Sepsis and the heart

被引：180

作者：

Hunter, J. D. ^{[1
]}

Doddi, M. ^{[1
]}

机构：

[1] Macclesfield Hosp, Macclesfield SK10 3BL, Cheshire, England

来源：

BRITISH JOURNAL OF ANAESTHESIA | 2010年 / 104卷 / 01期

关键词：

complications; hypotension; infection; heart; myocardial function; immune response; polypeptides; cytokines; CRITICALLY-ILL PATIENTS; NITRIC-OXIDE SYNTHASE; MYOCARDIAL DEPRESSANT SUBSTANCE; RIGHT-VENTRICULAR PERFORMANCE; SEPTIC SHOCK PATIENTS; NECROSIS-FACTOR-ALPHA; RAT CARDIAC MYOCYTES; TROPONIN-I; SEPSIS/SEPTIC SHOCK; DIASTOLIC FUNCTION;

D O I：

10.1093/bja/aep339

中图分类号：

R614 [麻醉学];

学科分类号：

100217 ;

摘要：

Septic shock, the most severe complication of sepsis, accounts for similar to 10% of all admissions to intensive care. Our understanding of its complex pathophysiology remains incomplete but clearly involves stimulation of the immune system with subsequent inflammation and microvascular dysfunction. Cardiovascular dysfunction is pronounced and characterized by elements of hypovolaemic, cytotoxic, and distributive shock. In addition, significant myocardial depression is commonly observed. This septic cardiomyopathy is characterized by biventricular impairment of intrinsic myocardial contractility, with a subsequent reduction in left ventricular (LV) ejection fraction and LV stroke work index. This review details the myocardial dysfunction observed in adult septic shock, and discusses the underlying pathophysiology. The utility of using the regulatory protein troponin for the detection of myocardial dysfunction is also considered. Finally, options for the management of sepsis-induced LV hypokinesia are discussed, including the use of levosimendan.

引用

页码：3 / 11

页数：9

共 111 条

[21] Levosimendan in septic shock: another piece in the puzzle, but many pieces are still lacking [J].

De Backer, Daniel ;

Taccone, Fabio Silvio ;

Radermacher, Peter .

INTENSIVE CARE MEDICINE, 2007, 33 (03) :403-405

[22]

Dellinger RP, 2008, INTENS CARE MED, V34, P783, DOI [10.1007/s00134-007-0934-2, 10.1007/s00134-008-1040-9, 10.1097/01.CCM.0000298158.12101.41]

[23] CORONARY HEMODYNAMICS AND MYOCARDIAL-METABOLISM OF LACTATE, FREE FATTY-ACIDS, GLUCOSE, AND KETONES IN PATIENTS WITH SEPTIC SHOCK [J].

DHAINAUT, JF ;

HUYGHEBAERT, MF ;

MONSALLIER, JF ;

LEFEVRE, G ;

AVASANTUCCI, JD ;

BRUNET, F ;

VILLEMANT, D ;

CARLI, A ;

RAICHVARG, D .

CIRCULATION, 1987, 75 (03) :533-541

[24] Rapid increase in hospitalization and mortality rates for severe sepsis in the United States: A trend analysis from 1993 to 2003 [J].

Dombrovskiy, Viktor Y. ;

Martin, Andrew A. ;

Sunderram, Jagadeeshan ;

Paz, Harold L. .

CRITICAL CARE MEDICINE, 2007, 35 (05) :1244-1250

[25] LEFT-VENTRICULAR PERFORMANCE IN SEPTIC SHOCK - REVERSIBLE SEGMENTAL AND GLOBAL ABNORMALITIES [J].

ELLRODT, AG ;

RIEDINGER, MS ;

KIMCHI, A ;

BERMAN, DS ;

MADDAHI, J ;

SWAN, HJC ;

MURATA, GH .

AMERICAN HEART JOURNAL, 1985, 110 (02) :402-409

[26] Peroxynitrite is a major contributor to cytokine-induced myocardial contractile failure [J].

Ferdinandy, P ;

Danial, H ;

Ambrus, I ;

Rothery, RA ;

Schulz, R .

CIRCULATION RESEARCH, 2000, 87 (03) :241-247

[27] Cardiac troponin: a new serum marker of myocardial injury in sepsis [J].

Fernandes, CJ ;

Akamine, N ;

Knobel, E .

INTENSIVE CARE MEDICINE, 1999, 25 (10) :1165-1168

[28] Sepsis-induced myocardial depression: Where is the missing link? [J].

Fernandes, Constantino Jose, Jr. .

CRITICAL CARE MEDICINE, 2007, 35 (03) :972-973

[29] NEGATIVE INOTROPIC EFFECTS OF CYTOKINES ON THE HEART MEDIATED BY NITRIC-OXIDE [J].

FINKEL, MS ;

ODDIS, CV ;

JACOB, TD ;

WATKINS, SC ;

HATTLER, BG ;

SIMMONS, RL .

SCIENCE, 1992, 257 (5068) :387-389

[30] Molecular events in the cardiomyopathy of sepsis [J].

Flierl, Michael A. ;

Rittirsch, Daniel ;

Huber-Lang, Markus S. ;

Sarma, J. Vidya ;

Ward, Peter A. .

MOLECULAR MEDICINE, 2008, 14 (5-6) :327-336

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