Francisco Baigorri

Pressure support ventilation via face mask in acute respiratory failure in hypercapnic COPD patients.

ObjectiveTo test whether non-invasive ventilation via facial mask could reduce the need for tracheal intubation via when mechanical ventilation must be initiated in COPD patients.DesignOpen prospective interventional study.SettingGeneral Intensive Care Service of a County Hospital.PatientsWe have studied 12 COPD patients during 14 episodes of acute exacerbation of chronic respiratory failure who failed to improve with intensive medical therapy and showed impairements in severe respiratory acidosis and/or hypercapnic encephalopathy leading their attending physicians to order mechanical ventilationInterventionsIn these circumstances, a trial of pressuresupport (PS) ventilation (Servo Ventilator 900Cℜ) via facial mask Vital Signs Inc.ℜ) was performed. The level of pressure support was adjusted to obtain a tidal volume>400 ml. If the patient deteriorated, tracheal intubation and standard mechanical ventilation were performed.Measurements and resultsMeasurements are presented as means±SEM. A pressure-support level of 14±3 cmH2O was used during a period of 8±4 h. Low levels of external PEEP were used in 4 patients, while it generated excessive leaks in the others. Significant differences (p<0.05 ANOVA for repeated measures) in data obtained on admission, when patients deteriorated and after pressure support was administered were only observed in PaCO2 (68±3 versus 92±3 versus 67±3 mmHg), arterial pH (7.27±0.03 versus 7.19±0.02 versus 7.31±0.01). SaO2 (60±4 versus 86±3 versus 92±1%) and respiratory rate (35±2 versus 32±2 versus 23±1 breaths·min−1). Three patients needed intubation and one of them died in the ICU.ConclusionNon-invasive ventilation (pressure-support) via face mask may reduce the need for tracheal intubation in the severe hypercapnic failure of COPD patients.

Effect of acute moderate changes in PaCO2 on global hemodynamics and gastric perfusion.

Objective: To describe global hemodynamics and splanchnic perfusion changes in response to acute modifications in PaCO2 in hemodynamically stable patients. Design: Prospective, randomized crossover study. Setting: Medical‐surgical intensive care unit at a community hospital (400,000 inhabitants). Patients: Ten critically III patients who were sedated, paralyzed, and mechanically ventilated. Interventions: Hypercapnia and hypocapnia were obtained by increasing and reducing instrumental deadspace in random order. After each intervention, patients returned to the basal condition. Each period lasted 80 min: 20 min to achieve stable PaCO2 and 60 min for tonometer equilibration. In each period, global hemodynamic variables and tonometric data were collected. The periods were compared using analysis of variance. Measurements and Main Results: Acute hypercapnia (PaCO2 from 40 ± 3 to 52 ± 3 torr, p < .05) increased cardiac index (3.43 ± 0.37 vs. 3.97 ± 0.43 mL/min/m2, p < .05), heart rate (95 ± 6 vs. 105 ± 3 beats/min, p < .05), and mean pulmonary artery pressure (21 ± 1 vs. 24 ± 1 mm Hg, p < .05) and reduced systemic vascular resistance (992 ± 98 vs. 813 ± 93 dyne‐sec/cm5, p < .05) and oxygen extraction ratio (27 ± 3% vs. 22 ± 2%, p < .05). Standardized intramucosal PCO2 increased from 49 ± 2 to 61 ± 3 torr (p < .05) with an associated decrease in calculated intramucosal pH ([pHi] 7.35 ± 0.03 vs. 7.25 ± 0.02, p < .05), but the gastro‐arterial PCO2 gradient (ΔPCO2) did not change. Acute hypocapnia (PaCO2 from 41 ± 3 to 34 ± 3 torr, p < .05; pH 7.41 ± 0.01 to 7.47 ± 0.02, p < .05) induced slight increments in systemic vascular resistance (995 ± 117 vs. 1088 ± 160 dyne·sec/cm5, p < .05) and oxygen extraction ratio (28 ± 2% vs. 30 ± 2%, p < .05). Standardized intramucosal PCO2 decreased (50 ± 4 vs. 44 ± 3 torr, p < .05), pHi increased (7.33 ± 0.03 vs. 7.36 ± 0.02; p < .05), but ΔPCO2 did not change. Conclusions: In this small group of stable patients, moderate acute variations in PaCO2 had a significant effect on global hemodynamics, but splanchnic perfusion, assessed by ΔPCO2, did not change. In these conditions, the use of pHi to evaluate gastric perfusion appears unreliable.

Role of bronchoalveolar lavage in mechanically ventilated patients with suspected pneumonia

To determine the usefulness of samples obtained by bronchoalveolar lavage (BAL) in establishing the diagnosis of ventilator-associated pneumonia, quantitative cultures of BAL and protected specimen brush (PSB) samples obtained via fiberoptic bronchoscope were compared in 42 patients with suspected ventilator-associated pneumonia. Direct examination of BAL fluid was also used to identify cells with intracellular organisms. Ventilator-associated pneumonia was diagnosed in 18 patients; a total of 39 microorganisms were recovered from BAL fluid and 29 from PSB specimens. Cultures of 21 BAL and 23 PSB specimens were sterile. Quantitative BAL and PSB cultures coincided in 76 % of cases. Sterile BAL and PSB cultures agreed in 87 % of cases. Cultures were completely discordant in only three cases. The sensitivity of BAL for diagnosis of ventilator-associated pneumonia using bacterial counts of ≥104 cfu/ml was 89 %, and specificity was 100 %. In 14 of the 18 patients with ventilator-associated pneumonia, the percentage of cells containing intracellular organisms in specimens recovered by BAL was 11.6 % versus 0.45 % in patients without pneumonia (p<0.05). In the remaining four patients, all of whom hadPseudomonas aeruginosa pneumonia, no intracellular organisms could be detected. Using a cut-off point of ≥ 5 % of cells with intracellular organisms, the sensitivity and specificity for the early diagnosis of ventilator-associated pneumonia was 67 % and 96 %, respectively. The results confirm the usefulness of the quantitative BAL culture (with a cut-off at 104 cfu/ml) for the diagnosis of ventilator-associated pneumonia. The identification of intracellular organisms in BAL fluid is a good early indicator of pneumonia, but the sensitivity of this technique may be lower forPseudomonas aeruginosa infections.

A modified McCabe score for stratification of patients after intensive care unit discharge: the Sabadell score

IntroductionMortality in the ward after an intensive care unit (ICU) stay is considered a quality parameter, and is described as a source of avoidable mortality. Additionally, the attending intensivist frequently anticipates fatal outcome after ICU discharge. Our objective was to test the ability of a new score to stratify patients according to ward mortality after ICU discharge.MethodsA prospective cohort study was performed in the general ICU of a university-affiliated hospital. In 2003 and 2004 we prospectively recorded the attending intensivists subjective prognosis at ICU discharge about the hospital outcome for each patient admitted to the ICU (the Sabadell score), which was later compared with the real hospital outcome.ResultsWe studied 1,521 patients with a mean age of 60.2 ± 17.8 years. The median (25–75% percentile) ICU stay was five (three to nine) days. The ICU mortality was 23.8%, with 1,156 patients being discharged to the ward. Post-ICU ward mortality was 9.6%, mainly observed in patients with a Sabadell score of 3 (81.3%) or a score of 2 (41.1%), whereas lower mortality was observed in patients scoring 1 (17.2%) and scoring 0 (1.7%). Multivariate analysis selected age and the Sabadell score as the only variables associated with ward mortality, with an area under the receiver operating curve of 0.88 (95% CI 0.84–0.93) for the Sabadell score.ConclusionThe Sabadell score at ICU discharge works effectively to stratify patients according to hospital outcome.

Lack of Oxygen Supply Dependency in Patients With Severe Sepsis: A Study of Oxygen Delivery Increased by Military Antishock Trouser and Dobutamine

BACKGROUND During severe sepsis, the existence of a pathologic oxygen supply dependency remains controversial. STUDY OBJECTIVE To evaluate the relationship between oxygen delivery (DO2) and oxygen consumption (VO2) during severe sepsis and to compare, in this respect, survivors and nonsurvivors and patients with normal or increased concentration of plasma lactate. STUDY DESIGN Cohort analytic study. SETTING Three European ICUs in university hospitals. PATIENTS Seventeen mechanically ventilated patients with severe sepsis (six with high blood lactate levels) studied within the first day of diagnosis. INTERVENTIONS AND MEASUREMENTS Pulmonary elimination of carbon dioxide, or carbon dioxide production (VCO2) and VO2 were measured by indirect calorimetry before and after two interventions designed to increase DO2 (calculated from the Fick equation): inflation of a military antishock trouser (MAST) and infusion of dobutamine. RESULTS During MAST inflation, DO2 increased by 19% in patients with a normal concentration of plasma lactate (p < 0.01), but remained unchanged in patients with high lactate levels. During dobutamine infusion, DO2 increased in both groups by 16% (p < 0.01) and 20% (p < 0.05), respectively. In both groups, we found that the VO2 and VCO2 were not affected by either the MAST or the dobutamine-induced increase in DO2. There was no difference between survivors and nonsurvivors. CONCLUSION There was no evidence of a pathologic oxygen supply dependency in patients with severe sepsis, even in those who had an elevated concentration of plasma lactate and in those who ultimately died. These results do not favor the conclusion that maximizing DO2 is a primary therapeutic objective in such patients.

Hemodynamic and gas exchange responses to inhalation of nitric oxide in patients with the acute respiratory distress syndrome and in hypoxemic patients with chronic obstructive pulmonary disease

AbstractObjective: Inhalation of nitric oxide (NO) can improve oxygenation and decrease mean pulmonary artery pressure (MPAP) in patients with the acute respiratory distress syndrome (ARDS). It is not known whether inhaled NO exerts a similar effect in hypoxemic patients with chronic obstructive pulmonary disease (COPD). Design: Prospective clinical study. Setting: General intensive care unit in Sabadell, Spain. Patients: Nine mechanically ventilated COPD patients (mean age 72±2 years; forced expiratory volume in 1 s 0.91±0.11 l) and nine ARDS patients (mean age 57±6 years; mean lung injury score 2.8±0.1) Measurements and results: We measured hemodynamic and gas exchange parameters before NO inhalation (basal 1), during inhalation of 10 ppm NO (NO-10), and 20 min after NO was discontinued (in basal 2) in the ARDS group. In the COPD group, these parameters were measured before NO inhalation (basal 1), during different doses of inhaled NO (10, 20, and 30 ppm), and 20 min after NO was discontinued (basal 2). A positive response to NO was defined as a 20% increment in basal arterial partial pressure of oxygen (PaO2). MPAP and pulmonary vascular resistance (PVR) decreased significantly, while other hemodynamic parameters remained unchanged after NO-10 in both groups. Basal oxygenation was higher in the COPD group (PaO2/FIO2 (fractional inspired oxygen) 190±18 mmHg) than in the ARDS group (PaO2/FIO2 98±12 mmHg), (p<0.01). After NO-10, PaO2/FIO2 increased (to 141±17 mmHg, p<0.01) and Qva/Qt decreased (39±3 to 34±3%, p<0.01) in the ARDS group. There were no changes in PaO2/FIO2 and Qva/Qt when the NO concentration was increased to 30 ppm in the COPD group. In both groups, a correlation was found between basal MPAP and basal PVR, and between the NO-induced decrease in MPAP and in PVR. The NO-induced increase in PaO2/FIO2 was not correlated with basal PaO2/FIO2. In the ARDS group, six of the nine patients (66%) responded to NO and in the COPD group, two of nine (22%) (p=0.05). Conclusions: NO inhalation had similar effects on hemodynamics but not on gas exchange in ARDS and COPD patients, and this response probably depends on the underlying disease.

