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Semin Respir Crit Care Med 2011; 32(2): 206-214
DOI: 10.1055/s-0031-1275533
© Thieme Medical Publishers

Management of Myocardial Dysfunction in Severe Sepsis

Mathieu Jozwiak1 , Romain Persichini1 , Xavier Monnet1 , 2 , Jean-Louis Teboul1 , 2
  • 1Assistance Publique-Hôpitaux de Paris (AP-HP), CHU Bicêtre, service de réanimation médicale, Le Kremlin-Bicêtre, France
  • 2Université Paris-Sud, Faculté de médecine Paris-Sud, Le Kremlin-Bicêtre, France
Further Information

Publication History

Publication Date:
19 April 2011 (online)

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ABSTRACT

Sepsis-induced cardiac dysfunction is a frequent and severe complication of septic shock. The mechanisms responsible for its development are complex and intricate. Echocardiography is the best method to make the diagnosis of cardiac dysfunction. Biomarkers (B-type natriuretic peptides and cardiac troponins) can alert clinicians of the possibility of cardiac dysfunction. Low plasma levels can serve to rule out a severe cardiac dysfunction. By contrast, high levels should prompt the performance of an echocardiographic examination. The transpulmonary thermodilution monitor and the pulmonary artery catheter can also be used to alert clinicians or to monitor the effects of inotropic therapy. Dobutamine is the first-line therapy. Its administration remains a matter of debate and should be carefully monitored in terms of efficacy and tolerance.

KEYWORDS

Sepsis - myocardial depression - echocardiography - B-type natriuretic peptide - dobutamine - levosimendan

