
revived the concept of gastric tonometry in the early 1980s. Their experiments involving sampling of saline solution directly from polytetrafluoroethylene balloons placed in the stomachs and small intestines of dogs demonstrated a novel method of measuring gastric intramucosal acidosis. The unit of measurement promoted in these studies was the gastric intramucosal pH (pHi), which was calculated using the measured gastric PCO2 levels and arterial bicarbonate concentrations in a modification of the Henderson-Hasselbalch equation:
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Validation
Follow-up studies demonstrated a high degree of correlation between the calculated pHi and pH microelectrode-calculated mucosal pH (R2 = 0.79). Progressive occlusion of the superior mesenteric arteries of dogs was noted to induce a sequential fall in pHi measured in the small intestine (R2 = 0.68), evidence that measured pHi had a strong correlation with intestinal ischemia.16
Intramucosal pH has, in fact, also been found to correlate well with histologic degree of ischemic mucosal injury.17
Clinical studies have also attempted to validate the tonometry tool by demonstrating associations between pHi measurements and patient outcomes. Critically ill patients with massive blood loss16 were observed to have significantly lower pHi readings than nonbleeding patients. Gastric mucosal pH was found to be a highly sensitive predictor for complications in 85 patients after elective cardiac surgery.18
A 1993 prospective cohort study7 followed 83 patients with acute circulatory failure in their first 24 h after hospital admission. Of all the indexes of perfusion, gastric mucosal pH was the most reliable indicator of adequacy of tissue oxygenation and predictor of mortality; arterial pH and standard base excess, although significantly different between survivors and nonsurvivors, were less predictive of outcome than gastric pHi. Lactate, which is known to rely on a few pathways of metabolic clearance, was found to be neither a sensitive nor specific marker of cellular hypoxia. The authors concluded that inadequate oxygenation of the gut is associated with poor outcome, and that inadequate regional blood flow as detected by reduction in gastric intramucosal pH, but not by systemic measures, is an important contributor to morbidity and mortality in ICUs.
In 1994 Roumen and colleagues10 undertook a prospective evaluation of pHi in 15 trauma patients. During the course of the study, three of eight patients with pHi < 7.32 died. All seven patients with pHi > 7.32 survived. The investigators found no correlation between pHi and injury severity score, clinical shock, APACHE (acute physiology and chronic health evaluation) II scores, lactate, or base deficit, suggesting that measurement of gastric intramucosal pH provides independent information from conventional indexes of perfusion. Because of the association of low pHi with death, the authors10 concluded that "monitoring gastric pHi is useful in severely injured patients admitted to the ICU."
Interestingly, these findings were challenged by the results of a prospective study of Boyd and colleagues19 of 20 patients. They found that systemic metabolic acidosis as reflected by changes in blood and extracellular fluid base deficits and bicarbonate concentrations significantly correlated with pHi through the range of acid-base conditions that their patients represented. A blood base deficit > 4.65 mmol/L and extracellular fluid > 6.13 estimated pHi < 7.32 with a sensitivity of 77%, and specificity of 96%. They concluded that information obtained from gastric tonometry can be more easily obtained from measurement of base deficit. They further argued that, on the basis of this data, significant splanchnic ischemia in the presence of a normal base deficit would be rare. The study of Boyd and colleagues19 suggested that information gleaned from tonometry does not improve on that provided by the usual systemic indicators of hypoperfusion (eg, base deficit).
Techniques
pHi is derived from the measurement of carbon dioxide in saline solution that is allowed to equilibrate with the gastric mucosa. Saline solution is instilled into a silicone balloon at the end of a nasogastric tonometer. Such tonometers (TRIP NGS catheter; Tonometric Division, Instrumentarium; Helsinki, Finland) are commercially available or can be synthesized from readily available materials in the ICU. As silicone is permeable to carbon dioxide, this molecule equilibrates between the balloon and the intraluminal fluid in a predictable, time-dependent manner. After the equilibration period (at least 30 min), the saline solution is anaerobically withdrawn from the balloon and its PCO2 is measured using standard blood gas techniques, and adjusted for equilibration time using a time-dependent correction factor. The resultant "steady-state" PCO2 is used along with the arterial bicarbonate level to calculate the pHi.
