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  • 1
    ISSN: 1432-1238
    Keywords: Acute respiratory failure ; Mechanical ventilation ; Nitric oxide (inhaled)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective To determine the dose-response curve of inhaled nitric oxide (NO) in terms of pulmonary vasodilation and improvement in PaO2 in adults with severe acute respiratory failure. Design Prospective randomized study. Setting A 14-bed ICU in a teaching hospital. Patients 6 critically ill patients with severe acute respiratory failure (lung injury severity score ≥2.5) and pulmonary hypertension. Interventions 8 concentrations of inhaled NO were administered at random: 100, 400, 700, 1000, 1300, 1600, 1900 and 5000 parts per billion (ppb). Control measurements were performed before NO inhalation and after the last concentration administered. After an NO exposure of 15–20 min, hemodynamic parameters obtained from a fiberoptic Swan-Ganz catheter, blood gases, methemoglobin blood concentrations and intratracheal NO and nitrogen dioxide (NO2) concentrations, continuously monitored using a bedside chemiluminescence apparatus, were recorded on a Gould ES 1000 recorder. In 2 patients end-tidal CO2 was also recorded. Results The administration of 100–2000 ppb of inhaled NO induced: i) a dose-dependent decrease in pulmonary artery pressure and in pulmonary vascular resistance (maximum decrease −25%); ii) a dose-dependent increase in PaO2 via a dose-dependent reduction in pulmonary shunt; iii) a slight but significant decrease in PaCO2 via a reduction in alveolar dead space; iv) a dose-dependent increase in mixed venous oxygen saturation (SVO2). Systemic hemodynamic variables and methemoglobin blood concentrations did not change. Maximum NO2 concentrations never exceeded 165 ppb. In 2 patients, 91% and 74% of the pulmonary vasodilation was obtained for inhaled NO concentrations of 100 ppb. Conclusion In hypoxemic patients with pulmonary hypertension and severe acute respiratory failure, therapeutic inhaled NO concentrations are in the range 100–2000 ppb. The risk of toxicity related to NO inhalation is therefore markedly reduced. Continuous SVO2 monitoring appears useful at the bedside for determining optimum therapeutic inhaled NO concentrations in a given patient.
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  • 2
    ISSN: 1432-1238
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
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  • 3
    ISSN: 1432-1238
    Keywords: Key words Nitric oxide ; Distribution ; Uptake ; Monitoring ; ARDS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Objectives : The concentrations of nitric oxide (NO) in the ventilatory circuits and the patient's airways were compared between sequential (SQA) and continuous (CTA) administration during inspiratory limb delivery. Design: Prospective controlled study. Setting: 14-bed Surgical Intensive Care Unit of a teaching University hospital. Patients and participants: Eleven patients with acute lung injury on mechanical ventilation and two healthy volunteers. Interventions: A prototype NO delivery device (Opti-NO) and César ventilator were set up in order to deliver 1, 3 and 6 parts per million (ppm) of NO into the bellows of a lung model in SQA and CTA. Using identical ventilatory and Opti-NO settings, NO was administered to the patients with acute lung injury. Measurements and results: NO concentrations measured from the inspiratory limb [INSP-NOMeas] and the trachea [TRACH-NOMeas] using fast response chemiluminescence were compared between the lung model and the patients using controlled mechanical ventilation with a constant inspiratory flow. INSP-NOMeas were stable during SQA and fluctuated widely during CTA (fluctuation at 6 ppm = 61 % in the lung model and 58 ± 3 % in patients). In patients, [TRACH-NOMeas] fluctuated widely during both modes (fluctuation at 6 ppm = 55 ± 3 % during SQA and 54 ± 5 % during CTA). The NO flow requirement was significantly lower during SQA than during CTA (74 ± 0.5 vs 158 ± 2.2 ml.min–1 to attain 6 ppm, p = 0.0001). INSP-NOMeas were close to the values predicted using a classical formula only during SQA (bias = –0.1 ppm, precision = ± 1 ppm during SQA; bias = 2.93 ppm and precision = ± 3.54 ppm during CTA). During SQA, INSP-NOMeas varied widely in healthy volunteers on pressure support ventilation. Conclusions: CTA did not provide homogenous mixing of NO with the tidal volume and resulted in fluctuating INSP-NOMeas. In contrast, SQA delivered stable and predictable NO concentrations during controlled mechanical ventilation with a constant inspiratory flow and was economical compared to CTA. However, SQA did not provide stable and predictable NO concentrations during pressure support ventilation.
