Skip to main content
SpringerLink
Log in

Sepsis und Herz

Sepsis and heart

  • Schwerpunkt
  • Published:
Der Internist Aims and scope Submit manuscript

Zusammenfassung

Bei Patienten mit schwerer Sepsis ist regelhaft auch eine Beeinträchtigung der Herzfunktion zu diagnostizieren. So wird häufig eine passagere Reduktion der kardialen Auswurffraktion beschrieben. Neben der gestörten Pumpleistung findet sich außerdem eine hochgradige prognoserelevante Reduktion der Herzfrequenzvariabilität. Bei der Verknüpfung von Inflammation und gestörter Herzfrequenzregulation könnte dem Endotoxin eine Schlüsselrolle zukommen. Experimentelle Untersuchungen belegen, dass es als Folge der komplexen Interaktion von Endotoxin, Schrittmacherstrom If und vegetativem Nervensystem zu einer Zunahme der Ruheherzfrequenz und gleichzeitig einer Herzfrequenzstarre kommt, wie dies typischerweise auch bei Patienten mit schwerer Sepsis beobachtet wird. Die Methode der Wahl zur Quantifizierung der septischen Kardiomyopathie auf der Intensivstation ist die Messung des Herzzeitvolumens in Relation zum systemischen Gefäßwiderstand. Klinische Studien zur kausalen Therapie der septischen Herzschädigung (Blockade der überschießenden Stickoxidbildung, Unterdrückung der Zytokinproduktion etc.) sind bislang leider enttäuschend verlaufen. Ein günstiger Behandlungseffekt kann für die Gabe von aktiviertem Protein C angenommen werden, was die Bedeutung der gestörten Mikrozirkulation bei der Genese der septischen Kardiomyopathie unterstreicht.

Abstract

In patients suffering from severe sepsis an impairment of cardiac function is seen constantly. Patients with septic shock often show a transient reduction of cardiac ejection fraction. Besides, a tremendous impairment of heart rate variability corresponding to a poor prognosis is often found. Endotoxin might play a pivotal role in the conjunction of inflammation and the disturbance of heart rate regulation. Experimental studies show that the complex interactions of endotoxin, the cardiac pacemaker current I f, and the autonomous nervous system lead to an increase of resting heart rate and in parallel to a decrease of heart rate variability – as typically seen in patients with severe sepsis. The method of choice to quantify the degree of septic cardiomyopathy at the intensive care unit certainly is to determine cardiac output in relation to systemic vascular resistance. Unfortunately, clinical trials aiming to influence the causal pathogenesis of septic cardiomyopathy (inhibition of excess formation of nitric oxide, suppression of cytokine release etc.) were rather disappointing so far. Positive effects might be assumed for the administration of activated protein C thereby underlining the role of microcirculatory alterations in the development of septic cardiomyopathy.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Abb. 1
Abb. 2
Abb. 3
Abb. 4
Abb. 5
Abb. 6

Literatur

  1. Babuin L, Vasile VC, Rio Perez JA et al (2008) Elevated cardiac troponin is an independent risk factor for short- and long-term mortality in medical intensive care unit patients. Crit Care Med 36:759–765

    Article  PubMed  CAS  Google Scholar 

  2. Bone RC, Balk RA, Cerra FB et al (1992) Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. Chest 101:1644–1655

    Article  PubMed  CAS  Google Scholar 

  3. Bouhemad B, Nicolas-Robin A, Arbelot C et al (2009) Acute left ventricular dilatation and shock-induced myocardial dysfunction. Crit Care Med 37:441–447

    Article  PubMed  Google Scholar 

  4. Brueckmann M, Huhle G, Lang S et al (2005) Prognostic value of plasma N-terminal pro-brain natriuretic peptide in patients with severe sepsis. Circulation 112:527–534

    Article  PubMed  CAS  Google Scholar 

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

    Article  PubMed  CAS  Google Scholar 

  6. Cotter G, Moshkovitz Y, Kaluski E et al (2003) The role of cardiac power and systemic vascular resistance in the pathophysiology and diagnosis of patients with acute congestive heart failure. Eur J Heart Fail 5:443–451

    Article  PubMed  Google Scholar 

  7. Cunnion RE, Schaer GL, Parker MM et al (1986) The coronary circulation in human septic shock. Circulation 73:637–644

    PubMed  CAS  Google Scholar 

  8. Elliott P, Andersson B, Arbustini E et al (2008) Classification of the cardiomyopathies: a position statement from the European Society Of Cardiology Working Group on Myocardial and Pericardial Diseases. Eur Heart J 29:270–276

    Article  PubMed  Google Scholar 

  9. Godin PJ, Fleisher LA, Eidsath A et al (1996) Experimental human endotoxemia increases cardiac regularity: results from a prospective, randomized, crossover trial. Crit Care Med 24:1117–1124

    Article  PubMed  CAS  Google Scholar 

  10. John J, Woodward DB, Wang Y et al (2010) Troponin-I as a prognosticator of mortality in severe sepsis patients. J Crit Care [Epub ahead of print]

  11. Kalla C, Raveh D, Algur N et al (2008) Incidence and significance of a positive troponin test in bacteremic patients without acute coronary syndrome. Am J Med 121:909–915

    Article  PubMed  Google Scholar 

  12. Levy MM, Macias WL, Vincent JL et al (2005) Early changes in organ function predict eventual survival in severe sepsis. Crit Care Med 33:2194–2201

    Article  PubMed  Google Scholar 

  13. Levy RJ, Piel DA, Acton PD et al (2005) Evidence of myocardial hibernation in the septic heart. Crit Care Med 33:2752–2756

    Article  PubMed  Google Scholar 

  14. Muller-Werdan U, Buerke M, Ebelt H et al (2006) Septic cardiomyopathy – A not yet discovered cardiomyopathy? Exp Clin Cardiol 11:226–236

    PubMed  CAS  Google Scholar 

  15. Muller-Werdan U, Pfeifer A, Hubner G et al (1997) Partial inhibition of protein synthesis by pseudomonas exotoxin a deranges catecholamine sensitivity of cultured rat heart myocytes. J Mol Cell Cardiol 29:799–811

    Article  PubMed  CAS  Google Scholar 

  16. Muller-Werdan U, Schumann H, Fuchs R et al (1997) Tumor necrosis factor alpha (TNF alpha) is cardiodepressant in pathophysiologically relevant concentrations without inducing inducible nitric oxide-(NO)-synthase (iNOS) or triggering serious cytotoxicity. J Mol Cell Cardiol 29:2915–2923

    Article  PubMed  CAS  Google Scholar 

  17. Muller-Werdan U, Werdan K (2000) Immune modulation by catecholamines – a potential mechanism of cytokine release in heart failure? Herz 25:271–273

    Article  PubMed  CAS  Google Scholar 

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

    PubMed  CAS  Google Scholar 

  19. Parrillo JE, Burch C, Shelhamer JH et al (1985) 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 76:1539–1553

    Article  PubMed  CAS  Google Scholar 

  20. Pirracchio R, Deye N, Lukaszewicz AC et al (2008) Impaired plasma B-type natriuretic peptide clearance in human septic shock. Crit Care Med 36:2542–2546

    Article  PubMed  CAS  Google Scholar 

  21. Rabuel C, Mebazaa A (2006) Septic shock: a heart story since the 1960s. Intensive Care Med 32:799–807

    Article  PubMed  CAS  Google Scholar 

  22. Reinhart K, Brunkhorst F, Bone H et al (2006) Diagnose und Therapie der Sepsis. S2-Leitlinien der Deutschen Sepsis-Gesellschaft e.V. (DSG) und der Deutschen Interdisziplinären Vereinigung für Intensiv- und Notfallmedizin (DIVI). Internist (Berl) 47:356–373

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

    Article  PubMed  CAS  Google Scholar 

  24. Rudiger A, Gasser S, Fischler M et al (2006) Comparable increase of B-type natriuretic peptide and amino-terminal pro-B-type natriuretic peptide levels in patients with severe sepsis, septic shock, and acute heart failure. Crit Care Med 34:2140–2144

    Article  PubMed  CAS  Google Scholar 

  25. Salman S, Bajwa A, Gajic O et al (2008) Paroxysmal atrial fibrillation in critically ill patients with sepsis. J Intensive Care Med 23:178–183

    Article  PubMed  Google Scholar 

  26. Schmidt H, Muller-Werdan U, Hoffmann T et al (2005) Autonomic dysfunction predicts mortality in patients with multiple organ dysfunction syndrome of different age groups. Crit Care Med 33:1994–2002

    Article  PubMed  Google Scholar 

  27. Schmidt H, Saworski J, Werdan K et al (2007) Decreased beating rate variability of spontaneously contracting cardiomyocytes after co-incubation with endotoxin. J Endotoxin Res 13:339–342

    Article  PubMed  CAS  Google Scholar 

  28. Tracey KJ (2007) Physiology and immunology of the cholinergic antiinflammatory pathway. J Clin Invest 117:289–296

    Article  PubMed  CAS  Google Scholar 

  29. Zorn-Pauly K, Pelzmann B, Lang P et al (2007) Endotoxin impairs the human pacemaker current If. Shock 28:655–661

    PubMed  CAS  Google Scholar 

Download references

Interessenkonflikte

Der korrespondierende Autor gibt Verbindungen zu folgenden Firmen an:

Fa. Boston Scientific (Kongressteilnahmen); Fa. Lilly (Kongressteilnahmen); Fa. MSD (Vortragshonorare).

Karl Werdan gibt Verbindungen zu folgenden Firmen an:

Fa. Servier (Vorträge, Advisory-Board-Tätigkeit, Forschungsunterstützung); Fa. Edwards (Vorträge, Forschungsunterstützung, Advisory-Board-Tätigkeit); Fa. Datascope (Vortragshonorare, Forschungsunterstützung, Advisory-Board-Tätigkeit); Fa. Biotest (Vorträge, Forschungsunterstützung, Advisory-Board-Tätigkeit).

Author information

Authors and Affiliations

  1. Klinik und Poliklinik für Innere Medizin III, Universitätsklinikum Halle (Saale), Ernst-Grube-Str. 40, 06097, Halle, Deutschland

    H. Ebelt & K. Werdan

Authors
  1. H. Ebelt
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. K. Werdan
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to H. Ebelt.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Ebelt, H., Werdan, K. Sepsis und Herz. Internist 51, 844–849 (2010). https://doi.org/10.1007/s00108-009-2560-2

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s00108-009-2560-2

Schlüsselwörter

Keywords

Search

Navigation