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

摘要:

ObjectiveTo compare a practice of protocol-directed weaning from mechanical ventilation implemented by nurses and respiratory therapists with traditional physician-directed weaning.DesignRandomized, controlled trial.SettingMedical and surgical intensive care units in two university-affiliated teaching hospitals.PatientsPatients requiring mechanical ventilation (n = 357).InterventionsPatients were randomly assigned to receive either protocol-directed (n = 179) or physician-directed (n = 178) weaning from mechanical ventilation.Measurements and Main ResultsThe primary outcome measure was the duration of mechanical ventilation from tracheal intubation until discontinuation of mechanical ventilation. Other outcome measures included need for reintubation, length of hospital stay, hospital mortality rate, and hospital costs. The median duration of mechanical ventilation was 35 hrs for the protocol-directed group (first quartile 15 hrs; third quartile 114 hrs) compared with 44 hrs for the physician-directed group (first quartile 21 hrs; third quartile 209 hrs). Kaplan-Meier analysis demonstrated that patients randomized to protocol-directed weaning had significantly shorter durations of mechanical ventilation compared with patients randomized to physician-directed weaning (chi squared = 3.62, p = .057, log-rank test; chi squared = 5.12, p = .024, Wilcoxon test). Cox proportional-hazards regression analysis, adjusting for other covariates, showed that the rate of successful weaning was significantly greater for patients receiving protocol-directed weaning compared with patients receiving physician-directed weaning (risk ratio 1.31; 95% confidence interval 1.15 to 1.50; p = .039). The hospital mortality rates for the two treatment groups were similar (protocol-directed 22.3% vs. physician-directed 23.6%; p = .779). Hospital cost savings for patients in the protocol-directed group were $42,960 compared with hospital costs for patients in the physician-directed group.ConclusionProtocol-guided weaning of mechanical ventilation, as performed by nurses and respiratory therapists, is safe and led to extubation more rapidly than physician-directed weaning. (Crit Care Med 1997; 25:567-574)

ISSN:0090-3493    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

ObjectivesTo determine if vecuronium doses individualized by peripheral nerve stimulation are lower than those doses chosen by standard clinical techniques; and to determine whether patients monitored by peripheral nerve stimulation exhibit shorter recovery times and less prolonged neuromuscular blockade after discontinuation of vecuronium than control patients.DesignA prospective, randomized, controlled, single-blind trial.SettingTwo ten-bed medical intensive care units of a 937-bed tertiary care, not-for-profit, teaching hospital and health system.PatientsMechanically ventilated patients requiring continuous neuromuscular blockade as part of their therapy.InterventionsAfter obtaining written, informed consent and baseline neurologic examinations, patients were randomized to treatment, where dosing was individualized by peripheral nerve stimulation or standard clinical assessment. Doses in the peripheral nerve stimulation group were adjusted to 90% blockade (Train-of-Four of 1/4). The standard clinical dosing group received doses individualized to clinical response by the medical team (blinded to Train-of-Four). Differences between groups were evaluated by Wilcoxon matched-pairs signed rank test.Measurements and Main ResultsA total of 77 patients (35 standard clinical patients vs. 42 peripheral nerve stimulation patients) were enrolled in the study. Despite no difference in initial doses and time to reach 90% blockade or clinical response between groups, the peripheral nerve stimulation group used less drug than the standard clinical group (0.040 +/- 0.028 vs. 0.070 +/- 0.030 mg/kg/hr, respectively, p = .001). The total cumulative amount of vecuronium for the episode of paralysis was greater in the control group (285.8 +/- 246.6 vs. 137.1 +/- 106.4 mg, p = .001). The peripheral nerve stimulation group recovered neuromuscular function (relative risk of 1.85, with 95% confidence interval [CI] of 1.02-3.35, p = .039) and spontaneous ventilation (relative risk of 1.86, 95% CI 1.00-3.45, p = .047) faster than the control group. In patients, adjusting for renal dysfunction, the likelihood of a faster recovery in the peripheral nerve stimulation group increased for neuromuscular function (relative risk of 1.89, 95% CI of 1.07-3.32, p = .018) and spontaneous ventilation (relative risk of 2.27, 95% CI of 1.23-4.21, p = .019). Patients with combined renal and liver failure similarly demonstrated a faster recovery in the peripheral nerve stimulation group. The recovery was affected to a lesser extent by adjusting for concurrent aminoglycoside and corticosteroid administration.ConclusionsUse of peripheral nerve stimulation for monitoring the degree of blockade and adjusting drug doses in continuously paralyzed critically ill medical patients results in lower doses of vecuronium to maintain a desired depth of paralysis, and allows a faster recovery of neuromuscular function and spontaneous ventilation. (Crit Care Med 1997; 25:575-583)

