Perioperative deterioration of the circulatory performance of patients
undergoing heart surgery ranges from transitory impairment in cardiac
output by deterioration of the compensation range of the oxygen trans
port system to manifest circulatory failure without previous myocardia
l damage and the acute decompensation of pre-existing chronic heart fa
ilure. On the basis of the current state of knowledge in this field, a
concept for rational staged treatment should be based on the differen
t myocardial beta-adrenoceptor conditions related to the type and stag
e of the individual underlying heart disease and on adrenoceptor subty
pe specific properties of positive inotropic drugs. 1. The therapy of
perioperative ''circulatory'' insufficiency after extra-corporal circu
lation consists of the use of drugs to adapt the performance of the ox
ygen transport system to increased overall oxygen demand. Simultaneous
volume loading (by CVP) and positive inotropic support with dobutamin
e are the best means of treating this (normally transitory) dysregulat
ion. 2. In the case of manifest severe circulatory insufficiency (low
cardiac output syndrome), sepsis or acute heart failure (e.g., followi
ng acute myocardial infarction), the use of a pulmonary artery cathete
r for determining perioperative cardiac output and resistance is essen
tial. In such cases, positive inotropic therapy is based on catecholam
ines of medium (dobutamine) to high (adrenaline) efficacy, because it
can be assumed that the beta-adrenoceptor pattern will remain normal w
ith regular functioning and regulation of the (remaining) myocardium u
p to the onset of acute heart failure. To reduce the work load on the
heart and to maintain adequate perfusion pressures, the peripheral vas
cular resistance is adjusted to 800 - 1200 dyn.s.cm(-5) using vasocons
trictors (phenylephrine, noradrenaline, depending on frequency) or dil
ators (nifedipine, nitroglycerine, possibly ACE inhibitors). 3. Severe
chronic heart failure with perioperative decompensation is accompanie
d by p-adrenoreceptor down-regulation of varying degress of severity a
nd a capacity for postreceptor stimulation which is, from a clinical s
tandpoint, largely unaffected. Except in the severest cases of cardiom
yopathy, there is little impact on cAMP/PDE-III interaction. In this s
ituation, we use PDE-III inhibitors as the sole therapy. 4. If the hem
odynamic improvement obtained is insufficient, the PDE-III inhibitors
is supplemented by low doses of catecholamines (adrenaline). This almo
st always produces sufficient improvement in circulatory performance.
In the overwhelming majority of cases, the situation can be brought un
der control by using this staged therapy program adapted to the cardia
c and circulatory condition to be expected in each case (after problem
s requiring surgery have been rigorously excluded). If this therapy is
unsuccessful, steps such as the use of mechanical support devices or
a transplant should be discussed.