title: Hypotension with dobutamine: beta-adrenergic antagonist selectivity at low doses of carvedilol.
abstract: OBJECTIVE
  To report a case of marked hypotension resulting from the concomitant use of low-dose carvedilol and intravenous dobutamine.
  
  
  METHODS
  A 54-year-old white man with severe heart failure was placed on carvedilol 3.125 mg orally twice a day; three days later the dosage was increased to 6.25 mg orally twice a day. His symptoms of heart failure worsened with increasing fluid retention, orthopnea, paroxysmal nocturnal dyspnea, and elevated blood urea nitrogen and creatinine. He was admitted for treatment of decompensated heart failure with intravenous dobutamine. With each increase in intravenous dobutamine, systolic blood pressure fell. Dobutamine was discontinued when systolic blood pressure reached 56 mm Hg. In a subsequent admission for decompensated heart failure, when the patient was not taking carvedilol, he was treated with intravenous dobutamine and systolic blood pressure increased.
  
  
  CONCLUSIONS
  Although carvedilol is a nonselective beta-adrenergic antagonist, at low doses it is a selective beta1-adrenergic antagonist. Dobutamine is a beta1-, beta2-, and alpha1-adrenergic agonist. Typically, patients with heart failure treated with intravenous dobutamine have a small increase in systolic blood pressure. We propose that the drop in blood pressure with dobutamine in this patient was caused by a fall in systemic vascular resistance due to vascular beta2-adrenergic receptor activation. The normal increase in cardiac output was partially blocked by selective beta1-adrenergic blockade at low doses of carvedilol.
  
  
  CONCLUSIONS
  Beta-adrenergic blockade with carvedilol is now common therapy for patients with congestive heart failure. Intravenous dobutamine is often used when these patients have worsening heart failure. Recognition that treatment with dobutamine in patients taking low doses of carvedilol may result in hypotension is important for appropriate monitoring and therapy.
authors.affiliation: Department of Medicine, Health Sciences Center, University of Colorado, Denver 80262, USA. JoAnn.Lindenfeld@UCHSC.edu
authors.forename: J
authors.initials: J
authors.lastname: Lindenfeld
authors.forename: B D
authors.initials: BD
authors.lastname: Lowes
authors.forename: M R
authors.initials: MR
authors.lastname: Bristow
mesh_terms: D000318:Adrenergic beta-Agonists / Q000009:adverse effects* / Q000627:therapeutic use; D000319:Adrenergic beta-Antagonists / Q000009:adverse effects* / Q000627:therapeutic use; D000328:Adult; D001794:Blood Pressure / Q000187:drug effects; D002227:Carbazoles / Q000009:adverse effects* / Q000627:therapeutic use; D002302:Cardiac Output / Q000187:drug effects; D000077261:Carvedilol; D004280:Dobutamine / Q000009:adverse effects* / Q000627:therapeutic use; D004347:Drug Interactions; D017809:Fatal Outcome; D006333:Heart Failure / Q000188:drug therapy; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D007022:Hypotension / Q000139:chemically induced* / Q000503:physiopathology; D008297:Male; D011412:Propanolamines / Q000009:adverse effects* / Q000627:therapeutic use
chemical_list: D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D002227:Carbazoles; D011412:Propanolamines; D000077261:Carvedilol; D004280:Dobutamine