Acceptable values for pHi have been conventionally considered to be within 2 SDs from mean pHi levels noted in healthy, ranitidine-treated volunteers; pHi < 7.32 is considered to represent mucosal acidosis by this criterion.8 Miller et al,20 on the basis of a prospective study of 114 trauma patients, have suggested that pHi < 7.25 or CO2 gap > 18 carries more prognostic significance than other conventionally used values.
Limitations
Technical limitations of gastric tonometry have been well described.21
The stomach is conveniently accessible for tonometric instrumentation, but because of its generous blood supply may respond slowly to hypoperfusion states. So far, this has not been found to be the case. Montgomery et al22
found a close correlation of pHi at various sites along the GI tract in a pig model of hemorrhagic shock. This finding may in part may be explained by the fact that cellular perfusion, and consequently ischemia, primarily depends on the configuration of blood supply at the microvascular level; the arrangement of single third-order capillaries in the GI tract may account for the observed similar patterns of hypoperfusion. pHi as measured by tonometric methods has also been shown to correlate well with directly measured pHi.16
Still, despite these validations, a few sources of measurement error (in arterial bicarbonate and saline solution sample carbon dioxide measurement) require consideration.
Bicarbonate
Administration of bicarbonate can alter the arterial bicarbonate, and falsely elevate the pHi. In addition, arterial bicarbonate may not reflect mucosal bicarbonate, which may be lower because of local ischemic lactic acidosis; pHi may consequently be overestimated. Because of these factors, arterial bicarbonate can be considered to be only an approximation of mucosal bicarbonate. The calculated pHi is therefore only an estimate of the true pHi. Despite this, animal studies23
have shown good correlation between tonometric and microelectrode measurements of mucosal pH in both low flow states and endotoxemia.
Carbon Dioxide
Equilibration of carbon dioxide between the gastric mucosa and the saline solution in the balloon is time dependent. Although optimum times along the GI tract may vary, in the stomach, equilibration times < 90 min may be too short. Furthermore, arterial sampling of bicarbonate reflects bicarbonate levels at a single point in time; it is difficult to know when it is best to draw an arterial sample. Results are also not immediately available as both saline solution and arterial samples must be analyzed separately in the laboratory; waiting times can adversely affect implementation of resuscitation measures. In addition, discrepancies in the PCO2 measurements between analyzers can introduce measurement error.
Duodenogastric reflux and the resulting reaction of pancreatic bicarbonate with gastric acid can generate an external source of carbon dioxide. This carbon dioxide will theoretically cause an elevation of carbon dioxide measured by the tonometer, and thereby result in an overestimation of intramucosal acidosis. To address this problem, numerous authorities have suggested the routine use of an histamine type-2 receptor antagonist to block gastric acid production and thereby limit intraluminal generation of carbon dioxide and artifactual reduction of pHi.16 Again, the fairly good correlation of tonometer and direct pHi measurements, even in the presence of varying concentrations of HCl and NaHCO3 in the stomach, suggests little quantitative importance of this effect.16 A 1998 randomized controlled trial24 of ranitidine vs placebo also demonstrated no effect of histamine type-2 blockers on pHi measurements.
The idea that shock states could cause stagnation of blood flow and result in accumulation of carbon dioxide from all sources was explored by Schlichtig and Bowles25 The accumulation of carbon dioxide from impaired clearance has the theoretical potential of causing on overestimate of mucosal acidosis. Stagnation of blood flow, however, was not found to be a significant contributor to mucosal carbon dioxide levels by these investigators.
Costs
The logistical awkwardness of gastric tonometry has probably been an important factor preventing its more widespread application. Costs from its use are attributable to the physical equipment, as well as to the measurement of saline sample carbon dioxide levels and arterial blood gases. But the maintenance of the tonometer, along with the collection of saline samples using strict protocols, and the follow-up of results with various therapeutic implications is labor intensive; nursing care applied to the collection of samples represents significant time and labor cost. New technological developments, including continuous automated measures of aliquots of air rather than saline solution, may reduce the labor investment required for the acquisition of this data.
