Cardiogenic shock is a syndrome of different etiologies resulting in t
he inability of the heart to provide adequate O-2 delivery to peripher
al organs and tissues with or without signs of severe pulmonary conges
tion or pulmonary edema. Clarification of the underlying etiologies is
essential for prognosis and therapy. Depending on the various etiolog
ies, the therapeutic procedure may be totally different. Furthermore,
it is decisive to differentiate between an acute shock (e.g., acute my
ocardial infarction) and the development of a cardiogenic shock state
on the basis of preexisting chronic congestive heart failure (e.g., co
ngestive cardiomyopathy). Whenever possible the underlying disease sho
uld be treated causally (e.g., PTCA or thrombolytic therapy in AM, lys
is in acute pulmonary embolism) in addition to symptomatic pharmacolog
ic treatment with vasodilators and/or inodilators. In myogenic cardiog
enic shock, the treatment with inotropic drugs (with and without vasod
ilatory potency) and, if necessary, in combination with additional vas
odilators may be life-saving. At present, there is no alternative to c
atecholamines in the acute state with apparent hemodynamic instability
. Catecholamines still represent the initial first line treatment. A S
wan-Ganz catheter is mandatory in such situations. In view of the rapi
d beta(1)-receptor down-regulation induced by endogenous catecholamine
s, long-term administration of exogenous catecholamines (adrenalin, do
pamine, dobutamine), seems essentially problematic, since these compou
nds intensify and accelerate this process. New beta(1)-receptor-indepe
ndent alternatives with considerable inotropic properties are beta(2)-
agonists (dopexamine), PDE-III-inhibitors (amrinone, milrinone, enoxim
one), and H-2-receptor agonists (impromidine, arpromidine), as well as
Ca++ sensitizers (Pimobendane). Initial results with these compounds
are promissing to decrease the present mortality rate of 85-95 %. The
availability of these new pharmacologic interventions and their applic
ation with mechanical left-heart assist devices (e.g. TABP, Hemopump,
percutaneous heart lung machine, Novacor) may profoundly increase ther
apeutic efficacy. Convicing results, however, have not yet been report
ed in the world literature.