REFERENCES

  • 1 Dellinger R P, Levy M M, Carlet J M International Surviving Sepsis Campaign Guidelines Committee et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008.  Crit Care Med. 2008;  36 (1) 296-327
    CrossrefPubMedGoogle Scholar
  • 2 Vieillard-Baron A, Caille V, Charron C, Belliard G, Page B, Jardin F. Actual incidence of global left ventricular hypokinesia in adult septic shock.  Crit Care Med. 2008;  36 (6) 1701-1706
    CrossrefPubMedGoogle Scholar
  • 3 Parker M M, Shelhamer J H, Bacharach S L et al.. Profound but reversible myocardial depression in patients with septic shock.  Ann Intern Med. 1984;  100 (4) 483-490
    CrossrefPubMedGoogle Scholar
  • 4 Parrillo J E. Pathogenetic mechanisms of septic shock.  N Engl J Med. 1993;  328 (20) 1471-1477
    CrossrefPubMedGoogle Scholar
  • 5 Zanotti Cavazzoni S L, Guglielmi M, Parrillo J E, Walker T, Dellinger R P, Hollenberg S M. Ventricular dilation is associated with improved cardiovascular performance and survival in sepsis.  Chest. 2010;  138 (4) 848-855
    CrossrefPubMedGoogle Scholar
  • 6 Bouhemad B, Nicolas-Robin A, Arbelot C, Arthaud M, Féger F, Rouby J J. Acute left ventricular dilatation and shock-induced myocardial dysfunction.  Crit Care Med. 2009;  37 (2) 441-447
    CrossrefPubMedGoogle Scholar
  • 7 Jardin F, Fourme T, Page B et al.. Persistent preload defect in severe sepsis despite fluid loading: a longitudinal echocardiographic study in patients with septic shock.  Chest. 1999;  116 (5) 1354-1359
    CrossrefPubMedGoogle Scholar
  • 8 Poelaert J, Declerck C, Vogelaers D, Colardyn F, Visser C A. Left ventricular systolic and diastolic function in septic shock.  Intensive Care Med. 1997;  23 (5) 553-560
    CrossrefPubMedGoogle Scholar
  • 9 Bouhemad B, Nicolas-Robin A, Arbelot C, Arthaud M, Féger F, Rouby J J. Isolated and reversible impairment of ventricular relaxation in patients with septic shock.  Crit Care Med. 2008;  36 (3) 766-774
    CrossrefPubMedGoogle Scholar
  • 10 Etchecopar-Chevreuil C, François B, Clavel M, Pichon N, Gastinne H, Vignon P. Cardiac morphological and functional changes during early septic shock: a transesophageal echocardiographic study.  Intensive Care Med. 2008;  34 (2) 250-256
    CrossrefPubMedGoogle Scholar
  • 11 Parker M M, McCarthy K E, Ognibene F P, Parrillo J E. Right ventricular dysfunction and dilatation, similar to left ventricular changes, characterize the cardiac depression of septic shock in humans.  Chest. 1990;  97 (1) 126-131
    CrossrefPubMedGoogle Scholar
  • 12 Vieillard Baron A, Schmitt J M, Beauchet A et al.. Early preload adaptation in septic shock? A transesophageal echocardiographic study.  Anesthesiology. 2001;  94 (3) 400-406
    CrossrefPubMedGoogle Scholar
  • 13 Rabuel C, Mebazaa A. Septic shock: a heart story since the 1960s.  Intensive Care Med. 2006;  32 (6) 799-807
    CrossrefPubMedGoogle Scholar
  • 14 Hunter J D, Doddi M. Sepsis and the heart.  Br J Anaesth. 2010;  104 (1) 3-11
    CrossrefPubMedGoogle Scholar
  • 15 Cunnion R E, Schaer G L, Parker M M, Natanson C, Parrillo J E. The coronary circulation in human septic shock.  Circulation. 1986;  73 (4) 637-644
    CrossrefPubMedGoogle Scholar
  • 16 Dhainaut J F, Huyghebaert M F, Monsallier J F et al.. Coronary hemodynamics and myocardial metabolism of lactate, free fatty acids, glucose, and ketones in patients with septic shock.  Circulation. 1987;  75 (3) 533-541
    CrossrefPubMedGoogle Scholar
  • 17 Lamia B, Chemla D, Richard C, Teboul J L. Clinical review: interpretation of arterial pressure wave in shock states.  Crit Care. 2005;  9 (6) 601-606
    CrossrefPubMedGoogle Scholar
  • 18 Lefer A M. Role of a myocardial depressant factor in the pathogenesis of circulatory shock.  Fed Proc. 1970;  29 (6) 1836-1847
    PubMedGoogle Scholar
  • 19 Parrillo J E, Burch C, Shelhamer J H, Parker M M, Natanson C, Schuette W. A circulating myocardial depressant substance in humans with septic shock: septic shock patients with a reduced ejection fraction have a circulating factor that depresses in vitro myocardial cell performance.  J Clin Invest. 1985;  76 (4) 1539-1553
    CrossrefPubMedGoogle Scholar
  • 20 Kumar A, Kumar A, Paladugu B, Mensing J, Parrillo J E. Transforming growth factor-beta1 blocks in vitro cardiac myocyte depression induced by tumor necrosis factor-alpha, interleukin-1beta, and human septic shock serum.  Crit Care Med. 2007;  35 (2) 358-364
    CrossrefPubMedGoogle Scholar
  • 21 Chensue S W, Terebuh P D, Remick D G, Scales W E, Kunkel S L. In vivo biologic and immunohistochemical analysis of interleukin-1 alpha, beta and tumor necrosis factor during experimental endotoxemia: kinetics, Kupffer cell expression, and glucocorticoid effects.  Am J Pathol. 1991;  138 (2) 395-402
