Katecholamine im kardiogenen Schock: hilfreich, nutzlos oder gefährlich?

Zusammenfassung

Der kardiogene Schock ist charakterisiert durch eine inadäquate Perfusion des Körpers und der Organe. Er hat seine Ursache in einer Pumpdysfunktion des Herzens, meist aufgrund eines akuten Myokardinfarktes. Die Letalität ist mit 50-70 % trotz optimaler Therapie sehr hoch. Eine rasche Diagnostik, aggressive Therapieansätze (invasive oder operative Revaskularisation, mechanische Pumpunterstützung) und die medikamentöse Unterstützung des Herz-Kreislaufsystems des Patienten sind notwendig, um die Prognose zu verbessern. Medikamentös werden zur Behandlung des kardiogenen Schocks an erster Stelle Katecholamine eingesetzt. Sie wirken über Beta- und Alpha-Rezeptoren auf die Inotropie, die Herzfrequenz, den myokardialen Sauerstoffverbrauch und den Gefäßtonus. Die Anwendung von Katecholaminen hat jedoch nicht nur Vorteile. Sicher führen sie zu einer Steigerung des Herzzeitvolumens (HZV) und des systemischen Blutdruckes. Aber in der Folge kann es durch den gesteigerten Sauerstoffbedarf zur Azidose, durch die Vasokonstriktion zur Minderperfusion und schließlich zu einer gesteigerten inflammatorischen Reaktion des Organismus kommen, wodurch die kardiale bzw. die globale Organfunktion weiter kompromittiert werden kann. Fazit: Derzeit sind Katecholamine wichtig und notwendig zur Therapie des kardiogenen Schocks - aber die Therapie mit Katecholaminen sollte nur so lange und hochdosiert wie nötig erfolgen.

Summary

Cardiogenic shock is characterized by inadequate organ and tissue perfusion, due to cardiac dysfunction, predominately following acute myocardial infarction. Mortality rates for patients with cardiogenic shock remain high, ranging from 50-70 % despite effective therapy. Rapid diagnostics, aggressive therapeutic approach (invasive or surgical revascularisation) and pharmacological support are currently used to improve the clinical outcome and survival. In the first line commonly sympathomimetics like dopamine, dobutamine, epinephrine and norepinephrine are used for the pharmacological treatment. They have a high affinity for alpha- and beta adrenergic receptors, leading to a positive inotropic cardiac function, an increase in heart rate, oxygen enhanced demand, and an increase in vasoconstriction. However, there are also some disadvantages in the use of sympathomimetics in patients with cardiogenic shock. Clearly, metabolic acidosis due to the increased oxygen demand can be observed. Vasoconstriction induced by sympathomimetics can lead to perfusion mismatch or even deficit within the microcirculation. Additionally, in some studies which give evidence that the use of sympathomimetics can directly lead to enhanced systemic inflammatory response due to an increased IL-6 expression.

However, sympathomimetics are still firstline therapeutics for treatment of cardiogenic shock - with respect to dosage and duration of treatment.

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