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Septische Kardiomyopathie

Septic cardiomyopathy

  • ÜBERSICHT
  • Published:
Intensivmedizin und Notfallmedizin

Summary

The existence of human septic myocardial depression was only unequivocally proven in the 1980s by the group of Parrillo, utilizing a nuclear imaging technique in intensive care patients. Heart failure in sepsis is frequently masked by a seemingly normal cardiac output. However, relative to the lowered systemic vascular resistance—resulting in a reduced afterload, cardiac outputs and ventricular ejection fractions of septic patients are often not adequately enhanced. This septic cardiomyopathy involves both the right and the left ventricle and is potentially reversible. In response to volume substitution, the hearts can be considerably enlarged. The disease is not primarily hypoxic in nature, but may be aggravated by ischemia. Autonomic dysfunction, documented by a reduced heart rate variability and impaired baro- and chemoreflex sensitivities, forms part of the disease entity. The severity of myocardial depression correlates with a poor prognosis. Non-infectious systemic inflammatory response syndrome (SIRS) can give rise to an analogous disease entity, namely SIRS cardiomyopathy.

The etiology of the disease is multifactorial. Several candidates with potential pathogenetic impact on the heart were identified: bacterial toxins, cytokines and mediators including tumor necrosis factor α, interleukin-1 and nitric oxide, cardiodepressant factors, oxygen reactive species, catecholamines. Symptomatic treatment consists of volume substitution and of catecholamine support; causal therapeutic approaches aiming at an interruption of the proinflammatory mediator cascades are being tested.

Zusammenfassung

Das Auftreten einer Myokarddepression in der Sepsis ist erst in den achtziger Jahren von der Gruppe um Parrillo gezeigt worden, indem sie die Herzfunktion von Intensivpatienten mit szintigraphischen Methoden untersucht haben. Die Einschränkung der Herzfunktion in der Sepsis wird häufig durch ein scheinbar normales Herzzeitvolumen maskiert. Berücksichtigt man jedoch die massive Nachlastsenkung infolge des stark verminderten systemischen Gefäßwiderstandes,—welche zu einer kompensatorischen Zunahme des Herzzeitvolumens führen sollte—so wird die häufig inadäquate Steigerung der Herzleistung rasch evident. Diese septische Kardiomyopathie involviert sowohl den linken als auch den rechten Ventrikel, und sie ist potenziell reversibel. Nach Volumengabe kann es zu einer ausgeprägten Herzdilatation kommen. Die septische Kardiomyopathie ist nicht primär hypoxischer Genese, sie kann aber durch eine gleichzeitig bestehende Myokardischämie verschlimmert werden. Eine das Herz betreffende autonome Dysfunktion – dokumentiert durch eine eingeschränkte Herzfrequenzvariabilität und eine gestörte Baro- und Chemoreflexsensitivität – ist Bestandteil der septischen Kardiomyopathie. Das Ausmaß der Herzfunktionseinschränkung korreliert mit einer ungünstigen Prognose. Nichtinfektiöse systemische Entzündungsreaktionen (SIRS) können eine der septischen Kardiomyopathie ähnliche „SIRS-Kardiomyopathie“ hervorrufen.

Die Ätiologie der Herzschädigung ist multifaktoriell. Mehrere Kandidaten mit einem pathogenen Potenzial auf das Herz wurden identifiziert: Bakterientoxine, Zytokine und Mediatoren einschließlich des Tumornektrosefaktor alpha, Interleukin-1 und Stickoxid, kardiodepressive Faktoren, reaktive Sauerstoffverbindungen und Katecholamine. Die symptomatische Behandlung der septischen Kardiomyopathie—eingebettet in das Gesamtkonzept der Herz-Kreislauftherapie—besteht in der Volumengabe und in der Unterstützung mit Katecholaminen. Kausale Therapieansätze zur Modulation des proinflammatorischen Toxin-Mediator-Netzwerkes befinden sich in der Anfangsphase.

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  1. Universitätsklinik und Poliklinik für Innere Medizin III, Universitätsklinikum der Martin-Luther-Universität Halle-Wittenberg, Ernst-Grube-Str. 40, 06096, Halle (Saale), Germany

    U. Müller-Werdan, M. Buerke, A. Christoph, R. R. Flieger, K. Heinroth, A. Herklotz, M. Ruß, A. Schlitt, H. Schmidt, G. Söffker & K. Werdan

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  1. U. Müller-Werdan
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  2. M. Buerke
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  3. A. Christoph
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  4. R. R. Flieger
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  6. A. Herklotz
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  8. A. Schlitt
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  9. H. Schmidt
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  11. K. Werdan
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Correspondence to U. Müller-Werdan.

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Serie: Die Intensivtherapie bei Sepsis und Multiorganversagen Herausgegeben von L. Engelmann (Leipzig)

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Müller-Werdan, U., Buerke, M., Christoph, A. et al. Septische Kardiomyopathie. Intensivmed 43, 486–497 (2006). https://doi.org/10.1007/s00390-006-0738-6

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  • DOI: https://doi.org/10.1007/s00390-006-0738-6

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