摘要:

ObjectiveTo determine the frequency, etiology, and risk factors of ventilator-associated pneumonia (VAP) and purulent tracheobronchitis (TBX) in patients who have undergone heart surgery. To study the predictive role of systematic surveillance cultures.DesignProspective study.SettingHeart surgery intensive care unit.PatientsIntubated heart surgical patients.InterventionsSystematic tracheal aspirate and protected brush catheter cultures of all intubated patients.Measurements and Main ResultsStudied were the frequency of lower respiratory tract infection in ventilated patients and the role of surveillance cultures. The frequency of VAP was 7.87% (34.5 per 1,000 days of mechanical ventilation), and the criteria for purulent tracheobronchitis was fulfilled by 8.15% of patients (31.13 per 1,000 days of mechanical ventilation). After multivariate analysis, the variables independently associated with the development of respiratory tract infection were central nervous system disorder (relative risk [RR] = 4.7), ulcer disease (RR = 3.6), New York Heart Association score ≥3 (RR = 4), need for mechanical circulatory support (RR = 6.8), duration of mechanical ventilation >96 hrs (RR = 12.3), and reintubation (RR = 63.7). Mortality in our study was as follows: VAP patients, 57.1%; purulent tracheobronchitis patients, 20.7%; colonized patients, 11.5%; and noncolonized patients, 1.6%. Regular surveillance cultures were taken from all ventilated patients to assess the anticipative value of the cultures in predicting respiratory tract infection. A total of 1,626 respiratory surveillance samples were obtained. Surveillance cultures effectively predicted only one episode of VAP and one of tracheobronchitis.ConclusionsPatients undergoing heart surgery have a high frequency of VAP. VAP is associated with a poor prognosis. In this study, surveillance cultures failed as an anticipative diagnostic method.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveUp to 20% of patients do not show improvements in health-related quality of life (HRQL) after cardiac surgery, despite apparently successful surgical procedures. We sought to determine whether failed improvements in HRQL after cardiac surgery are associated with the development of traumatic memories and chronic stress states as a result of high perioperative stress exposure.DesignProspective cohort study.SettingA 10-bed cardiovascular intensive care unit of a tertiary care university hospital.PatientsA total of 148 cardiac surgical patients.InterventionsNone.Measurements and Main ResultsThe patients were evaluated for traumatic memories from postoperative treatment in the cardiovascular intensive care unit (defined as the subjective recollection of pain, respiratory distress, anxiety/panic, and nightmares), symptoms of chronic stress, including those of posttraumatic stress disorder, and HRQL preoperatively (at baseline) and at 6 months after cardiac surgery. A state of chronic stress was defined as the development of posttraumatic stress disorder at 6 months after surgery. Factors predicting the decline in HRQL were determined by multivariable linear regression. Twenty-seven patients (18.2%) had posttraumatic stress disorder at 6 months after cardiac surgery; seven of these patients (4.8%) had evidence of preexisting posttraumatic stress disorder before undergoing cardiac surgery. Patients with new posttraumatic stress disorder at 6 months after cardiac surgery had a significantly higher number of traumatic memories from postoperative treatment in the cardiovascular intensive care unit (p= .01). A multiple regression model included the number of traumatic memories from the intensive care unit and stress symptom scores at 6 months after heart surgery as predictors for variations in physical HRQL outcome scores (R2= .30,p< .04). Stress symptom scores were the most significant predictors of mental health HRQL outcomes (R2= .52,p< .01).ConclusionsExposure to high stress in the cardiovascular intensive care unit can have negative effects on HRQL outcomes of cardiac surgery.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveTo describe characteristics of patients transferred from outside hospitals to a tertiary medical intensive care unit and to identify patient-level and system-level prognostic factors.DesignRetrospective cohort study.SettingTertiary university hospital.PatientsWe studied 3,347 patients who were transferred to the medical intensive care unit from outside hospitals from January 1990 through September 1999.InterventionsNone.Measurements and Main ResultsData collected included patient demographics, insurance type, discharge diagnoses, length of stay, mortality, admitting service, and distance traveled. The Charlson Comorbidity Score was used to adjust for comorbidity and the diagnostic related group risk level for risk of adverse outcome. Multivariate logistic models of early mortality (<72 hrs) and overall hospital mortality rate were developed. The most common major diagnostic categories included neurologic (10%), respiratory (10%), digestive diseases (10%), and drug overdose (10%). Most patients (70%) were transferred from >60 miles away. Mean medical intensive care unit length of stay was 5.3 days vs. 3.9 days for nontransfer patients. Transfer patients accounted for 49% of medical intensive care unit admits and 56% of intensive care unit patient-days. The overall mortality rate for transfer patients to the medical intensive care unit was 25% (95% confidence interval, 23–26), significantly higher than the 21% (95% confidence interval, 19–22) mortality rate among those admitted directly. Independent prognostic factors for early death (<72 hrs) included male gender, summer season, admitting service, diagnostic related group level, Charlson Comorbidity Score, insurance type, and major diagnostic category. Independent prognostic factors for overall hospital mortality rate included length of stay, medical complication, distance traveled, insurance type, and major diagnostic category.ConclusionsInterhospital transfers to the medical intensive care unit are patients at high risk for mortality and other adverse outcomes. System-level and patient-level characteristics influence both early and overall hospital mortality rates. These variables should be considered when risk stratifying medical intensive care unit patients and in studying outcomes of care.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveTo examine the mitochondrial function in the myocardium after hemorrhagic shock and reperfusion and to evaluate the protective effect of urinary trypsin inhibitor (UTI) on mitochondria.DesignAnimal experiment.SettingUniversity research laboratory.SubjectsWistar rats receiving 50,000 units/kg/hr of UTI (n = 27; UTI group) and control rats (n = 26; control group).InterventionsRats were subjected to low-perfusion ischemia with the left ventricular systolic pressure maintained at 50 mm Hg for 60 mins by bleeding, followed by a 60-min reperfusion by transfusion of shed blood. UTI was infused continuously from 10 mins before bleeding. Cardiac function was measured before bleeding, after bleeding, and after transfusion; at each determination point, the myocardial contents of adenosine triphosphate (ATP), creatine phosphate (P-Cr), pyruvate (Pyr), and lactate (Lac) were measured enzymatically. The cytosolic phosphorylation potential (PP) as well as the redox potential of the oxidized form of nicotinamide adenine dinucleotide/reduced form of nicotinamide adenine dinucleotide couple in mitochondria (EhNAD+/NADH) and change of Gibbs free energy in ATP hydrolysis (&Dgr;GATP hydrolysisenergy) were calculated.Measurements and Main ResultsCardiac function decreased during hemorrhagic shock but improved significantly in the UTI group after transfusion compared with the control group. Lac and the Lac/Pyr ratio were significantly lower in the UTI group than in the control group after transfusion. ATP and P-Cr were significantly higher in the UTI group than in the control group after transfusion. PP (×103M−1), EhNAD+/NADH(x− 1 mV), and &Dgr;GATP hydrolysis(x− 1 kcal/mol) were 1.9 ± 0.4, 266 ± 4, and 9.7 ± 0.2, respectively, in the control group and 4.0 ± 0.9, 274 ± 5 and 13.0 ± 0.2, respectively, in the UTI group after transfusion (p< .001,p< .001, andp< .001, respectively).ConclusionsIn reperfusion after hemorrhagic shock, oxidative phosphorylation in myocardial mitochondria is impaired and energy production remains reduced, even after reperfusion. UTI contributed to the recovery of cardiac function after reperfusion, probably by reducing the severity of mitochondrial dysfunction during a state of shock and by maintaining energy production.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveMany studies have investigated the protective role of positive end-expiratory pressure (PEEP) on ventilator-induced lung injury. Most assessed lung injury in protocols involving different ventilation strategies applied for the same length of time. This study, however, set out to investigate the protective role of PEEP with respect to the time needed to reach similar levels of lung injury.DesignProspective, randomized laboratory animal investigation.SettingThe University Laboratory of Ospedale Maggiore, Milano, IRCCS.SubjectsAnesthetized, paralyzed, and mechanically ventilated Sprague-Dawley rats.InterventionsThree groups of five Sprague-Dawley rats were ventilated using zero end-expiratory pressure ZEEP (PEEP of 0 cm H2O) and PEEP of 3 and 6 cm H2O and a similar index of lung overdistension (Pawp/P100≅ 1.1; where Pawpis peak airway pressure and P100is the pressure corresponding to total lung capacity). To obtain this, tidal volume was reduced depending on the