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31. |
Partial liquid ventilation enhances surfactant phospholipid production |
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Critical Care Medicine,
Volume 24,
Issue 7,
1996,
Page 1252-1256
David M. MD Steinhorn,
Corinne L. MD Leach,
Bradley P. MD Fuhrman,
Bruce A. PhD Holm,
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摘要:
ObjectiveTo study the effect of partial liquid ventilation on phospholipid metabolism.DesignProspective, controlled laboratory study.SettingUniversity-affiliated animal research facility.SubjectsMature New Zealand white rabbits (n equals 17).InterventionsThe rabbits were sedated, anesthetized, and instrumented with tracheostomy and the insertion of an arterial catheter. The rabbits were sequentially assigned to receive conventional mechanical ventilation or partial liquid ventilation with Perflubron (18 mL/kg by bolus fill). Ventilator strategies were identical in both groups and consisted of an FIO2of 0.5, positive end-expiratory pressure of 4 cm H2O, effective tidal volume of 8 to 13 mL/kg, and rate to maintain PCO2of 30 to 40 torr (4.0 to 5.3 kPa). Phosphatidylcholine was labeled in vivo by injection of3H-methylcholine (25 micro Ci/kg iv). Ventilation was continued for 5,5 hrs.Measurements and Main ResultsWhen animals were killed, phosphatidylcholine was extracted from the total lung lavage and from the pulmonary parenchyma. After the separation of phospholipids by thin-layer chromatography, the3H activity was determined by liquid scintillation counting. Inorganic phosphorus was also determined to assess the enrichment of the phosphatidylcholine. The3H-phosphatidylcholine activity in the partial liquid ventilation treated- vs. control rabbits demonstrated a 53% increase (p equals .051) in the lavage and a 48% increase (p equals .013) in the parenchyma for a net 50% (p equals .012) total pulmonary increase. The phospholipid content of the partial liquid ventilation treated- vs. the control rabbits demonstrated a 78% increase (p equals .046).ConclusionsWe conclude that partial liquid ventilation with Perflubron appears to have no negative impact on phospholipid metabolism but rather enhances surfactant phospholipid synthesis and secretion.(Crit Care Med 1996; 24:1252-1256)
ISSN:0090-3493
出版商:OVID
年代:1996
数据来源: OVID
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32. |
Mediastinal tube placement in children with pneumomediastinumHemodynamic changes and description of technique |
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Critical Care Medicine,
Volume 24,
Issue 7,
1996,
Page 1257-1260
Krishna M. MBBS Turlapati,
Robert M. MD Spear,
Bradley M. MD Peterson,
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摘要:
ObjectiveTo describe the technique, hemodynamic response, and complication rate after the insertion of a percutaneous mediastinal tube for drainage of pneumomediastinum.DesignA combined retrospective and prospective study in mechanically ventilated children with pneumomediastinum.SettingMultidisciplinary pediatric intensive care unit at a children's hospital.PatientsThe medical records and chest radiographs of 25 (15 retrospective and 10 prospective) patients who had placement of a mediastinal tube for drainage of pneumomediastinum from 1990 to 1995 were reviewed. Hemodynamic data were collected prospectively in the ten consecutive children from January 1994 to April 1995.InterventionMediastinal tube placement: The subxyphoid area was cleansed with povidone-iodine and draped. An 18-gauge, thin-walled introducer needle was inserted 1 to 2 cm below the xyphoid process at an angle of 20 degrees from the anterior abdominal wall, directed at the substernal space. Either a 9-Fr or 11-Fr pericardiocentesis catheter was inserted over a wire and advanced to the third intercostal space. The catheter was secured and connected to 10 cm H2O suction, using a standard thoracostomy tube drainage device.Measurements and Main ResultsThe size of the mediastinal air column on a lateral chest radiograph was measured before and after placement of the mediastinal tube. The mean change in the size of the mediastinal air column was minus 1.6 cm (median minus 1.5, p less than .001). In the ten prospective patients, hemodynamic data were recorded immediately before and after placement of a mediastinal tube from previously placed arterial and central venous pressure catheters. The mean hemodynamic changes after the mediastinal tube placement were: heart rate minus 4 beats/min (median equals minus 1, p equals .14); systolic blood pressure 16 mm Hg (median equals 10, p equals .007); diastolic blood pressure 11 mm Hg (median equals 11, p equals .005); mean arterial pressure 12 mm Hg (median equals 8, p equals .005); and central venous pressure minus 2 mm Hg (median equals minus 1, p equals .04). In four patients with pulmonary artery thermodilution catheters, the mean increase in cardiac index immediately following placement of the mediastinal tube was 34%. No complications, including bleeding, cardiac puncture, or infection occurred.ConclusionsThese findings suggest that hemodynamic compromise commonly accompanies pneumomediastinum in children. Decompression of the mediastinal space and drainage of the pneumomediastinum, using this simple bedside technique for continuous drainage, can be performed rapidly and safely in children, resulting in immediate hemodynamic improvement, and allowing for continuous drainage.(Crit Care Med 1996; 24:1257-1260)
