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Biomedical subjects

F Baigorri

Publications and source records attributed to F Baigorri.

At least 19 recordsLinked to original sources
PubMed2000

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 ill 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 x 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 (deltaPco2) 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 x 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 deltaPco2 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 deltaPco2, did not change. In these conditions, the use of pHi to evaluate gastric perfusion appears unreliable.

Acute Disease↗
PubMed2000

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 1,000 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.

APACHE↗
PubMed2000

Acute small bowel pseudo-obstruction due to AL amyloidosis: a case report and literature review.

Amyloidosis may uncommonly present with intestinal pseudo-obstruction. Previous reports have described an acute presentation with AA amyloid and a more chronic syndrome with AL amyloid. We report the case of a 78-yr-old man who presented with clinical and radiographic features of an acute small bowel obstruction and who, at laparotomy, was found to have intestinal pseudo-obstruction due to AL amyloidosis. We believe this case represents the first report of acute pseudo-obstruction from AL amyloidosis; awareness of this presentation may facilitate earlier diagnosis.

Acute Disease↗
PubMed1999

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.

Administration, Inhalation↗
PubMed1998

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.

APACHE↗
PubMed1997

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.

OBJECTIVE: 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.

Administration, Inhalation↗
PubMed1997

Effect of sucralfate on gastric intramucosal pH in critically ill patients.

OBJECTIVE: To determine whether sucralfate administration affects the tonometric measurement of gastric intramucosal pH (pHi). DESIGN: Non-randomized observational study. SETTING: General intensive care unit of a teaching hospital. PATIENTS: Twenty critically ill, mechanically ventilated, consecutively admitted patients requiring an arterial catheter and nasogastric tube. INTERVENTIONS: Tonometer placement and sucralfate administration. MEASUREMENTS AND MAIN RESULTS: We simultaneously determined tonometer saline PCO2 (PCO2i), arterial blood gases, pH of gastric juice and pHi. These parameters were evaluated immediately before sucralfate administration, and 2 h and 4 h after. We did not detect any change in either PCO2i or pHi after sucralfate administration (PCO2i: basal 6.4 +/- 1.7, 2 h 6.3 +/- 1.7, 4 h 6.3 +/- 1.7; pHi: basal 7.35 +/- 0.13, 2 h 7.36 +/- 0.12, 4 h 7.36 +/- 0.12). CONCLUSIONS: Sucralfate does not affect the tonometric measurement of PCO2i and pHi.

Adult↗
PubMed1996

Impact of using an indwelling introducer on diagnosis of Swan-Ganz pulmonary artery catheter colonization.

A prospective study was conducted to determine how the use of an indwelling introducer influences the diagnosis of pulmonary artery catheter (PAC) colonization. Sixty-six consecutive PACs and introducers were aseptically removed over a 15-month period. Two segments of the catheter and the catheter tip (a proximal segment from the portion of the catheter beneath the introducer) and two segments of the introducer (a proximal intradermal segment and the introducer tip) were cultured using a semiquantitative technique. Nineteen of 66 (28.7%) PACs showed colonization, representing an incidence of 5.6 episodes per 100 catheterization-days. Catheter tip cultures identified only 68% of colonized PACs; this yield rose to 91% when introducer tip cultures were added. These results indicate a need to evaluate both introducer tip cultures and catheter tip cultures for an accurate diagnosis of PAC colonization when an indwelling introducer is used.

Bacteria↗
PubMed1996

Oxygen delivery in critical illness.

Oxygen consumption is physiologically dependent on DO2 below the critical DO2. Thus, patients in overt shock have physiologic dependence of VO2 on DO2. The first priority of prevention and reversal of tissue hypoxia is to balance oxygen demand and oxygen supply. Pathologic dependence of VO2 on DO2 has not yet been demonstrated convincingly in critically ill patients. Furthermore, in our opinion, contradicting results of RCTs of supernormal DO2 versus normal DO2 do not support routine maintenance of supernormal levels of DO2. Finally, we suggest that intensivists continue to assess DO2 and VO2 carefully. Global assessment of VO2 and DO2 appears inadequate to detect occult tissue hypoxia in most critically ill patients. However, research focused on regional assessment such as gastric tonometer measurement of gastric mucosal PCO2 and pH provides opportunity for safe, convenient detection of occult tissue hypoxia in critically ill patients.

Critical Illness↗
PubMed1995

[Selective pulmonary vasodilator effect of inhaled nitric oxide in a patient with pulmonary thromboembolism].

The increase in pulmonary vascular resistences in acute pulmonary thromboembolism (APT) is the consequence of anatomical obstruction and pulmonary artery constriction. The administration of inhaled nitric oxide (NO) may be therapeutically useful in acute pulmonary hypertension by APT given its limited vasodilator effect on pulmonary circulation. A patient with APT in whom this selective vasodilator effect was observed is presented. The authors suggest that the administration of inhaled NO may be a potentially beneficial coadjuvant therapy in acute pulmonary hypertension induced by APT.

Administration, Inhalation↗
PubMed1995

Continuous aspiration of subglottic secretions in preventing ventilator-associated pneumonia.

OBJECTIVE: To determine whether continuous subglottic aspiration prevents nosocomial pneumonia in mechanically ventilated patients. DESIGN: A randomized, controlled, blinded study. SETTING: Medical-surgical intensive care unit. PATIENTS: 190 patients who were admitted to the intensive care unit during a 33-month period and whose condition suggested the need for prolonged intubation (> 3 days). INTERVENTION: 76 patients were randomly allocated to receive continuous aspiration of subglottic secretions, and 77 control patients were allocated to receive usual care. MEASUREMENTS: The numbers of cases of ventilator-associated pneumonia, ventilated days, days in intensive care unit, and deaths were recorded. The amount of subglottic secretions aspirated daily and surveillance cultures in the subglottic secretions were also obtained periodically. Etiologic diagnosis was based on the quantitative culture of secretions obtained by protected specimen brush or bronchoalveolar lavage. RESULTS: The incidence rate of ventilator-associated pneumonia was 19.9 episodes/1000 ventilator days in the patients receiving continuous aspiration of subglottic secretions and 39.6 episodes/1000 ventilator days in the control patients (relative risk, 1.98; 95% CI, 1.03 to 3.82). This difference was due to a significant (P < 0.03) reduction in the number of gram-positive cocci and Haemophilus influenzae organisms in the patients receiving continuous aspiration. However, no differences were observed in the number of Pseudomonas aeruginosa or Enterobacteriaceae organisms. Episodes of ventilator-associated pneumonia occurred later in patients receiving continuous aspiration (12.0 +/- 7.1 days) than in the control patients (5.9 +/- 2.1 days) (P = 0.003). The same microorganisms isolated from protected specimen brush or bronchoalveolar lavage cultures in patients with ventilator-associated pneumonia were previously isolated from cultures of subglottic secretions in 85% of cases. No significant differences in outcome were found. CONCLUSIONS: The incidence of nosocomial pneumonia in mechanically ventilated patients can be significantly reduced by using a simple method that decreases the chronic microaspirations through the cuff of endotracheal tubes.

Aged↗
PubMed1994

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 > or = 10(4) 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 had Pseudomonas aeruginosa pneumonia, no intracellular organisms could be detected. Using a cut-off point of > or = 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 10(4) 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 for Pseudomonas aeruginosa infections.

Adult↗
PubMed1994

Relationship between expired capnogram and respiratory system resistance in critically ill patients during total ventilatory support.

To examine the relationship of expired capnograms and respiratory system resistance (Rrs) in intubated critically ill patients, we consecutively studied 41 mechanically ventilated patients to (1) analyze the association between expired CO2 slope and auto-positive end-expiratory pressure (auto-PEEP), between Rrs and auto-PEEP, between Rrs and expired CO2 slope, and between Rrs and arterial minus end-tidal PCO2 gradient (PaCO2-PETCO2 gradient) and (2) to investigate the capacity of the expired CO2 slope and PaCO2-PETCO2 gradient to predict Rrs during mechanical ventilation. Regression analysis found a close correlation between Rrs and expired CO2 slope (r = 0.86; p < 0.001), between Rrs and auto-PEEP (r = 0.75; p < 0.001), and between auto-PEEP and expired CO2 slope (r = 0.74; p < 0.001). Weak correlation was found between Rrs and PaCO2-PETCO2 gradient (r = 0.48; p < 0.01). Prediction interval limits at 95 percent confidence level for Rrs are approximately +/- 7.39 cm H2O/L/s from the predicted value obtained by the regression equation, where Rrs = 11.42 + 2.28 expired CO2 slope. These observations suggest that CO2 elimination in critically ill patients is strongly modulated by lung, airway, endotracheal tube, and ventilator equipment resistances. Although continuous capnogram waveform monitoring at the bedside might be useful to assess Rrs, very accurate predictions could be done only in determinate patients.

