A Mas

Corporació Sanitària Parc Taulí, Catalonia, Spain

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Publications (9)44.56 Total impact

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    ABSTRACT: Objective: Inhaled nitric oxide (NO) and prone position improve arterial oxygenation in patients with the acute respiratory distress syndrome. This study was undertaken to assess the combined effects of NO and prone position in these patients. Design: Prospective clinical study. Setting: General intensive care service in a community teaching hospital. Patients: 14 mechanically ventilated adult patients with the acute respiratory distress syndrome (mean lung injury score 3.23 � 0.27). Measurements and results: We measured hemodynamic and oxygenation parameters in the supine position and 2 h later in the prone position, before and during inhalation of 10 ppm NO. A positive response in oxygenation was defined as a ≥ 20 % increment in the arterial oxygen tension/fractional inspired oxygen ratio (PaO2/FIO2). In the prone position PaO2/FIO2 increased significantly (from 110 � 55 to 161 � 89 mmHg, p p < 0.01) compared to the supine position. Ten of the 14 patients were responders in the prone position. In the supine position, inhalation of NO improved oxygenation to a lesser extent, increasing PaO2/FIO2 to 134 � 64 mmHg (p p p = 0.22). The combination of NO therapy and prone positioning was additive in increasing PaO2/FIO2 (197 � 92 mmHg) and decreasing venous admixture (27 � 8 %) (p < 0.01). This combination also showed a positive oxygenation response on compared to the supine value without NO in 13 of the 14 patients (93 %). NO-induced changes in PaO2/FIO2 were correlated to changes in pulmonary vascular resistance only in the prone position. Conclusions: In patients with the acute respiratory distress syndrome, the combination of NO and prone position is a valuable adjunct to mechanical ventilation.
    European Journal of Intensive Care Medicine 11/2011; · 5.17 Impact Factor
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    ABSTRACT: To describe global hemodynamics and splanchnic perfusion changes in response to acute modifications in Paco2 in hemodynamically stable patients. Prospective, randomized crossover study. Medical-surgical intensive care unit at a community hospital (400,000 inhabitants). Ten critically ill patients who were sedated, paralyzed, and mechanically ventilated. 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. 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. 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.
    Critical Care Medicine 02/2000; 28(2):360-5. · 6.12 Impact Factor
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    ABSTRACT: Inhaled nitric oxide (NO) and prone position improve arterial oxygenation in patients with the acute respiratory distress syndrome. This study was undertaken to assess the combined effects of NO and prone position in these patients. Prospective clinical study. General intensive care service in a community teaching hospital. 14 mechanically ventilated adult patients with the acute respiratory distress syndrome (mean lung injury score 3.23+/-0.27). We measured hemodynamic and oxygenation parameters in the supine position and 2 h later in the prone position, before and during inhalation of 10 ppm NO. A positive response in oxygenation was defined as a > or =20% increment in the arterial oxygen tension/fractional inspired oxygen ratio (PaO2/FIO2). In the prone position PaO2/FIO2 increased significantly (from 110+/-55 to 161+/-89 mm Hg, p<0.01) and venous admixture decreased (from 38+/-12 to 30+/-7%, p<0.01) compared to the supine position. Ten of the 14 patients were responders in the prone position. In the supine position, inhalation of NO improved oxygenation to a lesser extent, increasing PaO2/FIO2 to 134+/-64 mm Hg (p<0.01) and decreasing venous admixture to 35+/-12%, (p<0.01). Five of the 14 patients responded to NO inhalation supine and 8 of 14 responded prone (p = 0.22). The combination of NO therapy and prone positioning was additive in increasing PaO2/FIO2 (197+/-92 mm Hg) and decreasing venous admixture (27+/-8%) (p<0.01). This combination also showed a positive oxygenation response on compared to the supine value without NO in 13 of the 14 patients (93 %). NO-induced changes in PaO2/FIO2 were correlated to changes in pulmonary vascular resistance only in the prone position. In patients with the acute respiratory distress syndrome, the combination of NO and prone position is a valuable adjunct to mechanical ventilation.
