#PAGE_PARAMS# #ADS_HEAD_SCRIPTS# #MICRODATA#

Myocardial dysfunction in sepsis –  diagnostics and therapy


Authors: J. Maláska;  M. Slezák;  K. Muriová;  J. Stašek;  P. Ševčík
Authors place of work: Klinika anesteziologie, resuscitace a intenzivní medicíny Lékařské fakulty MU a FN Brno, pracoviště Bohunice, přednosta prof. MU Dr. Pavel Ševčík, CSc.
Published in the journal: Vnitř Lék 2010; 56(3): 226-232
Category: Reviews

Summary

Incidence of myocardial dysfunction in studies with severe sepsis patients is up to two thirds of patients. On the other side, patients with normal echocardiography have some type of myocardial injury, which can be detected by elevated serum levels of troponins and natriuretic peptides. Strong prognostic value of these markers regarding morbidity and mortality of septic patients indicates an important role of this „occult“ myocardial injury. Therapeutical interventions should take place only in situation in that low cardiac output is not capable to ensure metabolic demands of tissues. Nowadays, because of detrimental effects of classical inotropes, new strategies are under investigation. Namely levosimendan is promising alternative, not only related to its inotropic effects. Early diagnostics, assessment of prognosis and therapeutic strategy in patients with SMD are challenging for continuing research and for clinicians of different specialities.

Key words:
sepsis –  myocardial dysfunction –  troponin –  BN –  echocardiography –  inotropes –  levosimendan


Zdroje

1. Clec’h C, Ferriere F, Karoubi P et al. Diagnostic and prognostic value of procalcitonin in patients with septic shock. Crit Care Med 2004; 32: 1166– 1169.

2. Charpentier J, Luyt CE, Fulla Y et al. Brain natriuretic peptide: A marker of myocardial dysfunction and prognosis during severe sepsis. Crit Care Med 2004; 32: 660– 665.

3. Presneill JJ, Waring PM, Layton JE et al. Plasma granulocyte colony‑ stimulating factor and granulocyte‑ macrophage colony‑ stimulating factor levels in critical illness including sepsis and septic shock: relation to disease severity, multiple organ dysfunction, and mortality. Crit Care Med 2000; 28: 2344– 2354.

4. Mehta NJ, Khan IA, Gupta V et al. Cardiac troponin I predicts myocardial dysfunction and adverse outcome in septic shock. Int J Cardiol 2004; 95: 13– 17.

5. King DA, Codish S, Novack V et al. The role of cardiac troponin I as a prognosticator in critically ill medical patients: a prospective observational cohort study. Crit Care 2005; 9: R390– R395.

6. ver Elst KM, Spapen HD, Nguyen DN et al. Cardiac troponins I and T are bio­logical markers of left ventricular dysfunction in septic shock. Clin Chem 2000; 46: 650– 657.

7. Parker MM. Myocardial dysfunction in sepsis: injury or depression? Crit Care Med 1999; 27: 2035– 2036.

8. Turner A, Tsamitros M, Bellomo R. Myocardial cell injury in septic shock. Crit Care Med 1999; 27: 1775– 1780.

9. Soriano FG, Nogueira AC, Caldini EG et al. Potential role of poly (adenosine 5’‑ diphosphate‑ ribose) polymerase activation in the pathogenesis of myocardial contractile dysfunction associated with human septic shock. Crit Care Med 2006; 34: 1073– 1079.

10. Maeder M, Fehr T, Rickli H et al. Sepsis‑associated myocardial dysfunction: diagnostic and prognostic impact of cardiac troponins and natriuretic peptides. Chest 2006; 129: 1349– 1366.

11. Singh S, Evans TW. Organ dysfunction during sepsis. Intensive Care Med 2006; 32: 349– 360.

12. Witthaut R, Busch C, Fraunberger P et al. Plasma atrial natriuretic peptide and brain natriuretic peptide are increased in septic shock: impact of interleukin‑6 and sepsis‑associated left ventricular dysfunction. Intensive Care Med 2003; 29: 1696– 1702.

13. Cuthbertson BH, Patel RR, Croal BL et al. B‑type natriuretic peptide and the prediction of outcome in patients admitted to intensive care. Anaesthesia 2005; 60: 16– 21.

14. Forfia PR, Watkins SP, Rame JE et al. Relationship between B‑type natriuretic peptides and pulmonary capillary wedge pressure in the intensive care unit. J Am Coll Cardiol 2005; 45: 1667– 1671.

15. Jefic D, Lee JW, Savoy‑ Moore RT et al. Utility of B‑type natriuretic peptide and N‑terminal pro B‑type natriuretic peptide in evaluation of respiratory failure in critically ill patients. Chest 2005; 128: 288– 295.

16. Lubien E, DeMaria A, Krishnaswamy P et al. Utility of B‑ natriuretic peptide in detecting diastolic dysfunction: comparison with Doppler velocity recordings. Circulation 2002; 105: 595– 601.

17. Poelaert J, Declerck C, Vogelaers D et al. Left ventricular systolic and diastolic function in septic shock. Intensive Care Med 1997; 23: 553– 560.

18. Hartemink KJ, Groeneveld AB, de Groot MC et al. Alpha‑ atrial natriuretic peptide, cyclic guanosine monophosphate, and endothelin in plasma as markers of myocardial depression in human septic shock. Crit Care Med 2001; 29: 80– 87.

19. Roch A, Allardet‑ Servent J, Michelet P et al. NH2 terminal pro‑brain natriuretic peptide plasma level as an early marker of prognosis and cardiac dysfunction in septic shock patients. Crit Care Med 2005; 33: 1001– 1007.

20. Mitaka C, Hirata Y, Makita K et al. Endothelin‑1 and atrial natriuretic peptide in septic shock. Am Heart J 1993; 126: 466– 468.

21. Morgenthaler NG, Struck J, Christ‑ Crain M et al. Pro‑atrial natriuretic peptide is a prognostic marker in sepsis, similar to the APACHE II score: an observational study. Crit Care 2005; 9: R37– R45.

22. Dellinger RP, Levy MM, Carlet JM et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008. Intensive Care Med 2008; 34: 17– 60.

23. Parker MM, Shelhamer JH, Bacharach SL et al. Profound but reversible myocardial depression in patients with septic shock. Ann Intern Med 1984; 100: 483– 490.

24. Singer M. Catecholamine treatment for shock ‑  equally good or bad? Lancet 2007; 370: 636– 637.

25. Duranteau J, Sitbon P, Teboul JL et al. Effects of epinephrine, norepinephrine, or the combination of norepinephrine and dobutamine on gastric mucosa in septic shock. Crit Care Med 1999; 27: 893– 900.

26. Krejci V, Hiltebrand LB, Sigurdsson GH. Effects of epinephrine, norepinephrine, and phenylephrine on microcirculatory blood flow in the gastrointestinal tract in sepsis. Crit Care Med 2006; 34: 1456– 1463.

27. Pullamsetti SS, Maring D, Ghofrani HA et al. Effect of nitric oxide synthase (NOS) inhibition on macro‑ and microcirculation in a model of rat endotoxic shock. Thromb Haemost 2006; 95: 720– 727.

28. Landry DW, Levin HR, Gallant EM et al. Vasopressin deficiency contributes to the vasodilation of septic shock. Circulation 1997; 95: 1122– 1125.

29. Barrett LK, Orie NN, Taylor V et al. Differential effects of vasopressin and norepinephrine on vascular reactivity in a long‑term rodent model of sepsis. Crit Care Med 2007; 35: 2337– 2343.

30. Russell JA. Vasopressin in vasodilatory and septic shock. Curr Opin Crit Care 2007; 13: 383– 391.

31. Takeuchi K, del Nido PJ, Ibrahim AE et al. Increased myocardial calcium cycling and reduced myofilament calcium sensitivity in early endotoxemia. Surgery 1999; 126: 231– 238.

32. Dong LW, Wu LL, Ji Y et al. Impairment of the ryanodine‑ sensitive calcium release channels in the cardiac sarcoplasmic reticulum and its underlying mechanism during the hypodynamic phase of sepsis. Shock 2001; 16: 33– 39.

33. Cariello C, Guarracino F, Giannecchini Let al. Hemodynamic and cardiac peptide in septic myocardial depression: the effects of calcium sensitizer. Critical Care 2007; 11 (Suppl 2): P39.

34. Faivre V, Kaskos H, Callebert J et al. Cardiac and renal effects of levosimendan, arginine vasopressin, and norepinephrine in lipopolysaccharide‑treated rabbits. Ane­sthesiology 2005; 103: 514– 521.

35. Kevelaitis E, Peynet J, Mouas C et al. Opening of potassium channels: the common cardioprotective link between preconditioning and natural hibernation? Circulation 1999; 99: 3079– 3085.

36. Dubin A, Murias G, Sottile JP et al. Effects of levosimendan and dobutamine in experimental acute endotoxemia: a preliminary controlled study. Intensive Care Med 2007; 33: 485– 494.

37. Matejovic M, Krouzecky A, Radej J et al. Successful reversal of resistent hypodynamic septic shock with levosimendan. Acta Anaesthesiol Scand 2005; 49: 127– 128.

38. Noto A, Giacomini M, Palandi A et al. Levosimendan in septic cardiac failure. Intensive Care Med 2005; 31: 164– 165.

39. Powell BP, De Keulenaer BL. Levosimendan in septic shock: a case series. Br J Anaesth 2007; 99: 447– 448.

40. Morelli A, De Castro S, Teboul JL et al. Effects of levosimendan on systemic and regional hemodynamics in septic myocardial depression. Intensive Care Med 2005; 31: 638– 644.

41. Morelli A, Teboul JL, Maggiore SM et al. Effects of levosimendan on right ventricular afterload in patients with acute respiratory distress syndrome: a pilot study. Crit Care Med 2006; 34: 2287– 2293.

42. Bakker J, Grover R, McLuckie A et al. Administration of the nitric oxide synthase inhibitor NG‑ methyl‑  l‑ arginine hydrochloride (546C88) by intravenous infusion for up to 72 hours can promote the resolution of shock in patients with severe sepsis: Results of a randomized, double‑blind, placebo‑ controlled multicenter study (study no. 144– 002)*. Crit Care Med 2004; 32: 1– 12.

43. Lopez A, Lorente JA, Steingrub J et al. Multiple‑ center, randomized, placebo‑ controlled, double‑blind study of the nitric oxide synthase inhibitor 546C88: effect on survival in patients with septic shock. Crit Care Med 2004; 32: 21– 30.

44. Solomon SB, Minneci PC, Deans KJ et al. Effects of intra‑ aortic balloon counterpulsation in a model of septic shock. Crit Care Med 2009; 37: 7– 18.

Štítky
Diabetology Endocrinology Internal medicine

Článok vyšiel v časopise

Internal Medicine

Číslo 3

2010 Číslo 3
Najčítanejšie tento týždeň
Najčítanejšie v tomto čísle
Prihlásenie
Zabudnuté heslo

Zadajte e-mailovú adresu, s ktorou ste vytvárali účet. Budú Vám na ňu zasielané informácie k nastaveniu nového hesla.

Prihlásenie

Nemáte účet?  Registrujte sa

#ADS_BOTTOM_SCRIPTS#