Intravenous diltiazem worsens regional function in compromised myocardium

Anesth Analg. 1988 Mar;67(3):205-10.

Abstract

The effect of intravenous diltiazem on regional myocardial function was assessed in a canine model of critical constriction of the left anterior descending coronary artery (LAD). Maintenance anesthesia with fentanyl (1.5 micrograms.kg-1.min-1), 60% inspired nitrous oxide, and 0.7% inspired halothane resulted in regional dysfunction, measured as postsystolic shortening (20.6 +/- 10.7%), which was significantly worsened after 0.1 mg/kg (48.7 +/- 12.5%, P less than 0.05) and after 0.2 mg/kg (68.8 +/- 11.7%, P less than 0.05) intravenous diltiazem. Systolic shortening in the compromised LAD territory was substantially depressed after 0.1 mg/kg diltiazem (8.2 +/- 0.6% to 5.3 +/- 1.3%, P less than 0.05) and was essentially abolished after 0.2 mg/kg diltiazem (8.2 +/- 0.6% to 0.7 +/- 2.3%, P less than 0.05). At the higher dose of diltiazem, cardiac output was substantially decreased (1.37 +/- 0.23 L/min to 0.88 +/- 0.30 L/min, P less than 0.05) and LV dP/dtmax significantly depressed (1090 +/- 90 mm Hg/sec to 744 +/- 80 mm Hg/sec, P less than 0.05). These results demonstrate significant depression of regional systolic shortening and substantial worsening of regional dysfunction in myocardium with a compromised blood supply, in association with significant depression of left ventricular performance, with intravenous diltiazem administration during anesthesia.

MeSH terms

  • Anesthesia, Inhalation
  • Anesthetics / toxicity*
  • Animals
  • Coronary Disease / physiopathology*
  • Diltiazem / toxicity*
  • Dogs
  • Drug Interactions
  • Fentanyl / toxicity
  • Halothane / toxicity
  • Heart / drug effects*
  • Heart / physiopathology
  • Hemodynamics / drug effects
  • Infusions, Intravenous
  • Nitrous Oxide / toxicity

Substances

  • Anesthetics
  • Diltiazem
  • Nitrous Oxide
  • Fentanyl
  • Halothane