摘要:

ObjectivesTo determine the use of commonly used diagnostic criteria for adult/acute respiratory distress syndrome (ARDS), evaluate physiologic variables of most value in diagnosing ARDS, and assess the frequency of newly diagnosed ARDS.DesignSelf-administered questionnaire by mail.SettingHospital intensive care units (ICUs).SubjectsIntensive care physicians (n equals 923) in the United States listed as ICU directors in the Society of Critical Care Medicine Membership Directory.InterventionsNone.Measurements and Main ResultsA total of 448 (48.5%) physicians responded, with 301 questionnaires completed. Bilateral infiltrates on chest radiograph, the PaO2/FIO2ratio, and pulmonary artery occlusion pressure were the most commonly used diagnostic criteria. However, the actual values used to diagnose ARDS were highly variable. The most important clinical physiologic variable used in determining the respiratory status of the ARDS patient was the PaO2/FIO2ratio, followed by shunt fraction, alveolar-arterial oxygen tension gradient, FIO2, PaO2, respiratory system compliance, and minute ventilation. Respondents indicated that 9% of ICU beds at their institutions were occupied by a patient diagnosed with ARDS within the previous 7 days and 18.6% of all mechanically ventilated patients had ARDS by their own criteria. Based on the total number of ICU beds, the predicted incidence of ARDS would be approximate 275,000 patients per year in the United States.ConclusionA wide range of diagnostic criteria are utilized by clinicians in the diagnosis of ARDS.(Crit Care Med 1996; 24:247-251)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo describe the clinical characteristics of a group of patients infected with the newly recognized hantavirus in the Southwestern United States.DesignCase series.SettingTertiary referral center.PatientsAll patients with confirmed hantavirus infection admitted to the University of New Mexico Hospital between May 1, 1993 and January 1, 1994.InterventionsRecords of patients with hantavirus infection were reviewed to collect all pertinent clinical data.Measurements and Main ResultsPulmonary disease in these patients was characterized by hypoxemia covering a wide range of severity. The cause of hypoxemia was an increased permeability (noncardiac) pulmonary edema which could be differentiated from hydrostatic (cardiac) pulmonary edema by its association with low pulmonary artery occlusion pressures and increased protein content of edema fluid. Hemodynamic measurements in severe cases showed a shock state characterized by a low cardiac index (range 1.6 to 3.0 L/min/m2), a low stroke volume index (range 10.5 to 29 mL/m2), and high systemic vascular resistance index (range 1653 to 2997 dyne centered dot sec/cm5centered dot m2). Progression to death was associated with worsening cardiac dysfunction unresponsive to treatment and causing oxygen debt and lactic acidosis.ConclusionsThe two major life-threatening pathophysiologic changes in Hantavirus Pulmonary Syndrome are increased permeability pulmonary edema, and an atypical form of septic shock caused by myocardial depression and hypovolemia.(Crit Care Med 1996; 24:252-258)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo study the catalytic activity of phospholipase A2and the concentrations of group I and group II phospholipases A2in the sera of patients during and after coronary artery bypass surgery.DesignProspective study.SettingUniversity hospital and research laboratory.PatientsFourteen consecutive patients operated on for ischemic heart disease.InterventionsThe catalytic activity of phospholipase A2and the serum concentrations of group I and group II phospholipases A2were measured before, during, and after the operation until the seventh postoperative day. A total of 196 blood samples were taken from 14 patients.Measurements and Main ResultsThe catalytic activity of phospholipase A2and the concentration of group II phospholipase A2increased in the sera of patients after coronary artery bypass surgery. The concentration of group I phospholipase A2did not change. The catalytic activity of phospholipase A2correlated significantly with group II but not with group I phospholipase A2values.ConclusionsThe increase in the catalytic activity of phospholipase A2in serum after coronary artery bypass surgery is due to group II phospholipase A2. The present results suggest that group II phospholipase A2is responsible for the physiologic and pathophysiologic effects of catalytically active phospholipase A2after coronary artery bypass surgery.(Crit Care Med 1996; 24:259-262)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo test the hypothesis that pulmonary vasodilator responses to pentoxifylline are dependent on the synthesis of nitric oxide from L-arginine and are independent of the release of cyclooxygenase products.DesignProspective study.SettingResearch laboratory.SubjectsIsolated lobar lung preparation, using mongrel cats.InterventionsIn separate experiments, the effects of NG-L-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthase, and the effects of a cyclooxygenase blocker, meclofenamate, were investigated on pulmonary arterial responses to pentoxifylline, acetylcholine, and isoproterenol during increased tone conditions induced by the thromboxane A2mimic, U46619, in the pulmonary vascular bed of the cat.Measurements and Main ResultsLobar arterial perfusion pressure, systemic pressure, and left atrial pressure were continuously monitored, electronically averaged, and permanently recorded.Under increased tone conditions in the isolated left lower lobe vascular bed of the cat, N sup G-L-nitro-L-arginine methyl ester significantly reduced the vasodilator responses to pentoxifylline and to acetylcholine, whereas NG-L-nitro-L-arginine methyl ester had no significant effect on the vasodilator responses to isoproterenol. Vasodilator responses to pentoxifylline and acetylcholine were not significantly changed in the presence of meclofenamate, whereas meclofenamate markedly reduced the vasopressor effects of arachidonic acid.ConclusionsThese data show that pentoxifylline has significant vasodilator activity in the pulmonary vascular bed of the cat. The present data also suggest that responses to pentoxifylline during increased tone conditions may, in part, be mediated by the release of nitric oxide and are independent of the release of cyclooxygenase products.(Crit Care Med 1996; 24:263-267)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo compare compliance and end-expiratory lung volume during reexpansion of normal and surfactant-deficient ex vivo atelectatic lungs with either gas or total liquid ventilation.DesignControlled, animal study using an ex vivo lung preparation.SettingA research laboratory at a university medical center.SubjectsThirty-six adult cats, weighing 2.5 to 4.0 kg.InterventionsHeparin (300 U/kg) was administered, cats were killed, and lungs were excised en bloc. Normal lungs and salinelavaged, surfactant-deficient lungs were allowed to passively collapse and remain atelectatic for 1 hr. Lungs then were placed in a plethysmogragh and ventilated for 2 hrs with standardized volumes of either room air or perfluorocarbon. Static pulmonary compliance and end-expiratory lung volume were measured every 30 mins.Measurements and Main ResultsReexpansion of normal atelectatic lungs with total liquid ventilation was associated with an 11-fold increase in end-expiratory lung volume when compared with the increase in end-expiratory lung volume observed with gas ventilation (total liquid ventilation 50 plus minus 14 mL, gas ventilation 4 plus minus 9 mL, p less than .0001). The difference was even more pronounced in the surfactant-deficient lungs with an approximate 19-fold increase in end-expiratory lung volume observed in the total liquid ventilated group, compared with the gas ventilated group (total liquid ventilation 44 plus minus 17 mL, gas ventilation 2 plus minus 8 mL, p equals .0001). Total liquid ventilation was associated with an increase in pulmonary compliance when compared with gas ventilation in both normal and surfactant-deficient lungs (normal: gas ventilation 6 plus minus 1 mL/cm H2O, total liquid ventilation 14 plus minus 4 mL/cm H2O, p less than .0001; surfactant-deficient: gas ventilation 4 plus minus 1 mL/cm H2O, total liquid ventilation 9 plus minus 3 mL/cm H2O, p less than .01).ConclusionsEnd-expiratory lung volume and static compliance are increased significantly following attempted reexpansion with total liquid ventilation when compared with gas ventilation in normal and surfactant-deficient, atelectatic lungs. The ability of total liquid ventilation to enhance recruitment of atelectatic lung regions may be an important means by which gas exchange is improved during total liquid ventilation when compared with gas ventilation in the setting of respiratory failure.(Crit Care Med 1996; 24:268-273)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectivesTo investigate the effects of partial liquid ventilation (i.e., mechanical ventilation in combination with intratracheal administration of perfluorocarbon) on lung function, with particular attention to the integrity of the alveolocapillary membrane in healthy adult animals.DesignProspective, randomized, controlled study.SettingLaboratory at the Department of Experimental Anesthesiology, Erasmus University Rotterdam.SubjectsTen adult male New Zealand rabbits.InterventionsFive rabbits were intratracheally treated with 12 mL/kg of perfluorocarbon while conventional mechanical ventilation (volume-controlled, tidal volume of 12 mL/kg, respiratory rate of 30 breaths/min, inspiration/expiration ratio of 1:2, positive endexpiratory pressure of 2 cm H2O, and an FIO2of 1.0) was applied for 3 hrs. To assess the permeability of the alveolocapillary membrane, pulmonary clearance of inhaled technetium-99m-labeled diethylenetriamine pentaacetic acid (sup 99m Tc-DTPA) measurements were performed at 3 hrs and compared with data from the control group (n equals 5) treated with mechanical ventilation only, using the same ventilatory parameters.Measurements and Main ResultsPulmonary gas exchange and lung mechanical parameters were measured in both groups at 30-min intervals. Mean values for PaO2in the perfluorocarbon group, although at adequate levels, were less than those values of the control group during the 3-hr study period (370 plus minus 44 vs. 503 plus minus 44 torr at 3 hrs [49.3 plus minus 5.9 vs. 67.1 plus minus 5.9 kPa]). Peak and mean airway pressures were higher in the perfluorocarbon group (ranging from 1.9 to 3.4 cm H2O and 0.7 to 1.3 cm H2O, respectively) compared with the control group, while end-inspiratory airway pressure was similar in both groups. The half-life of99mTc-DTPA was 83.7 plus minus 24.5 mins in the control group, which was significantly longer (p less than .01) than in the perfluorocarbon group (49.8 plus minus 6.1 mins).ConclusionsThese findings suggest that partial liquid ventilation with perfluorocarbons lowers pulmonary gas exchange in healthy animals, and the increased pulmonary clearance of99mTc-DTPA after 3 hrs of this type of ventilatory support may reflect minimal reversible changes in the lung surfactant system.(Crit Care Med 1996; 24:274-279)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo determine whether intubation and ventilation with either conventional mechanical ventilation or high-frequency jet ventilation, using dry or humidified gas, could induce regional tracheal ischemia and serve as a basis for the tracheal necrosis observed clinically during ventilation.DesignProspective, multiple group, controlled experimental study.SettingMedical school research laboratory.SubjectsTwenty, 3- to 5-wk-old suckling pigs.InterventionsAnesthetized, closed-chest piglets were intubated and ventilated for 30 mins with conventional mechanical ventilation and then ventilated for 2 additional hrs with either conventional mechanical ventilation or high-frequency jet ventilation. Groups were also ventilated, using both modes of ventilation, with either 37 degrees C humidified gas or 25 degrees C dry gas.Measurements and Main ResultsBlood flow groups were compared during spontaneous breathing, conventional mechanical ventilation, high-frequency jet ventilation and both ventilation modes, using 37 degrees C humidified or 22 degrees C dry inspired gas. Groups were compared, using an analysis of variance with a Newman-Keul's post-test. Regional tracheal blood flow was measured, using radioactive microspheres. Cardiac output and organ blood flows were also monitored. Tracheal blood flow increased 10.3-fold within 30 mins after intubation, but there were no significant differences in regional or total tracheal blood flow between conventional mechanical ventilation and high-frequency jet ventilation, using 37 degrees C humidified gas. Tracheal blood flow was increased further using high-frequency jet ventilation and 25 degrees C dry gas but not conventional mechanical ventilation with dry gas. Although ventilation reduced cardiac output by approximate 30%, there were no significant differences in organ distribution between modes of ventilation.ConclusionsAcute tracheal hyperemia occurred with intubation and ventilation with both conventional mechanical ventilation and high-frequency jet ventilation but no differences were observed between ventilation modes. Hyperemia was further increased with cool, dry inspired gas, using high-frequency jet ventilation but not conventional mechanical ventilation. Although acute tracheal ischemia was not produced by high-frequency jet ventilation or conventional mechanical ventilation, factors which alter the balance between arterial supply and metabolic demand or induce inflammation may contribute to the tracheal necrosis reported during sustained ventilation.(Crit Care Med 1996; 24:280-286)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

Objectivesa) To determine the response of endotoxin-exposed vascular smooth muscle to exogenous vasoconstrictors during concomitant exposure to an inhaled anesthetic (halothane); and b) to determine if excess nitric oxide production is responsible for any altered response.DesignIn vitro, prospective, repeated-measures, dose-response study.SettingUniversity/medical school experimental physiology laboratory.SubjectsAdult male Sprague-Dawley rats, whose aortae were studied in an in vitro preparation.InterventionsThoracic aortae were excised from anesthetized animals and cut into 3-mm rings. After incubation in aerated organ baths containing a modified essential medium with or without Escherichia coli lipopolysaccharide (100 micro gram/mL) at 37 degrees C for 5 hrs, the rings were removed and suspended in separate baths for isometric tension recording. Phenylephrine dose-response data (10minus10 to 10minus5 M) were determined for lipopolysaccharide- and nonlipopolysaccharide-treated rings. After washout and equilibration, two vessels (one each lipopolysaccharide- and nonlipopolysaccharide-treated) were additionally exposed to 2% halothane and phenylephrine dose-response determinations were repeated for all vessels. This procedure was repeated for 1% halothane in a separate experiment. In some experiments, the nitric oxide synthase inhibitor, Nomega-nitro-L-arginine (3 times 10minus4 M), was added to the bath after the washout from the second phenylephrine dose-response determination. Then, a third phenylephrine dose-response determination was performed, with and without 2% halothane.Measurements and Main ResultsDose-response curves were evaluated using a logistic regression analysis. In addition, absolute and percentage changes in tension were compared between the first and second contractions. Exposure to lipopolysaccharide resulted in a decrease in the maximum tension from 2.07 plus minus 0.03 (controls) to 1.24 plus minus 0.04 g/mg of vessel dry weight and an increase in the dose at which the contraction is 50% of maximum (ED50) from 3.78 times 10minus8 to 2.05 times 10minus7 M (p less than .05). Exposure to 2% halothane produced significant reductions in the maximum tensions in both groups. The lipopolysaccharide-treated vessels showed not only a proportionately larger decrease (minus 51 plus minus 5% vs. minus 18 plus minus 2% in the control plus halothane group), but also a significantly greater absolute decrease (0.59 plus minus 0.09 vs. 0.34 plus minus 0.04 g/mg in the control plus halothane group). The addition of 1% halothane produced less pronounced decreases in tension, with only an additive effect in the lipopolysaccharide-treated vessels. The addition of Nomega-nitro-L-arginine resulted in a reversal of the lipopolysaccharide-induced decrease in tension. However, 2% halothane still had a significantly greater effect on the lipopolysaccharide-exposed rings.ConclusionsExposure of rat aortic rings to lipopolysaccharide in vitro decreased the contractile response to phenylephrine. The addition of 2% halothane resulted in a more than additive decrease in tension in the lipopolysaccharide-treated vessels. Patients in septic or endotoxic shock are sensitive to most anesthetic regimens, and some of this sensitivity may be due to an altered vasoconstrictive response induced by lipopolysaccharide exposure. The inability of nitric oxide synthase inhibition to reverse this response completely suggests that induction of nitric oxide synthase and increased production of nitric oxide are not solely responsible for this finding.(Crit Care Med 1996; 24:287-293)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectivesIn septic shock, the principal source of increased plasma concentrations of tumor necrosis factor alpha (TNF) is considered to be the macrophage. Release from the macrophage is stimulated by bacterial lipopolysaccharide (endotoxin). We tested the hypothesis that vascular tissue also responds to endotoxin by releasing TNF.DesignProspective repeated measures analysis of timed-release curves.SettingAnesthesia research laboratory in an academic medical center.SubjectsWith Institutional Review Board approval and patient consent, segments of internal mammary artery and saphenous vein were obtained during coronary artery bypass surgery.InterventionsNone.Measurements and Main ResultsSegments of saphenous veins were incubated for 24 hrs in the presence or absence of bacterial lipopolysaccharide. At 0.5, 1, 3, 6, and 24 hrs, medium was assayed for TNF. In other experiments, smooth muscle cells were cultured from saphenous veins, incubated with or without bacterial lipopolysaccharide, and a time-course of TNF release determined. Bacterial lipopolysaccharide (20 micro gram/mL) significantly stimulated release of TNF from venous tissue in a time-dependent manner. At 0.5 hrs, TNF was undetectable in untreated tissue and was 48 plus minus 8 U/g wet tissue weight in the presence of bacterial lipopolysaccharide. At 3 hrs, TNF was 43 plus minus 27 U/g wet tissue weight in untreated and 388 plus minus 185 U/g wet tissue weight in treated (p less than .01 vs. control) tissue. Segments of internal mammary artery responded in a similar manner. In smooth muscle cells cultured from saphenous vein and internal mammary artery, bacterial lipopolysaccharide triggered the release of TNF. At 3 hrs, the release of TNF in control cells was 0.2 plus minus 0.15 U/mg cell protein and 17 plus minus 2 U/mg in the presence of 20 micro gram/mL of bacterial lipopolysaccharide (p less than .01 vs. control).ConclusionsHuman blood vessels, both artery and vein, produce TNF potentially from a smooth muscle cell source in response to bacterial lipopolysaccharide.(Crit Care Med 1996; 24:294-297)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo investigate the role of the brain gamma-aminobutyric acid receptor system in septic shock.DesignProspective, controlled study.SettingAnimal laboratory.SubjectsTwenty-one male Wistar rats (7 wks old) were randomized to three groups: group 1 (n equals 7, control); group 2 (n equals 7, sham-operated); group 3 (n equals 7, cecal ligation and puncture group).InterventionsUnder light ether anesthesia, the rats were treated as described above. Twenty-four hours after treatment, the rats were killed by decapitation. Plasma amino acid concentrations were measured using the collected blood. The brain was excised as rapidly as possible, and separated into forebrain, cerebellum, and brain stem. The brain gamma-aminobutyric acid concentration was measured at each of the three regions. Using3H-musimol, which is a gamma-aminobutyric acid receptor agonist, as a radioligand, the gamma-aminobutyric receptor densities were measured in these three regions by a radio-receptor assay.Measurements and Main ResultsThe concentrations of the branch-chain amino acids (leucine, isoleucine, valine) were lower in the cecal ligation and puncture group than in the control and sham-operated groups. The concentrations of the sulfur-containing amino acids (cysteine and taurine) were increased in the cecal ligation and puncture group compared with the other two groups, but the methionine concentration was increased in the shamoperated and the cecal ligation and puncture groups compared with the control group (p less than .05). The plasma gamma-aminobutyric acid concentration was not detectable in any of the three groups. The ammonia concentration was greater in the cecal ligation and puncture group than in the other two groups.There was no significant difference in the brain gamma-aminobutyric acid concentration among the three groups.The maximum number of binding sites in the forebrain of the cecal ligation and puncture group was higher than in the other two groups at both high-and low-affinity sites (control group: high-affinity sites 0.34 plus minus 0.03, low-affinity sites 2.93 plus minus 0.28; shamoperated group: high-affinity sites 0.35 plus minus 0.03, low-affinity sites 2.73 plus minus 0.18; cecal ligation and puncture group: high-affinity sites 0.59 plus minus 0.13, low-affinity sites 3.53 plus minus 0.21; mean plus minus SEM pmol/mg protein) (p less than .05). There were no significant differences observed in other regions of the brain (cerebellum and brain stem) in the three groups. The dissociation constants for3H-musimol were almost unchanged in the three groups.ConclusionsAn increase in the gamma-aminobutyric acid-A receptor density was observed in the forebrain of the cecal ligation and puncture model rats. This alteration may be closely related to the pathogenesis of brain dysfunction during septic shock.(Crit Care Med 1996; 24:298-305)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID