| Class | Inotrope |
|---|---|
| Chemistry |
Synthetic catecholamine
|
| Routes of administration |
IV |
| Absorption |
Basically zero oral availability due to destruction by brush border enzymes in the gut (COMT)
|
| Solubility |
pKa = 10.14; sparingly soluble in water
|
| Distribution |
VOD ~ 0.2 L/kg (Majerus et al, 1989)
|
| Metabolism |
Metabolised rapidly by COMT-mediated methylation and conjugation
|
| Elimination |
Metabolites are renally excreted. Half-life is ~2 minutes
|
| Time course of action |
Very short acting, very rapid onset of effect
|
| Target receptor |
Dobutamine is a racemic mixture of stereoisomers; net effect is a partial alpha-1 agonist effect, a full beta-1 agonist effect, and a weak beta-2 agonist effect |
| Mechanism of action |
By binding to the beta-1 receptor, dobutamine causes an increase in intracellular cAMp, which leads to increased calcium availability inside the cardiac myocytes, and therefore increased contractility and pacemaker automaticity |
| Clinical effects |
Increased heart rate, increased contractility, increased lusitopy; decreased peripheral vascular resistance due to beta-2 effect |
| Literature reference |
TGA PI document |
| CICM details of understanding | Level 3 |
| Mentioned around Deranged Physiology | |
| Related SAQs |
Question 15 from the second paper of 2016: dobutamine vs. noradrenaline Question 14 from the second paper of 2011: dobutamine vs. milrinone |