The effects of short-term norepinephrine up-titration on hemodynamics in cardiogenic shock

Physiol Res. 2010;59(3):373-378. doi: 10.33549/physiolres.931804. Epub 2009 Aug 12.

Abstract

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.

Publication types

  • Clinical Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adrenergic alpha-Agonists / administration & dosage*
  • Adult
  • Aged
  • Blood Pressure / drug effects
  • Cardiac Output / drug effects
  • Critical Care
  • Female
  • Heart Rate / drug effects
  • Hemodynamics / drug effects*
  • Humans
  • Male
  • Middle Aged
  • Monitoring, Physiologic
  • Norepinephrine / administration & dosage*
  • Prospective Studies
  • Respiration, Artificial
  • Shock, Cardiogenic / drug therapy*
  • Shock, Cardiogenic / physiopathology
  • Time Factors
  • Treatment Outcome
  • Vascular Resistance / drug effects

Substances

  • Adrenergic alpha-Agonists
  • Norepinephrine