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  • 1
    Electronic Resource
    Electronic Resource
    Effects of rapid permissive hypercapnia on hemodynamics, gas exchange, and oxygen transport and consumption during mechanical ventilation for the acute respiratory distress syndrome (1996)
    Springer
    Intensive care medicine 22 (1996), S. 182-191 
    Details
    ISSN: 1432-1238
    Keywords: Permissive hypercapnia ; Mechanical ventilation ; Alveolar hypoventilation ; Oxygen transport ; Oxygen consumption ; DO2/VO2 relationship ; Hemoglobin dissociation curve ; ARDS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective To measure the effects of rapid permissive hypercapnia on hemodynamics and gas exchange in patients with acute respiratory distress syndrome (ARDS). Design Prospective study.Setting: 18-bed, medical intensive care unit, university hospital. Patients 11 mechanically ventilated ARDS patients. Intervention Patients were sedated and ventilated in the controlled mode. Hypercapnia was induced over a 30–60 min period by decreasing tidal volume until pH decreased to 7.2 and/or P50 increased by 7.5 mmHg. Settings were then maintained for 2 h. Results Minute ventilation was reduced from 13.5±6.1 to 8.2±4.1l/min (mean±SD), PaCO2 increased (40.3±6.6 to 59.3±7.2 mmHg), pH decreased (7.40±0.05 to 7.26±0.05), and P50 increased (26.3±2.02 to 31.1±2.2 mmHg) (p〈0.05). Systemic vascular resistance decreased (865±454 to 648±265 dyne·s·cm−5, and cardiac index (CI) increased (4±2.4 to 4.7±2.4 l/min/m2) (p〈0.05). Mean systemic arterial pressure was unchanged. Pulmonary vascular resistance was unmodified, and mean pulmonary artery pressure (MPAP) increased (29±5 to 32±6 mmHg,p〈0.05). PaO2 remained unchanged, while saturation decreased (93±3 to 90±3%,p〈0.05), requiring an increase in FIO2 from 0.56 to 0.64 in order to maintain an SaO2〉90%. PvO2 increased (36.5±5.7 to 43.2±6.1 mmHg,p〈0.05), while saturation was unmodified. The arteriovenous O2 content difference was unaltered. Oxygen transport (DO2) increased (545±240 to 621±274 ml/min/m2,p〈0.05), while the O2 consumption and extraction ratio did not change significantly. Venous admixture (Qva/Qt) increased (26.3±12.3 to 32.8±13.2,p〈0.05). Conclusions These data indicate that acute hypercapnia increases DO2 and O2 off-loading capacity in ARDS patients with normal plasma lactate, without increasing O2 extraction. Whether this would be beneficial in patients with elevated lactate levels, indicating tissue hypoxia, remains to be determined. Furthermore, even though hypercapnia was well tolerated, the increase in Qva/Qt, CI, and MPAP should prompt caution in patients with severe hypoxemia, as well as in those with depressed cardiac function and/or severe pulmonary hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01712235
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Effects of rapid permissive hypercapnia on hemodynamics, gas exchange, and oxygen transport and consumption during mechanical ventilation for the acute respiratory distress syndrome (1996)
    Springer
    Intensive care medicine 22 (1996), S. 182-191 
    Details
    ISSN: 1432-1238
    Keywords: Key words Permissive hypercapnia ; Mechanical ventilation ; Alveolar hypoventilation ; Oxygen transport ; Oxygen consumption ; DO2/VO2 relationship ; Hemoglobin dissociation curve ; ARDS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: To measure the effects of rapid permissive hypercapnia on hemodynamics and gas exchange in patients with acute respiratory distress syndrome (ARDS). Design: Prospective study. Setting: 18-bed, medical intensive care unit, university hospital. Patients: 11 mechanically ventilated ARDS patients. Intervention: Patients were sedated and ventilated in the controlled mode. Hypercapnia was induced over a 30–60 min period by decreasing tidal volume until pH decreased to 7.2 and/or P50 increased by 7.5 mmHg. Settings were then maintained for 2 h. Results: Minute ventilation was reduced from 13.5±6.1 to 8.2±4.1 l/min (mean±SD), PaCO2 increased (40.3±6.6 to 59.3± 7.2 mmHg), pH decreased (7.40±0.05 to 7.26±0.05), and P50 increased (26.3±2.02 to 31.1± 2.2 mmHg) (p〈0.05). Systemic vascular resistance decreased (865±454 to 648±265 dyne·s·cm–5, and cardiac index (CI) increased (4±2.4 to 4.7±2.4 l/min/m2) (p〈0.05). Mean systemic arterial pressure was unchanged. Pulmonary vascular resistance was unmodified, and mean pulmonary artery pressure (MPAP) increased (29±5 to 32± 6 mmHg, p〈0.05). PaO2 remained unchanged, while saturation decreased (93±3 to 90±3%, p〈0.05), requiring an increase in FIO2 from 0.56 to 0.64 in order to maintain an SaO2〉90%. PvO2 increased (36.5±5.7 to 43.2± 6.1 mmHg, p〈0.05), while saturation was unmodified. The arteriovenous O2 content difference was unaltered. Oxygen transport (DO2) increased (545±240 to 621± 274 ml/min/m2, p〈0.05), while the O2 consumption and extraction ratio did not change significantly. Venous admixture (Qva/Qt) increased (26.3±12.3 to 32.8±13.2, p〈0.05). Conclusions: These data indicate that acute hypercapnia increases DO2 and O2 off-loading capacity in ARDS patients with normal plasma lactate, without increasing O2 extraction. Whether this would be beneficial in patients with elevated lactate levels, indicating tissue hypoxia, remains to be determined. Furthermore, even though hypercapnia was well tolerated, the increase in Qva/Qt, CI, and MPAP should prompt caution in patients with severe hypoxemia, as well as in those with depressed cardiac function and/or severe pulmonary hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01712235
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    The repeated measurement of vital capacity is a poor predictor of the need for mechanical ventilation in myasthenia gravis (1995)
    Springer
    Intensive care medicine 21 (1995), S. 663-668 
    Details
    ISSN: 1432-1238
    Keywords: Myasthenia gravis ; Vital capacity ; Mechanical ventilation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective Testing the hypothesis that, in myasthenia gravis (MG), repeated measurements of vital capacity (VC) and various parameters derived from this measurement [median or lowest value of measured VCs during hospitalization, VC values〈20ml/kg body weight (BW) or〈13ml/kg BW, or an index assessing the variability of VC values during the whole ICU stay] could predict the need for intubation and mechanical ventilation (MV), as has been shown in other neuromuscular diseases with respiratory failure.Design: Retrospective study with medical chart revision of all the patients with MG and respiratory failure admitted to our intensive care unit between 1985 and 1993.Setting: Medical intensive care unit (15 beds) of a nuniversity hospital.Patients and methods: Five patients suffering from ten episodes of acute respiratory failure due to their decompensated MG. Repeated measurements of arterial blood gases and VC by trained respiratory therapists, at least every 4h.Results: There was no difference in any of these parameters between patients eventually requiring MV (four episodes) and those in whom mechanical ventilation was not necessary (six episodes).Conclusions: VC repeated measurements is a poor predictor of the need for further MV in MG patients. This can probably be ascribed to the erratic nature of MG, a disease whose course is largely influenced by many parameters (infection, treatment modifications, initiation of corticosteroid therapy, stress, psychological factors, etc.). Early admissions to the ICU of MG patients with respiratory dysfunction is thus recommended.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01711545
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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