| Class | Inotrope |
|---|---|
| Chemistry |
Phenylethylamine |
| Routes of administration |
IV, s/c, IM |
| Absorption |
Good oral bioavailability (88%) |
| Solubility |
pKa = 10.25; highly water soluble, but also reasonably lipid soluble, so it crosses the blood brain barrier |
| Distribution |
VOD=3L:/kg, minimally protein-bound (~4-6%) |
| Metabolism |
A small and variable quantity is metabolised into norephedrine, but otherwise it is eliminated unchanged |
| Elimination |
Mostly eliminated as unchanged drug in the urine |
| Time course of action |
Average half-life is about 6 hours |
| Target receptor |
Directly acts on beta-1 receptors, but this is not the main mechanism of effect |
| Mechanism of action |
By acting as a false neurotransmitter, ephedrine displaces noradrenaline from storage vesicles in noradrenergic synapses, therefore increasing the synaptic and systemic noradrenaline concenttration. Because it has effecs on all classes of noradrenaline receptor, the clinical effect is similar to adrenaline. |
| Clinical effects |
Slightly increased peripheral resistance and afterload, increased blood pressure; redistribution of blood flow from splanchnic circulation and skeletal muscle. Increased heart rate, contractility, and cardiac output. Ephedrine has |
| Literature reference |
Limberger et al (2013) |
| CICM details of understanding | Level 2 |
| Mentioned around Deranged Physiology |
Sympathomimetics, as it is one of those; but otherwise only Classification of inotropes and vasopressors |
| Related SAQs |
Question 13 from the second paper of 2022 |