ISSN:0090-3493
出版商:OVID
年代:1996
数据来源: OVID
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33. |
An intrinsic positive end-expiratory pressure lung model, with and without flow limitation |
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Critical Care Medicine,
Volume 24,
Issue 7,
1996,
Page 1261-1265
Karl L. MD Yang,
Chen MD Wang,
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摘要:
ObjectiveTo design an intrinsic positive end-expiratory pressure (PEEP) lung model that has the property of air flow limitation.DesignMechanlcal lung model study of intrinsic PEEP.SettingLung models were set up in the research laboratory.InterventionsIntrinsic PEEP lung models were created with and without flow limitation. In the model with flow limitation, intrinsic PEEP was created by replacing a portion of the expiratory circuit with a collapsible Penrose tube and by placing this portion the circuit under water. The expiratory circuit became a part of the respiratory airway, with flow limitation occurring at the Penrose drain. In the model without flow limitation, intrinsic PEEP was generated with a fixed linear resistor, which was inserted in the expiratory circuit to produce a similar level of intrinsic PEEP. Multiple levels of external PEEP, both above and below the initial intrinsic PEEP, were applied.Measurements and Main ResultsAt each level of external PEEP, peak airway pressure, plateau airway pressure, isovolume air flow, internal lung pressure, and intrinsic PEEP were measured.Peak airway pressure, plateau pressure, and internal lung pressure were minimally affected if the external PEEP was less than the intrinsic PEEP in the lung model with flow limitation. Intrinsic PEEP was reduced with external PEEP. However, if intrinsic PEEP was induced without dynamic airway closure or flow limitation, any level of external PEEP caused an immediate increase in peak airway pressure, plateau airway pressure, and internal lung pressure and a decrease in isovolume flow. External PEEP has little effect on the levels of intrinsic PEEP.ConclusionsWe demonstrated two different models of an intrinsic PEEP lung model. The interactions between intrinsic PEEP and externally applied PEEP were different. The lung model with collapsible tube closely simulated the human respiratory system with flow limitation. This lung model may be useful for the future study of intrinsic PEEP and pulmonary mechanics.(Crit Care Med 1996; 24:1261-1265)
ISSN:0090-3493
出版商:OVID
年代:1996
数据来源: OVID
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34. |
Doxacurium-corticosteroid acute myopathyAnother piece to the puzzle |
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Critical Care Medicine,
Volume 24,
Issue 7,
1996,
Page 1266-1267
Paul E. MBBCh Marik,
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ISSN:0090-3493
出版商:OVID
年代:1996
数据来源: OVID
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35. |
Cisapride-induced dysrhythmia in a pediatric patient receiving extracorporeal life support |
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Critical Care Medicine,
Volume 24,
Issue 7,
1996,
Page 1268-1271
Robert MD Pettignano,
Robert C. MD Chambliss,
Edress PharmD Darsey,
Michael RN Heard,
Reese MD Clark,
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ISSN:0090-3493
出版商:OVID
年代:1996
数据来源: OVID
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36. |
Multiple Organ Dysfunction Score |
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Critical Care Medicine,
Volume 24,
Issue 7,
1996,
Page 1272-1272
John C. MD Marshall,
Deborah J. MD Cook,
Nicolas V. MD Christou,
Gordon R. MD Bernard,
Charles L. MD Sprung,
William J. MD Sibbald,
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ISSN:0090-3493
出版商:OVID
年代:1996
数据来源: OVID
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37. |
Role of Cerebral Perfusion Pressure in Acute Brain Trauma |
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Critical Care Medicine,
Volume 24,
Issue 7,
1996,
Page 1273-1274
Andrea MD Halliday,
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ISSN:0090-3493
出版商:OVID
年代:1996
数据来源: OVID
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38. |
Role of Cerebral Perfusion Pressure in Acute Brain Trauma |
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Critical Care Medicine,
Volume 24,
Issue 7,
1996,
Page 1274-1274
Michael J. MD Rosner,
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ISSN:0090-3493
出版商:OVID
年代:1996
数据来源: OVID
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39. |
Role of Cerebral Perfusion Pressure in Acute Brain Trauma |
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Critical Care Medicine,
Volume 24,
Issue 7,
1996,
Page 1275-1276
Julio MD Cruz,
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ISSN:0090-3493
出版商:OVID
年代:1996
数据来源: OVID
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40. |
Teaching Medical Students |
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Critical Care Medicine,
Volume 24,
Issue 7,
1996,
Page 1276-1276
David MD Kaufman,
Paul MBBCh Marik,
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ISSN:0090-3493
出版商:OVID
年代:1996
数据来源: OVID
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