Effect of ranitidine on gastric intramucosal pH in critically ill patients

Objective: To determine whether ranitidine a) increases the values of gastric intramucosal pH (pHi) in critically ill patients, as determined by tonometry; b) reduces the variability of these measurements. Design: Prospective, double blind, randomized, placebo-controlled study. Setting: General Intensive Care Unit of a teaching hospital. Patients: Twenty-five critically ill, mechanically ventilated patients requiring arterial catheter and nasogastric tube. Interventions: Tonometer placement; blind, random administration of intravenous ranitidine (50 mg) or placebo. Measurements and main results: Tonometer saline PCO2 (PCO2i), arterial blood gases, gastric juice pH and pHi were determined immediately before, and 2, 4, 6 and 8 h after, ranitidine (12 patients) or placebo (13 patients). Ranitidine significantly increased gastric juice pH, but did not affect PCO2i or pHi; pHi was 7.34 ± 0.14 before ranitidine, and 7.30 ± 0.12, 7.31 ± 0.11, 7.31 ± 0.14 and 7.31 ± 0.12 – 2, 4, 6 and 8 h, respectively, after ranitidine administration (p = 0.55). Ranitidine did not modify the coefficients of variation of PCO2i or pHi, either. No significant changes in gastric juice pH, PCO2i or pHi were observed in the placebo group. Conclusions: In critically ill patients, ranitidine has no effect on pHi values, and does not increase the reproducibility of pHi measurements.

Central venous-to-arterial carbon dioxide difference combined with arterial-to-venous oxygen content difference is associated with lactate evolution in the hemodynamic resuscitation process in early septic shock.

IntroductionSince normal or high central venous oxygen saturation (ScvO2) values cannot discriminate if tissue perfusion is adequate, integrating other markers of tissue hypoxia, such as central venous-to-arterial carbon dioxide difference (PcvaCO2 gap) has been proposed. In the present study, we aimed to evaluate the ability of the PcvaCO2 gap and the PcvaCO2/arterial-venous oxygen content difference ratio (PcvaCO2/CavO2) to predict lactate evolution in septic shock.MethodsObservational study. Septic shock patients within the first 24 hours of ICU admission. After restoration of mean arterial pressure, and central venous oxygen saturation, the PcvaCO2 gap and the PcvaCO2/CavO2 ratio were calculated. Consecutive arterial and central venous blood samples were obtained for each patient within 24 hours. Lactate improvement was defined as the decrease ≥ 10% of the previous lactate value.ResultsThirty-five septic shock patients were studied. At inclusion, the PcvaCO2 gap was 5.6 ± 2.1 mmHg, and the PcvaCO2/CavO2 ratio was 1.6 ± 0.7 mmHg · dL/mL O2. Those patients whose lactate values did not decrease had higher PcvaCO2/CavO2 ratio values at inclusion (1.8 ± 0.8vs. 1.4 ± 0.5, p 0.02). During the follow-up, 97 paired blood samples were obtained. No-improvement in lactate values was associated to higher PcvaCO2/CavO2 ratio values in the previous control. The ROC analysis showed an AUC 0.82 (p < 0.001), and a PcvaCO2/CavO2 ratio cut-off value of 1.4 mmHg · dL/mL O2 showed sensitivity 0.80 and specificity 0.75 for lactate improvement prediction. The odds ratio of an adequate lactate clearance was 0.10 (p < 0.001) in those patients with an elevated PcvaCO2/CavO2 ratio (≥1.4).ConclusionIn a population of septic shock patients with normalized MAP and ScvO2, the presence of elevated PcvaCO2/CavO2 ratio significantly reduced the odds of adequate lactate clearance during the following hours.

