A higher mean arterial pressure (MAP) achieved by
norepinephrine up-titration may improve organ blood flow in
critically ill, whereas norepinephrine-induced afterload rise might
worsen myocardial function. Our aim was to assess the effects of
norepinephrine dose titration on global hemodynamics in
cardiogenic shock. We prospectively evaluated 12 mechanically
ventilated euvolemic patients (aged 67±12 years) in cardiogenic
shock (10 patients acute myocardial infarction, 1 patient dilated
cardiomyopathy, 1 patient decompensated aortic stenosis).
Hemodynamic monitoring included arterial and Swan-Ganz
catheters. The first data were obtained at MAP of 65 mm Hg,
then the norepinephrine dose was increased over 40 min to
achieve MAP of 85 mm Hg. Finally, the norepinephrine-dose was
tapered over 40 min to achieve MAP of 65 mm Hg.
Norepinephrine up-titration increased MAP to the predefined
values in all patients with concomitant mild increase in filling
pressures and heart rate. Systemic vascular resistance increased,
whereas cardiac output remained unchanged. During
norepinephrine down-titration, all hemodynamic parameters
returned to baseline values. We observed no changes in lactate
levels and mixed venous oxygen saturation. Our data suggest
that short-term norepinephrine dose up-titration in cardiogenic
shock patients treated or pretreated with inotropes was tolerated
well by the diseased heart.
After transradial primary percutaneous coronary intervention, early patent hemostasis and short artery compression times were associated with a higher incidence of local hematomas. The incidence of hematomas was dependent on the use of abciximab, but unrelated to the type of P2Y12 inhibitor used. All hematomas were without clinical consequences.
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