    PubMedGoogle Scholar
  • 22 Abi-Gerges N, Tavernier B, Mebazaa A et al.. Sequential changes in autonomic regulation of cardiac myocytes after in vivo endotoxin injection in rat.  Am J Respir Crit Care Med. 1999;  160 (4) 1196-1204
    PubMedGoogle Scholar
  • 23 Tavernier B, Li J M, El-Omar M M et al.. Cardiac contractile impairment associated with increased phosphorylation of troponin I in endotoxemic rats.  FASEB J. 2001;  15 (2) 294-296
    PubMedGoogle Scholar
  • 24 Reithmann C, Hallström S, Pilz G, Kapsner T, Schlag G, Werdan K. Desensitization of rat cardiomyocyte adenylyl cyclase stimulation by plasma of noradrenaline-treated patients with septic shock.  Circ Shock. 1993;  41 (1) 48-59
    PubMedGoogle Scholar
  • 25 Silverman H J, Penaranda R, Orens J B, Lee N H. Impaired beta-adrenergic receptor stimulation of cyclic adenosine monophosphate in human septic shock: association with myocardial hyporesponsiveness to catecholamines.  Crit Care Med. 1993;  21 (1) 31-39
    CrossrefPubMedGoogle Scholar
  • 26 Tang C, Liu M S. Initial externalization followed by internalization of beta-adrenergic receptors in rat heart during sepsis.  Am J Physiol. 1996;  270 (1 Pt 2) R254-R263
    PubMedGoogle Scholar
  • 27 Kumar A, Paladugu B, Mensing J, Kumar A, Parrillo J E. Nitric oxide-dependent and -independent mechanisms are involved in TNF-alpha -induced depression of cardiac myocyte contractility.  Am J Physiol Regul Integr Comp Physiol. 2007;  292 (5) R1900-R1906
    CrossrefPubMedGoogle Scholar
  • 28 Vona-Davis L, Wearden P, Hill J, Hill R. Cardiac response to nitric oxide synthase inhibition using aminoguanidine in a rat model of endotoxemia.  Shock. 2002;  17 (5) 404-410
    CrossrefPubMedGoogle Scholar
  • 29 Lancel S, Tissier S, Mordon S et al.. Peroxynitrite decomposition catalysts prevent myocardial dysfunction and inflammation in endotoxemic rats.  J Am Coll Cardiol. 2004;  43 (12) 2348-2358
    CrossrefPubMedGoogle Scholar
  • 30 Ahmad R, Rasheed Z, Ahsan H. Biochemical and cellular toxicology of peroxynitrite: implications in cell death and autoimmune phenomenon.  Immunopharmacol Immunotoxicol. 2009;  31 (3) 388-396
    CrossrefPubMedGoogle Scholar
  • 31 Carlson D L, Willis M S, White D J, Horton J W, Giroir B P. Tumor necrosis factor-alpha-induced caspase activation mediates endotoxin-related cardiac dysfunction.  Crit Care Med. 2005;  33 (5) 1021-1028
    CrossrefPubMedGoogle Scholar
  • 32 Nevière R, Fauvel H, Chopin C, Formstecher P, Marchetti P. Caspase inhibition prevents cardiac dysfunction and heart apoptosis in a rat model of sepsis.  Am J Respir Crit Care Med. 2001;  163 (1) 218-225
    PubMedGoogle Scholar
  • 33 Vieillard-Baron A. Assessment of right ventricular function.  Curr Opin Crit Care. 2009;  15 (3) 254-260
    CrossrefPubMedGoogle Scholar
  • 34 Combes A, Berneau J B, Luyt C E, Trouillet J L. Estimation of left ventricular systolic function by single transpulmonary thermodilution.  Intensive Care Med. 2004;  30 (7) 1377-1383
    PubMedGoogle Scholar
  • 35 Jabot J, Monnet X, Bouchra L, Chemla D, Richard C, Teboul J L. Cardiac function index provided by transpulmonary thermodilution behaves as an indicator of left ventricular systolic function.  Crit Care Med. 2009;  37 (11) 2913-2918
    CrossrefPubMedGoogle Scholar
  • 36 Charpentier J, Luyt C E, Fulla Y et al.. Brain natriuretic peptide: a marker of myocardial dysfunction and prognosis during severe sepsis.  Crit Care Med. 2004;  32 (3) 660-665
    CrossrefPubMedGoogle Scholar
  • 37 Brueckmann M, Huhle G, Lang S et al.. Prognostic value of plasma N-terminal pro-brain natriuretic peptide in patients with severe sepsis.  Circulation. 2005;  112 (4) 527-534
    CrossrefPubMedGoogle Scholar
  • 38 Maeder M, Fehr T, Rickli H, Ammann P. Sepsis-associated myocardial dysfunction: diagnostic and prognostic impact of cardiac troponins and natriuretic peptides.  Chest. 2006;  129 (5) 1349-1366
    CrossrefPubMedGoogle Scholar
  • 39 Ma K K, Ogawa T, de Bold A J. Selective upregulation of cardiac brain natriuretic peptide at the transcriptional and translational levels by pro-inflammatory cytokines and by conditioned medium derived from mixed lymphocyte reactions via p38 MAP kinase.  J Mol Cell Cardiol. 2004;  36 (4) 505-513
    CrossrefPubMedGoogle Scholar
  • 40 Pirracchio R, Deye N, Lukaszewicz A C et al.. Impaired plasma B-type natriuretic peptide clearance in human septic shock.  Crit Care Med. 2008;  36 (9) 2542-2546
    CrossrefPubMedGoogle Scholar
  • 41 Fernandes Jr C J, Akamine N, Knobel E. Cardiac troponin: a new serum marker of myocardial injury in sepsis.  Intensive Care Med. 1999;  25 (10) 1165-1168
    CrossrefPubMedGoogle Scholar
  • 42 Røsjø H, Varpula M, Hagve T A The FINNSEPSIS Study Group et al. Circulating high sensitivity troponin T in severe sepsis and septic shock: distribution, associated factors, and relation to outcome.  Intensive Care Med. 2011;  37 (1) 77-85
    CrossrefPubMedGoogle Scholar
  • 43 Ammann P, Maggiorini M, Bertel O et al.. Troponin as a risk factor for mortality in critically ill patients without acute coronary syndromes.  J Am Coll Cardiol. 2003;  41 (11) 2004-2009
    CrossrefPubMedGoogle Scholar
  • 44 Turner A, Tsamitros M, Bellomo R. Myocardial cell injury in septic shock.  Crit Care Med. 1999;  27 (9) 1775-1780
    CrossrefPubMedGoogle Scholar
  • 45 Merx M W, Weber C. Sepsis and the heart.  Circulation. 2007;  116 (7) 793-802
    CrossrefPubMedGoogle Scholar
  • 46 Hayes M A, Timmins A C, Yau E H, Palazzo M, Hinds C J, Watson D. Elevation of systemic oxygen delivery in the treatment of critically ill patients.  N Engl J Med. 1994;  330 (24) 1717-1722
    CrossrefPubMedGoogle Scholar
  • 47 Boyd J H, Forbes J, Nakada T A, Walley K R, Russell J A. Fluid resuscitation in septic shock: a positive fluid balance and elevated central venous pressure are associated with increased mortality.  Crit Care Med. 2011;  39 (2) 259-265
    CrossrefPubMedGoogle Scholar
  • 48 Monnet X, Teboul J L. Volume responsiveness.  Curr Opin Crit Care. 2007;  13 (5) 549-553
    CrossrefPubMedGoogle Scholar
  • 49 Rivers E, Nguyen B, Havstad S Early Goal-Directed Therapy Collaborative Group et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock.  N Engl J Med. 2001;  345 (19) 1368-1377
    CrossrefPubMedGoogle Scholar
  • 50 Teboul J L, Mercat A, Lenique F, Berton C, Richard C. Value of the venous-arterial PCO2 gradient to reflect the oxygen supply to demand in humans: effects of dobutamine.  Crit Care Med. 1998;  26 (6) 1007-1010
    CrossrefPubMedGoogle Scholar
  • 51 Kumar A, Schupp E, Bunnell E, Ali A, Milcarek B, Parrillo J E. Cardiovascular response to dobutamine stress predicts outcome in severe sepsis and septic shock.  Crit Care. 2008;  12 (2) R35
    CrossrefPubMedGoogle Scholar
  • 52 Barraud D, Faivre V, Damy T et al.. Levosimendan restores both systolic and diastolic cardiac performance in lipopolysaccharide-treated rabbits: comparison with dobutamine and milrinone.  Crit Care Med. 2007;  35 (5) 1376-1382
    CrossrefPubMedGoogle Scholar
  • 53 Morelli A, De Castro S, Teboul J L et al.. Effects of levosimendan on systemic and regional hemodynamics in septic myocardial depression.  Intensive Care Med. 2005;  31 (5) 638-644
    CrossrefPubMedGoogle Scholar
  • 54 Morelli A, Teboul J L, Maggiore S M et al.. Effects of levosimendan on right ventricular afterload in patients with acute respiratory distress syndrome: a pilot study.  Crit Care Med. 2006;  34 (9) 2287-2293
    CrossrefPubMedGoogle Scholar
  • 55 Hamzaoui O, Georger J F, Monnet X et al.. Early administration of norepinephrine increases cardiac preload and cardiac output in septic patients with life-threatening hypotension.  Crit Care. 2010;  14 (4) R142
    CrossrefPubMedGoogle Scholar
  • 56 Annane D, Vignon P, Renault A CATS Study Group et al. Norepinephrine plus dobutamine versus epinephrine alone for management of septic shock: a randomised trial.  Lancet. 2007;  370 (9588) 676-684
    CrossrefPubMedGoogle Scholar
  • 57 Levy B, Bollaert P E, Charpentier C et al.. Comparison of norepinephrine and dobutamine to epinephrine for hemodynamics, lactate metabolism, and gastric tonometric variables in septic shock: a prospective, randomized study.  Intensive Care Med. 1997;  23 (3) 282-287
    CrossrefPubMedGoogle Scholar
  • 58 Levy B, Mansart A, Bollaert P E, Franck P, Mallie J P. Effects of epinephrine and norepinephrine on hemodynamics, oxidative metabolism, and organ energetics in endotoxemic rats.  Intensive Care Med. 2003;  29 (2) 292-300
    PubMedGoogle Scholar
  • 59 Duranteau J, Sitbon P, Teboul J L et al.. Effects of epinephrine, norepinephrine, or the combination of norepinephrine and dobutamine on gastric mucosa in septic shock.  Crit Care Med. 1999;  27 (5) 893-900
    CrossrefPubMedGoogle Scholar
  • 60 Creagh-Brown B C, Quinlan G J, Evans T W, Burke-Gaffney A. The RAGE axis in systemic inflammation, acute lung injury and myocardial dysfunction: an important therapeutic target?.  Intensive Care Med. 2010;  36 (10) 1644-1656
    CrossrefPubMedGoogle Scholar

Jean-Louis TeboulM.D. Ph.D. 

Service de réanimation médicale, CHU Bicêtre

78, rue du Général Leclerc, 94 270 Le Kremlin-Bicêtre, France

Email: jean-louis.teboul@bct.aphp.fr