Volume expansion using pentastarch does not change gastric-arterial CO2 gradient or gastric intramucosal pH in patients who have sepsis syndrome.

Objective In hypovolemic patients with sepsis syndrome, to determine the effects of colloid volume infusion using 10% pentastarch on abnormal gastric tonometer measurements (gastric intramucosal CO2 tension, gastric intramucosal-arterial Pco2 gradient, and gastric intramucosal pH [pHi]) and on cardiac index, global oxygen delivery, and hemoglobin. Design Prospective prepost intervention study. Setting Tertiary care, university-affiliated 15-bed general systems intensive care unit. Patients Patients were studied who had sepsis syndrome, who had pulmonary arterial catheters in place, who were hypovolemic (pulmonary arterial occlusion pressure [PAOP] <15 mm Hg), and who had a gastric arterial Pco2 gradient >10 mm Hg. Interventions Baseline measurements of gastric intramucosal CO2 tension, gastric intramucosal-arterial Pco2 gradient, and pHi, as well as arterial lactate, pulmonary arterial occlusion, central venous and systemic arterial pressures, thermodilution cardiac output, and temperature. Boluses of 500 mL pentastarch were administered to a total of 1000 mL or until PAOP was >18 mm Hg. Measurements were repeated at 30 mins and 120 mins postinfusion of pentastarch. Main Results Volume infusion using pentastarch did not change gastric Pco2, gastric-arterial Pco2 gradient, or pHi. Volume expansion with pentastarch significantly increased cardiac index, global oxygen delivery, and PAOP. Administration of pentastarch decreased hemoglobin and arterial lactate at 30 mins but not at 120 mins. Conclusions Volume expansion using a colloidal solution of 10% pentastarch does not change abnormal intramucosal CO2 tension, gastric-arterial Pco2 gradient, or pHi in critically ill hypovolemic patients who have sepsis syndrome despite increasing cardiac index, oxygen delivery, and pulmonary artery occlusion pressure.

Inhaled nitric oxide does not improve cardiac or pulmonary function in patients with an exacerbation of chronic obstructive pulmonary disease.

OBJECTIVE To determine whether inhaled nitric oxide (NO) improves right ventricular function in mechanically ventilated patients with severe chronic obstructive pulmonary disease (COPD). DESIGN Open, prospective, controlled trial. SETTING General intensive care unit of a community hospital. PATIENTS Twelve patients with acute respiratory failure caused by acute exacerbation of COPD requiring mechanical ventilation. INTERVENTIONS Insertion of a pulmonary artery catheter modified with a rapid response thermistor and a radial arterial catheter. Nitric oxide was then administered to the patient via a T piece placed between the Y piece of the ventilator and the endotracheal tube. MEASUREMENTS AND MAIN RESULTS Hemodynamic and gasometric variables were recorded before NO inhalation, during administration of inhaled NO (20 ppm, 20 mins), and 20 mins after NO discontinuation. Inhaled NO reduced pulmonary artery pressure from 26 +/- 6 to 22 +/- 5 mm Hg (p = .0004), but arterial oxygenation, cardiac output, and right ventricular ejection fraction remained unmodified (41% +/- 9% vs. 41% +/- 8%; not significant). Calculated pulmonary vascular resistance decreased from 453 +/- 233 to 348 +/- 108 dyne x sec/cm5 x m2 (p = .02), and right ventricular volumes did not change. Subsequently, right ventricular end-systolic pressure/volume ratio decreased from 0.52 +/- 0.22 to 0.44 +/- 0.19 mm Hg/mL/m2 (p = .01). No significant correlation was observed between the changes of pulmonary artery pressure (or pulmonary vascular resistance) and changes of right ventricular ejection fraction. CONCLUSION Inhalation of NO does not seem to improve either right ventricular function or arterial oxygenation in patients with acute respiratory failure caused by acute exacerbation of COPD.