Pathophysiology of Septic Shock

被引：91

作者：

Russell, James A. ^{[1
]}

Rush, Barret ^{[2
]}

Boyd, John ^{[1
]}

机构：

[1] St Pauls Hosp, Ctr Heart Lung Innovat, Dept Med, 1081 Burrard St, Vancouver, BC V6Z 1Y6, Canada

[2] St Pauls Hosp, Div Crit Care Med, 1081 Burrard St, Vancouver, BC V6Z 1Y6, Canada

来源：

CRITICAL CARE CLINICS | 2018年 / 34卷 / 01期

关键词：

Septic shock; Sepsis; Vasodilation; Permeability; Cardiac dysfunction; Contractility; Nitric oxide; Cytokines; LEFT-VENTRICULAR CONTRACTILITY; NECROSIS-FACTOR-ALPHA; ACTIVATED PROTEIN-C; GOAL-DIRECTED RESUSCITATION; HEPARIN-BINDING PROTEIN; NITRIC-OXIDE SYNTHESIS; LOW-DOSE VASOPRESSIN; SPHINGOSINE; 1-PHOSPHATE; CARDIAC MYOCYTES; HYDROXYETHYL STARCH;

D O I：

10.1016/j.ccc.2017.08.005

中图分类号：

R4 [临床医学];

学科分类号：

1002 ; 100602 ;

摘要：

The fundamental features of septic shock are vasodilation, increased permeability, hypovolemia, and ventricular dysfunction. Vasodilation owing to increased nitric oxide and prostaglandins is treated with vasopressors (norepinephrine first). Increased permeability relates to several pathways (Slit/Robo4, vascular endothelial growth factor, angiopoietin 1 and 2/Tie2 pathway, sphingosine-1-phosphate, and heparin-binding protein), some of which are targets for therapies. Hypovolemia is common, and crystalloid is recommended for fluid resuscitation. Cardiomyocyte-inflammatory interactions decrease contractility, and dobutamine is recommended to increase cardiac output. There is benefit in decreasing the heart rate in selected patients with esmolol. Ivabradine is a novel agent for heart rate reduction without decreasing contractility.

引用

页码：43 / +

页数：20

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