Résumés
Résumé
Le profil hémodynamique du choc septique, influencé par de multiples variations physiologiques induites par l’infection, est caractérisé par l’association à des degrés variables de composantes hypovolémique, obstructive, cardiogénique, distributive ou cytotoxique. Ce profil est modifié par la restauration volémique, mais la persistance d’une hypotension signe le choc septique. Même si le débit cardiaque semble normal, voire élevé, des arguments solides témoignent d’une altération des propriétés contractiles du myocarde. Si le dysfonctionnement purement myocardique est rarement la cause directe du décès, il peut largement y contribuer. Faute d’une connaissance suffisante des phénomènes qui concourent à son développement, l’utilisation de substances visant à le corriger peut parfois s’avérer délétère. Une intégration plus précise de la physiopathologie du dysfonctionnement myocardique au cours du choc septique devrait permettre d’améliorer sa prise en charge.
Summary
Myocardial dysfunction frequently accompanies severe sepsis and septic shock. It is now clear that such a myocardial depression, as evidenced by biventricular alteration, is present during the early phase of sepsis in most patients. Myocardial depression exists despite a fluid loading-dependent hyperdynamic state and usually recovers within 7 to 10 days in survivors. Myocardial dysfunction does not appear to be due to irreversible structural abnormalities nor to myocardial hypoperfusion, but rather linked to many circulating mediators including cytokines. At a cellular level, reduced myocardial contractility could be related in part to apoptosis and induced by both nitric oxide-dependent and nitric oxide-independent mechanisms. However, whatever the mechanism involved, it leads to calcium homeostasis abnormality. The present review describes both the diagnosis procedure and the molecular and cellular pathways of sepsis-induced myocardial depression.
Parties annexes
Références
- 1. Friedman G, Silva E, Vincent JL. Has the mortality of septic shock changed with time? Crit Care Med 1998 ; 26 : 2078-86.
- 2. Parker MM, Shelhamer JH, Bacharach SL, et al. Profound but reversible myocardial depression in patients with septic shock. Ann Intern Med 1984 ; 100 : 483-9.
- 3. Robotham JL, Takata M, Berman M, Harasawa Y. Ejection fraction revisited. Anesthesiology 1991 ; 74 : 172-83.
- 4. Ognibene FP, Parker MM, Natanson C, et al. Depressed left ventricular performance. Response to volume infusion in patients with sepsis and septic shock. Chest 1988 ; 93 : 903-10.
- 5. Cariou A, Vinsonneau C, Chiche D, et al. L’élastance ventriculaire gauche est-elle altérée au cours du sepsis ? Réanim Urgences 2000 ; 9 (suppl 2) : 91S.
- 6. Poelaert J, Declerck C, Vogelaers D, et al. Left ventricular systolic and diastolic function in septic shock. Intensive Care Med 1997 ; 23 : 553-60.
- 7. Vincent JL, Reuse C, Frank N, et al. Right ventricular dysfunction in septic shock: Assessment by measurements of right ventricular ejection fraction using the thermodilution technique. Acta Anesthesiol Scand 1989 ; 33 : 34-8.
- 8. Fernandes CJ Jr, Iervolino M, Neves RA, et al. Interstitial myocarditis in sepsis. Am J Cardiol 1994 ; 74 : 958
- 9. Turner A, Tsamitros M, Bellomo R. Myocardial cell injury in septic shock. Crit Care Med 1999 ; 27 : 1775-80.
- 10. Yu P, Boughner DR, Sibbald WJ, et al. Myocardial collagen changes and edema in rats with hyperdynamic sepsis. Crit Care Med 1997 ; 25 : 657-62.
- 11. Neviere R, Fauvel H, Chopin C, et al. Caspase inhibition prevents cardiac dysfunction and heart apoptosis in a rat model of sepsis. Am J Respir Crit Care Med 2001 ; 163 : 218-25.
- 12. Taylor FB, Haddad PA, Hack E, et al. Two-stage response to endotoxin infusion into normal human subjects: correlation of blood phagocyte luminescence with clinical and laboratory markers of the inflammatory, hemostatic response. Crit Care Med 2001 ; 29 : 326-34.
- 13. Dinarello CA. Proinflammatory and anti-inflammatory cytokines as mediators in the pathogenesis of septic shock. Chest 1997 ; 112 (suppl 6) : S321-9.
- 14. Lesur O, F Chagnon, B Lévy, et al. Myocardial dysfunction in experimental septic shock: Effect of macrophage inhibitory factor (MIF) neutralization. Am J Respir Crit Care Med 2002 ; 165 : A176.
- 15. Paulus WJ, Vantrimpont PJ, Shah AM. Paracrine coronary endothelial control of left ventricular function in humans. Circulation 1995 ; 92 : 2119-26.
- 16. Tavernier B, Li JM, El-Omar MM, et al. Cardiac contractile impairment associated with increased phosphorylation of troponine I in endotoxemic rats. FASEB J 2001 ; 15 : 294-6.
- 17. Abi-Gerges N, Tavernier B, Mebazaa A, et al. Sequential changes in autonomic regulation of cardiac myocytes after in vivo endotoxin injection in rats. Am J Respir Crit Care Med 1999 ; 160 : 1196-204.
- 18. Tavernier B, Abi-Gerges N, Mebazaa A. Alteration of beta-adrenergic pathway in the septic heart. In : Vincent JL, ed. Yearbook of intensive care and emergency medicine. Berlin : Springer-Verlag, 1999 : 504-18.
- 19. Ming MJ, Hu DY, Chen HS, et al. Effects of MCI-154, a calcium sensitizer, on calcium sensitivity of myocardial fibers in endotoxic shock rats. Shock 2000 ; 14 : 652-6.
- 20. Landry DW, Levin HR, Gallant EM, et al. Vasopressin deficiency contributes to vasodilatation of septic shock. Circulation 1997 ; 95 : 1122-5.
- 21. Dunser MW, Mayr AJ, Ulmer H, et al. Arginine vasopressin in advanced vasodilatory shock. A prospective, randomized controlled study. Circulation 2003 ; 107 : 2313-9.