ISSN:0090-3493    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

ObjectiveTo determine if, and by what mechanisms, inhaled nitric oxide attenuates acute lung injury in a porcine model of adult respiratory distress syndrome induced by Gram-negative sepsis.DesignNonrandomized, controlled study.SettingLaboratory at a university medical center.SubjectsThirty pathogen-free Yorkshire swine (15 to 20 kg).InterventionsFour groups of swine were anesthetized, mechanically ventilated, and studied for 5 hrs. Both control-nitric oxide and septic-nitric oxide animals received inhaled nitric oxide at 20 parts per million throughout the study. Control (n = 10) and control-nitric oxide (n = 5) animals received a 1-hr infusion of sterile saline. Sepsis was induced in septic (n = 10) and septic-nitric oxide (n = 5) animals with a 1-hr intravenous infusion of live Pseudomonas aeruginosa.Measurements and Main ResultsUntreated septic animals developed a progressive decrease in PaO2that was prevented in septic-nitric oxide animals (73 +/- 4 vs. 214 +/- 23 torr [9.7 +/- 0.5 vs. 28.5 +/- 3.1 kPa], respectively, at 5 hrs, p < .05). Untreated septic animals showed a significant increase in bronchoalveolar lavage protein and neutrophil count at 5 hrs, compared with the baseline value, indicating acute lung injury. Septic-nitric oxide animals showed no significant increase in these parameters. Peripheral blood neutrophils from untreated septic animals and septic-nitric oxide animals exhibited significant (p < .05) up-regulation of CD18 receptor expression and oxidant activity (10.5 +/- 0.9 and 5.0 +/- 0.9 nmol of superoxide anion/106neutrophils/10 mins, respectively) compared with both control and control-nitric oxide animals (3.0 +/- 0.6 and 2.6 +/- 0.2 nmol of superoxide anion/10 sup 6 neutrophils/10 mins, respectively). Also, priming for the oxidant burst at 5 hrs was decreased by 50% in septic-nitric oxide animals compared with untreated septic animals. Both untreated septic and septic-nitric oxide animals showed a significant increase in pulmonary arterial pressure at 30 mins (47.5 +/- 2.4 and 51.0 +/- 3.0 mm Hg, respectively), followed by a progressive decrease (32.8 +/- 2.6 and 31.3 +/- 5.4 mm Hg, respectively, at 5 hrs). Both of these changes were significant (p < .05) compared with baseline values and compared with the control groups. There was no significant difference in pulmonary arterial pressure or systemic arterial pressure at any time between untreated septic and septic-nitric oxide animals.ConclusionsThese results demonstrate that inhaled nitric oxide attenuates alveolar-capillary membrane injury in this porcine model of Gram-negative sepsis but does not adversely affect systemic hemodynamics. The data suggest that inhaled nitric oxide preserves alveolar-capillary membrane integrity by the following means: a) inhibiting transendothelial migration of activated, tightly adherent neutrophils; and b) possibly by attenuating the neutrophil oxidant burst. (Crit Care Med 1997; 25:584-593)

ISSN:0090-3493    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

ObjectiveTo quantitate gelsolin concentrations in serum of patients with a variety of conditions involving actin release into the circulation.DesignProspective evaluation of sera on consecutive patients.SettingMetropolitan county hospital.PatientsNinety hospital patients with a variety of well-characterized diseases.InterventionsNone.Measurements and Main ResultsSera were studied from patients with acute liver failure (n = 18), chronic hepatitis (n = 17), cirrhosis of varying etiology (n = 17), pancreatitis (n = 10), acute myocardial infarction (n = 10), myonecrosis due either to polymyositis or crush injuries (n = 12), and septic shock (n = 6); results were compared with sera from healthy individuals (n = 25). Gelsolin was quantified by Western blotting with monoclonal anti-gelsolin and laser densitometry.Significant reductions in mean gelsolin concentrations compared with healthy controls were observed in patients with acute liver failure (47%), myocardial infarction (69%), sepsis (51%), and myonecrosis (66%). An inverse correlation was observed between gelsolin concentration and severity of illness, as indicated by the magnitude of serum enzyme concentrations.ConclusionsGelsolin depletion occurs in a variety of tissue injury syndromes. Depletion of actin-scavenger capacity in the presence of continued actin release may affect outcome in situations of severe organ damage. (Crit Care Med 1997; 25:594-598)