    Intensive Care Medicine 01/1999; 25(1):29-36. · 5.54 Impact Factor
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    ABSTRACT: Hydrochlorothiazide-induced pulmonary edema is an unusual but life-threatening adverse reaction. It causes hypoxemia, hypotension, tachycardia, fever, and occasionally electrocardiographic and echocardiographic abnormalities. The mechanism of production is, probably, idiosyncratic.
    Intensive Care Medicine 05/1998; 24(4):363-5. · 5.54 Impact Factor
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    ABSTRACT: 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. Prospective, double blind, randomized, placebo-controlled study. General Intensive Care Unit of a teaching hospital. Twenty-five critically ill, mechanically ventilated patients requiring arterial catheter and nasogastric tube. Tonometer placement; blind, random administration of intravenous ranitidine (50 mg) or placebo. 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. In critically ill patients, ranitidine has no effect on pHi values, and does not increase the reproducibility of pHi measurements.
    Intensive Care Medicine 01/1998; 24(1):12-7. · 5.54 Impact Factor
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    ABSTRACT: Changing the position from supine to prone is an emerging strategy to improve gas exchange in patients with the acute respiratory distress syndrome (ARDS). The aim of this study was to evaluate the acute effects on gas exchange, hemodynamics, and respiratory system mechanics of turning critically ill patients with ARDS from supine to prone. Open, prospective study. General intensive care units. 23 patients [mean age 56 +/- 17 (SD) years] who met ARDS criteria and had a Lung Injury Score > 2.5 (mean 3.25 +/- 0.3). The decision to turn a patient was made using a protocol based on impaired oxygenation despite the use of positive end-expiratory pressure and a fractional inspired oxygen (FIO2) of 1. We measured gas exchange and hemodynamic variables in all patients and in 16 patients calculated respiratory system compliance when they were supine and 60 to 90 min after turning them to a prone position. This latter position was remarkably well tolerated and no clinically relevant complications or events were detected either during turning or while prone. The partial pressure of oxygen in arterial blood (PaO2)/FIO2 ratio improved from 78 +/- 37 mm Hg supine to 115 +/- 31 mm Hg prone (p < 0.001), and intrapulmonary shunt decreased from 43 +/- 11 to 34 +/- 8% (p < 0.001). Cardiac output and other hemodynamic parameters were not affected. Respiratory system compliance slightly improved from 24.7 +/- 10.2 ml/cmH20 supine to 27.8 +/- 13.2 ml/cmH20 prone (p < 0.05). An improvement in PaO2/FIO2 of more than 15% from changing from supine to prone was found in 16 patients (responders). Responders had more hypoxemia (PaO2/FIO2 70 +/- 23 vs 99 +/- 53 mm Hg in non-responders, p < 0.01), more hypercapnia (partial pressure of carbon dioxide in arterial blood (70 +/- 27 vs 64 +/- 9 mm Hg, p < 0.01) and a shorter elapsed time to the onset of ARDS and turning to the prone position (11.8 +/- 16 vs 32.8 +/- 42 days, p < 0.01). Turning critically ill, severely hypoxemic patients from the supine to the prone position is a safe and useful therapeutic intervention. Our data suggest that prone positioning should be carried out early in the course of ARDS.
    Intensive Care Medicine 10/1997; 23(10):1033-9. · 5.54 Impact Factor
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    ABSTRACT: To determine whether sucralfate administration affects the tonometric measurement of gastric intramucosal pH (pHi). Non-randomized observational study. General intensive care unit of a teaching hospital. Twenty critically ill, mechanically ventilated, consecutively admitted patients requiring an arterial catheter and nasogastric tube. Tonometer placement and sucralfate administration. 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). Sucralfate does not affect the tonometric measurement of PCO2i and pHi.
    Intensive Care Medicine 08/1997; 23(7):738-42. · 5.54 Impact Factor
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    ABSTRACT: 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). Prospective clinical study. General intensive care unit in Sabadell, Spain. 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). 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). 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.
    Intensive Care Medicine 01/1997; 23(1):51-7. · 5.54 Impact Factor
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