Infarktbedingter kardiogener Schock

Kernaussagen

Bedeutung. Der kardiogene Schock tritt in 7 - 10 % nach akutem Myokardinfarkt auf und hat eine hohe Sterblichkeit (50 - 80 %)

Pathophysiologie. Neben der primären Einschränkung der Pumpfunktion durch die Ischämie tritt zunehmend die systemische Entzündungsreaktion in den Mittelpunkt der pathophysiologischen Grundlagen des kardiogenen Schocks. In der Frühphase sind vielfältige hämodynmische Konstellationen möglich (z. B. Hypoperfusion bei niedrig-normalem Blutdruck). Dies kann das Krankheitsbild verschleiern.

Diagnostik. Klinische Zeichen des Schocks (u. a. arterielle Hypotonie, Oligurie, Verwirrung) stehen im Mittelpunkt der Diagnostik. Hämodynamische Messungen (Pulmonalarterienkatheter) können die klinische Diagnose bestätigen und erleichtern eine rationale Therapie.

Die Echokardiographie gibt grundlegende Informationen zur Pumpfunktion und zu mechanischen Infarktkomplikationen (z. B. Ventrikelseptumdefekt, akute Mitralinsuffizienz, Ventrikelperforation).

Therapie. Die frühzeitige Rekanalisierung des infarktverursachenden Gefäßes - meist durch eine perkutane Koronarintervention (PCI) - ist die Therapie der Wahl. Sie darf nicht unnötig verzögert werden.

Die medikamentöse Therapie zielt auf die Etablierung eines minimal suffizienten Kreislaufs unter maximaler Restriktion der Katecholamine. Hierzu ist auch eine optimale Einstellung des Volumenstatus notwendig. Die adäquate Behandlung eines sich oft ausbildenden Multiorgandysfunktionssyndroms ist überlebenswichtig.

Literatur

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