摘要:

Objective:The nitric oxide synthase inhibitor L-NG-methylarginine hydrochloride (L-NMMA HC1 546C88) causes reductions in cardiac output (CO), a potential limitation to clinical application. This drop in CO exceeds that from phenylephrine at matched systemic arterial pressure. We tested the hypothesis that the greater fall in CO attributable to L-NMMA primarily reflects a difference in venoconstriction between agents, such that phenylephrine produces larger increases in preload (an independent determinant of CO).Design:Random infusion of phenylephrine or L-NMMA.Setting:An animal research laboratory.Subjects:Eight healthy, conscious, male dogs.Interventions:L-NG-methylarginine hydrochloride (20 mg/kg for 1 hr) and phenylephrine (0.5 to 3 μg/kg/min) were administered into eight dogs chronically instrumented to measure left ventricular pressure and dimension. Data were measured at a constant heart rate (140 beats/min) to render CO proportional to stroke dimension.Measurements and Main Results:At a matched increase in afterload (effective arterial elastance), L-NMMA increased preload (end-diastolic dimension) to a lesser degree (3.8% ± 1.5%,p< .05) than phenylephrine (9.6% ± 1.6%,p< .05 vs. L-NMMA). Neither L-NMMA nor phenylephrine affected the slope of the end-systolic pressure dimension relationship, although L-NMMA shifted the relationship rightward (1.7 ± 0.7 mm,p< .05), consistent with a mild negative inotropic effect. L-NMMA decreased the stroke dimension to a greater extent than phenylephrine (−24.1% ± 6.8% and −10.6% ± 3.4%, respectively,p< .05).Conclusions:Differential CO responses to phenylephrine and L-NMMA were primarily attributable to changes in preload. Variable venular vs. arteriolar constrictor effects must be considered when evaluating the integrated cardiovascular response to a vasoactive agent.

ISSN:0090-3493    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Objectives:To assess the success rate of pressure support ventilation (PSV) in acute lung injury patients undergoing continuous positive pressure ventilation (CPPV), to study physiologic changes after the transition from CPPV to PSV, and to investigate differences between patients who succeed and patients who fail PSV according to predetermined criteria.Design:Observational study.Setting:General intensive care unit in a teaching hospital.Subjects:We studied 48 patients having acute lung injury, as defined by a PaO2/FIO2<300 mm Hg and the presence of bilateral infiltrates on chest radiograph, and ventilated with CPPV. We included patients with PaO2>80 mm Hg, at positive end-expiratory pressure of <15 cm H2O and with FIO2up to 1.0.Interventions:After enrollment, PSV was instituted and patients were strictly monitored during the following 48 hrs. Subjects who met any of the predefined PSV failure criteria during this period were returned to CPPV (Group F). PSV was continued in the remaining patients (Group S).Measurements and Main Results:Gas exchange, respiratory mechanics, and hemodynamics measurements were collected before switching from CPPV to PSV and were repeated at 24 hrs after beginning PSV, or immediately before return to CPPV in Group F patients. The physiologic deadspace volume to tidal volume ratio (VD/VT) was obtained by the Enghoff's equation from the measurement of the mixed expired CO2fraction.PSV resulted in a significant PaCO2decrease (49.2 ± 10.9 mm Hg to 44.4 ± 7.2 mm Hg) and significant increases in minute volume (&OV0312;E) (9.0 ± 2.3 L/min to 12.0 ± 4.0 L/min) and arterial blood pH (7.405 ± 0.054 to 7.435 ± 0.064), with stable oxygenation and hemodynamics. In patients who were hypercapnic (PaCO2>50 mm Hg) during CPPV, the &OV0312;Eincrease was higher than in normocapnic patients. In the latter patients, PaCO2and pH did not change significantly going from CPPV to PSV. A total of 38 patients (79%) were allocated to Group S and the remaining 10 patients were included in Group F. In Group S, positive endexpiratory pressure of 9.4 ± 2.9 cm H2O (range, 3-14 cm H2O) and a PSV level of 14.9 ± 3.8 cm H2O (range, 9-22 cm H2O) were applied. In Group F, positive end-expiratory pressure of 8.9 ± 3.1 cm H2O (range, 5-15 cm H2O) and a PSV level of 21.6 ± 4.6 cm H2O (range, 16-31 cm H2O) were adopted. Compared with Group S, Group F had a longer duration of intubation (20.2 ± 19.2 days vs. 9.2 ± 13.5 days), a lower static compliance of the respiratory system (30.4 ± 16.5 mL/cm H2O vs. 41.7 ± 15.0 mL/cm H2O), and a higher VD/VT(0.70 ± 0.09 vs. 0.52 ± 0.10), but similar oxygenation and positive end-expiratory pressure. &OV0312;Ewas higher in Group F during both CPPV and PSV.Conclusions:In a relatively high proportion of the investigated patients, PSV was successful. The institution of PSV led to no major changes in oxygenation or in hemodynamics. PSV was associated with increases in &OV0312;Eand respiratory frequency. In patients who had been hypercapnic during CPPV, PaCO2decreased despite a compensated pH. Compared with PSV success patients, patients who failed PSV appeared to be sicker, as shown by the higher duration of respiratory support, increased ventilatory needs, and decreased respiratory system compliance, despite similar arterial oxygenation and positive end-expiratory pressure.

ISSN:0090-3493    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Objectives:To document changes in serum secretory leukocyte protease inhibitor (SLPI) in human sepsis and in experimental endotoxemiain vivo.To compare changes in serum SLPI in human sepsis with changes in interleukin (IL)-6, IL-10, and tumor necrosis factor (TNF)-α. To determine whether or not changes in SLPI correlate with the severity of multiple organ dysfunction syndrome as measured by the maximal multiple organ dysfunction score. Finally, because neutrophils have been implicated in tissue injury associated with organ dysfunction, to determine whether recombinant human SLPI blocks activation of isolated human neutrophils.Design:Case-control study andex-vivocellular assay.Setting:Surgical intensive care unit and clinical research center of university hospitals; laboratory of a medical school.Interventions:None.Measurements and Main Results:There was a significant dose-dependent elevation (50.2 ± 4.0 ng/mL,p= .01) in plasma SLPI 12 hrs after administration of lipopolysaccharide to seven healthy adults (36.4 ± 2.3 ng/mL). Further, serum concentrations of SLPI (132 ± 15 ng/mL) were elevated in septic surgical patients compared with healthy controls (43 ± 2 ng/mL,p< .01) and nonseptic surgical controls (69 ± 10 ng/mL,p= .01). Serum SLPI concentrations correlated (r2= .71,p< .01) better with organ dysfunction as measured by maximal multiple organ dysfunction score than did serum IL-6 (r2= .49,p< .01), IL-10 (r2= .05,p= .22), or TNF-α (r2= .02,p= .44). We found that recombinant human SLPIin vitroinhibits TNF-α-induced hydrogen peroxide production by human neutrophils (ID50= 1-2 μg/mL).Conclusions:Serum SLPI is elevated in human sepsis and experimental endotoxemia. Maximal concentrations of serum SLPI correlate significantly with maximal multiple organ dysfunction scores in patients with sepsis. Secretory leukocyte protease inhibitor may function to limit ongoing neutrophil-mediated tissue injury associated with organ dysfunction.

ISSN:0090-3493    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Objective:To examine which recumbent position can lead to the highest vagal modulation in patients during the acute phase of myocardial infarction.Design:Descriptive study.Setting:Intensive care unit in a medical center.Patients:A total of 52 patients admitted to the intensive care unit because of acute myocardial infarction (AMI), 41 patients with coronary artery disease (CAD), and 28 patients with patent coronary arteriogram.Interventions:None.Measurements and Main Results:Heart rate variability analysis was performed in patients with AMI, patients with CAD, and patent coronary controls in supine, left lateral decubitus, and right lateral decubitus positions in random order. In the right lateral decubitus position, the vagal modulation was the highest and the sympathetic modulation was the lowest among three recumbent positions in three groups of patients. When the position was changed from supine to right lateral decubitus, the increase in vagal modulation was greater in patients who had more severely depressed vagal modulation in the supine position and the rate of increase was the greatest in patients with AMI, followed by patients with CAD and patent coronary controls. Detailed analysis showed that the vagal enhancing and sympathetic suppression effect of the right lateral decubitus position applied to patients with Q wave myocardial infarctions.Conclusions:The right lateral decubitus position can lead to the highest vagal modulation and the lowest sympathetic modulation among three recumbent positions in patients with Q wave myocardial infarction. The right lateral decubitus position can be used as an effective vagal enhancer in patients with Q wave myocardial infarction but without severe bradycardia or atrioventricular block.

ISSN:0090-3493    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Objective:To examine the mechanisms contributing to decreased microvascular blood flow in cardiogenic shock by comparing patients with cardiogenic shock with critically ill controls and with patients with septic shock.Design:Prospective, consecutive entry of patients meeting the criteria for septic shock, cardiogenic shock, and critical illness without coexisting infection or shock.Setting:University hospital, medical intensive care unit, coronary care unit, and respiratory care unit.Patients:Eight patients with cardiogenic shock secondary to acute myocardial infarction, six critically ill controls, and six patients with septic shock.Measurements and Main Results:Forearm blood flow was measured at rest and during reactive hyperemia by venous air plethysmography. Red cell deformability was determined by filtration. Leukocyte aggregation was detected by the leukergy test. Neutrophil CD11b/CD18 expression and soluble intercellular adhesion molecule-1 levels were also measured.In cardiogenic shock, forearm arterial resistance was significantly increased at rest and during reactive hyperemia compared with controls and patients with septic shock. The response to reactive hyperemia was attenuated in cardiogenic and septic shock patients, as measured by the absolute change in forearm blood flow from baseline, which was significantly less as compared with controls (p< .01). The percent change in forearm blood flow during reactive hyperemia compared with forearm blood flow at rest was significantly lower in cardiogenic shock (60 ± 10) and in septic shock (50 ± 11) compared with controls at baseline (145 ± 20;p< .01). Red cell deformability was significantly decreased in cardiogenic shock (1.2 ± 0.2 mL/min;p< .05) and septic shock (1.1 ± 0.2 mL/min;p< .05), compared with controls (1.8 ± 0.1 mL/min). Neutrophil CD11b/CD18 expression, leukergy, and serum intercellular adhesion molecule-1 levels in cardiogenic shock patients were not significantly different from controls.Conclusion:These data suggest that the response to reactive hyperemia is attenuated in cardiogenic shock. This appears to reflect increased vasoconstriction and an impaired capacity for vasodilation. Decreased erythrocyte deformability may also be important in limiting systemic microvascular flow. However, evidence supporting a role for neutrophil-endothelial cell interactions was not observed.

ISSN:0090-3493    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Objective:Manifestation of intraoperative fever is impaired by volatile anesthetics and muscle relaxants. Opioids are common anesthetic adjuvants and remain the dominant treatment for postoperative surgical pain and sedation of critically ill patients. The effect of opioids on normal thermoregulatory control is well established. However, the extent to which these drugs might inhibit fever remains unknown. Accordingly, we tested the hypothesis that relatively low plasma concentrations of the μ-receptor agonist alfentanil reduce fever magnitude.Design:Prospective, randomized, crossover study.Setting:Outcomes Research Laboratory, at the Department of Anesthesia and Perioperative Care, University of California, San Francisco.Patients:Eight healthy male volunteers, aged 25-31 yrs, each studied on three separate days.Intervention:Each volunteer was given an intravenous injection of 30 IU/g interleukin (IL)-2, followed 2 hrs later by 70 IU/g. One hour after the second dose, the volunteers were randomly assigned to three doses of alfentanil: a) none (control); b) a target plasma concentration of 100 ng/mL; and c) a target concentration of 200 ng/mL. Opioid administration continued for 5 hrs.Methods and Main Results:Alfentanil significantly reduced the febrile response to pyrogen, decreasing integrated tympanic membrane temperatures from 7.5 ± 2.2°C·hr on the control day, to 4.9 ± 1.5°C·hr with 100 ng/mL alfentanil, and to 5.1 ± 1.7°C·hr with 200 ng/mL alfentanil (p= .011). Peak temperatures were also significantly reduced from 38.5 ± 0.4°C on the control day, to 38.0 ± 0.4°C on the 100 ng/mL-alfentanil day and 38.0 ± 0.6°C on the 200-ng/mL day (p= .019). Plasma cytokine concentrations increased after IL-2 administration, roughly in proportion to the elevation in core temperature. However, cytokine concentrations did not differ significantly among the treatment groups.Conclusion:Alfentanil significantly reduced the febrile response to IL-2 administration. However, the reduction was comparable at plasma concentrations near 100 and 200 ng/mL. These data indicate that concentrations of opioids commonly observed in critical care patients significantly inhibit the manifestation of fever.

ISSN:0090-3493    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Objective:Improved pathophysiologic insight and prognostic information regarding in-hospital risk of mortality among stroke patients admitted to an intensive care unit.Design:Retrospective analysis.Setting:Neurology/neurosurgery intensive care unit in a tertiary care university medical center.Patients:A total of 63 consecutive ischemic stroke patients.Interventions:Patients were classified according to in-hospital mortality. Charts were reviewed to retrospectively generate an admitting Acute Physiology and Chronic Health Evaluation (APACHE) II score. The APACHE II score and its individual components were assessed for predicting subsequent death.Measurements and Main Results:Of 63 patients, 13 died and 50 survived to either discharge or surgical intervention. The mean admitting APACHE II score of survivors (6.9) was lower than that of patients who died (17.2;p< .0001). None of the 33 patients with a score <9 died, compared with 43% of those with a score ≥9. A score ≥18 was uniformly associated with fatal outcome (n = 8). Univariate analysis identified APACHE II total score, Glasgow Coma Scale score, temperature, pH, and white blood cell count as significant predictors of death. Among multivariate logistic regression models examining the components of the APACHE II score, the model containing white blood cells, temperature, and creatinine best predicted death.Conclusions:Several features of the APACHE II score are associated with risk of death in this patient population. The findings suggest particular physiologic derangements that are associated with, and may contribute to, increased mortality in critically ill patients with acute ischemic stroke.

ISSN:0090-3493    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Objective:To assess whether clinical variables might be useful in selecting patients who will have an acute intracranial abnormality seen in head computed tomographic scans (HCT).Design:Retrospective study.Setting:Medical intensive care unit (MICU) in a tertiary teaching hospital.Measurements:Medical records of patients admitted to the MICU who underwent HCT between January 1, 1994, and December 31, 1995, were reviewed. Patients with acute intracranial abnormalities (HCT-positive) and those without new acute findings (HCT-negative) were compared on various clinical variables, including demographics, indications for obtaining the HCT (mental status change, neurologic deficit, fever, seizures), coagulation profiles, when the HCT was performed (at admission or after admission), and ordering physician.Main Results:Of 297 HCTs obtained in 230 patients, 37% (109/297) were positive. When the clinical variables were examined univariately, only the presence of a neurologic deficit (70% vs. 37%; difference, 33%;p< .001) differed significantly between positive and negative HCTs. Multivariate analysis confirmed that only the frequency of a new neurologic deficit differed significantly in the two groups (p< .001; odds ratio, 3.9; 95% confidence interval, 2.3-6.4). In patients without neurologic deficits, only the presence of seizures was associated with a positive HCT (p< .01: logistic regression). The presence of either neurologic deficit or seizures best predicted a positive HCT: sensitivity 0.81, specificity 0.53, positive predictive value 0.50, and negative predictive value 0.83.Conclusion:Among MICU patients, the presence of either neurologic deficit or seizures is associated with the presence of an acute intracranial abnormality seen in HCT, but the association is not powerful enough to reliably depend on these clinical variables to select patients for HCTs in the MICU.

ISSN:0090-3493    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Objective:Evaluation of changes in the peak latencies of sensory evoked potentials in different patient groups, to evaluate differences in metabolic encephalopathy of critically ill patients with multiple organ failure as a result of septic or nonseptic conditions.Design:Prospective cohort study.Setting:Intensive care units of the university hospital, Vienna.Patients:Patients (n = 103) treated on an intensive care unit because of multiple organ failure with additional metabolic encephalopathy. Multiple organ failure was induced by sepsis (group A; n = 56), surgery (group B; n = 29), or both (group C; n = 18).Interventions:None.Measurements and Main Results:Metabolic encephalopathy was determined by measuring median nerve-stimulated short-latency and long-latency sensory evoked potentials. No differences in the peak latencies of the sensory evoked potentials were detected among the groups. Septic patients had a N70 peak latency of 131 ± 21 msecs, nonseptic postsurgical patients of 132 ± 17 msecs, and septic postsurgical patients of 134 ± 17 msecs. The cervicomedullary N13 to cortical N20 conduction times were 6.4 ± 1 msec, 6.4 ± 1.4 msecs, and 6.8 ± 1.2 msecs, respectively. All measured peak latencies were significantly prolonged compared with peak latencies of healthy controls. The severity of illness assessed by the Acute Physiology and Chronic Health Evaluation III score was not different between the three groups. An increase of the delay of N70 peak latencies was significantly correlated with the severity of illness (r2= .15;p< .00005).Conclusion:There was no difference in sensory evoked potential measurements detectable among septic patients with multiple organ failure, nonseptic postsurgical patients with multiple organ failure, and septic postsurgical patients with multiple organ failure. The N70 peak latency was significantly correlated with the severity of illness but not with the presence or absence of sepsis. In postsurgical patients with multiple organ failure and superimposed sepsis, the N70 peak latencies were not further prolonged compared with postsurgical patients without sepsis.

ISSN:0090-3493    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Objective:To determine the 1-day prevalence of community-acquired, hospital-acquired, or intensive care unit (ICU)-acquired infections in Mexican ICUs. To identify associated risk factors, predominant infecting organisms, and mortality rates.Design:A 1-day point-prevalence study.Setting:A total of 254 adult ICUs in Mexico.Patients:Adult patients hospitalized in the participating ICUs.Results:A total of 895 patients were studied, of whom 521 patients (58.2%) were infected. Community-acquired infection occurred in 214 patients (23.9%), non-ICU nosocomial infection occurred in 99 patients (11.1%), and 208 patients had at least one ICU-acquired infection (23.2%; 1.45 episodes/patient). The most frequently reported ICU-acquired infections were pneumonia (39.7%), urinary tract infections (20.5%), wound infection (13.3%), and bacteremia (7.3%). The mortality rate for the ICU-acquired infections after 6 wks of follow-up was 25.5%. Multivariate regression analysis showed the following risk factors for ICU-acquired infections: neurologic failure as a primary cause of admission (odds ratio [OR], 1.697; 95% confidence interval [CI], 1.001-2.839); length of stay in ICU (OR, 1.119; 95% CI, 1.091-1.151); number of therapeutic and/or diagnostic interventions during the preceding week (OR, 1.118; 95% CI, 1.016-1.231); peripherally administered infusion of hyperosmolar solutions (OR, 6.93; 95% CI, 2.452-21.661); sedative usage in the preceding week (OR, 1.751; 95% CI, 1.183-2.602); history of an emergency surgery in the preceding month (OR, 1.875; 95% CI, 1.251-2.813). The administration of antimicrobial treatment if there was an infection decreased the risk of death (OR, 0.406; 95% CI, 0.204-0.755).Conclusions:Evidence of a high frequency of nosocomial infections was found, and potential risk factors for acquiring infections and mortality were identified. Mortality rates according to the hierarchy of the systemic inflammatory response syndrome in Latin American ICUs are reported.

ISSN:0090-3493    

出版商:OVID    

年代:2000

数据来源: OVID