摘要:

ObjectiveAn overview of the importance of understanding mechanisms occurring in the microcirculation during septic and endotoxic shock. The thesis of the paper is to place emphasis on this important vascular network to ultimately benefit the patient.Data SourcesEarly descriptions of vascular reactions to endotoxin which suggest that the microcirculation is a major site of attack during shock. More recent studies were sought out and examined as to their possible impacts on the microcirculation.Study SelectionEarly comprehensive studies concerning vascular reactions in the microcirculation during shock were selected. Subsequent studies identified from the mainstream scientific medical literature describe the actions of blood, cells, and the emerging significant role of the vascular endothelium among other factors. A consensus view is identified, pointing to the causes of a malfunctioning microcirculation during shock.Data ExtractionData gathered from reports in the mainstream, well-established basic and clinical literature, from reviews and forum reports, from studies by well-established investigators, and from more recent reports of excellent quality.Data SynthesisThe microcirculation undergoes massive alterations during sepsis/septic shock. There are numerous changes, including slowing of capillary blood flow due to depressed perfusion pressure as a result of systemic pressure reduction and local arteriolar constriction. Observations suggest that the microcirculation is shut off early in severe sepsis, allowing the effects of hypoperfusion and attacks by microorganisms to prevail in their destructive capabilities. Widespread capillary dilation may ultimately occur. However, with blood flow diverted through some arteriovenous channels, important areas of capillary exchange are bypassed. Decreased capillary blood flow during shock results from failure to allow normal passage of cellular elements, including erythrocytes and neutrophils. This defect occurs, in part, because of decreased perfusion pressure, decreased deformability of red and white cells, constricted arterioles, circulating obstructive fragments (including hemoglobin), and plugging of microvessels with ``sludge.'' Other factors are adherence of cells to capillary and venular epithelial membranes creating increased resistance to flow, loss of fluid through abnormal transcapillary exchange, differential vascular resistance changes between various beds (e.g., intestinal vs. muscle), and the relative absence of regulatory neurohumoral control of small vessel segments of the circulation. During sepsis/septic shock, endothelial cells are reported to modulate vascular tone, control local blood flow, influence the rate of leakage of fluids and plasma proteins into tissues, modulate the accumulation and extravasation of white cells into tissues, and influence white cell activation. As a result of the predominance of many destructive factors, a subsequent round of tissue damage may occur. Because of prolonged capillary vascular stasis, deficient flow, and factors released from injured cells, the microcirculation becomes a trap for uncontrolled bacterial growth enhanced by sustained hypoxemia, acidosis, and toxemia. These events may combine to contribute to the loss of normal cell integrity and death of the host.ConclusionsThe purpose of this review is to draw the readers' attention to the growing list of adverse factors occurring in the microcirculation during sepsis/septic shock. A further aim is to point to the realization of the complexity of factors which may contribute to the importance of a well-functioning microcirculation.(Crit Care Med 1996; 24:1072-1078)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectivesTo determine curriculum requirements and educational methods used by Critical Care fellowship training programs in fulfilling Residency Review Committee requirements for a research experience during Critical Care subspecialty training.Data SourceResponses from 163 (67%) of the 245 directors of accredited Anesthesiology, Medicine, Pediatric, and Surgical Critical Care fellowship training programs listed in the American Medical Association Graduate Medical Education Directory.Data ExtractionSurvey information accepted as valid for each program was tabulated to answer study questions.Data SynthesisMost (89%) Critical Care programs with 2- or 3-yr curricula meet Residency Review Committee requirements and provide nonclinical time for research. Only 63% of 1-yr curricula from Anesthesiology and Medicine provide a required research experience. Formal instruction in research topics is provided by lecture, journal club, or research conference in approximate 90% of fellowships. Academic productivity from fellowship programs is high, but not correlated with a program's requirement for research.ConclusionCompliance with current Residency Review Committee requirements for active participation in research is poor for 1-yr fellowship curricula. Reasons for this failure are discussed and a modified requirement is proposed.(Crit Care Med 1996; 24:1079-1082)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo investigate the functional status of arteries in patients with septic shock, each of whom suffered from severe hypotension.DesignExperimental, comparative study.SettingLaboratory in a university hospital.SubjectsMesenteric artery resected from omentum was obtained from patients (n equals 3) with or without (n equals 4) sepsis.InterventionsTo study the effect of modification of the nitric oxide system in human arteries during sepsis, changes in norepinephrine-evoked isometric tension in mesenteric arterial rings were measured.Measurements and Main ResultsMesenteric arteries were isolated from omentum resected from three patients with septic shock and from four patients with no inflammatory conditions; in each case, during an intestinal anastomosis. In arterial rings, after a 1-hr equilibration with Krebs solution, changes in isometric tension evoked by norepinephrine were measured for 5 mins every 20 mins. The tension initially evoked in rings from septic patients was lower than in those rings from nonseptic patients and, unlike the controls, it decreased with a short time course. The addition of 300 micro mol/L of NG-nitro-L-arginine methyl ester or 10 micro mol/L of methylene blue reversed this decrease.ConclusionThese results indicate that in patients with septic shock, the main cause of reduced sensitivity to pressor agents may be a massive generation of nitric oxide via the L-arginine pathway.(Crit Care Med 1996; 24:1083-1086)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID