Central Venous-to-Arterial PCO2 Difference and Central Venous Oxygen Saturation in the Detection of Extubation Failure in Critically Ill Patients.

OBJECTIVES: To evaluate the ability of central venous-to-arterial carbon dioxide pressure difference, central venous oxygen saturation, and the combination of these two parameters to detect extubation failure in critically ill patients. DESIGN: Multicentric, prospective, observational study. SETTING: Three ICUs. PATIENTS: All patients who received mechanical ventilation for more than 48 hours and tolerated spontaneous breathing trials with a T-piece for 60 minutes. INTERVENTIONS: Extubation after successful spontaneous breathing trials. Extubation failure was defined as the need for mechanical ventilation within 48 hours. MEASUREMENTS AND MAIN RESULTS: The oxygen delivery index, oxygen consumption index, central venous oxygen saturation, central venous-to-arterial carbon dioxide pressure difference, and oxygen extraction were measured immediately before spontaneous breathing trials and at 60 minutes after spontaneous breathing trials initiation. Seventy-five patients were enrolled, and extubation failure was noted in 18 (24%) patients. Oxygen consumption index increased significantly during spontaneous breathing trials in the failure group. Oxygen delivery index increased in both success and failure groups. Oxygen extraction increased in the failure group (p = 0.005) and decreased in the success group (p = 0.001). Central venous oxygen saturation decreased in the failure group and increased in the success group (p = 0.014). ΔPCO2 value increased in the extubation failure group and decreased in the success group (p = 0.002). Changes in ΔPCO2 (Δ - ΔPCO2) and central venous oxygen saturation (ΔScvO2) during spontaneous breathing trials were independently associated with extubation failure (odds ratio, 1.02; 95% CI, 1.01-1.05; p = 0.006, and odds ratio, 0.84; 95% CI, 0.70-0.95; p = 0.02, respectively). Δ - ΔPCO2 and central venous oxygen saturation could predict extubation failure with areas under the curve of 0.865 and 0.856, respectively; however, their combined areas under the curve was better at 0.940. CONCLUSIONS: We found that Δ - ΔPCO2 and central venous oxygen saturation, during spontaneous breathing trials, were independent predictors of weaning outcomes. Combination analysis of both parameters enhanced their diagnostic performance and provided excellent predictability in extubation failure detection in critically ill patients.

Central venous-to-arterial carbon dioxide partial pressure difference in early resuscitation from septic shock: a prospective observational study.

BACKGROUND: Central venous-to-arterial carbon dioxide partial pressure difference (ΔPCO2) can be used as a marker for the efficacy of venous blood in removing the total CO2 produced by the tissues. To date, this role of ΔPCO2 has been assessed only in patients after resuscitation from septic shock with already normalised central venous oxygen saturation (ScvO2 ≥70%). There are no reports on the behaviour of ΔPCO2 and its relationship to cardiac index (CI) and clinical outcome before normal ScvO2 has been achieved. OBJECTIVES: To investigate the behaviour of ΔPCO2 and its relationship to CI, blood lactate concentration and 28-day mortality during resuscitation in the very early phase of septic shock. To examine whether patients who normalise both ΔPCO2 and ScvO2 during the first 6  h of resuscitation will have a greater percentage decrease in blood lactate concentration than those who only achieve normal ScvO2. DESIGN: Prospective observational study. SETTING: Intensive Care Unit (ICU) in a university hospital. PATIENTS: Eighty patients with septic shock were consecutively recruited. INTERVENTIONS: Patients were resuscitated in accordance with the recommendations of the Surviving Sepsis Campaign. MAIN OUTCOME MEASURES: Blood lactate concentrations, and haemodynamic and oxygen-derived variables were obtained at ICU admission (T0) and 6  h after admission (T6). Lactate decrease was defined as the percentage decrease in lactate concentration from T0 to T6. All cause 28-day mortality was also recorded. RESULTS: Data are presented as median (interquartile range). At T0, there were significant differences (P < 0.0001) between normal (ΔPCO2 ≤0.8 kPa) and high ΔPCO2 groups for CI (3.9 [3.3 to 4.7] vs. 2.9 [2.3 to 3.1] l min m) and ScvO2 (73 [65 to 80] vs. 61 [53 to 63]%). The correlation between changes in CI and ΔPCO2 was r  =  -0.62, P < 0.0001. Patients who reached a normal ΔPCO2 at T6 had larger decreases in blood lactate concentration and Sequential Organ Failure Assessment scores on day 1. The lactate decrease was greatest in the subgroup achieving both normal ScvO2 and ΔPCO2 at T6. Lactate decrease, unlike ΔPCO2 and ScvO2, was an independent predictor of 28-day mortality. CONCLUSION: Monitoring ΔPCO2 may be a useful tool to assess the adequacy of tissue perfusion during resuscitation. The normalisation of both ΔPCO2 and ScvO2 is associated with a greater decrease in blood lactate concentration than ScvO2 alone. The lactate decrease is an independent predictor of 28-day mortality. Further research is needed to confirm this hypothesis.

Rescue therapy by switching to total face mask after failure of face mask-delivered noninvasive ventilation in do-not-intubate patients in acute respiratory failure.

OBJECTIVE: To evaluate the impact of switching to total face mask in cases where face mask-delivered noninvasive mechanical ventilation has already failed in do-not-intubate patients in acute respiratory failure. DESIGN AND SETTING: Prospective observational study in an ICU and a respiratory stepdown unit over a 12-month study period. INTERVENTION: Switching to total face mask, which covers the entire face, when noninvasive mechanical ventilation using facial mask (oronasal mask) failed to reverse acute respiratory failure. PATIENTS: Seventy-four patients with a do-not-intubate order and treated by noninvasive mechanical ventilation for acute respiratory failure. MAIN RESULTS: Failure of face mask-delivered noninvasive mechanical ventilation was associated with a three-fold increase in in-hospital mortality (36% vs. 10.5%; p = 0.009). Nevertheless, 23 out of 36 patients (64%) in whom face mask-delivered noninvasive mechanical ventilation failed to reverse acute respiratory failure and, therefore, switched to total face mask survived hospital discharge. Reasons for switching from facial mask to total face mask included refractory hypercapnic acute respiratory failure (n = 24, 66.7%), painful skin breakdown or facial mask intolerance (n = 11, 30%), and refractory hypoxemia (n = 1, 2.7%). In the 24 patients switched from facial mask to total face mask because of refractory hypercapnia, encephalopathy score (3 [3-4] vs. 2 [2-3]; p < 0.0001), PaCO2 (87 ± 25 mm Hg vs. 70 ± 17 mm Hg; p < 0.0001), and pH (7.24 ± 0.1 vs. 7.32 ± 0.09; p < 0.0001) significantly improved after 2 hrs of total face mask-delivered noninvasive ventilation. Patients switched early to total face mask (in the first 12 hrs) developed less pressure sores (n = 5, 24% vs. n = 13, 87%; p = 0.0002), despite greater length of noninvasive mechanical ventilation within the first 48 hrs (44 hrs vs. 34 hrs; p = 0.05) and less protective dressings (n = 2, 9.5% vs. n = 8, 53.3%; p = 0.007). The optimal cutoff value for face mask-delivered noninvasive mechanical ventilation duration in predicting facial pressure sores was 11 hrs (area under the receiver operating characteristic curve, 0.86 ± 0.04; 95% confidence interval 0.76-0.93; p < 0.0001; sensitivity, 84%; specificity, 71%). CONCLUSION: In patients in hypercapnic acute respiratory failure, for whom escalation to intubation is deemed inappropriate, switching to total face mask can be proposed as a last resort therapy when face mask-delivered noninvasive mechanical ventilation has already failed to reverse acute respiratory failure. This strategy is particularly adapted to provide prolonged periods of continuous noninvasive mechanical ventilation while preventing facial pressure sores.

Effects of sitting position and applied positive end-expiratory pressure on respiratory mechanics of critically ill obese patients receiving mechanical ventilation*.

OBJECTIVE: To evaluate the extent to which sitting position and applied positive end-expiratory pressure improve respiratory mechanics of severely obese patients under mechanical ventilation. DESIGN: Prospective cohort study. SETTINGS: A 15-bed ICU of a tertiary hospital. PARTICIPANTS: Fifteen consecutive critically ill patients with a body mass index (the weight in kilograms divided by the square of the height in meters) above 35 were compared to 15 controls with body mass index less than 30. INTERVENTIONS: Respiratory mechanics was first assessed in the supine position, at zero end-expiratory pressure, and then at positive end-expiratory pressure set at the level of auto-positive endexpiratory pressure. Second, all measures were repeated in the sitting position. MEASUREMENTS AND MAIN RESULTS: Assessment of respiratory mechanics included plateau pressure, auto-positive end-expiratory pressure, and flow-limited volume during manual compression of the abdomen, expressed as percentage of tidal volume to evaluate expiratory flow limitation. In supine position at zero end-expiratory pressure, all critically ill obese patients demonstrated expiratory flow limitation (flow-limited volume, 59.4% [51.3-81.4%] vs 0% [0-0%] in controls; p < 0.0001) and greater auto-positive end-expiratory pressure (10 [5-12.5] vs 0.7 [0.4-1.25] cm H2O in controls; p < 0.0001). Applied positive end-expiratory pressure reverses expiratory flow limitation (flow-limited volume, 0% [0-21%] vs 59.4% [51-81.4%] at zero end-expiratory pressure; p < 0.001) in almost all the obese patients, without increasing plateau pressure (24 [19-25] vs 22 [18-24] cm H2O at zero end-expiratory pressure; p = 0.94). Sitting position not only reverses partially or completely expiratory flow limitation at zero end-expiratory pressure (flow-limited volume, 0% [0-58%] vs 59.4% [51-81.4%] in supine obese patients; p < 0.001) but also results in a significant drop in auto-positive end-expiratory pressure (1.2 [0.6-4] vs 10 [5-12.5] cm H2O in supine obese patients; p < 0.001) and plateau pressure (15.6 [14-17] vs 22 [18-24] cm H2O in supine obese patients; p < 0.001). CONCLUSIONS: In critically ill obese patients under mechanical ventilation, sitting position constantly and significantly relieved expiratory flow limitation and auto-positive end-expiratory pressure resulting in a dramatic drop in alveolar pressures. Combining sitting position and applied positive end-expiratory pressure provides the best strategy.

Defining metabolic acidosis in patients with septic shock using Stewart approach.

PURPOSE: The aim of this study was to define the nature of metabolic acidosis in patients with septic shock on admission to intensive care unit (ICU) using Stewart method. We also aimed to compare the ability of standard base excess (SBE), anion gap (AG), and corrected AG for albumin and lactate (AGcorr) to accurately predict the presence of unmeasured anions (UA). PATIENTS AND METHODS: Thirty consecutive patients with septic shock were prospectively included on ICU admission. Stewart equations modified by Figge were used to calculate the strong ion difference and the strong ion gap (SIG). RESULTS: Most patients had multiple underlying mechanisms explaining the metabolic acidosis. Unmeasured anions and hyperchloremia were present in 70% of the patients. Increased UA were present in 23% of patients with normal values of SBE and [HCO3-]. In these patients, plasma [Cl-] was significantly lower compared with patients with low SBE and increased UA (103 [102-106.6] vs 108 [106-111] mmol/L; P=.01, respectively). Corrected AG for albumin and lactate had the best correlation with SIG (r²=0.94; P<.0001) with good agreement (bias, 0, and precision, 1.22) and highest area under the receiver operating characteristic curve (0.995; 95% confidence interval, 0.87-1) to discriminate SIG acidosis. CONCLUSIONS: Patients with septic shock exhibit a complex metabolic acidosis at ICU admission. High UA may be present with normal values of SBE and [HCO3-] as a result of associated "relative" hypochloremic alkalosis. Corrected AG for albumin and lactate offers the most accurate bedside alternative to Stewart calculation of UA.

Central venous-to-arterial PCO2 difference as a marker to identify fluid responsiveness in septic shock.

Defining the hemodynamic response to volume therapy is integral to managing critically ill patients with acute circulatory failure, especially in the absence of cardiac index (CI) measurement. This study aimed at investigating whether changes in central venous-to-arterial CO2 difference (Δ-ΔPCO2) and central venous oxygen saturation (ΔScvO2) induced by volume expansion (VE) are reliable parameters to define fluid responsiveness in sedated and mechanically ventilated septic patients. We prospectively studied 49 critically ill septic patients in whom VE was indicated because of circulatory failure and clinical indices. CI, ΔPCO2, ScvO2, and oxygen consumption (VO2) were measured before and after VE. Responders were defined as patients with a > 10% increase in CI (transpulmonary thermodilution) after VE. We calculated areas under the receiver operating characteristic curves (AUCs) for Δ-ΔPCO2, ΔScvO2, and changes in CI (ΔCI) after VE in the whole population and in the subgroup of patients with an increase in VO2 (ΔVO2) ≤ 10% after VE (oxygen-supply independency). Twenty-five patients were fluid responders. In the whole population, Δ-ΔPCO2 and ΔScvO2 were significantly correlated with ΔCI after VE (r = - 0.30, p = 0.03 and r = 0.42, p = 0.003, respectively). The AUCs for Δ-ΔPCO2 and ΔScvO2 to define fluid responsiveness (increase in CI > 10% after VE) were 0.76 (p < 0.001) and 0.68 (p = 0.02), respectively. In patients with ΔVO2 ≤ 10% (n = 36) after VE, the correlation between ΔScvO2 and ΔCI was 0.62 (p < 0.001), and between Δ-ΔPCO2 and ΔCI was - 0.47 (p = 0.004). The AUCs for Δ-ΔPCO2 and ΔScvO2 were 0.83 (p < 0.001) and 0.73 (p = 0.006), respectively. In these patients, Δ-ΔPCO2 ≤ -37.5% after VE allowed the categorization between responders and non-responders with a positive predictive value of 100% and a negative predictive value of 60%. In sedated and mechanically ventilated septic patients with no signs of tissue hypoxia (oxygen-supply independency), Δ-ΔPCO2 is a reliable parameter to define fluid responsiveness.

A comparison between measured and calculated central venous oxygen saturation in critically ill patients.

BACKGROUND: Central venous oxygen saturation (ScvO2) is often used to help to guide resuscitation of critically ill patients. The standard gold technique for ScvO2 measurement is the co-oximetry (Co-oximetry_ScvO2), which is usually incorporated in most recent blood gas analyzers. However, in some hospitals, those machines are not available and only calculated ScvO2 (Calc_ScvO2) is provided. Therefore, we aimed to investigate the agreement between Co-oximetry_ScvO2 and Calc_ScvO2 in a general population of critically ill patients and septic shock patients. METHODS: A total of 100 patients with a central venous catheter were included in the study. One hundred central venous blood samples were collected and analyzed using the same point-of-care blood gas analyzer, which provides both the calculated and measured ScvO2 values. Bland and Altman plot, intra-class correlation coefficient (ICC), and Cohen's Kappa coefficient were used to assess the agreement between Co-oximetry_ScvO2 and Calc_ScvO2. Multiple linear regression analysis was performed to investigate the independent explanatory variables of the difference between Co-oximetry_ScvO2 and Calc_ScvO2. RESULTS: In all population, Bland and Altman's analysis showed poor agreement (+4.5 [-7.1, +16.1]%) between the two techniques. The ICC was 0.754 [(95% CI: 0.393-0.880), P< 0.001], and the Cohen's Kappa coefficient, after categorizing the two variables into two groups using a cutoff value of 70%, was 0.470 (P <0.001). In septic shock patients (49%), Bland and Altman's analysis also showed poor agreement (+5.6 [-6.7 to 17.8]%). The ICC was 0.720 [95% CI: 0.222-0.881], and the Cohen's Kappa coefficient was 0.501 (P <0.001). Four independent variables (PcvO2, Co-oximetry_ScvO2, venous pH, and Hb) were found to be associated with the difference between the measured and calculated ScvO2 (adjusted R2 = 0.8, P<0.001), with PcvO2 being the main independent explanatory variable because of its highest absolute standardized coefficient. The area under the receiver operator characteristic curves (AUC) of PcvO2 to predict Co-oximetry_ScvO2 ≥ 70% was 0.911 [95% CI: 0.837-0.959], in all patients, and 0.903 [95% CI: 0.784-0.969], in septic shock patients. The best cutoff value was ≥ 36 mmHg (sensitivity, 88%; specificity, 83%), in all patients, and ≥ 35 mmHg (sensitivity, 94%; specificity, 71%) in septic shock patients. CONCLUSIONS: The discrepancy between the measured and calculated ScvO2 is clinically not acceptable. We do not recommend the use of calculated ScvO2 to guide resuscitation in critically ill patients. In situations where the Co-oximetry technique is not available, relying on PcvO2 to predict the measured ScvO2 value above or below 70% could be an option.

Acute hyperventilation increases the central venous-to-arterial PCO2 difference in stable septic shock patients.

BACKGROUND: To evaluate the effects of acute hyperventilation on the central venous-to-arterial carbon dioxide tension difference (∆PCO2) in hemodynamically stable septic shock patients. METHODS: Eighteen mechanically ventilated septic shock patients were prospectively included in the study. We measured cardiac index (CI), ∆PCO2, oxygen consumption (VO2), central venous oxygen saturation (ScvO2), and blood gas parameters, before and 30 min after an increase in alveolar ventilation (increased respiratory rate by 10 breaths/min). RESULTS: Arterial pH increased significantly (from 7.35 ± 0.07 to 7.42 ± 0.09, p < 0.001) and arterial carbon dioxide tension decreased significantly (from 44.5 [41-48] to 34 [30-38] mmHg, p < 0.001) when respiratory rate was increased. A statistically significant increase in VO2 (from 93 [76-105] to 112 [95-134] mL/min/m2, p = 0.002) was observed in parallel with the increase in alveolar ventilation. While CI remained unchanged, acute hyperventilation led to a significant increase in ∆PCO2 (from 4.7 ± 1.0 to 7.0 ± 2.6 mmHg, p < 0.001) and a significant decrease in ScvO2 (from 73 ± 6 to 67 ± 8%, p < 0.001). A good correlation was found between changes in arterial pH and changes in VO2 (r = 0.67, p = 0.002). Interestingly, we found a strong association between the increase in VO2 and the increase in ∆PCO2 (r = 0.70, p = 0.001). CONCLUSIONS: Acute hyperventilation provoked a significant increase in ∆PCO2, which was the result of a significant increase in VO2 induced by hyperventilation. The clinician should be aware of the effects of acute elevation of alveolar ventilation on ∆PCO2.

Use of venous-to-arterial carbon dioxide tension difference to guide resuscitation therapy in septic shock.

The mixed venous-to-arterial carbon dioxide (CO2) tension difference [P (v-a) CO2] is the difference between carbon dioxide tension (PCO2) in mixed venous blood (sampled from a pulmonary artery catheter) and the PCO2 in arterial blood. P (v-a) CO2 depends on the cardiac output and the global CO2 production, and on the complex relationship between PCO2 and CO2 content. Experimental and clinical studies support the evidence that P (v-a) CO2 cannot serve as an indicator of tissue hypoxia, and should be regarded as an indicator of the adequacy of venous blood to wash out the total CO2 generated by the peripheral tissues. P (v-a) CO2 can be replaced by the central venous-to-arterial CO2 difference (ΔPCO2), which is calculated from simultaneous sampling of central venous blood from a central vein catheter and arterial blood and, therefore, more easy to obtain at the bedside. Determining the ΔPCO2 during the resuscitation of septic shock patients might be useful when deciding when to continue resuscitation despite a central venous oxygen saturation (ScvO2) > 70% associated with elevated blood lactate levels. Because high blood lactate levels is not a discriminatory factor in determining the source of that stress, an increased ΔPCO2 (> 6 mmHg) could be used to identify patients who still remain inadequately resuscitated. Monitoring the ΔPCO2 from the beginning of the reanimation of septic shock patients might be a valuable means to evaluate the adequacy of cardiac output in tissue perfusion and, thus, guiding the therapy. In this respect, it can aid to titrate inotropes to adjust oxygen delivery to CO2 production, or to choose between hemoglobin correction or fluid/inotrope infusion in patients with a too low ScvO2 related to metabolic demand. The combination of P (v-a) CO2 or ΔPCO2 with oxygen-derived parameters through the calculation of the P (v-a) CO2 or ΔPCO2/arteriovenous oxygen content difference ratio can detect the presence of global anaerobic metabolism.

Ratios of central venous-to-arterial carbon dioxide content or tension to arteriovenous oxygen content are better markers of global anaerobic metabolism than lactate in septic shock patients.

BACKGROUND: To evaluate the ability of the central venous-to-arterial CO2 content and tension differences to arteriovenous oxygen content difference ratios (∆ContCO2/∆ContO2 and ∆PCO2/∆ContO2, respectively), blood lactate concentration, and central venous oxygen saturation (ScvO2) to detect the presence of global anaerobic metabolism through the increase in oxygen consumption (VO2) after an acute increase in oxygen supply (DO2) induced by volume expansion (VO2/DO2 dependence). METHODS: We prospectively studied 98 critically ill mechanically ventilated patients in whom a fluid challenge was decided due to acute circulatory failure related to septic shock. Before and after volume expansion (500 mL of colloid solution), we measured cardiac index, VO2, DO2, ∆ContCO2/∆ContO2 and ∆PCO2/∆ContO2 ratios, lactate, and ScvO2. Fluid-responders were defined as a ≥15 % increase in cardiac index. Areas under the receiver operating characteristic curves (AUC) were determined for these variables. RESULTS: Fifty-one patients were fluid-responders (52 %). DO2 increased significantly (31 ± 12 %) in these patients. An increase in VO2 ≥ 15 % ("VO2-responders") concurrently occurred in 57 % of the 51 fluid-responders (45 ± 16 %). Compared with VO2-non-responders, VO2-responders were characterized by higher lactate levels and higher ∆ContCO2/∆ContO2 and ∆PCO2/∆ContO2 ratios. At baseline, lactate predicted a fluid-induced increase in VO2 ≥ 15 % with AUC of 0.745. Baseline ∆ContCO2/∆ContO2 and ∆PCO2/∆ContO2 ratios predicted an increase of VO2 ≥ 15 % with AUCs of 0.965 and 0.962, respectively. Baseline ScvO2 was not able to predict an increase of VO2 ≥ 15 % (AUC = 0.624). CONCLUSIONS: ∆ContCO2/∆ContO2 and ∆PCO2/∆ContO2 ratios are more reliable markers of global anaerobic metabolism than lactate. ScvO2 failed to predict the presence of global tissue hypoxia.

Repeatability of blood gas parameters, PCO2 gap, and PCO2 gap to arterial-to-venous oxygen content difference in critically ill adult patients.

The objective of this study was to examine the repeatability of blood gas (BG) parameters and their derived variables such as the central venous-to-arterial carbon dioxide tension difference (▵PCO2) and the ratio of ▵PCO2 over the central arteriovenous oxygen content difference (▵PCO2/C(a-cv)O2) and to determine the smallest detectable changes in individual patients.A total of 192 patients with arterial and central venous catheters were included prospectively. Two subsequent arterial and central venous blood samples were collected immediately one after the other and analyzed using the same point-of-care BG analyzer. The samples were analyzed for arterial and venous BG parameters, ▵PCO2, and ▵PCO2/C(a-cv)O2 ratio. Repeatability was expressed as the smallest detectable difference (SDD) and the least significant change (LSC). A change in value of these parameters exceeding the SDD or the LSC should be regarded as real.The SDDs for arterial carbon dioxide tension, arterial oxygen saturation, central venous oxygen saturation (ScvO2), and ▵PCO2 were small: ±2.06 mm Hg, ±1.23%, 2.92%, and ±1.98 mm Hg, respectively, whereas the SDDs for arterial oxygen tension (PaO2) and ▵PCO2/C(a-cv)O2 were high: ±9.09 mm Hg and ±0.57 mm Hg/mL, respectively. The LSCs (%) for these variables were 5.06, 1.27, 4.44, 32.4, 9.51, and 38.5, respectively.The repeatability of all these variables was good except for PaO2 and ▵PCO2/C(a-cv)O2 ratio for which we observed an important inherent variability. Expressed as SDD, a ScvO2 change value of at least ±3% should be considered as true. The clinician must be aware that an apparent change in these variables in an individual patient might represent only an inherent variation.

Time course of central venous-to-arterial carbon dioxide tension difference in septic shock patients receiving incremental doses of dobutamine.

PURPOSE: To assess the time course of the central venous-arterial carbon dioxide tension difference (∆PCO2)-as an index of the carbon dioxide production (VCO2)/cardiac index (CI) ratio-in stable septic shock patients receiving incremental doses of dobutamine. METHODS: Twenty-two hemodynamically stable septic shock patients with no signs of global tissue hypoxia, as testified by normal blood lactate levels, were prospectively included. A dobutamine infusion was administered at a dose of up to 15 µg/kg/min in increments of 5 µg/kg/min every 30 min. Complete hemodynamic and gas measurements were obtained at baseline, and at each dose of dobutamine. RESULTS: Dobutamine induced a significant dose-dependent increase of CI from 0 to 15 µg/kg/min (P < 0.001). Oxygen consumption (VO2) and VCO2 were progressively increased by dobutamine. These increases were more marked between 10 and 15 µg/kg/min (8.3 and 8.6 %, respectively) than between the lower doses. ∆PCO2 and oxygen extraction (EO2) significantly decreased between 0 (8.0 ± 2.0 mmHg and 43.8 ± 13.4 %, respectively) and 10 µg/kg/min of dobutamine (4.2 ± 1.6 mmHg and 28.9 ± 7.9 %, respectively), but remained unchanged from 10 to 15 µg/kg/min (5.4 ± 2.4 mmHg and 29.5 ± 8.2 %, respectively). The central venous oxygen saturation significantly (ScvO2) increased from 0 to 10 µg/kg/min and remained unchanged from 10 to 15 µg/kg/min. Time courses of ∆PCO2, ScvO2, and EO2 were linked therefore to the biphasic changes of VO2 and VCO2. CONCLUSION: ∆PCO2 is a good indicator of the change of VCO2 induced by dobutamine. Measurement of ∆PCO2, along with ScvO2 and EO2, may be presented as a useful tool to assess the adequacy of oxygen supply versus metabolic and oxygen demand.

Use of sodium-chloride difference and corrected anion gap as surrogates of Stewart variables in critically ill patients.

INTRODUCTION: To investigate whether the difference between sodium and chloride ([Na(+)] - [Cl(-)]) and anion gap corrected for albumin and lactate (AG(corr)) could be used as apparent strong ion difference (SID(app)) and strong ion gap (SIG) surrogates (respectively) in critically ill patients. METHODS: A total of 341 patients were prospectively observed; 161 were allocated to the modeling group, and 180 to the validation group. Simple regression analysis was used to construct a mathematical model between SID(app) and [Na(+)] - [Cl(-)] and between SIG and AG(corr) in the modeling group. Area under the receiver operating characteristic (ROC) curve was also measured. The mathematical models were tested in the validation group. RESULTS: in the modeling group, SID(app) and SIG were well predicted by [Na(+)] - [Cl(-)] and AG(corr) (R(2) = 0.973 and 0.96, respectively). Accuracy values of [Na(+)] - [Cl(-)] for the identification of SID(app) acidosis (<42.7 mEq/L) and alkalosis (>47.5 mEq/L) were 0.992 (95% confidence interval [CI], 0.963-1) and 0.998 (95%CI, 0.972-1), respectively. The accuracy of AG(corr) in revealing SIG acidosis (>8 mEq/L) was 0.974 (95%CI: 0.936-0.993). These results were validated by showing excellent correlations and good agreements between predicted and measured SID(app) and between predicted and measured SIG in the validation group (R(2) = 0.977; bias = 0±1.5 mEq/L and R(2) = 0.96; bias = -0.2±1.8 mEq/L, respectively). CONCLUSIONS: SID(app) and SIG can be substituted by [Na(+)] - [Cl(-)] and by AG(corr) respectively in the diagnosis and management of acid-base disorders in critically ill patients.

Extravascular lung water indexed or not to predicted body weight is a predictor of mortality in septic shock patients.

PURPOSE: The purpose was to investigate whether extravascular lung water (EVLW) indexed to actual body weight (EVLWa) is an independent predictor of mortality in patients with septic shock, to determine the relationship between EVLWa and other markers of lung injury, and to test if indexing EVLW with predicted body weight (EVLWp) strengthens its predictive power. METHODS: Extravascular lung water, pulmonary vascular permeability index, and other markers of lung injury were measured prospectively in 55 patients with septic shock for 3 days. RESULTS: At day 1, EVLWa, EVLWp, and pulmonary vascular permeability index were not significantly different between survivors and nonsurvivors. However, in parallel to the course of septic shock, these variables decreased only in the survivors and remained elevated in the nonsurvivors, reaching intergroup difference by day 3. In multiple logistic regression analysis, both EVLWa and EVLWp (at day 3) were predictors of mortality with an odds ratio of 2 (95% confidence interval, 1.12-3.7) and 1.7 (95% confidence interval, 1.1-2.5) per SD increase, respectively. The receiver operating characteristic curve analysis showed that EVLWp did not improve the discriminative power of EVLW to predict mortality. Extravascular lung water indexed to actual body weight correlated with lung injury score and with the ratio of arterial oxygen partial pressure to inspired oxygen fraction but not with static respiratory compliance. Indexing EVLW to predicted body weight did not ameliorate these correlations. CONCLUSIONS: Extravascular lung water indexed or not to predicted body weight is an independent predictor of mortality in patients with septic shock. Repeated measurements of EVLW indexes over time, rather than a too-early measurement, seem to be more appropriate for predicting outcome.

The repeatability of Stewart's parameters and anion gap in a cohort of critically ill adult patients.

PURPOSE: To examine the repeatability of Stewart's parameters and anion gap in a cohort of critically ill patients and to determine the smallest detectable changes in individual patients. METHODS: A total of 161 patients were included prospectively. They underwent two subsequent blood samplings within 10 min of each other and samples were analyzed using the same central laboratory analyzer. Measured and calculated parameters from the two samples were compared. The repeatability was expressed as the smallest detectable difference (SDD), coefficient of variation (CV) and intraclass correlation coefficient (ICC). RESULTS: The mean differences ± SD (mEq/L) for the repeated measurements were 0.1 ± 0.76, 0.12 ± 0.68, -0.02 ± 1.02, and -0.08 ± 1.05 for the apparent strong ion difference (SID(app)), effective strong ion difference (SID(eff)), strong ion gap (SIG), and albumin-corrected anion gap (AG(corr)), respectively. The SDDs (mEq/L) for SID(app), SID(eff), SIG, and AG(corr), were ±1.49, ±1.33, ±2, and ±2.06, respectively. The CVs (%) for these variables were 1.4, 1.45, 13.3, and 4.15, respectively. The ICCs for all these variables were high, largely above 0.75. CONCLUSIONS: The repeatability of all these calculated variables was good. In repeated measurements, a change in value of these parameters exceeding 1.96√2 CV (%), the least significant change (LSC) or the SDD should be regarded as significant. Use of SDD is preferable to CV and LSC (%) because of its independence from the levels of variables and its expression in absolute units. Expressed as SDD, a SIG change value, e.g., of at least ±2 mEq/L should be significant.