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DOI: 10.1055/s-0029-1214836
© Georg Thieme Verlag KG Stuttgart · New York
Differenzieller Einsatz von Inotropika, Vasopressoren und Inodilatoren im septischen und kardiogenen Schock
Publication History
Publication Date:
01 July 2009 (online)
![](https://www.thieme-connect.de/media/kardiologie-u2d/200902/lookinside/thumbnails/10.1055-s-0029-1214836-1.jpg)
Abstract
For hemodynamic stabilization of patients in a life-threatening situation such as septic or cardiogenic shock, the use of vasopressors, inotropics and sometimes inodilators is essential although not well supported by randomized studies. As the substances used have no effect on disease progression, they can only serve as hemodynamic „bridges” to gain time for causal therapies to act or until the bodies defense mechanisms have changed the course of the disease.
A differential therapeutic approach, which is useful and often necessary, takes the ventricular-arterial coupling of a damaged heart as well as the microcirculatory changes during shock, especially within the hepato-splanchnic tissue, into account.
During septic shock, inotropics and vasopressors are used in an evidence-based algorithm to achieve a timely optimization of the hemodynamic situation („early goal directed therapy”). To date, noradrenalin (alternatively, adrenalin or dopamine) and dobutamin are the inotropics of choice. During cardiogenic shock, however, only the concept of early revascularization and implantation of an intra-aortic counter pulsation is established by clinical studies. Therefore, pharmacologic stabilization can only serve to bridge the time to immediate coronary angiography and revascularization. In this situation, the use of dobutamin, if necessary in combination with noradrenalin, is judged clinically (RRsyst≥ 90 mmHg). After successful revascularization, however, pharmacologic therapy should be monitored and guided via extended hemodynamic monitoring (cardiac output, wedge pressure). Noradrenalin must be added, if arterial mean pressure remains < 65 mmHg despite an adequate fluid management, dobutamine use, and intra-aortic counter pulsation. Although currently not approved in Germany, the calcium-sensitizer levosimendan represents an interesting and potent therapeutic additive (or alternative) to achieve an adequate cardiac output. The (accurately timed) use of mechanical assist devices is only indicated after failure of above-mentioned recommendations.
Kernaussagen
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Zur hämodynamischen Stabilisierung lebensbedrohlicher Zustände wie dem septischen oder kardiogenen Schock ist der Einsatz von Vasopressoren, Inotropika und teilweise Inodilatoren essenziell, wenn auch in der Regel nicht durch große randomisierte Studien abgesichert.
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Diese Substanzen wirken nicht kausal heilend, sondern sie bauen „hämodynamische und zeitliche Brücken”, um die grundsätzliche Voraussetzung für den vollen Wirkeintritt ursächlicher Therapien oder körpereigener Erholungsmechanismen zu schaffen.
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Ein differenzieller Einsatz der Substanzen ist möglich und zumeist auch notwendig. Stets bedürfen hierbei die adäquate Kopplung von myokardialer Funktion und vaskulärer Nachlast (ventrikuloarterielle Kopplung) bei myokardialer Schädigung sowie die mikrovaskuläre Zirkulation, insbesondere im Hepatikosplanchnikusgebiet, besondere Beachtung.
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Beim septischen Schock ordnet sich die Gabe von Inotropika/Vasopressoren in einen evidenzbasierten Maßnahmenkatalog zur frühen Optimierung der Hämodynamik ein („early goal directed therapy”). Derzeit wird zumeist Noradrenalin als Vasopressor (alternativ Adrenalin, Dopamin) und Dobutamin als Inotropikum der Wahl bevorzugt.
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Beim kardiogenen Schock ist derzeit nur das Konzept der frühen Revaskularisierung sowie die frühe Implantation einer intraaortalen Gegenpulsation (IABP) durch Studien und große Register abgesichert. Die pharmakologische Strategie zur initialen Stabilisierung hat als primäres Ziel den sicheren und schnellen Zugang ins Herzkatheterlabor. Der Einsatz von Dobutamin, wenn nötig in Kombination mit Noradrenalin, wird klinisch gesteuert (RRsyst ≥ 90 mmHg). Nach der Revaskularisierung wird die weitere Therapie mittels erweiterten hämodynamischen Monitoring gesteuert. Bleibt der arterielle Mitteldruck trotz Vor- und Nachlastkorrektur und trotz Dobutamin und IABP weiter unter 65 mmHg, muss Noradrenalin eingesetzt werden. Um außerdem ein adäquates Herz-Zeit-Volumen zu generieren, existiert heute insbesondere mit dem Kalziumsensitizer Levosimendan (als Heilversuch, da bisher in Deutschland nicht zugelassen) eine sehr interessante und potente Therapiealternative. Der (rechtzeitige) Einsatz mechanischer Assistsysteme kommt erst nach Ausschöpfung der o. g. therapeutischen Kaskade infrage.
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PD Dr. med. Alexander Schmeisser
Universitätsklinikum Magdeburg
Klinik für Kardiologie, Angiologie und Pneumologie
Otto-von-Guericke Universität Magdeburg
Leipzigerstraße 44
39120 Magdeburg
Email: Alexander.Schmeisser@med.orga.de