Pathophysiology of Septic Shock - 22/11/17

Doi : 10.1016/j.ccc.2017.08.005

James A. Russell, MD ^a,^⁎ , Barret Rush, MD ^b, John Boyd, MD ^a
^a Department of Medicine, Centre for Heart Lung Innovation, St. Paul’s Hospital, 1081 Burrard Street, Vancouver, British Columbia V6Z 1Y6, Canada
^b Division of Critical Care Medicine, St. Paul’s Hospital, 1081 Burrard Street, Vancouver, British Columbia V6Z 1Y6, Canada

^∗Corresponding author. Centre for Heart Lung Innovation, Division of Critical Care Medicine, St. Paul’s Hospital, 1081 Burrard Street, Vancouver, British Columbia V6Z 1Y6, Canada.Centre for Heart Lung InnovationDivision of Critical Care MedicineSt. Paul’s Hospital1081 Burrard StreetVancouverBritish ColumbiaV6Z 1Y6Canada

Résumé

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 heart rate in selected patients with esmolol. Ivabradine is a novel agent for heart rate reduction without decreasing contractility.

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Keywords : Septic shock, Sepsis, Vasodilation, Permeability, Cardiac dysfunction, Contractility, Nitric oxide, Cytokines