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J L Teboul

Publications and source records attributed to J L Teboul.

At least 19 recordsLinked to original sources
PubMed2006

Meaning of arterio-venous PCO2 difference in circulatory shock.

The arterovenous difference in carbon dioxide tension (DeltaPCO2) can be calculated after simultaneous sampling of arterial blood (PaCO2) and of mixed venous blood from the distal of a pulmonary artery catheter (PvCO2). Under physiological conditions, DeltaPCO2 ranges from 2 to 5 mmHg. The DeltaPCO2 depends on carbon dioxide and cardiac output by a complex fashion. In this article, we detail the influence of these factors on DeltaPCO2 in normoxic conditions and in hypoxic conditions. We bring evidence that DeltaPCO2 cannot serve as a marker of tissue hypoxia contrary to what was initially thought. However, DeltaPCO2 can be considered as a marker of the adequacy of venous blood flow (i.e. cardiac output) to remove the total CO2 produced by the peripheral tissues. In this regard, the knowledge of DeltaPCO2 should help the clinicians for the decision of giving therapy aimed at increasing cardiac output.

Animals↗
PubMed2005

Rapid and beneficial hemodynamic effects of activated protein C in septic shock patients.

OBJECTIVE: Because recombinant human activated protein C (rhAPC) reduces NO production during sepsis, it could improve the vascular tone. We tested whether rhAPC reduces the dose of norepinephrine required to maintain mean arterial pressure (MAP) in septic shock patients. DESIGN AND SETTING: Retrospective study in intensive care unit of two university hospitals. PATIENTS: Twenty-two septic shock patients with at least two organ failures were retrospectively investigated for MAP and the required dose of norepinephrine before and 24 h after rhAPC administration. A control group of 22 septic shock patients with at least two organ failures who did not receive rhAPC was matched on age, SAPS II, MAP, and norepinephrine dose at the time of the theoretical start of rhAPC. MEASUREMENTS AND RESULTS: The MAP remained stable and similar in the two groups (86+/-16 vs. 89+/-9 mmHg at 24 h). The required dose of norepinephrine increased in the control group (+38%, from -41% to +38%) but decreased in the treated group (-33%, from -74% to +11%). CONCLUSIONS: rhAPC rapidly improved the vascular tone in septic shock patients as assessed by a decrease in the norepinephrine dose required to maintain arterial pressure.

Blood Pressure↗
PubMed2001

Effects of tidal volume reduction in acute respiratory distress syndrome on gastric mucosal perfusion.

OBJECTIVE: This study was conducted with the aim of testing the effects of a reduction in tidal volume (V(T)) on gastric mucosal perfusion using laser-Doppler flowmetry in patients with acute respiratory distress syndrome (ARDS). DESIGN: It was designed as a prospective study. PATIENTS: Seventeen patients with ARDS were enrolled in the study. All patients were mechanically ventilated in volume-controlled mode. Before the start of the protocol, V(T) was set at 9 ml/kg body weight. INTERVENTION: V(T) was reduced to 6 ml/kg body weight. MEASUREMENTS AND RESULTS: Measurements of systemic hemodynamic parameters and gastric mucosal blood flow (GMBF) were obtained before and after reduction of V(T). Cardiac index, heaart rate and pulmonary arterial pressure increased significantly after V(T) reduction. The increase in cardiac output was observed in all patients. However, despite a mean 25% increase in cardiac output after V(T) reduction, no significant increase in mean GMBF was observed, and individual GMBF responses were heterogeneous. CONCLUSION: V(T) reduction in patients with ARDS, despite resulting in an increase in cardiac output, did not change gastric mucosal perfusion. The heterogeneity in the individual response of GMBF to V(T) reduction could be due to opposite direct (i.e., local vasodilatory effect) and indirect (i.e., global sympathetic stimulation) effects of hypercapnia on gut vessels.

Adult↗
PubMed2001

Extending inspiratory time in acute respiratory distress syndrome.

OBJECTIVE: To assess the short-term effects of extending inspiratory time by lengthening end-inspiratory pause (EIP) without inducing a clinically significant increase in intrinsic positive end-expiratory pressure (PEEPi) in patients with acute respiratory distress syndrome (ARDS). DESIGN: Controlled, randomized, crossover study. SETTING: Two medical intensive care units of university hospitals. PATIENTS: Sixteen patients with early (< or =48 hrs) ARDS. INTERVENTION: We applied two durations of EIP (0.2 secs and extended) each for 1 hr while keeping all the following ventilatory parameters constant: FIO2, total PEEP (PEEPtot = applied PEEP + PEEPi), tidal volume, inspiratory flow, and respiratory rate. The duration of extended EIP was titrated to avoid an increase of PEEPi of > or =1 cm H2O. MEASUREMENTS AND MAIN RESULTS: Despite an increase in mean airway pressure (20.6 +/- 2.3 vs. 17.6 +/- 2.1 cm H2O, p < .01), extended EIP did not significantly improve PaO2 (93 +/- 21 vs. 86 +/-16 torr [12.40 +/- 2.80 vs. 11.46 +/- 2.13 kPa] with 0.2 secs EIP, NS). However, although the difference in PaO2 between the two EIP durations was <20 torr (<2.66 kPa) in 14 patients, two patients exhibited a >40 torr (>5.33 kPa) increase in PaO2 with extended EIP. Extended EIP decreased PaCO2 (62 +/- 13 vs. 67 +/- 13 torr [8.26 +/- 1.73 vs. 8.93 +/- 1.73 kPa] with 0.2 secs EIP, p < .01), which resulted in a higher pH (7.22 +/- 0.10 vs. 7.19 +/- 0.09 with 0.2 secs EIP, p < .01) and contributed to a slight increase in arterial hemoglobin saturation (94 +/- 3 vs. 93 +/- 3% with 0.2 EIP, p < .01). No significant difference in hemodynamics was observed. CONCLUSION: In patients with ARDS, extending EIP without inducing a clinically significant increase in PEEPi does not consistently improve arterial oxygenation but enhances CO2 elimination.

Adult↗
PubMed2001

Respiratory changes in aortic blood velocity as an indicator of fluid responsiveness in ventilated patients with septic shock.

STUDY OBJECTIVE: To investigate whether the respiratory changes in peak velocity (Vpeak) of aortic blood flow could be related to the effects of volume expansion on cardiac index. DESIGN: Prospective clinical study. SETTING: Medical ICUs of a university hospital (20 beds) and of a nonuniversity hospital (15 beds). PATIENTS: Nineteen sedated septic shock patients who were receiving mechanical ventilation and who had preserved left ventricular (LV) systolic function. INTERVENTION: Volume expansion. MEASUREMENTS AND RESULTS: Analysis of aortic blood flow by transesophageal echocardiography allowed beat-to-beat measurement of Vpeak before and after volume expansion. Maximum values of Vpeak (Vpeakmax) and minimum values of Vpeak (Vpeakmin) were determined over one respiratory cycle. The respiratory changes in Vpeak (Delta Vpeak) were calculated as the difference between Vpeakmax and Vpeakmin divided by the mean of the two values and were expressed as a percentage. The indexed LV end-diastolic area (EDAI) and cardiac index were obtained at the end of the expiratory period. The volume expansion-induced increase in cardiac index was > or = 15% in 10 patients (responders) and < 15% in 9 patients (nonresponders). Before volume expansion, Delta Vpeak was higher in responders than in nonresponders (20 +/- 6% vs 10 +/- 3%; p < 0.01), while EDAI was not significantly different between the two groups (9.7 +/- 3.7 vs 9.7 +/- 2.4 cm(2)/m(2)). Before volume expansion, a Delta Vpeak threshold value of 12% allowed discrimination between responders and nonresponders with a sensitivity of 100% and a specificity of 89%. Volume expansion-induced changes in cardiac index closely correlated with the Delta Vpeak before volume expansion (r(2) = 0.83; p < 0.001). CONCLUSION: Analysis of respiratory changes in aortic blood velocity is an accurate method for predicting the hemodynamic effects of volume expansion in septic shock patients receiving mechanical ventilation who have preserved LV systolic function.

Aorta, Thoracic↗
PubMed2001

[Mechanical ventilation-related variability of stroke volume. Clinical evaluation and therapeutic implications].

Mechanical ventilation induces cyclic changes in left ventricular stroke volume. These variations are mainly related to the expiratory decrease in left ventricular preload following the inspiratory decrease in right ventricular filling and ejection. Therefore, the magnitude of the respiratory changes in left ventricular stroke volume reflect the sensitivity of the heart to the cyclic changes in preload induced by mechanical insufflation. At the bedside, the respiratory changes in left ventricular stroke volume can be assessed by the analysis of the arterial pressure (arterial catheter) or aortic blood velocity (echocardiography) wave forms. The respiratory changes in arterial pressure and in aortic blood velocity have been shown to be accurate predictors of fluid responsiveness and of the hemodynamic effects of positive end-expiratory pressure.

Blood Pressure↗
PubMed2000

Using heart-lung interactions to assess fluid responsiveness during mechanical ventilation.

According to the Frank-Starling relationship, a patient is a 'responder' to volume expansion only if both ventricles are preload dependent. Mechanical ventilation induces cyclic changes in left ventricular (LV) stroke volume, which are mainly related to the expiratory decrease in LV preload due to the inspiratory decrease in right ventricular (RV) filling and ejection. In the present review, we detail the mechanisms by which mechanical ventilation should result in greater cyclic changes in LV stroke volume when both ventricles are 'preload dependent'. We also address recent clinical data demonstrating that respiratory changes in arterial pulse (or systolic) pressure and in Doppler aortic velocity (as surrogates of respiratory changes in LV stroke volume) can be used to detect biventricular preload dependence, and hence fluid responsiveness in critically ill patients.

Aorta↗
PubMed2000

Estimating cardiac filling pressure in mechanically ventilated patients with hyperinflation.

OBJECTIVE: When positive end-expiratory pressure (PEEP) is applied, the intracavitary left ventricular end-diastolic pressure (LVEDP) exceeds the LV filling pressure because pericardial pressure exceeds 0 at end-expiration. Under those conditions, the LV filling pressure is itself better reflected by the transmural LVEDP (tLVEDP) (LVEDP minus pericardial pressure). By extension, end-expiratory pulmonary artery occlusion pressure (eePAOP), as an estimate of end-expiratory LVEDP, overestimates LV filling pressure when pericardial pressure is >0, because it occurs when PEEP is present. We hypothesized that LV filling pressure could be measured from eePAOP by also knowing the proportional transmission of alveolar pressure to pulmonary vessels calculated as index of transmission = (end-inspiratory PAOP--eePAOP)/(plateau pressure--total PEEP). We calculated transmural pulmonary artery occlusion pressure (tPAOP) with this equation: tPAOP = eePAOP--(index of transmission x total PEEP). We compared tPAOP with airway disconnection nadir PAOP measured during rapid airway disconnection in subjects undergoing PEEP with and without evidence of dynamic pulmonary hyperinflation. DESIGN: Prospective study. SETTING: Medical intensive care unit of a university hospital. PATIENTS: We studied 107 patients mechanically ventilated with PEEP for acute respiratory failure. Patients without dynamic pulmonary hyperinflation (group A; n = 58) were analyzed separately from patients with dynamic pulmonary hyperinflation (group B; n = 49). INTERVENTION: Transient airway disconnection. MEASUREMENTS AND MAIN RESULTS: In group A, tPAOP (8.5+/-6.0 mm Hg) and nadir PAOP (8.6+/-6.0 mm Hg) did not differ from each other but were lower than eePAOP (12.4+/-5.6 mm Hg; p < .05). The agreement between tPAOP and nadir PAOP was good (bias, 0.15 mm Hg; limits of agreement, -1.5-1.8 mm Hg). In group B, tPAOP (9.7+/-5.4 mm Hg) was lower than both nadir PAOP and eePAOP (12.1+/-5.4 and 13.9+/-5.2 mm Hg, respectively; p < .05 for both comparisons). The agreement between tPAOP and nadir PAOP was poor (bias, 2.3 mm Hg; limits of agreement, -0.2-4.8 mm Hg). CONCLUSIONS: Indexing the transmission of proportional alveolar pressure to PAOP in the estimation of LV filling pressure is equivalent to the nadir method in patients without dynamic pulmonary hyperinflation and may be more reliable than the nadir PAOP method in patients with dynamic pulmonary hyperinflation.