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  • 4
    ISSN: 1432-1238
    Keywords: Nosocomial bronchopneumonia ; Mechanical ventilation ; Intratracheal colistin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective To evaluate the efficiency of intratracheal colistin in preventing nosocomial bronchopneumonia (BPN) in the critically ill. Design Study evaluating the clinical incidence of nosocomial BPN in 2 groups of critically ill patients who receive or did not receive intratracheal colistin. BPN was assessed clinically in survivors and histologically in nonsurvivors. Setting A 14-bed surgical intensive care unit. Patients 598 consecutive critically ill patients were studied during a prospective non-randomized study over a 40-month period. Interventions 251 patients — 31 non-survivors and 220 survivors — did not receive intratracheal colistin and 347 — 42 non-survivors and 305 survivors — received intratracheal colistin for a 2-week period (16000000 units per 24h). Measurements and results The incidence of nosocomial BPN was evaluated clinically in survivors, using repeated protected minibronchoalveolar lavages, and histologically in non-survivors via an immediate postmortem pneumonectomy (histologic and semi-quantitative bacteriologic analysis of one lung). The clinical incidence of nosocomial BPN was of 37% in coli (−) survivors and of 27% in coli (+) survivors (p〈0.01). This result was histologically confirmed in non-survivors, where the incidence of histologic BPN was of 61% in coli (−) patients and of 36% in coli (+) patients (p〈0.001). Emergence of BPN due to colistin-resistant micro-organisms was not observed. Because colistin was successful in preventing Gram-negative BPN and did not change the absolute number of Gram-positive BPN, the proportion of BPN caused bystaphylococcus species was higher in group coli (+) patients (33% vs 16%). Mortality was not significantly influenced by the administration of colistin. Conclusion This study suggests that the administration of intratracheal colistin during a 2-week period significantly reduces the incidence of Gram-negative BPN without creating an increasing number of BPN due to colistin-resistant micro-organism.
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  • 5
    ISSN: 1432-1238
    Keywords: Key words Computed tomography ; Lung morphology ; Functional residual capacity ; Acute respiratory distress syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: To compare the computed tomographic (CT) analysis of the distribution of gas and tissue in the lungs of patients with ARDS with that in healthy volunteers. Design: Prospective study over a 53-month period.¶Setting: Fourteen-bed surgical intensive care unit of a university hospital. Patients and participants: Seventy-one consecutive patients with early ARDS and 11 healthy volunteers. Measurements and results: A lung CT was performed at end-expiration in patients with ARDS (at zero PEEP) and healthy volunteers. In patients with ARDS, end-expiratory lung volume (gas + tissue) and functional residual capacity (FRC) were reduced by 17 % and 58 % respectively, and an excess lung tissue of 701 ± 321 ml was observed. The loss of gas was more pronounced in the lower than in the upper lobes. The lower lobes of 27 % of the patients were characterized by “compression atelectasis,” defined as a massive loss of aeration with no concomitant excess in lung tissue, and “inflammatory atelectasis,” defined as a massive loss of aeration associated with an excess lung tissue, was observed in 73 % of the patients. Three groups of patients were differentiated according to the appearance of their CT: 23 % had diffuse attenuations evenly distributed in the two lungs, 36 % had lobar attenuations predominating in the lower lobes, and 41 % had patchy attenuations unevenly distributed in the two lungs. The three groups were similar regarding excess lung tissue in the upper and lower lobes and reduction in FRC in the lower lobes. In contrast, the FRC of the upper lobes was markedly lower in patients with diffuse or patchy attenuations than in healthy volunteers or patients with lobar attenuations. Conclusions: These results demonstrate that striking differences in lung morphology, corresponding to different distributions of gas within the lungs, are observed in patients whose respiratory condition fulfills the definition criteria of ARDS.
