| Class | Concentrated electrolyte |
|---|---|
| Chemistry |
Monovalent cation salt |
| Routes of administration |
IV only (specifically, can only be administered through CVC) |
| Absorption |
Well absorbed in the small intestine. largely because of paracellular transport (high concentration). Good bioavailability |
| Solubility |
pKa 3.09; good water solubility |
| Distribution |
VOD=0.2L/kg, basically confined to the extracellular fluid |
| Metabolism |
Does not undergo any metabolism; excreted unchanged in the urine |
| Elimination |
Elininated renally, where specific reabsorption mechanisms in the renal tubule regulate the rate of sodium and chloride excretion |
| Time course of action |
For control of intracranial pressure, onset of effect is very rapid (within tens of seconds of the infusion starting) |
| Target receptor |
Mechanism of action does not involve receptor binding; you might say the target is the blood brain barrier |
| Mechanism of action |
Increases the osmolality of the extracellular fluid, and therefore decreases the volume of the intracellular compartment by producing an osmotic shift of intracellular water of of the cells. This produces the desirable clinical effect of decreasing the volume of brain tissue, and therefore reducing the intracranial pressure. |
| Clinical effects |
Increase in serum osmolality, which produces the desireable osmotic decrease in intracranial pressure. |
| Literature reference |
TGA PI document |
| CICM details of understanding | Level 1 |
| Mentioned around Deranged Physiology | |
| Related SAQs |
Question 10 from the first paper of 2015; also, from the Second Part exam, Question 5 from the second paper of 2017, Question 4 from the first paper of 2007 and Question 8 from the first paper of 2001. |