Effect of vasopressin on hemodynamics in patients with refractory cardiogenic shock complicating acute myocardial infarction

Am J Cardiol. 2005 Dec 15;96(12):1617-20. doi: 10.1016/j.amjcard.2005.07.076. Epub 2005 Oct 21.

Abstract

In a retrospective study of 36 patients who developed cardiogenic shock after myocardial infarction, intravenous vasopressin therapy increased mean arterial pressure from 56 to 73 mm Hg at 1 hour (p < 0.001) and maintained it for 24 hours without changing pulmonary capillary wedge pressure, cardiac index, urine output, or other inotropic requirements. After norepinephrine administration, mean pulmonary capillary wedge pressure increased at 1 hour from 21 to 24 mm Hg (p = 0.04); however, this increase was not sustained at 12 and 24 hours. Norepinephrine was associated with a significant increase in cardiac power index at 24 hours, whereas there was only a trend for an increase in cardiac power with vasopressin therapy. In a cohort of patients who developed refractory cardiogenic shock after myocardial infarction, vasopressin was associated with increased mean arterial pressure and no adverse effect on other hemodynamic parameters.

Publication types

  • Comparative Study

MeSH terms

  • Aged
  • Blood Pressure / drug effects*
  • Cardiac Output / drug effects*
  • Female
  • Follow-Up Studies
  • Humans
  • Male
  • Myocardial Infarction / complications
  • Myocardial Infarction / physiopathology
  • Norepinephrine / therapeutic use
  • Pulmonary Wedge Pressure / drug effects*
  • Retrospective Studies
  • Shock, Cardiogenic / drug therapy*
  • Shock, Cardiogenic / etiology
  • Shock, Cardiogenic / physiopathology
  • Treatment Outcome
  • Vasoconstrictor Agents / therapeutic use*
  • Vasopressins / therapeutic use*

Substances

  • Vasoconstrictor Agents
  • Vasopressins
  • Norepinephrine