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  • 6
    ISSN: 1432-1238
    Keywords: Key words Adult respiratory distress syndrome ; Outcome ; Computed tomography ; Lung morphology ; Lung mechanics ; Lung volumes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objectives: (a) To assess whether differences in lung morphology observed in patients with adult respiratory distress syndrome (ARDS) are associated with differences in cardiorespiratory parameters, lung mechanics, and outcome. (b) To propose a new ARDS Severity Score to identify patients with a high mortality risk. Design: Prospective study over a 53-month period. Setting: Fourteen-bed surgical intensive care unit of a university hospital. Patients and participants: Seventy-one consecutive patients with early ARDS. Measurements and results: Cardiorespiratory parameters were measured using a Swan-Ganz catheter, the pressure-volume (PV) curve was measured using the gross syringe method, and fast spiral computed tomography (CT) was performed. Patients with diffuse attenuations (n = 16) differed from patients with lobar attenuations (n = 26) regarding: (a) mortality rate (75 % vs. 42 %, p = 0.05), (b) incidence of primary ARDS (82 % vs. 50 %, p = 0.03), (c) respiratory compliance (47 ± 12 vs. 64 ± 16 ml per cmH2O–1 p = 0.04), and (d) lower inflexion point (8.4 ± 2.0 vs. 4.6 ± 2.0 cmH2O, p = 0.001). A third group of patients with patchy attenuations (n = 29) had a mortality rate of 41 %, a respiratory compliance of 56 ± 18 ml per cmH2O–1 and a lower inflexion point of 6.3 ± 2.7 cmH2O. The bedside chest radiograph accurately assessed lung morphology in only 42 % of the patients. In contrast to the scores based on the bedside chest radiograph, a new ARDS Severity Score based on CT lung morphology and cardiorespiratory parameters identified a subgroup of patients with a high mortality rate (≥ 60 %). Conclusions: In patients with ARDS, differences in lung morphology are associated with differences in outcome and lung mechanics. A new ARDS Severity Score based on CT lung morphology and cardiorespiratory parameters accurately identified patients with the most severe forms of ARDS and a mortality rate above 60 %.
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  • 7
    ISSN: 1432-1238
    Keywords: Key words Acute respiratory distress syndrome ; Positive end-expiratory pressure ; Computed tomography ; Alveolar recruitment ; Lung overdistension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: To determine whether differences in lung morphology assessed by computed tomography (CT) affect the response to positive end-expiratory pressure (PEEP).¶Design: Prospective study over a 53-month period.¶Setting: Fourteen-bed surgical intensive care unit of a university hospital.¶Patients and participants: Seventy-one consecutive patients with early adult respiratory distress syndrome (ARDS).¶Measurements and results: Fast spiral thoracic CT was performed at zero end-expiratory pressure (ZEEP) and after implementation of PEEP 10 cmH2O. Hemodynamic and respiratory parameters were measured in both conditions. PEEP-induced overdistension and alveolar recruitment were quantified by specifically designed software (Lungview). Overdistension occurred only in the upper lobes and was significantly correlated with the volume of lung, characterized by a CT attenuation ranging between –900 and –800 HU in ZEEP conditions. Cardiorespiratory effects of PEEP were similar in patients with primary and secondary ARDS. PEEP-induced alveolar recruitment of the lower lobes was significantly correlated with their lung volume (gas + tissue) at functional residual capacity. PEEP-induced alveolar recruitment was greater in the lower lobes with “inflammatory atelectasis” than in the lower lobes with “mechanical atelectasis.” Lung morphology as assessed by CT markedly influenced the effects of PEEP: in patients with diffuse CT attenuations PEEP induced a marked alveolar recruitment without overdistension, whereas in patients with lobar CT attenuations PEEP induced a mild alveolar recruitment associated with overdistension of previously aerated lung areas. These results can be explained by the uneven distribution of regional compliance characterizing patients with lobar CT attenuations (compliant upper lobes and stiff lower lobes) contrasting with a more even distribution of regional compliances observed in patients with diffuse CT attenuations.¶Conclusions: In patients with ARDS, the cardiorespiratory effects of PEEP are affected by lung morphology rather than by the cause of the lung injury (primary versus secondary ARDS). The regional distribution of the loss of aeration and the type of atelectasis –“mechanical” with a massive loss of lung volume, or “inflammatory” with a preservation of lung volume – characterizing the lower lobes are the main determinants of the cardiorespiratory effects of PEEP.