PEEP. To reach similar levels of lung injury, we measured respiratory system elastance while ventilating the animals and killed them when respiratory system elastance was 150% of baseline. Once target respiratory system elastance was reached, the lung wet-to-dry ratio was obtained.ResultsRats were ventilated with comparable high airway pressure (Pawpof 42.8 ± 3.1, 43.5 ± 2.6, and 46.2 ± 4.4, respectively, for PEEP 0, 3, and 6) obtaining similar overdistension (Pawp/P100− index of overdistension: 1.17 ± 0.2, 1.06 ± 0.1, and 1.19 ± 0.2). The respiratory system elastance target was reached and wet-to-dry ratio was not different in the three groups, suggesting a similar degree of lung damage. The time taken to achieve the target respiratory system elastance was three times longer with PEEP 3 and 6 (55 ± 14 mins and 60 ± 17) as compared with zero end-expiratory pressure (18 ± 3 mins,p< .001).ConclusionThese findings confirm that PEEP is protective against ventilator-induced lung injury and may enable the clinician to “buy time” in the progression of lung injury.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveTo compare the effects of fenoldopam and dopamine on gastric mucosal and systemic oxygenation, and to identify the receptors involved.DesignRandomized controlled animal study.SettingUniversity research department of experimental anesthesiology.SubjectsSeven anesthetized dogs with chronically implanted ultrasound flow probes around the pulmonary artery for continuous measurement of cardiac output.InterventionsOn different days, the dogs received in random order either the selective DA1-agonist fenoldopam (0.1 and 1.0 &mgr;g·kg−1·min−1, with or without DA1-blocker pretreatment), dopamine (2.5 and 5.0 &mgr;g·kg−1·min−1, with or without &agr;1-blocker pretreatment), or saline (control).Measurements and Main ResultsWe continuously measured regional microvascular hemoglobin oxygen saturation (&mgr;HbO2) in gastric mucosa by reflectance spectrophotometry, and systemic oxygen delivery. Fenoldopam increased gastric mucosal &mgr;HbO2by approximately 20%, and this effect was prevented by selective DA1-receptor blockade. In contrast, dopamine neither alone nor during &agr;1-blockade altered &mgr;HbO2. With respect to systemic measures of oxygen transport, fenoldopam had negligible effects, whereas dopamine (with and without &agr;1-blocker pretreatment) dose-dependently increased cardiac output and systemic oxygen delivery by approximately 30%.ConclusionsFenoldopam dose-dependently increased microvascular oxygenation of the gastric mucosa without changing systemic oxygen transport, i.e., this drug actedselectivelyon the splanchnic mucosa. The increase in gastric mucosal oxygenation was mediated by DA1-receptors. In contrast, dopamine markedly increased systemic oxygen transport, but did not affect microvascular oxygenation of gastric mucosa. This lacking effect on gastric mucosal oxygenation was not caused by &agr;1-mediated vasoconstriction. The regional effects of both catecholamines could not be deduced from systemic hemodynamics and oxygenation.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveTo compare gas exchange with heliox and oxygen-enriched air during high-frequency oscillatory ventilation, while controlling for tidal volume, in a pediatric swine model of acute lung injury. We hypothesized that when tidal volume delivery is held constant, heliox does not alter gas exchange.DesignRandomized, crossover trial.SettingUniversity animal research laboratory.SubjectsTen swine (4.4–5.4 kg).InterventionsAcute lung injury (A-a gradient of >300 mm Hg) was created using repeated saline lavage during conventional mechanical ventilation. The animals were then administered high-frequency oscillatory ventilation and ventilated with 60% oxygen/40% helium and 60% oxygen/40% nitrogen in a randomized, crossover trial. When changing gas mixtures within each animal, mean airway pressure (Paw = 16.8 ± 0.3 cm H2O) and frequency (10 Hz) were held constant. Oscillation amplitude (&Dgr;P) was adjusted to maintain constant tidal volume delivery as measured by respiratory inductive plethysmography. Next, the animals were ventilated with 40% oxygen/60% helium and 40% oxygen/60% nitrogen in a randomized crossover trial, again controlling for tidal volume.Measurements and Main ResultsGas exchange was assessed by arterial blood gas analysis after ventilation with each gas mixture. We demonstrated no significant difference in Paco2or Pao2between the heliox and oxygen-enriched air with either the 40% or 60% oxygen mixtures. The oscillation amplitude required to achieve the same tidal volume delivery was significantly less with heliox.ConclusionsWe conclude that if tidal volume delivery is maintained constant, heliox does not alter gas exchange when compared with oxygen-enriched air. However, to achieve the same tidal volume delivery, a lower oscillation amplitude is required with heliox. The clinical benefit of heliox administration during high-frequency oscillatory ventilation has yet to be determined. Possible advantages of heliox include improved ventilation of larger patients when approaching the power limitations of the Sensormedics 3100A oscillator and a potential reduction in the oscillation amplitude delivered to the more proximal gas exchange units.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveTo investigate the role of endothelial cyclooxygenase in the antiaggregatory effect of nitric oxide, and to investigate the significance of the time span between contact of nitric oxide and platelets and laboratory evaluation by platelet aggregation.DesignProspective, controlled,in vitrostudy.SettingResearch laboratory of a university hospital.ParticipantsThree healthy volunteers.InterventionsIncubation of platelets with different concentrations (30 &mgr;M, 100 &mgr;M, 500 &mgr;M, 1000 &mgr;M) of the nitric oxide-donorS-nitroso-N-acetyl-d,l-penicillamine (SNAP) for varying incubation times (0 hrs, 1 hr, 2 hrs, 4 hrs) with and without endothelial cells. Induction of platelet aggregation with adenosine diphosphate. Inhibition of the effect of SNAP by 100 &mgr;M of the guanylate cyclase inhibitor 1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one (ODQ). Inhibition of prostacyclin production by endothelial cells with COX inhibitors acetyl salicylic acid (1 mM) and indomethacin (10 &mgr;M).Measurements and Main ResultsIncubation with endothelial cells (= controls) had no effect on platelet aggregation. Platelet aggregation was significantly inhibited by all concentrations of SNAP. Time course studies with 30 &mgr;M of SNAP showed an inhibitory effect only after 0, 1, and 2 hrs of incubation, whereas after 4 hrs of incubation the inhibition of platelet aggregation could not be detected any more. Endothelial cells significantly increased the inhibitory effect of SNAP after 1 and 2 hrs of incubation. Incubation with ODQ with and without endothelial cells reversed the SNAP-mediated inhibition of maximum platelet aggregation regardless of the incubation time. Pretreatment of the endothelial cells with the COX inhibitors acetyl salicylic acid and indomethacin blocked the increased inhibitory effect of the endothelial cells after 1 and 2 hrs of incubation.ConclusionsThe time span between nitric oxide contact with platelets and induction of platelet aggregation by adenosine 5′-diphosphate is important for correct estimation of the antiaggregatory effect of nitric oxide. Endothelial cyclooxygenase plays an important role in the nitric oxide-mediated inhibition of platelet aggregation.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveIn the pathogenesis of septic shock, caused by either bacterial toxins or trauma, increased production of multiple proinflammatory mediators, such as phospholipase A2(PLA2), cytokines, and chemokines, is known to be of major importance. The present study was undertaken to investigate the influence of a newly designed extracellular PLA2inhibitor (ExPLI) on synthesis of proinflammatory mediators and mortality rate in a rat sepsis model.DesignProspective, randomized animal study.SettingExperimental laboratory.SubjectsMale Wistar-rats weighing 200–300 g.InterventionsMortality was induced by intraperitoneal bolus administration of lipopolysaccharide 15 mg/kg in 22 rats that were pretreated with NaCl or ExPLI (150 mg/kg). Furthermore, nine rats received a sublethal bolus of lipopolysaccharide (7.5 mg/kg) and nine rats received lipotechoic acid (8 mg/kg) simultaneously with or after ExPLI administration. Blood samples were collected from these rats, and cytokine concentrations were assessed by enzyme-linked immunosorbent assay. Lung and kidney were removed for RNA isolation and immunohistological analysis.Measurements and Main ResultsExPLI treatment significantly reduced lipopolysaccharide-induced mortality of rats (90.9 and 36.4%,p< .05). Up-regulation of tumor necrosis factor-&agr; and interleukin-6 production in serum after endotoxin treatment was significantly inhibited when ExPLIs were administered at the time of or before sepsis induction by using lipopolysaccharide or lipotechoic acid (p< .01). Similarly, messenger RNA expression of secreted PLA2-IIA, interleukin-1, or inducible nitric oxide synthase and the expression of intercellular adhesion molecule-1 were significantly down-regulated in lung and kidney of ExPLI-treated rats, as demonstrated by RNase protection assay, reverse transcription-polymerase chain reaction, or immunohistochemistry.ConclusionsExPLIs may be considered as potentially effective compounds to prevent the production of inflammatory mediators and to improve mortality rate in septic patients.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID