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Pharmakotherapie der akuten schweren Herzinsuffizienz

Katecholamine, Katecholamine, Katecholamine–hat sich nichts geändert?

Therapy of acute severe heart failure: catecholamines, catecholamines, catecholamines–has nothing changed?

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Intensivmedizin und Notfallmedizin

Abstract

The severe acute heart failure is characterized by the heart's limited ability to sustain adequate organ perfusion. Acute heart failure is based on myocardial dysfunction, a patient's negative outcome often results from peripheral circulatory derangements. The positive inotropic effect of beta-receptor agonists is associated with chronotropic and arrhythmogenic properties by which myocardial oxygen demand is increased. Moreover, myocardial beta-adrenoceptor population may be reduced in patients with myocardial heart disease (“down regulation”). Compounds inhibiting phosphodiesterase (PDE) may be useful to increase contractility. They improve cardiac performance without increasing myocardial oxygen demand, because the expected increase in myocardial oxygen consumption is compensated by a decrease in ventricular pre- and afterload. Combination of PDE III inhibitors and catecholamines appears to be useful because PDE inhibitors inhibit the destruction of cAMP, whereas catecholamines stimulate cAMP production. The Ca++-sensitizer levosimendan is another promising approach to treat acute heart failure aside from catecholamines. Levosimendan simultaneously increases myocardial contractility while additionally protecting the heart from ischemia. Levosimendan was proposed especially for patients requiring inotropic support showing myocardial ischemia simultaneously. Aside from exclusively using increasing doses of catecholamines, both classes of substances seem tobe an alternative or additive tool for treating acute heart failure.

Zusammenfassung

Die akute schwere Herzinsuffizienz basiert häufig auf einem myokardialen Pumpversagen und dominiert als „low output“ Syndrom (LOS). Katecholamine sind seit langem etablierte Therapeutika in dieser Situation. Unter Berücksichtigung der pathophysiologischen Mechanismen beim akuten myokardialen Pumpversagen muss ein differential-therapeutisches Konzept bezüglich der Indikation der einzelnen Substanzen erstellt werden. Die Fortschritte der pharmakologischen Intervention müssen sich dabei an den pathophysiologischen Erkenntnissen orientieren. Aufgrund der Veränderungen des normalen Adrenozeptor-Systems („down“–Regulation Phänomen) bzw. gleichzeitiger beta-Blockade muss die klassische katecholaminorientierte Therapie der akuten, schweren Herzinsuffizienz neu überdacht werden. Phosphodiesterase (PDE) III Hemmer und Ca++-Sensitizer (Levosimendan) stellen neue Behandlungskonzepte in dieser Situation dar. Sie führen zu einer Verbesserung der Hämodynamik mit Steigerung der linksventrikulären Funktion und Senkung erhöhter Gefäßwiderstände verbunden zu einer Verbesserung der Organperfusion. Ca++-Sensitizer führen darüberhinaus zu einer Verbesserung der diastolischen Funktion und besitzen myokard-protektive Effekte. PDE III Hemmern bzw. Ca++-Sensitizer in Kombination mit Katecholaminen bieten sich aus pharmakologischer Sicht als aussichtsreiche Therapieform bei akuter Herzinsuffizienz mit LOS an und sollten die ausschließliche Gabe von Katecholaminen ergänzen.

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  1. Klinikum der Stadt Ludwigshafen GmbH, Klinik für Anästhesiologie und Operative Intensivmedizin, Bremserstr. 79, 67063, Ludwigshafen am Rhein, Germany

    J. Boldt & A. Lehmann

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  1. J. Boldt
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  2. A. Lehmann
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Correspondence to J. Boldt.

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Boldt, J., Lehmann, A. Pharmakotherapie der akuten schweren Herzinsuffizienz. Intensivmed 44, 11–19 (2007). https://doi.org/10.1007/s00390-006-0730-1

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  • DOI: https://doi.org/10.1007/s00390-006-0730-1

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