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  • 8
    ISSN: 1432-1238
    Keywords: Ventilation ; Airway pressure release ventilation ; Continuous positive airway pressure ; Positive end-expiratory pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Intermittent Mandatory Pressure Release Ventilation (IMPRV) is a positive pressure spontaneous breathing ventilatory mode in which airway pressure is released intermittently and synchronously with patient's spontaneous expiration in order to provide ventilatory assistance. Eight critically ill patients free of any factor known to alter chest wall mechanics (group 1) and 8 critically ill patients whose spontaneous respiratory activity was markedly altered by a flail chest, or by a C5 quadraplegia and/or by the administration of opioids (group 2) were studied prospectively. CPAP and IMPRV were administered to each patient in a random order during a 1 h period using a CESAR ventilator. Gas flow, tidal volume, tracheal pressure, esophageal pressure, end-expiratory lung volume and hemodynamic parameters were measured. In group 1 patients, the ventilatory assistance provided by IMPRV was associated with a significant decrease in spontaneous tidal volume whereas all other respiratory parameters remained unchanged. In group 2 patients, IMPRV increased minute ventilation from 8.0±2.61/min to 12.2±1.81/min (p〈0.05), decreased PaCO2 from 46±7.3 mmHg to 38±6.8 mmHg (p〈0.05) and reduced respiratory frequency from 21±10 bpm to 14±5.7 bpm (p〈0.07). These results show that IMPRV provides significant ventilatory assistance to patients with mild acute respiratory failure either by decreasing patient's contribution to minute ventilation or by increasing alveolar ventilation in presence of respiratory depression of central or peripheral origin.
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  • 9
    ISSN: 1432-1238
    Keywords: Mechanical ventilation ; Barotrauma ; Respiratory failure ; Alveolar overdistension ; Pneumothorax
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective To describe histologically pulmonary barotrauma in mechanically ventilated patients with severe acute respiratory failure. Design Assessment of histologic pulmonary barotrauma. Setting A 14-bed surgical intensive care unit (SICU). Patients The lungs of 30 young critically ill patients (mean age 34±10 years) were histologically examined in the immediate post-mortem period. None of them were suspected of pre-existing emphysema. Measurements and results Clinical events and ventilatory settings used during mechanical ventilation were compared with lung histology. Airspace enlargement, defined as the presence of either alveolar overdistension in aerated lung areas or intraparenchymal pseudocysts in nonaerated lung areas, was found in 26 of the 30 lungs examined (86%). Patients with severe airspace enlargement (2.6–40 mm internal diameter) had a significantly greater incidence of pneumothorax (8 versus 2,p〈0.05), were ventilated using higher peak airway pressures (56±18 cmH2O versus 44±10 cmH2O,p〈0.05) and tidal volumes (12±3 ml/kg, versus 9±2ml/kg,p〈0.05) were exposed significantly longer to toxic levels of oxygen (8.6±9.4 days versus 1.9±2 days at FIO2〉0.6,p〈0.05) and lost more weight (6.3±9.2 kg versus 0.75±5.8 kg,p〈0.05) than patients with mild airspace enlargement (1–2.5 mm internal diameter). Conclusion Underlying histologic lesions responsible for clinical lung barotrauma consist of pleural cysts, bronchiolar dilatation, alveolar overdistension and intraparenchymal pseudocysts. Mechanical ventilation appears to be an aggravating factor, particularly when high peak airway pressures and large tidal volumes are delivered by the ventilator.
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Intensivmedizin und Notfallmedizin 34 (1997), S. 179-197 
    ISSN: 1435-1420
    Keywords: Schlüsselwörter Hypoxämie ; ARDS ; Stickstoffmonoxid ; Inhalation ; Almitrine ; Cyclooxygenase-Inhibitoren ; Key words Hypoxemia ; ARDS ; nitric ; oxide ; inhaled ; almitrine ; cyclooxygenase inhibitors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary The use of selective pulmonary vasodilators or vasoconstrictors is a new therapeutic option to improve arterial oxygenation in patients with ARDS through a redistribution of ventilation/perfusion ratios. The objective of such a therapy is to reduce the need for high O2 concentrations and airway pressures, thereby decreasing ventilator-induced lung injury. Nitric oxide (NO) is one part of this approach. It is administered through the inhalation route in mechanically ventilated patients. It reduces the vasomotor tone of pulmonary vessels from the ventilated part of the lung. It also reduces pulmonary arterial pressure and alveolar deadspace. Alveolar recruitment potentiates the effects of NO on arterial oxygenation but not on pulmonary circulation. For NO concentrations as low as 0.45 ppm, inhaled NO induces a significant decrease in platelet aggregation. In patients with ARDS and septic shock receiving a continuous intravenous infusion of norepinephrine, there is a concentration-dependent increase in oxygenation in the range of 0.1–150 ppm, whereas a plateau effect is observed for concentrations below 5 ppm in patients in shock. Sequential mode of administration of inhaled NO (only during the inspiratory phase) provides stable and predictible concentrations of NO within the inspiratory limb. Aerosolized prostacyclin in doses as low as 2 µg ⋅ kg–1⋅ min–1 is another means to improve arterial oxygenation through a dilation of the vessels located in the ventilated part of the lung. At the opposite, almitrine improves arterial oxygenation by reinforcing hypoxic pulmonary vasoconstriction. When combined with inhaled NO, the beneficial effect of almitrine on arterial oxygenation is potentiated while its detrimental effects on the pulmonary circulation are blunted. Maximal effect on PaO2 and shunt are observed at a dose of 4 µg ⋅ kg–1⋅ min–1. Due to its large volume of distribution and low plasma clearance, prolonged administration of almitrine in patients with ARDS should be regarded with caution. Cyclooxygenase inhibitors also improve arterial oxygenation by reinforcing hypoxic pulmonary vasoconstriction. All these new treatments have profoundly changed the therapeutic strategy aimed at correcting life-threatening hypoxemia in patients with severe ARDS.
