This Article  • Abstract  • PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Citing articles on ISI (4)  • Contact me when this article is cited  Related Content  • Related letters  • Similar articles in this journal  Topic Collections  • Surgical Physiology, Other  • Critical Care/ Intensive Care Medicine  • Alert me on articles by topic

Matthew J. Martin, MD; Elizabeth FitzSullivan, BS; Ali Salim, MD; Thomas V. Berne, MD; Shirin Towfigh, MD

Arch Surg. 2005;140:745-751.

ABSTRACT
Hypothesis  Serum bicarbonate (HCO₃) measurement may accurately and reliably be substituted for the arterial base deficit (BD) assay in the surgical intensive care unit (ICU).

Design  Retrospective criterion standard analysis.

Setting  Surgical ICU in a tertiary care facility.

Patients  Consecutive sample of non–trauma-related surgical ICU admissions from January 1996 to January 2004 with simultaneously obtained serum HCO₃ and arterial BD levels.

Main Outcome Measures  Correlation between HCO₃ and BD at admission and during the ICU stay; predictive value of serum HCO₃ for significant metabolic acidosis and ICU mortality.

Results  The study included 2291 patients with 26 063 sets of paired laboratory data. The mean ± SD age was 52 ± 16 years and mean ICU stay was 5.8 ± 9.8 days. There were 174 ICU deaths (8%). Serum HCO₃ levels showed significant correlation with arterial BD levels both at admission (r = 0.85, R² = 0.72, P<.001) and throughout the ICU stay (r = 0.88, R² = 0.77, P<.001). Serum HCO₃ reliably predicted the presence of significant metabolic acidosis (BD > 5) with an area under the receiver operating characteristic curve (AUC) of 0.93 at admission and 0.95 overall (both P<.001), outperforming pH (AUC, 0.80), anion gap (AUC, 0.70), and lactate (AUC, 0.70). The admission serum HCO₃ level predicted ICU mortality as accurately as the admission arterial BD (AUCs of 0.68 and 0.70, respectively) and more accurately than either admission pH or anion gap.

Conclusions  Serum HCO₃ provides equivalent information to the arterial BD and may be used as an alternative predictive marker or guide to resuscitation. Low HCO₃ levels should prompt immediate metabolic acidosis evaluation and management.

INTRODUCTION

Jump to Section  • Top  • Introduction  • Methods  • Results  • Comment  • Author information  • References  • Discussion

Acid-base disturbances are commonly encountered in all critically ill patient populations. Early and accurate identification and correction of significant metabolic acidoses are particularly relevant to patients in the surgical intensive care unit (ICU).¹ An arterial blood gas and serum chemistry profile are commonly used to classify the types of acid-base disequilibrium. The arterial base deficit (BD) is directly calculated from the blood gas analyzer from the PCO₂, pH, and serum bicarbonate (HCO₃) values as applied to a standard nomogram and represents the number of milliequivalents of additional base that must be added to a liter of blood to normalize the pH. An elevated BD is thought to represent the presence of unmeasured anions and is usually taken as a surrogate marker of lactic acidosis.²

The severity of metabolic acidosis as indicated by the measurement has been demonstrated to predict ICU and hospital mortality,^3-6 length of stay and hospital morbidity,^{5, 7-8} severity of sepsis and organ failure,⁹ the presence of bowel ischemia,¹⁰ and transfusion requirements¹¹ in both medical and surgical or trauma ICU populations. In addition to providing prognostic information, many centers use normalization of the BD over multiple measurements as an end point of therapy or resuscitation.^{6, 12-15} However, measurement of the arterial BD requires an arterial puncture and often necessitates multiple arterial punctures or placement of an indwelling arterial catheter. This has been associated with significant pain, increased hospital costs, and complications such as infection, pseudoaneurysm, distal embolization, and, in rare cases, hand or limb loss.^16-20 In addition, arterial blood gas measurement is not routinely performed in all ICU patients, which could result in a failure or delay in the diagnosis of significant acidosis.

The increased concentrations of plasma hydrogen ions with metabolic acidosis are buffered by a variety of homeostatic mechanisms, including plasma bicarbonates (HCO₃).²¹ Serum HCO₃ levels have been shown to decrease in a linear fashion with increasing acid loads^22-23 and theoretically should provide information similar to the arterial BD. In addition, plasma HCO₃ measurement is part of the routine chemistry panel obtained on nearly all ICU admissions, does not require any separate equipment to obtain or perform analysis, and does not require arterial puncture or catheterization. The aims of this study were to examine the degree of correlation between the arterial BD and serum HCO₃ levels, to analyze the accuracy of serum HCO₃ in identifying significant metabolic acidosis, and to compare their ability to predict mortality in a surgical ICU population.

METHODS

Jump to Section  • Top  • Introduction  • Methods  • Results  • Comment  • Author information  • References  • Discussion

This study was designed as a retrospective criterion standard analysis to compare the use of serum HCO₃ levels with the standard measure of arterial BD in an ICU population. The Los Angeles County Hospital (Los Angeles, Calif) is a large tertiary care facility and level I trauma center with a 16-bed surgical ICU. The study population included all adult (>14 years) patients admitted to the surgical ICU by either the Emergency Non-Trauma Surgery Service or one of the general surgical specialty services (Thoracic Foregut, Hepatobiliary, Colorectal, or Vascular) from January 1, 1996, to January 1, 2004. Only patients with an ICU stay longer than 24 hours and adequate laboratory data for analysis were included.

Patients were identified from a prospectively maintained clinical and laboratory database of all surgical ICU admissions. Patients who met the foregoing criteria and had at least 1 simultaneously drawn arterial blood gas determination (with BD) and serum chemistry panel (with HCO₃) were included. Laboratory, demographic, and outcome data for each patient were entered into a computerized spreadsheet. The Simplified Acute Physiology Score II and the Acute Physiology and Chronic Health Evaluation II score at 24 hours after ICU admission were calculated and recorded.^24-25 The correlation between HCO₃ and BD was assessed by calculation of the Pearson correlation coefficient (r) and the coefficient of determination (R²), and linear regression analysis was used to develop a predictive equation for BD. The predictive ability of HCO₃ and 3 conventional measures (pH, lactate, and anion gap [AG]) of severe metabolic acidosis and mortality were examined by calculating the area under the receiver operating characteristic curve (AUC). Severe metabolic acidosis was defined as a BD greater than 5. The AG was calculated with the following formula:

AG = (Na + K) – (Cl + HCO₃),

where Na indicates the level of sodium; K, of potassium; and Cl, of chloride. Linear variables are reported as the mean value ± 1 SD and AUC with 95% confidence intervals. All statistical analysis was performed with SPSS 12.0 for Windows (SPSS Inc, Chicago, Ill), and statistical significance was set at P<.05. This study was reviewed and approved with waiver of informed consent by the hospital’s institutional review board.

RESULTS

Jump to Section  • Top  • Introduction  • Methods  • Results  • Comment  • Author information  • References  • Discussion

Among 7241 surgical ICU admissions, 2291 patients (32%) were identified who met the inclusion criteria and had adequate laboratory data for analysis. These patients had a total of 26 063 sets of simultaneously obtained paired laboratory data, including an arterial blood gas and serum chemistry panel with serum HCO₃. The patient demographics are shown in Table 1. The majority of patients (56%) were admitted to the Emergency Non-Trauma Surgery Service for major abdominal surgery or disease. There were 174 deaths in the ICU, for an overall ICU mortality rate of 8%.

View this table: [in this window] [in a new window] Table 1. Patient Demographics

Table 2 shows the mean relevant laboratory values for the study population, for both the ICU admission laboratory studies only and for the entire ICU stay. There was a mean BD of 1.9 at ICU admission, which improved to 0.1 for the ICU stay. Similarly, the mean HCO₃ level at admission was 19.8 mEq/L, with improvement to a mean of 23.9 mEq/L for the ICU stay. Correlation and regression analysis demonstrated a very strong correlation between the arterial BD and the simultaneously measured serum HCO₃ levels. Figure 1 shows the strong linear correlation between the BD and serum HCO₃ level drawn at the time of ICU admission, with a correlation coefficient of 0.85 (R² = 0.72, P<.001). This linear relationship was retained throughout the early resuscitation period and for the entire ICU stay, with a correlation coefficient of 0.88 (R² = 0.77, P<.001) for all ICU laboratory measures obtained during the study period. The regression equation derived from this analysis allows prediction of the arterial BD from the serum HCO₃ level by the following formula:

View this table: [in this window] [in a new window] Table 2. Mean Laboratory Values at ICU Admission and During ICU Stay*

View larger version (35K): [in this window] [in a new window] Figure 1. Scatterplot of the admission base deficit (BD) vs the admission serum bicarbonate level (HCO3) with regression line and correlation coefficients.

BD = 21.5 – (0.79 x HCO₃).

From this equation, 2 important cutoff points for clinical use would be a serum HCO₃ level of 22 mEq/L, which equals a BD of 0, and a serum HCO₃ level of 18 mEq/L, which equates to a BD of 5.

We then assessed the accuracy and reliability of serum HCO₃ level for the identification of significant metabolic acidoses (BD > 5) and compared this with other conventional measures of acidosis such as pH, anion gap, and lactate. The serum HCO₃ level reliably and accurately identified the presence of a significant acidosis, with an AUC of 0.93 (95% confidence interval, 0.92-0.94; P<.001) for the ICU admission laboratory studies and 0.95 (95% confidence interval, 0.94-0.96; P<.001) for the entire data set (Figure 2). The serum HCO₃ significantly outperformed the other conventional acid-base measures examined, including the arterial pH (AUC, 0.80), serum anion gap (AUC, 0.70), and arterial lactate (AUC, 0.70).

View larger version (19K): [in this window] [in a new window] Figure 2. Receiver operating characteristic curve for the prediction of significant metabolic acidosis (base deficit >5) by the serum bicarbonate level. AUC indicates area under the receiver operating characteristic curve.

The study laboratory values were then analyzed for their ability to predict ICU mortality. Nonsurvivors were older, had a higher Simplified Acute Physiology Score II and Acute Physiology and Chronic Health Evaluation II score, and demonstrated significant differences in pH, anion gap, HCO₃, BD, and lactate at the time of ICU admission compared with survivors (Table 3). The receiver operating characteristic curves for mortality prediction demonstrated that the serum HCO₃ performed as well as the arterial BD, with AUCs of 0.68 and 0.70 (both P<.001), respectively (Figure 3). Both measures outperformed the admission arterial pH (AUC, 0.61) and serum anion gap (AUC, 0.59) for predicting ICU deaths. Analysis of the entire data set demonstrated that BD and HCO₃ level maintained similar predictive power throughout the ICU stay, with an AUC of 0.64 for BD and 0.63 for serum HCO₃ level (both P<.001).

View this table: [in this window] [in a new window] Table 3. Comparison of ICU Survivors and Nonsurvivors*

View larger version (20K): [in this window] [in a new window] Figure 3. Receiver operating characteristic curves comparing the prediction of intensive care unit mortality by the serum bicarbonate (HCO3) level and the arterial base deficit (BD).

COMMENT

Jump to Section  • Top  • Introduction  • Methods  • Results  • Comment  • Author information  • References  • Discussion

The diagnosis and management of major disturbances in acid-base homeostasis are a routine aspect of caring for critically ill or injured patients across all medical and surgical specialties. Acute changes in pH can produce significant alterations in the physical and electrochemical functions from the cellular to the organ and system levels.^{21, 23, 26-27} Metabolic acidosis remains one of the more concerning acid-base disturbances in the acutely ill surgical patient, as it often reflects ongoing tissue or organ hypoperfusion, which can result in organ failure or death if not promptly corrected.^5-6,15 Multiple techniques to identify the presence of acidosis and/or tissue hypoperfusion have been studied and used, including systemic markers such as the arterial BD,²⁸ anion gap,²⁹ lactate,³⁰ and mixed venous oxygen saturation,¹⁵ as well as tissue- or organ-specific measures such as gastric tonometry,³¹ sublingual capnometry,³² and transcutaneous oxygen or carbon dioxide monitoring.³³ Although there is ongoing debate about the relative merits of each measure, the ideal marker would be easily obtained and analyzed, provide accurate and reliable clinical information, and be cost-effective.

The arterial BD remains one of the most commonly used markers in the ICU both to diagnose the presence of metabolic acidosis and to guide resuscitation or therapy. Although an elevated BD is often taken as a surrogate marker for lactic acidosis in the perioperative or acute illness setting, a variety of mechanisms contribute to metabolic acidosis in the surgical ICU.^{4, 34-36} Thus, while the level of serum lactate appears to be a more specific predictor of ICU and hospital mortality,^{5, 37-38} the arterial BD remains a more sensitive measure of the overall degree of metabolic acidosis from all causes.²³ In trauma patients, several series have demonstrated that the admission BD is predictive of hospital mortality and morbidity and that normalization of the BD during the initial resuscitation correlates with improved outcomes.^{6, 28, 39-40}

The BD has also been used extensively in other medical and surgical ICU populations. In a series of 104 patients with acute pancreatitis, Sanchez-Lozada et al⁷ reported that the admission arterial BD predicted disease severity with a sensitivity of 71% and mortality with a sensitivity of 100%. Takeuchi et al¹⁰ found that the BD predicted the presence of intestinal gangrene in a series of patients with small-bowel obstruction and that the absolute level of BD correlated with the size of the necrotic segment of bowel. Other series have demonstrated that BD independently predicts perioperative mortality after ruptured abdominal aortic aneurysm repair,⁸ predicts mortality and the development of multiple organ dysfunction after thermal injury,⁹ and correlates with the ICU length of stay after cardiac surgery.⁴¹ In a study of 438 patients undergoing elective noncardiac surgery, Bennett-Guerrero et al⁴² found that BD independently predicted postoperative complications and increased length of stay (P = .008), whereas standard variables such as heart rate, blood pressure, temperature, and urine output did not. In addition, the BD has been shown to be superior to other conventional measures of acidosis, such as the arterial pH or the serum anion gap.^{4, 28, 43-44} Our data confirm that nonsurvivors in a surgical ICU population have significant BD elevations, that both the admission and serially obtained BDs are predictive of ICU mortality, and that the BD clearly outperforms other measures such as pH and anion gap.

Although the arterial BD has demonstrated utility for diagnosis, for prognosis, and as a guide to therapy, there are several drawbacks to its use. The main drawbacks involve the need for arterial puncture (single or multiple) or arterial catheterization. In an audit of patients undergoing arterial puncture, 49% recalled pain levels greater than 5 of 10, and 49% were poorly informed regarding the procedure.¹⁶ Although infrequent, other complications associated with arterial puncture or catheterization can range from minor hematoma formation to devastating ischemia and limb loss.^17-20,45 Patient factors such as obesity, diminutive arteries, and hypovolemia may make obtaining an adequate specimen difficult or impossible. In addition, processing of the arterial sample requires specialized equipment for collection, storage, and analysis, with resultant increase in costs to the hospital and patient.⁴⁶ The substitution of an easily measured value from a venous sample, such as the serum HCO₃, would overcome most of these drawbacks if it provided clinical information equivalent to the arterial BD.

There are few published data examining the utility of using the serum HCO₃ to provide information equivalent to the arterial BD in the ICU. In patients with chronic acidosis undergoing dialysis, serum HCO₃ levels have been demonstrated to correlate with nutritional status, hospitalization rates, and mortality.^47-48 In a large series of patients with septic shock, serum HCO₃ levels demonstrated a moderate correlation with the degree of lactic acidosis but were not directly compared with BD.³⁸ Eachempati et al¹² performed the only study to date that has objectively described the relationship between simultaneously measured arterial BD and serum HCO₃ levels, which served as the impetus for this study. They found a strong linear correlation between the 2 measures (r = 0.91, R² = 0.83) in a mixed trauma and surgical ICU population, and derived a regression equation to predict the BD from a known HCO₃ level. Although they demonstrated a high degree of overall correlation, they did not analyze the performance of the serum HCO₃ in the most clinically important area, identifying or excluding a significant metabolic acidosis. In addition, inclusion of a more homogeneous population (trauma) with a more mixed group of patients (nontrauma surgical) could potentially overestimate the degree of correlation and utility of serum HCO₃ in the nontrauma patients.

Our results do demonstrate a strong linear correlation between these 2 measures in a nontrauma surgical ICU population, with correlation coefficients only slightly weaker (r = 0.88 vs 0.91 and R² = 0.77 vs 0.83) than those reported by Eachempati et al.¹² Our receiver operating characteristic curves for prediction of significant acidosis and mortality also demonstrate that serum HCO₃ measurement provides nearly identical information as arterial BD in this patient population, both at the time of ICU admission and throughout the ICU stay. The serum HCO₃ level also provided better diagnostic and prognostic information than other conventional measures, such as the arterial pH and the serum anion gap.

This study has several limitations. Although a strong and reliable relationship was found between the 2 main study variables in the entire population, there may have been unidentified subgroups of patients in whom this relationship may have been altered or even invalid. Measurement of the arterial BD is only one of several major indications for arterial puncture or catheterization in the ICU population, and adoption of this practice would potentially decrease but would not eliminate the need for arterial puncture. Because of the nature of this retrospective review, we are unable to comment on the percentage of patients in this study who had other indications for arterial catheterization, such as hemodynamic or respiratory instabililty. Although we have identified several local complications from arterial manipulation in these patients, including hand ischemia, our database did not track the overall number or type of arterial-related complications.

In conclusion, these results indicate that the serum HCO₃ determination may be safely and reliably substituted for measurement of arterial BD in the surgical ICU patient. Potential advantages of this approach include increased patient comfort, avoidance of complications associated with arterial puncture and cannulation, and cost savings in terms of both time and equipment. These data should also improve the understanding that low serum HCO₃ levels accurately identify metabolic acidosis and should prompt immediate evaluation and potential interventions.

AUTHOR INFORMATION

Jump to Section  • Top  • Introduction  • Methods  • Results  • Comment  • Author information  • References  • Discussion

Correspondence: Matthew J. Martin, MD, Department of Surgery, Los Angeles County Hospital + USC Medical Center, 1200 N State St, Room 10-750, Los Angeles, CA 90033 (docmartin2{at}yahoo.com).

Accepted for Publication: April 5, 2005.

Previous Presentation: This paper was presented at the 76th Annual Meeting of the Pacific Coast Surgical Association; February 20, 2005; Dana Point, Calif; and is published after peer review and revision. The discussions that follow this article are based on the originally submitted manuscript and not the revised manuscript.

Author Affiliations: Division of Trauma and Surgical Critical Care (Drs Martin and Salim and Ms FitzSullivan) and Division of Emergency Non-Trauma Surgery (Drs Berne and Towfigh), Department of Surgery, Keck School of Medicine, University of Southern California, and the Los Angeles County Hospital + USC Medical Center, Los Angeles.

REFERENCES

Jump to Section  • Top  • Introduction  • Methods  • Results  • Comment  • Author information  • References  • Discussion

1. Wilson RF, Sibbald WJ. Approach to acid-base problems in the critically ill and injured. JACEP. 1976;5:515-522. PUBMED 2. Balasubramanyan N, Havens PL, Hoffman GM. Unmeasured anions identified by the Fencl-Stewart method predict mortality better than base excess, anion gap, and lactate in patients in the pediatric intensive care unit. Crit Care Med. 1999;27:1577-1581. FULL TEXT | ISI | PUBMED 3. Kincaid EH, Miller PR, Meredith JW, Rahman N, Chang MC. Elevated arterial base deficit in trauma patients: a marker of impaired oxygen utilization. J Am Coll Surg. 1998;187:384-392. FULL TEXT | ISI | PUBMED 4. Rocktaeschel J, Morimatsu H, Uchino S, Bellomo R. Unmeasured anions in critically ill patients: can they predict mortality? Crit Care Med. 2003;31:2131-2136. FULL TEXT | ISI | PUBMED 5. Husain F, Martin M, Mullenix P, Steele S, Elliott D. Serum lactate and base deficit as predictors of mortality and morbidity. Am J Surg. 2003;185:485-491. FULL TEXT | ISI | PUBMED 6. Randolph LC, Takacs M, Davis KA. Resuscitation in the pediatric trauma population: admission base deficit remains an important prognostic indicator. J Trauma. 2002;53:838-842. ISI | PUBMED 7. Sanchez-Lozada R, Chapa-Azuela O, Gutierrez-Vega R, Fernandez-Hidalgo E. Use of base deficit as a prognosis factor for acute pancreatitis [in Spanish]. Gac Med Mex. 2003;139:108-111. PUBMED 8. Piper G, Patel NA, Chandela S, et al. Short-term predictors and long-term outcome after ruptured abdominal aortic aneurysm repair. Am Surg. 2003;69:703-710. ISI | PUBMED 9. Fitzwater J, Purdue GF, Hunt JL, O’Keefe GE. The risk factors and time course of sepsis and organ dysfunction after burn trauma. J Trauma. 2003;54:959-966. ISI | PUBMED 10. Takeuchi K, Tsuzuki Y, Ando T, et al. Clinical studies of strangulating small bowel obstruction. Am Surg. 2004;70:40-44. ISI | PUBMED 11. Rutherford EJ, Morris JA, Reed GW, Hall KS. Base deficit stratifies mortality and determines therapy. J Trauma. 1992;33:417-423. ISI | PUBMED 12. Eachempati SR, Reed RL, Barie PS. Serum bicarbonate concentration correlates with arterial base deficit in critically ill patients. Surg Infect (Larchmt). 2003;4:193-197. PUBMED 13. Davis JW, Kaups KL, Parks SN. Effect of alcohol on the utility of base deficit in trauma. J Trauma. 1997;43:507-510. ISI | PUBMED 14. Spain DA. When is the seriously ill patient ready to be fed? JPEN J Parenter Enteral Nutr. 2002;26(suppl):S62-S68. 15. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345:1368-1377. FREE FULL TEXT 16. Crawford A. An audit of the patient’s experience of arterial blood gas testing. Br J Nurs. 2004;13:529-532. PUBMED 17. Wallach SG. Cannulation injury of the radial artery: diagnosis and treatment algorithm. Am J Crit Care. 2004;13:315-319. FREE FULL TEXT 18. Rodriguez Montalban R, Martinez de Guerenu Alonso AM, Perez-Cerda Silvestre F, et al. Acute ischemia of the hand as a complication of radial artery catheterization: apropos of 2 cases following abdominal sarcoma surgery [in Spanish]. Rev Esp Anestesiol Reanim. 2000;47:480-484. PUBMED 19. Matthews JI, Gibbons RB. Embolization complicating radial artery puncture. Ann Intern Med. 1971;75:87-88. PUBMED 20. Okeson GC, Wulbrecht PH. The safety of brachial artery puncture for arterial blood sampling. Chest. 1998;114:748-751. FREE FULL TEXT 21. Kellum JA. Determinants of blood pH in health and disease. Crit Care. 2000;4:6-14. ISI | PUBMED 22. Wiederseiner JM, Muser J, Lutz T, Hulter HN, Krapf R. Acute metabolic acidosis: characterization and diagnosis of the disorder and the plasma potassium response. J Am Soc Nephrol. 2004;15:1589-1596. FREE FULL TEXT 23. Sterns RH. Fluid, electrolyte, and acid-base disturbances. J Am Soc Nephrol. 2003;2:1-33. PUBMED 24. Knaus WA, Draper EA, Wagner DP, et al. APACHE II: a severity of disease classification system. Crit Care Med. 1985;13:818-829. ISI | PUBMED 25. Le Gall JR, Lemeshow S, Saulnier F. A new Simplified Acute Physiology Score (SAPS II) based on a European/North American multicenter study. JAMA. 1993;270:2957-2963. ABSTRACT 26. Kellum JA. Diagnosis and treatment of acid-base disorders. In: Grenvik A, Shoemaker PK, Ayers S, Holbrook PR, eds. Textbook of Critical Care. Philadelphia, Pa: WB Saunders Co; 1999:839-853. 27. Cavaliere F. Effects of acid-base abnormalities on blood capacity of transporting CO₂: adverse effects of metabolic acidosis. Intensive Care Med. 2002;28:609-615. FULL TEXT | ISI | PUBMED 28. Davis JW, Kaups KL, Parks SN. Base deficit is superior to pH in evaluating clearance of acidosis after traumatic shock. J Trauma. 1998;44:114-118. ISI | PUBMED 29. Gabow PA, Kaehny WD, Fennessey PV, et al. Diagnostic importance of an increased serum anion gap. N Engl J Med. 1980;303:854-858. ISI | PUBMED 30. Smith I, Kumar P, Molloy S, et al. Base excess and lactate as prognostic indicators for patients admitted to intensive care. Intensive Care Med. 2001;27:74-83. FULL TEXT | ISI | PUBMED 31. Heard SO. Gastric tonometry: the hemodynamic monitor of choice. Chest. 2003;123(suppl):469S-474S. FREE FULL TEXT 32. Boswell SA, Scalea TM. Sublingual capnometry: an alternative to gastric tonometry for the management of shock resuscitation. AACN Clin Issues. 2003;14:176-184. PUBMED 33. Shoemaker WC, Wo CJ, Chan L, et al. Outcome prediction of emergency patients by noninvasive hemodynamic monitoring. Chest. 2001;120:528-537. FREE FULL TEXT 34. Fencl V, Jabor A, Kazda A, Figge J. Diagnosis of metabolic acid-base disturbances in critically ill patients. Am J Respir Crit Care Med. 2000;162:2246-2251. FREE FULL TEXT 35. Brill SA, Stewart TR, Brundage SI, Schreiber MA. Base deficit does not predict mortality when secondary to hyperchloremic acidosis. Shock. 2002;17:459-462. FULL TEXT | ISI | PUBMED 36. Verma RK, Williams B, Welsby IJ. Differential diagnosis of perioperative metabolic acidosis [abstract]. Crit Care Med. 1999;27:A42. 37. Mikulaschek A, Henry SM, Donovan R, et al. Serum lactate is not predicted by anion gap or base excess after trauma resuscitation. J Trauma. 1996;40:218-224. ISI | PUBMED 38. Wira CR, Rivers EP, Donnino MW, et al. Surrogate markers for lactic acidosis in patients with severe sepsis and septic shock [abstract]. Crit Care Med. 2004;32:A151. 39. Croce MA, Fabian TC, Davis KA, Gavin TJ. Early and late acute respiratory distress syndrome: two distinct clinical entities. J Trauma. 1999;46:361-368. ISI | PUBMED 40. Davis JW, Kaups KL. Base deficit in the elderly: a marker of severe injury and death. J Trauma. 1998;45:873-877. ISI | PUBMED 41. Hugot P, Sicsic JC, Schaffuser A, et al. Base deficit in immediate postoperative period of coronary surgery with cardiopulmonary bypass and length of stay in intensive care unit. Intensive Care Med. 2003;29:257-261. ISI | PUBMED 42. Bennett-Guerrero E, Welsby I, Dunn TJ, et al. The use of a postoperative morbidity survey to evaluate patients with prolonged hospitalization after routine, moderate-risk, elective surgery. Anesth Analg. 1999;89:514-519. FREE FULL TEXT 43. Iberti TJ, Leibowitz AB, Papadakos PJ, et al. Low sensitivity of the anion gap as a screen to detect hyperlactatemia in critically ill patients. Crit Care Med. 1990;18:275-277. ISI | PUBMED 44. Salem MM, Mujais SK. Gaps in the anion gap. Arch Intern Med. 1992;152:1625-1629. ABSTRACT 45. Barnes DJ. Brachial artery puncture for blood sampling. Chest. 1999;115:1484. FREE FULL TEXT 46. Asimos AW, Gibbs MA, Marx JA, et al. Value of point-of-care blood testing in emergent trauma management. J Trauma. 2000;48:1101-1108. ISI | PUBMED 47. Bommer J, Locatelli F, Satayathum S, et al. Association of predialysis serum bicarbonate levels with risk of mortality and hospitalization in the Dialysis Outcomes and Practice Patterns Study (DOPPS). Am J Kidney Dis. 2004;44:661-671. FULL TEXT | ISI | PUBMED