Cardiogenic Shock - Diagnosis and Treatment

64 Part III / Contemporary Treatment
who had anterior myocardial infarction with radiological pulmonary edema); thus, it is
not possible to assess its impact on 12-mo mortality rates (4).
Although no randomized studies have evaluated the benefits of accurate hemody-
namic assessment, we recommend the use of pulmonary artery catheters in patients
without major bleeding contraindications.
GLYCOPROTEIN IIb/IIIa RECEPTOR ANTAGONISTS
There is considerable evidence that outcomes are improved by the use of glycopro-
tein IIb/IIIa receptor antagonists prior to (30) and at the time of percutaneous coronary
intervention (31). (See a further discussion of glycoprotein IIb/IIIa receptor inhibitors
in Chapter 3.) In the setting of acute myocardial infarction and cardiogenic shock,
microvascular flow (32–35) may be enhanced (36,37). Recently, several small nonran-
domized studies have reported improved outcomes with abciximab in patients under-
going percutaneous intervention for cardiogenic shock complicating acute myocardial
infarction (38,39).
When the SHOCK Trial commenced in 1993, the use of IIb/IIIa antagonists (pre-
dominantly abciximab) was rare, but by the final year of the trial in 1998, 61% of
patients undergoing percutaneous intervention were treated with a IIb/IIIa antagonist
(4). However, this treatment was not randomized, so it is not possible to evaluate its
contribution to the better outcomes achieved by emergency revascularization.
In the PURSUIT Trial of 9449 patients with acute coronary syndromes without per-
sistent ST elevation, eptifibatide had no effect on the incidence of cardiogenic shock
(1.2% vs 1.3% with placebo, odds ratio-0.95, 95% CI-0.72–1.25, p = 0.71), but it did
reduce the mortality rate at 30 d (odds ratio-0.51, 95% CI-0.28–0.94, p = 0.03) (40).
The available data favor administration of a IIb/IIIa antagonist, particularly abcix-
imab, in patients with cardiogenic shock who are undergoing percutaneous interven-
tion, unless the risk of bleeding is considered to be too great. It has not yet been defined
just how soon IIb/IIIa antagonists can be safely administered after full-dose throm-
bolytic theraphy.
INOTROPES AND VESOPRESSORS
In patients with cardiogenic shock, a mean arterial pressure of 60 mm Hg is gener-
ally necessary for tissue perfusion. Studies in patients with septic shock have shown
that further elevation of the mean blood pressure by norepinephrine did not improve
systemic perfusion but did increase myocardial oxygen demands (41).
Dopamine and dobutamine are the most commonly used inotropic agents. They have
different effects on the hemodynamics, cardiac output, and systemic vascular resis-
tance (Table 1).
Low-dose dopamine (0.5–2 µg/kg/min) acts on the dopaminergic receptors, causing
vasodilatation and theoretically preserving renal blood flow and natriuresis, an obser-
vation based mainly on data from human volunteers (42). However, a recent Australasian
placebo-controlled trial in intensive care patients reported no nephro-protective benefit
from low-dose dopamine (43). Dopamine’s myocardial inotropic and chronotropic
effects are mediated through several myocardial β-1-adrenergic receptors and are most
evident with doses above 5 µg/kg/min. As the infusion rate rises, peripheral α-adrener-
gic vasoconstriction activity increases, raising the blood pressure. Because dopamine
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