Adult↗
PubMed1994

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.

Acute Disease↗
PubMed1994

Hemodynamic responses to external counterbalancing of auto-positive end-expiratory pressure in mechanically ventilated patients with chronic obstructive pulmonary disease.

OBJECTIVE: To study the effect of positive end-expiratory pressure (PEEP) on right ventricular hemodynamics and ejection fraction in patients with chronic obstructive pulmonary disease and positive alveolar pressure throughout expiration by dynamic hyperinflation (auto-PEEP). DESIGN: Open, prospective, controlled trial. SETTING: General intensive care unit of a community hospital. PATIENTS: Ten patients sedated and paralyzed with an acute exacerbation of chronic obstructive pulmonary disease undergoing mechanical ventilation. INTERVENTIONS: Insertion of a pulmonary artery catheter modified with a rapid response thermistor and a radial arterial catheter. PEEP was then increased from 0 (PEEP 0) to auto-PEEP level (PEEP = auto-PEEP) and 5 cm H2O above that (PEEP = auto-PEEP +5). MEASUREMENTS: At each level of PEEP, airway pressures, flow and volume, hemodynamic variables (including right ventricular ejection fraction by thermodilution technique), and blood gas analyses were recorded. MAIN RESULTS: The mean auto-PEEP was 6.6 +/- 2.8 cm H2O and the total PEEP reached was 12.2 +/- 2.4 cm H2O. The degree of lung inflation induced by PEEP averaged 145 +/- 87 mL with PEEP = auto-PEEP and 495 +/- 133 mL with PEEP = auto-PEEP + 5. The PEEP = auto-PEEP caused a right ventricular end-diastolic pressure increase, but there was no other significant hemodynamic change. With PEEP = auto-PEEP + 5, there was a significant increase in intravascular pressures; this amount of PEEP reduced cardiac output (from 4.40 +/- 1.38 L/min at PEEP 0 to 4.13 +/- 1.48 L/min; p < .05). The cardiac output reduction induced by PEEP = auto-PEEP + 5 was > 10% in only five cases and this group of patients had significantly lower right ventricular volumes than the group with less cardiac output variation (right ventricular end-diastolic volume: 64 +/- 9 vs. 96 +/- 26 mL/m2; right ventricular end-systolic volume: 38 +/- 6 vs. 65 +/- 21 mL/m2; p < .05) without significant difference in the other variables that were measured. Neither right ventricular ejection fraction nor right ventricle volumes changed as PEEP increased, but there were marked interpatient differences and also pronounced changes in volume between stages in individual patients. CONCLUSIONS: In the study conditions, PEEP application up to values approaching auto-PEEP did not result in the impairment of right ventricular hemodynamics, while higher levels reduced cardiac output in selected patients.

APACHE↗
PubMed1993

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

OBJECTIVE: To test whether non-invasive ventilation via facial mask could reduce the need for tracheal intubation when mechanical ventilation must be initiated in COPD patients. DESIGN: Open prospective interventional study. SETTING: General Intensive Care Service of a County Hospital. PATIENTS: We 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 impairments in severe respiratory acidosis and/or hypercapnic encephalopathy leading their attending physicians to order mechanical ventilation. INTERVENTIONS: In these circumstances, a trial of pressure-support (PS) ventilation (Servo Ventilator 900C) via facial mask Vital Signs Inc.) 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 RESULTS: Measurements 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. CONCLUSION: Non-invasive ventilation (pressure-support) via face mask may reduce the need for tracheal intubation in the severe hypercapnic failure of COPD patients.

Acute Disease↗