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  • 1
    Electronic Resource
    Electronic Resource
    Inhaled nitric oxide in acute respiratory failure: Dose-response curves (1994)
    Springer
    Intensive care medicine 20 (1994), S. 319-327 
    Details
    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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01720903
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  • 2
    Electronic Resource
    Electronic Resource
    Distribution of inhaled nitric oxide during sequential and continuous administration into the inspiratory limb of the ventilator (1997)
    Springer
    Intensive care medicine 23 (1997), S. 849-858 
    Details
    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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001340050421
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    Paper (German National Licenses)
    Fulltext
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