摘要:

ObjectiveTo determine the role of nitric oxide as a mediator of lipopolysaccharide-induced myocardial depression.DesignProspective, controlled study.SettingUniversity research laboratory.SubjectsMale and female Hartley guinea pigs.InterventionsAnimals (n = 97) received intraperitoneal injections of either saline or Escherichia coli lipopolysaccharide (2 mg/kg). Some (n = 5) animals received two injections of dexamethasone before lipopolysaccharide. Left atria were harvested 6 hrs (n = 20) or 16 hrs (n = 77) later and placed in a tissue bath with Krebs-Henseleit buffer. Contractile tension was measured in the presence or absence of two inhibitors of nitric oxide synthase (NG-nitroarginine [NNA] or aminoguanidine). Atrial and serum nitrite/nitrate and atrial cyclic guanosine monophosphate (cGMP) concentrations were assayed.Measurements and Main ResultsLipopolysaccharide caused significant atrial contractile depression at 16 hrs but not 6 hrs compared with control animals. Neither NNA nor aminoguanidine reversed the depression in atrial function. In contrast, exposure of control atria to NNA worsened contractile function. There were no significant differences between control and lipopolysaccharide-treated animals in atrial and serum nitrite/nitrate and atrial cGMP concentrations.ConclusionsNitric oxide does not mediate lipopolysaccharide-induced myocardial depression in this animal model. Basal concentrations of nitric oxide may be important since NNA worsened contractile function in control atria. (Crit Care Med 1997; 25:684-688)

ISSN:0090-3493    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

ObjectivesTo quantify CO2removal using an extracorporeal low-resistance membrane gas exchanger placed in an arteriovenous shunt and evaluate its effects on the reduction of ventilatory volumes and airway pressures during severe respiratory failure induced by smoke inhalation injury.DesignProspective study.SettingResearch laboratory.SubjectsAdult female sheep (n = 5).InterventionsAnimals were instrumented with femoral and pulmonary arterial catheters and underwent an LD50cotton smoke inhalation injury via a tracheostomy under halothane anesthesia. Twenty-four hours after smoke inhalation injury, the animals were reanesthetized and systemically heparinized for cannulation of the left carotid artery and common jugular vein to construct a simple arteriovenous shunt. A membrane gas exchanger was interposed within the arteriovenous shunt, and blood flow produced by the arteriovenous pressure gradient was unrestricted at the time of complete recovery from anesthesia. CO2removal by the gas exchanger was measured as the product of the sweep gas flow (FIO2of 1.0 at 2.5 to 3.0 L/min) and the exhaust CO2content measured with an inline capnometer. CO2removed by the animal's lungs was determined by the expired gas CO2content in a Douglas bag. We made stepwise, 20% reductions in ventilator support hourly. We first reduced the tidal volume to achieve a peak inspiratory pressure of <30 cm H2O, and then we reduced the respiratory rate while maintaining normocapnia. PaO2was maintained by adjusting the FIO2and the level of positive end-expiratory pressure.Measurements and Main ResultsMean blood flow through the arteriovenous shunt ranged from 1154 +/- 82 mL/min (25% cardiac output) to 1277 +/- 38 mL/min (29% cardiac output) over the 6-hr study period. The pressure gradient across the gas exchanger was always <10 mm Hg. Maximum arteriovenous CO2removal was 102.0 +/- 9.5 mL/min (96% of total CO2production), allowing minute ventilation to be reduced from 10.3 +/- 1.4 L/min (baseline) to 0.5 +/- 0.0 L/min at 6 hrs of arteriovenous CO2removal while maintaining normocapnia. Similarly, peak inspiratory pressure decreased from 40.8 +/- 2.1 to 19.7 +/- 7.5 cm H2O. PaO213.3 kPa) at maximally reduced ventilator support. Mean arterial pressure and cardiac output did not change significantly as a result of arteriovenous shunting.ConclusionsExtracorporeal CO2removal using a low-resistance gas exchanger in a simple arteriovenous shunt allows significant reduction in minute ventilation and peak inspiratory pressure without hypercapnia or the complex circuitry and monitoring required for conventional extracorporeal membrane oxygenation. Arteriovenous CO2removal can be applied as an easy and cost-effective treatment to minimize ventilator-induced barotrauma and volutrauma during severe respiratory failure. (Crit Care Med 1997; 25:689-695)

ISSN:0090-3493    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

ObjectivesTo determine the exposure to, and evaluate the potential toxicity from, the plasticlzer, di(2-ethylhexyl)phthalate (DEHP) during extracorporeal membrane oxygenation (ECMO) therapy.DesignProtocol 1 consisted of a prospective comparison of three ECMO circuit designs in vitro. Protocol 2 consisted of a prospective, comparative clinical study evaluating DEHP plasma concentrations in ECMO vs. non-ECMO patients with respiratory failure.SettingNeonatal intensive care unit at The Children's National Medical Center, Washington, DC.PatientsIn protocol 2, 28 consecutive term infants were referred for ECMO therapy. Eighteen infants required ECMO; ten control patients received conventional ventilation and improved without ECMO.InterventionsIn protocol 1, three ECMO circuit designs were primed in vitro with normal saline, albumin, and human blood, which was maintained at 37 degrees C and recirculated at 400 mL/min for 48 hrs. Plasma samples were obtained at time 0, 1 hr, and every 6 hrs. In protocol 2, ventilatory and cardiovascular management of the patients in the study was conducted by the attending physician. Patients were placed on ECMO when they met the institutional criteria for ECMO therapy. Daily plasma concentrations for DEHP were collected until 3 days after decannulation from bypass in the ECMO group. Control patients were sampled daily until extubation. Evidence of cardiac, liver, or lung toxicity was evaluated by Chest Radiographic Scores, liver function studies, and echocardiograms obtained on day 1, day 3, and the day of decannulation in the ECMO group, or at the time of extubation in the control group. Sedation, blood product transfusions as indicated, antibiotics, and hyperalimentation were administered to all patients.Measurements and Main ResultsAll DEHP plasma concentrations were measured by gas chromatography. In protocol 1, three circuits were studied: circuit A (small surface area); circuit B (larger surface area); and circuit C (surface area of A but with heparin-bonded tubing in the circuit). DEHP leached from circuit A at 0.32 +/- 0.12 micro g/mL/hr, compared with 0.57 +/- 0.14 micro g/mL/hr from circuit B (p < .05). This amount of DEHP extrapolates in the ECMO patient to a potential exposure of 20 to 70 times that exposure from other medical devices or procedures, such as transfusions, dialysis, or short-term cardiopulmonary bypass. Circuit C showed almost no leaching from the circuit; DEHP concentrations decreased at a rate of 0.2 +/- 0.04 micro g/mL/hr. In protocol 2, DEHP was undetected in the control patients. DEHP concentrations in ECMO patients were greater in the early course of ECMO. However, most patients cleared this compound from the plasma before decannulation. In contrast to the in vitro results in protocol 1, the average highest concentration at any time on bypass was 8.3 +/- 5.7 micro g/mL or 2 mg/kg.ConclusionsDEHP leaches from ECMO circuits, with potential exposure concentrations related to the surface area of the tubing in the ECMO circuit. Heparin bonding of the tubing eliminates this risk. Although significant concentrations of DEHP leach from the nonheparin-bonded circuits over time, our in vivo studies showed that the DEHP plasma concentrations were less than the previously reported values and do not correlate with any observable short-term toxicity. This compound may be either efficiently metabolized by the newborn, or redistributed into various tissues. Although signs of toxicity were not found in this study, long-term complications from chronic exposure to DEHP have not been determined. (Crit Care Med 1997; 25:696-703)

ISSN:0090-3493    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

ObjectiveTo assess the relationship between the experience of pediatric housestaff and tests ordered on infants in the neonatal intensive care unit (ICU).DesignProspective, cohort study over one full academic year.SettingOne academic Level III neonatal intensive care nursery.PatientsData were collected prospectively on all 785 infants admitted to the neonatal ICU from July 1993 to June 1994. These infants were cared for by 14 different categorical pediatric housestaff.Measurements and Main ResultsOur neonatal ICU has either a resident or an intern on-call by himself/herself at night, affording us a natural setting to compare intern vs. resident test ordering. The outcomes of interest were number of arterial blood gases, radiographs, and electrolytes ordered per infant by the on-call pediatric houseofficer, as tabulated the morning after the call night. Control variables included the severity-of-illness of the individual infant (using the Neonatal Therapeutic Intervention Scoring System), the workload of the houseofficer (number of patients, number of admissions), and supervision (rounding frequency and on-call attending). Controlling for the severity-of-illness of the infant, the workload on the call night, and supervision with multiple linear regression, we found that interns ordered significantly (p = .02) greater numbers of arterial blood gases per infant than residents, amounting to some 0.33 blood gases per infant per call night (3.22 vs. 2.89 arterial blood gases per infant per night). This increase of 0.33 blood gases per infant amounts to interns ordering $169 more arterial blood gases per call night at our institution. There was no difference between interns and residents in ordering radiographs or electrolytes.ConclusionInterns order significantly more arterial blood gases per infant than junior and senior residents on-call in the neonatal ICU. Additional study is required to see if the experience of housestaff is associated with a broader array of neonatal outcomes, such as morbidity and mortality. (Crit Care Med 1997; 25:704-709)

ISSN:0090-3493    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1997

数据来源: OVID