    Notes: Zusammenfassung Bei der Verabreichung selektiver pulmonaler Vasodilatoren oder Vasokonstriktoren handelt es sich um eine neue therapeutische Möglichkeit zur Verbesserung der arteriellen Sauerstoffzufuhr bei Patienten mit ARDS mittels einer Umverteilung der Ventilations-/Perfusionsquotienten. Das Ziel einer solchen Therapie ist es, die Notwendigkeit hoher O2-Konzentrationen und Druckwerte in den Luftwegen zu reduzieren und dadurch Lungenverletzungen durch den Ventilator zu vermindern. Stickstoffmonoxid (NO) ist Bestandteil dieses Vorgehens. Es wird bei mechanisch ventilierten Patienten bei der Inhalation verabreicht. Es reduziert den vasomotorischen Tonus der pulmonalen Gefäße im beatmeten Teil der Lungen. Es senkt außerdem den pulmonalen arteriellen Druck und den alveolären Totraum. Das alveoläre Rekruitment verstärkt die Wirkung des Stickstoffmonoxids auf die arterielle Sauerstoffzufuhr, hingegen nicht aber auf die die pulmonale Zirkulation. In Konzentrationen von nur 0,45 ppm inhaliertem Stickstoffmonoxid bewirkt NO eine signifikante Abnahme der Thrombozytenaggregation. Bei Patienten mit akutem Atemnotsyndrom (ARDS) und septischem Schock, die eine intravenöse Norepinephrin-Dauerinfusion erhalten, kommt es zu einer konzentrationsabhängigen Zunahme der Sauerstoffzufuhr im Bereich von 0,1–150 ppm, während bei Patienten ohne Schock für Konzentrationen unter 5 ppm eine Plateauwirkung beobachtet wird. Die sequentielle Methode der Verabreichung von inhalierten NO (lediglich während der Inspiration) liefert in der Inspirationsphase stabile und vorhersagbare NO-Konzentrationen. Prostacyclin-Aerosol in niedrigen Dosen von nur 2 µg ⋅ kg–1⋅ min–1 kann ebenfalls zur Verbesserung der arteriellen Sauerstoffzufuhr verwendet werden, da es im ventilierten Abschnitt der Lungen eine Gefäßdilatation bewirkt. Andererseits verbessert Almitrine die arterielle Sauerstoffzufuhr, indem es die hypoxische pulmonale Vasokonstriktion verstärkt. Kombiniert man es mit der NO-Inhalation, wird die günstige Wirkung von Almitrine auf die arterielle Sauerstoffzufuhr verstärkt, wohingegen die schädlichen Wirkungen auf die pulmonale Zirkulation abgeschwächt werden. Maximale Effekte auf den PaO2-Shunt werden bei Dosen von 4 µg ⋅ kg–1⋅ min–1 registriert. Wegen seines großen Verteilungsvolumens und seiner langsamen Plasma-Clearance sollte die längere Anwendung von Almitrine bei Patienten mit ARDS vorsichtig erfolgen. Cyclooxygenase-Inhibitoren verbessern ebenfalls die arterielle Sauerstoffzufuhr, indem sie die hypoxische pulmonale Vasokonstriktion verstärken. Sämtliche neuen Behandlungsmethoden haben die Behandlungsstrategien der Beseitigung lebensbedrohlicher Hypoxämien bei Patienten mit schwerem ARDS grundlegend verändert.
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