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Tonometry-Directed Therapy: Review of the Evidence |
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Interventional studies in which specific efforts were made to alter gastric pHi were predated by clinical studies that prospectively documented pHi in patients in shock and followed their outcomes while attempting to demonstrate associations. Doglio et al,26 in a 1991 prospective study of 80 patients, showed that mortality, sepsis, and multiple organ failure were high in the group of patients who presented with a low pHi. Persistent depression of pHi was associated with higher mortality than when pHi was correctable by standard resuscitative measures. Patients whose pHi was not correctable had a mortality rate of 86.7%, while those who corrected within the first 12 h had a lower mortality rate (36.4%). Patients with an initially normal pHi who subsequently sustained a decrease in pHi had a 68.4% mortality rate.
A similar prospective study by Chang and colleagues21 of 20 critically ill trauma patients noted higher mortality rates in subjects with low initial pHi which did not correct within 24 h (50% vs 0%) as well as a higher incidence of organ dysfunction. A poor correlation between pHi and measured systemic indexes of acidosis and systemic hemodynamic and oxygen transport variables was observed. Only pHi, mixed venous oxygen saturation, and base deficit were noted to be significant predictors of mortality at regression analysis. Of all of the indexes of oxygen delivery, only pHi was different between subjects with multiple organ failure at 24 h and those without multiple organ failure. The authors argued that on the basis of their findings, splanchnic perfusion is an important factor in the pathogenesis of multiple organ failure, and that an indicator of gastric ischemia provides useful prognostic information in underperfused patients.
These prospective observational studies imply that correctable pHi carries a better prognosis than noncorrectable mucosal acidosis, and that resuscitation titrated to changes in pHi could be more beneficial than conventional strategies with their inherent risks of underresuscitation or overresuscitation. This is a plausible hypothesis, but is of value only if an intervention is found that can alter mucosal perfusion in a meaningful way. Systemic measures of increasing oxygen delivery could fail for the same reasons that systemic indexes of perfusion are considered to be inadequate: they are systemic, and they may not address problems of hypoperfusion in important microvascular beds.
A few studies have attempted to define therapeutic measures which may have a specific pHi-altering effect, and the randomized trials conducted to date in this area have based their interventions on some of these modalities. Silva et al27 conducted a meta-analysis of pHi studies, showing that vasoactive agents have a variable effect on pHi; dobutamine increases pHi, as does norepinephrine in septic patients. Epinephrine was found to have detrimental effects on gastric perfusion, while prostacycline possibly increased pHi in the analysis of available data. Dopamine was least likely to increase pHi, a finding that was supported by a crossover study of dopamine and dobutamine by Neviere et al.28 There was insufficient evidence for evaluation of nitric oxide donors, pentoxifylline, and N-acetylcysteine, although a randomized trial conducted by Molnar et al29 found no benefit from the use of acetylcysteine in shock patients. It is clear that more information on therapeutic modalities is required before the threshold to rational pHi-based intervention can be successfully crossed.
One of the first prospective randomized trials on tonometry-directed therapy was published in 1992 by Gutierrez et al.30 Two hundred sixty medical and surgical patients with APACHE scores of 15 to 20 were randomized to receive tonometry-directed therapy (dobutamine and saline solution infusions) or standard ICU management. Patients with low hospital admission pHi (< 7.35) had similar survival rates in both trial arms, whereas patients in the intervention arm with normal hospital admission pHi had increased survival (58% vs 42%). Based on the latter finding, the authors concluded that "prompt therapeutic action, when pHi falls, to increase systemic oxygen transport could protect patients" from disorders such as systemic inflammatory response syndrome and multiple organ failure, both of which could result as a direct consequence of global hypoperfusion or reperfusion, or specifically from underperfusion of the gut. The article argued that tonometry-directed therapy could avoid the potential pitfalls of indiscriminate use of pHi optimizing strategies (fluid overload, myocardial work [from use of dobutamine], blood transfusion-related complications) by reserving them for patients with documented intramucosal acidosis.
A prospective trial conducted by Ivatury et al randomized 57 trauma patients to receive therapies aimed at the following: (1) normalization and maintenance of pHi (blood, IV fluids, dobutamine), or (2) maintenance of O2 index of 600 or O2 index of 150. In this trial, whose primary focus was trauma, mortality and single-organ failure differences among the two groups did not reach statistical significance (although the latter outcome trended toward significance). No differences in any end points apart from pHi were observed between groups. Subgroup analysis demonstrated that the mortality rate from multiple organ failure was higher in patients whose pHi did not correct to 7.3 at 24 h (54% vs 6.8%) and that longer optimization times were predictive of mortality on multiple regression. The multiple organ dysfunction scores were higher in patients whose pHi did not correct within 24 h. Persistently low pHi was frequently associated with intra-abdominal anastomotic leak, compartment syndrome, abscess formation, or other complications. The authors31
concluded that "gastric mucosal pH may be an important marker to assess adequacy of resuscitation." This tentative conclusion possibly reflects insufficient power of the study to discern survival differences between the trial arms. Alternatively, it could result from insufficient correction of mucosal acidosis due to an inadequate intervention. The possibility that the intervention was found to be of no benefit because of underlying fallacies in the theories supporting gut ischemia as a sentinel of correctable shock might, however, be refuted by proponents of gastric tonometry because of the additional data that this trial provided in the subgroup analyses which support the mucosal acidosis-mortality association.
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Discussion and Future Directions |
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TOPAbstractIntroductionThe Problem of Occult...Gastric TonometryTonometry-Directed Therapy:...Discussion and Future DirectionsReferences |
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O2 DebateO2; Shoemaker et al33
and Moore et al34
initially found lower multiple organ dysfunction rates in subjects receiving or responding to supernormal O2. Such global therapy may ignore the divide between capillary bed-rich and bed-poor tissues and may result in potentially toxic oversupply of oxygen to some tissues and continued deprivation in some tissues, while subjecting a hemodynamically unstable environment to inappropriate fluid resuscitation and inotropic support with their associated risks. Sensitive tissue beds such as the GI tract could perpetuate systemic organ failure as barrier function declines and bacterial toxins and cytokines are leaked. Indiscriminate maximization of oxygen transport in heterogeneous ICU populations has, in fact, met with disappointing results and pharmacologic increases in cardiac output. Although believed to be beneficial by some investigators,35 it may actually result in increased mortality.8 These findings have formed the central premise for tonometry as an early warning of systemic catastrophe and as a guide for more directed therapy, and have paved the way for its application in the prediction of intestinal ischemia in various settings, including abdominal aortic aneurysm surgery, GI ulceration, weaning from ventilatory support,36 trauma outcomes, mortality in the ICU, liver transplant outcome, and surgical complications.
It is interesting that, despite extensive experience with gastric tonometry, no trial has documented better outcomes with tonometry-directed therapy, and that there is not much evidence from randomized studies that intramucosal pH can be reproducibly, favorably influenced relative to placebo. Gomersall et al37 speculated that failure of their trial to document a difference in outcome could have been the result of inability to produce a significant change in pHi using dobutamine and colloid, or because pHi is a marker of disease and itself not a factor in the pathogenesis of multiple organ failure as suggested by proponents of the gut-motor hypothesis.
Unpublished data from a prospective randomized study of trauma patients from our institution suggests that even a comprehensive intervention to correct gastric pHi in surgical patients does not significantly reduce mortality rates. In this trial, 151 critically ill trauma patients were randomized in three arms to receive standard therapy, placement of a gastric tonometer with otherwise routine management, or gastric pHi-directed therapy with inotropic agents, vasodilators, an infusion of agents designed to limit free-radical damage to the gut mucosa (including mannitol, vitamin C, selenium, and polymyxin B), and supplementation of enteral feeds with glutamine, N-acetylcysteine, and vitamins A and E. No significant difference was observed between the groups in rates of multiple organ failure, or mortality.
It is clear that to date, despite measurable associations of low pHi and mortality, currently available interventions designed for correction of regional acidosis do not influence mortality. Better data are needed on the role of intestinal ischemia in the progression of shock to multiple organ failure, and on the modifiable determinants of regional perfusion prior to the more widespread implementation of gastric tonometry technology.
Refinements in Gastric Tonometry
New developments in measurement strategies and the tonometry instrument itself may make measurements more precise, and may make it more easy to use. Some investigators38
have suggested that the tissue-arterial carbon dioxide partial pressure difference may be a better measure of mucosal acidosis than pHi as excess carbon dioxide levels have been shown to primarily correlate with anaerobic metabolism as opposed to blood flow stagnation and because calculation of pHi requires the assumption that arterial bicarbonate can be used as an estimate of tissue bicarbonate. Capnometric recirculating gas tonometry, an automated technique that pumps air into a gastric balloon and measures equilibrated carbon dioxide levels using infrared analysis, circumvents some of the criticisms of conventional tonometry by providing continuous data output that is rapidly interpretable.8
Other GI Monitoring Sites
Carbon dioxide is measurable in other tissue beds, and the principles first described for gastric tonometry have been extrapolated to other sites in the GI tract. Again, early detection of oxygen debt in the gut may have implications in the prevention of multiple organ dysfunction syndrome. Walley et al,39
after studying the properties of small-bowel tonometry, concluded that gastric tonometry measurements are excessively noisy and inaccurate in the detection of gut ischemia when compared to small-bowel tonometry. Unfortunately, placement of tonometers in the small bowel is more problematic than placement in the stomach.
Jacques et al40 studied a more accessible tissue bed, the sigmoid colon. Aortic cross-clamping in pigs predictably resulted in steady gastric pHi and consistent depression of sigmoid pHi, but 63% remained within the baseline range. The authors suggested that wide variation in sigmoid pHi limits the value of individual pHi measurement in the detection of ischemia. The tongue and esophagus have also been used as sites of measurement of regional perfusion.15
New Techniques
Balloonless tonometry and the use of fiberoptic carbon dioxide sensors have been described as methods of measurement of the O2-O2 balance41
42
; the inflection point of the delivery-consumption curve may be used as a sensitive indicator of tissue-specific flow-dependent O2 and increased prominence of anaerobic metabolism. Interestingly, abnormalities in oxygen supply may not be strictly limited to the GI tract. In a study of 16 septic patients and 10 nonseptic ICU control subjects, Neviere et al43
demonstrated that skeletal muscle microvascular perfusion is reduced in septic patients despite normal or elevated whole-body O2 (at rest and during reactive hyperemia). The application of near infrared spectroscopy techniques44
to various tissue beds may demonstrate similar findings in other regions. Such microvascular abnormalities are postulated to compromise tissue nutrient flow and to contribute to the development of multiple organ failure in septic patients.
Regardless of the measurement technique used, it is becoming clear that the concept of shock as the presence of inadequate organ perfusion and tissue oxygenation resulting from a limiting abnormality of the circulatory system is applicable at the microvascular level and that detection of microvascular hypoperfusion correlates with increased mortality. Redistribution of blood flow to sustain vital organs necessarily implies that certain tissue beds become deprived. Redistribution of detectable magnitude may signal severity of compensated shock and therefore herald mortality, or it may, through mechanisms such as bacterial translocation or liberation of cytokines, contribute to the progression of shock to multiple organ dysfunction. Rational approaches to these circulatory abnormalities will depend on an accurate understanding of the determinants of regional blood flow and on whether specific treatments to improve regional blood flow can alter shock pathophysiology. These controversies can be resolved by continued work at the cellular level, and through the use of well-designed clinical studies with adequate power to detect outcome differences. The diagnosis and management of shock is at another complex and exciting threshold.
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Footnotes |
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O2 = oxygen delivery; pHi = intramucosal pH; O2 = oxygen consumption |
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TOPAbstractIntroductionThe Problem of Occult...Gastric TonometryTonometry-Directed Therapy:...Discussion and Future DirectionsReferences |
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This article has been cited by other articles:
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  Y.-C. T. Huang Monitoring Oxygen Delivery in the Critically Ill Chest, November 1, 2005; 128(5_suppl_2): 554S - 560S. [Abstract] [Full Text] [PDF]
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