ISSN:0090-3493    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

ObjectiveTo develop and evaluate a new method for blood volume measurements using hydroxyethyl starch as a dilution marker.DesignLaboratory and clinical investigation.SettingNeurosurgical operating rooms and anesthesiological laboratories of a university hospital.PatientsTwelve patients who underwent a neurosurgical operation.InterventionsAnesthesia and operations were carried out by physicians who were not involved in the study. In addition, blood samples were drawn from 50 volunteers.Measurements and Main ResultsBlood volume measurements by the hydroxyethyl starch method were validated in vivo by comparison with a conventional carbon monoxide technique. Patients were intravenously injected with hydroxyethyl starch (100 mL) and received simultaneously an injection of carbon monoxide (50 mL) into a closed-circuit ventilation system. Blood samples obtained before and 5 mins after injection were analyzed for carboxyhemoglobin and glucose plasma concentrations after acidic hydrolysis of hydroxyethyl starch. Blood volume was calculated from the difference between glucose concentrations measured after hydrolysis in the plasma, before and after the addition of hydroxyethyl starch.In vitro, the hydroxyethyl starch method had an error and a precision of [approximately]2%. In vivo, simultaneous measurements of blood volume using hydroxyethyl starch and carbon monoxide demonstrated a high correlation (r2= .96, p < .001) between these methods. The mean difference between the two methods relative to their average value was 1.0 +/- 3.5%; the bias was 52.3 mL, and the 95% confidence interval was -64.0 to +168.7 mL.ConclusionsBlood volume determination by the hydroxyethyl starch method is accurate and rapid and may enhance perioperative monitoring of fluid and blood therapy. (Crit Care Med 1997; 25:599-606)

ISSN:0090-3493    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

ObjectivesTo determine and compare the respective concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, soluble TNF receptors, nitrite/nitrate (NO2sup -/NO3sup -), and procalcitonin in the plasma of patients with septic shock, cardiogenic shock, and bacterial pneumonia without shock; and to assess the predictive value of these mediators in defining patients with septic shock.DesignCohort study, comparing normal volunteers (controls) and patients with septic shock, cardiogenic shock, and bacterial pneumonia.SettingA collaborative study among an intensive care unit, an emergency room, and three research laboratories.PatientsMediators were measured at various times in 15 patients with septic shock (during the shock phase and during the recovery phase), in seven patients with cardiogenic shock during the shock phase, and in seven patients with severe bacterial pneumonia on day 1 of admission.InterventionsBlood samples were collected at various times during the course of the disease.Measurements and Main ResultsTNF-alpha values were highest in the acute phase of septic shock (53 to 131 pg/mL during septic shock), while patients with bacterial pneumonia had intermediate concentrations (32 pg/mL). TNF-alpha concentrations were normal in patients with cardiogenic shock. IL-6 concentrations were highest in patients with acute septic shock (85 to 385 pg/mL). However, in contrast to TNF-alpha concentrations, IL-6 concentrations were normal in patients with bacterial pneumonia and increased in patients with cardiogenic shock (78 pg/mL). Soluble TNF receptors were increased in all three groups vs. controls, with the highest increase in patients with septic shock. NO2sup -/NO3sup - concentrations were highest (72 to 140 mM) in patients with septic shock, and were <40 mM in the other groups of patients. Procalcitonin concentrations were only markedly increased in patients with septic shock (72 to 135 ng/mL, compared with [approximately] 1 ng/mL in the three other groups). The best predictive value for septic shock was found to be the measurements of NO2sup -/NO3sup - and procalcitonin concentrations.ConclusionsThese observations showed that increase of proinflammatory cytokines was a consequence of inflammation, not of shock. In this study comparing various shock and infectious states, measurements of NO2sup -/NO3sup - concentration and procalcitonin concentration represented the most suitable tests for defining patients with septic shock. (Crit Care Med 1997; 25:607-613)

ISSN:0090-3493    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

ObjectiveTo identify areas requiring the most urgent improvement in the intensive care unit (ICU); and to accurately determine the positive predictive value of routine critical care patient monitoring alarms, as well as the common causes for false-positive alarms.DesignProspective, observational study.SettingA multidisciplinary ICU in a university-affiliated children's hospital (excluding children with primary heart disease).InterventionsThe occurrence rate, cause, and appropriateness of all alarms from tracked monitors were recorded by a trained observer and validated by the bedside nurse over a 10-wk period for a single bedspace at a time.Measurements and Main ResultsAfter 298 monitored hrs, 86% of a total 2,942 alarms were found to be false-positive alarms, while an additional 6% were classified as clinically irrelevant true alarms. Only 8% of all alarms tracked during the study period were determined to be true alarms with clinical significance. Alarms were also classified according to whether they were clearly associated with a "patient intervention" (18%), were clearly not associated with a patient intervention (74%), or had unclear association to interventions (8%). While 11% of "nonpatient intervention" alarms were clinically significant true alarms, only 2% of "patient intervention" alarms were so. Positive predictive values for the various devices ranged from <1% for the pulse oximeter's heart rate signal to 74% for the arterial catheter's mean systemic blood pressure signal during periods free from patient interventions. The pulse oximeter caused false-positive alarms most frequently, with common reasons being bad data format/bad connection and poor contact.ConclusionEfforts to develop intelligent monitoring systems have more potential to deliver significantly improved patient care by initially targeting especially weak areas in ICU monitoring, such as pulse oximetry reliability. (Crit Care Med 1997; 25:614-619)

ISSN:0090-3493    

出版商:OVID    

年代:1997

数据来源: OVID