Aged↗
PubMed2000

Venoarterial CO(2) difference during regional ischemic or hypoxic hypoxia.

To test the role of blood flow in tissue hypoxia-related increased veno-arterial PCO(2) difference (DeltaPCO(2)), we decreased O(2) delivery (&Ddot;O(2)) by either decreasing flow [ischemic hypoxia (IH)] or arterial PO(2) [hypoxic hypoxia (HH)] in an in situ, vascularly isolated, innervated dog hindlimb perfused with a pump-membrane oxygenator system. Twelve anesthetized and ventilated dogs were studied, with systemic hemodynamics maintained within normal range. In the IH group (n = 6), hindlimb DO(2) was progressively lowered every 15 min by decreasing pump-controlled flow from 60 to 10 ml. kg(-1). min(-1), with arterial PO(2) constant at 100 Torr. In the HH group (n = 6), hindlimb DO(2) was progressively lowered every 15 min by decreasing PO(2) from 100 to 15 Torr, when flow was constant at 60 ml. kg(-1). min(-1). Limb DO(2), O(2) uptake (VO(2)), and DeltaPCO(2) were obtained every 15 min. Below the critical DO(2), VO(2) decreased, indicating dysoxia, and O(2) extraction ratio (VO(2)/DO(2)) rose continuously and similarly in both groups, reaching a maximal value of approximately 90%. DeltaPCO(2) significantly increased in IH but never differed from baseline in HH. We conclude that absence of increased DeltaPCO(2) does not preclude the presence of tissue dysoxia and that decreased flow is a major determinant in increased DeltaPCO(2).

Analysis of Variance↗
PubMed2000

Relation between respiratory changes in arterial pulse pressure and fluid responsiveness in septic patients with acute circulatory failure.

In mechanically ventilated patients with acute circulatory failure related to sepsis, we investigated whether the respiratory changes in arterial pressure could be related to the effects of volume expansion (VE) on cardiac index (CI). Forty patients instrumented with indwelling systemic and pulmonary artery catheters were studied before and after VE. Maximal and minimal values of pulse pressure (Pp(max) and Pp(min)) and systolic pressure (Ps(max) and Ps(min)) were determined over one respiratory cycle. The respiratory changes in pulse pressure (DeltaPp) were calculated as the difference between Pp(max) and Pp(min) divided by the mean of the two values and were expressed as a percentage. The respiratory changes in systolic pressure (DeltaPs) were calculated using a similar formula. The VE-induced increase in CI was >/= 15% in 16 patients (responders) and < 15% in 24 patients (nonresponders). Before VE, DeltaPp (24 +/- 9 versus 7 +/- 3%, p < 0.001) and DeltaPs (15 +/- 5 versus 6 +/- 3%, p < 0.001) were higher in responders than in nonresponders. Receiver operating characteristic (ROC) curves analysis showed that DeltaPp was a more accurate indicator of fluid responsiveness than DeltaPs. Before VE, a DeltaPp value of 13% allowed discrimination between responders and nonresponders with a sensitivity of 94% and a specificity of 96%. VE-induced changes in CI closely correlated with DeltaPp before volume expansion (r(2) = 0. 85, p < 0.001). VE decreased DeltaPp from 14 +/- 10 to 7 +/- 5% (p < 0.001) and VE-induced changes in DeltaPp correlated with VE-induced changes in CI (r(2) = 0.72, p < 0.001). It was concluded that in mechanically ventilated patients with acute circulatory failure related to sepsis, analysis of DeltaPp is a simple method for predicting and assessing the hemodynamic effects of VE, and that DeltaPp is a more reliable indicator of fluid responsiveness than DeltaPs.

Adolescent↗
PubMed1999

Association of TNF2, a TNF-alpha promoter polymorphism, with septic shock susceptibility and mortality: a multicenter study.

CONTEXT: Tumor necrosis factor alpha (TNF-alpha) is believed to be a cytokine central to pathogenesis of septic shock. TNF2, a polymorphism within the TNF-alpha gene promoter, has been associated with enhanced TNF-alpha production and negative outcome in some severe infections. OBJECTIVES: To investigate the frequency of the TNF2 allele in patients with septic shock and to determine whether the allele is associated with the occurrence and outcome of septic shock. DESIGN: Multicenter case-control study conducted from March 1996 to June 1997. SETTING: Seven medical intensive care units in university hospitals. SUBJECTS: Eighty-nine patients with septic shock and 87 healthy unrelated blood donors. MAIN OUTCOME MEASURES: Frequency of the TNF2 allele among patients with septic shock and among those who died and the level of corresponding TNF-alpha concentrations. RESULTS: Mortality among patients with septic shock was 54%, consistent with the predicted mortality from the Simplified Acute Physiologic Score (SAPS II) value. The polymorphism frequencies of the controls and the patients with septic shock differed only at the TNF2 allele (39% vs 18% in the septic shock and control groups, respectively, P =.002). Among the septic shock patients, TNF2 polymorphism frequency was significantly greater among those who had died (52% vs 24% in the survival group, P =.008). Concentrations of TNF-alpha were higher in 68% and 52% with the TNF2 and TNF1 polymorphisms, respectively, but their median values (48 pg/mL vs 29 pg/mL) were not statistically different (P = .31). After controlling for age and the probability of death, derived by the SAPS II score, multiple logistic regression analysis showed that, for the same rank of SAPS II value, patients with the TNF2 allele had a 3.7-fold risk of death (95% confidence interval, 1.37-10.24). CONCLUSION: The TNF2 allele is strongly associated with susceptibility to septic shock and death due to septic shock.

Alleles↗
PubMed1999

Hemodynamic effects of fluid loading in acute massive pulmonary embolism.

OBJECTIVE: To assess the hemodynamic effects of fluid loading in patients with acute circulatory failure caused by acute massive pulmonary embolism (AMPE). DESIGN: Prospective study. SETTING: Respiratory critical care unit of a university hospital. PATIENTS: Thirteen patients free of previous cardiopulmonary disease with angiographically proven AMPE (Miller index = 24 +/- 1), with acute circulatory failure defined by a cardiac index (CI) lower than 2.5 L/min/m2. INTERVENTION: Infusion of 500 mL of dextran 40 over 20 mins. MEASUREMENTS AND MAIN RESULTS: Fluid loading induced a substantial increase in right atrial pressure from 9 +/- 1 mm Hg to 17 +/- 1 mm Hg and in right ventricular end-diastolic volume index from 123 +/- 14 mL/m2 to 150 +/- 11 mL/m2 (p < .05 for both comparisons). The increase in right ventricular preload was associated with an increase in Cl from 1.6 +/- 0.1 to 2.0 +/- 0.1 L/min/m2 (p < .05), whereas right ventricular ejection fraction (15 +/- 3% at baseline vs. 16 +/- 3% after fluid loading) and total pulmonary vascular resistance index (1689 +/- 187 dyne x sec/cm5 x m2 at baseline vs. 1492 +/- 166 dyne x sec/ cm5 x m2 after fluid loading) remained unchanged. The increase in Cl induced by fluid loading was inversely correlated to baseline right ventricular end-diastolic volume index (r = -.89 ; p< .05). CONCLUSIONS: These results suggest that fluid loading can improve hemodynamic status in patients with acute circulatory failure caused by AMPE.

Acute Disease↗
PubMed1999

Effects of epinephrine, norepinephrine, or the combination of norepinephrine and dobutamine on gastric mucosa in septic shock.

OBJECTIVES: To compare in the same patient with septic shock, respective effects of epinephrine, norepinephrine, and the combination of norepinephrine and dobutamine (5 microg/kg/min) on systemic hemodynamic parameters and gastric mucosal perfusion using gastric tonometry and laser-Doppler flowmetry techniques. DESIGN: Prospective, controlled, randomized, crossover study. SETTING: University hospital intensive care unit. PATIENTS: Twelve patients with septic shock. INTERVENTIONS: Each patient received in a random succession epinephrine, norepinephrine, and norepinephrine plus dobutamine. Dosages of epinephrine and norepinephrine were adjusted to achieve a mean arterial pressure between 70 and 80 mm Hg. A laser-Doppler probe and a tonometer were introduced into the gastric lumen. MEASUREMENTS AND MAIN RESULTS: The increase in gastric mucosal perfusion detected by laser-Doppler flowmetry was higher with epinephrine and the combination of norepinephrine and dobutamine than with norepinephrine alone (p < .05). In addition, the ratio of gastric mucosal perfusion (local oxygen delivery) to systemic oxygen delivery was increased after norepinephrine plus dobutamine as compared with norepinephrine alone and epinephrine (p< .05). Although values of intramucosal pH and gastroarterial PCO2 tended to be higher with norepinephrine plus dobutamine compared with those obtained with norepinephrine and epinephrine, differences were not statistically significant. CONCLUSIONS: For the same mean arterial pressure in patients with septic shock, our study showed that administration of epinephrine increased gastric mucosal perfusion more than norepinephrine administration alone. Addition of dobutamine (5 microg/kg/ min) to norepinephrine improved gastric mucosal perfusion. This result could be explained by a vasodilating effect of dobutamine on gastric mucosal microcirculation.

Adrenergic beta-Agonists↗
PubMed1999

Clinical use of respiratory changes in arterial pulse pressure to monitor the hemodynamic effects of PEEP.

In ventilated patients with acute lung injury (ALI) we investigated whether respiratory changes in arterial pulse pressure (DeltaPP) could be related to the effects of PEEP and fluid loading (FL) on cardiac index (CI). Measurements were performed before and after application of a PEEP (10 cm H2O) in 14 patients. When the PEEP-induced decrease in CI was > 10% (six patients), measurements were also performed after FL. Maximal (PPmax) and minimal (PPmin) values of pulse pressure were determined over one respiratory cycle and DeltaPP was calculated: DeltaPP (%) = 100 x ((PPmax - PPmin)/ ([PPmax + PPmin]/2)). PEEP decreased CI from 4.2 +/- 1.1 to 3.8 +/- 1.3 L/min/m2 (p < 0.01) and increased DeltaPP from 9 +/- 7 to 16 +/- 13% (p < 0.01). The PEEP-induced changes in CI correlated with DeltaPP on ZEEP (r = -0.91, p < 0.001) and with the PEEP-induced increase in DeltaPP (r = -0.79, p < 0.001). FL increased CI from 3.5 +/- 1.1 to 4.2 +/- 0.9 L/min/m2 (p < 0.05) and decreased DeltaPP from 27 +/- 13 to 14 +/- 9% (p < 0.05). The FL-induced changes in CI correlated with DeltaPP before FL (r = 0.97, p < 0.01) and with the FL-induced decrease in DeltaPP (r = -0.85, p < 0.05). In ventilated patients with ALI, DeltaPP may be useful in predicting and assessing the hemodynamic effects of PEEP and FL.

Adult↗
PubMed1998

Relation between dicrotic notch and mean pulmonary artery pressure studied by using a Swan-Ganz catheter in critically ill patients.

OBJECTIVE: It has been recently shown that there is a match between dicrotic notch and mean pulmonary artery (PA) pressures in spontaneously breathing patients studied by means of high-fidelity pressure catheters. The aim of the study was to analyze the relation between mean PA pressure and PA pressure at the incisura by using a Swan-Ganz catheter in critically ill, mechanically ventilated patients. MEASUREMENTS AND RESULTS: Fluid-filled PA pressures were obtained over four ventilatory cycles in 32 consecutive, mechanically ventilated patients in the intensive care unit. We measured mean PA pressure and dicrotic notch pressure. We also calculated the widely used approximation of mean PA pressure (mean PAPapprox = diastolic + 1/3 pulse pressure). Cardiac output was measured in triplicate by using the thermodilution technique. Dicrotic notch was clearly identified in 30 of 32 patients. Mean PA pressure (32.1 +/- 10.2 mm Hg) and PA dicrotic notch pressure (31.8 +/- 10.4 mm Hg) were linearly related (r = 0.989, p < 0.001). Agreement between dicrotic notch and mean PA pressures was suggested (mean difference +/- SD = -0.3 +/- 1.5 mm Hg). Similar agreement was found between mean PAPapprox and mean PA pressure (mean difference +/- SD = -0.7 +/- 0.8 mm Hg; p = 0.20). CONCLUSION: By using a Swan-Ganz catheter we found that dicrotic notch pressure equalled mean PA pressure in the critically ill, mechanically ventilated patients studied. This indicated that right-sided ejection was completed at a PA pressure equal to mean PA pressure in these patients.

Aged↗
PubMed1998

Value of the venous-arterial PCO2 gradient to reflect the oxygen supply to demand in humans: effects of dobutamine.

OBJECTIVE: To test the value of venous-arterial PCO2 gradient (deltaPCO2) measurements to reflect the adequacy of cardiac index (CI) to oxygen demand in patients submitted to rapid changes of CI and oxygen demand. DESIGN: Prospective, comparative study. SETTING: Medical intensive care unit of a university hospital. PATIENTS: Ten patients with congestive heart failure exhibiting low baseline CI (< or =2.5 L/min/m2) but no evidence of global tissue hypoxia, as attested by the absence of clinical signs of shock and by normal blood lactate concentrations. INTERVENTIONS: Infusion of incremental doses of dobutamine: 0 (D0), 5 (D5), 10 (D10), and 15 (D15) microg/kg/min. MEASUREMENTS AND MAIN RESULTS: The CI increased by a linear fashion from D0 (1.6+/-0.1 L/min/m2) to D15 (2.4+/-0.2 L/min/m2) (p< .05). The mixed venous oxygen saturation (SVO2) increased from D0 (49+/-2%) to D10 (61+/-2%) (p < .05) and remained unchanged from D10 to D15 (60+/-2%). The oxygen extraction ratio (O2 ER) and the deltaPCO2 decreased from D0 (48+/-2% and 9+/-1 torr [1.2+/-0.3 kPa], respectively) to D10 (36+/-2% and 5+/-1 torr [0.7+/-0.1 kPa], respectively) (p < .05 for both comparisons) and remained unchanged from D10 to D15 (36+/-2% and 6+/-1 torr [0.8+/-0.1 kPa], respectively). The biphasic courses of SVO2, O2 ER, and deltaPCO2 were related to the course of oxygen consumption that remained constant from D0 (113+/-9 mL/min/m2) to D10 (112+/-8 mL/min/m2) and significantly increased from D10 to D15 (127+/-10 mL/min/m2) (p <.05). CONCLUSIONS: deltaPCO2 can be reliably used at the bedside for informing on the adequacy of CI with respect to a given metabolic condition, and particularly for detecting changes in oxygen demand (e.g., the changes accompanying drug-induced changes in CI). In this regard, deltaPCO2, together with O2 ER and SVO2, can help to assess the adequacy of CI to global oxygen demand.

Adult↗