K2i / 15A22: Dexemdetomidine v Ketamine
15A22: Exam Report
Compare and contrast dexmedetomidine and ketamine
50% of candidates passed this question.
The majority of candidates were able to describe the mechanism of action, uses, dose and some side effects of each drug. The better answers were in a table format. It is of course possible to include much of the relevant information without using a table; however without the visual prompt of a table it makes it likely sections will be omitted.
When comparing two drugs it would be useful to note that though they both provide sedation with analgesia they are used in different circumstances. In ICU, dexmedetomidine is mainly used for sedation peri-extubation and may be continued post-extubation but this was not often mentioned.
The pharmacodynamic effects often omitted the cardiovascular and respiratory effects of ketamine (particularly bronchodilation).
The pharmacokinetic information required was not detailed but only minimal marks can be awarded for ‘administered IV with 100% bioavailability, liver metabolism and renal excretion’ which was a common answer. Noting dexmedetomidine is metabolised to inactive metabolites and ketamine is metabolised to norketamine gained marks, specific pathways were not required. Both drugs are licenced for administration intravenously (and ketamine may be administered IM); however other routes of administration are emerging in clinical practice for both drugs.
K2i / 15A22: Compare and contrast Dexemdetomidine and Ketamine
Chemical
Dexmedetomidine
Ketamine
Use
Dexmedetomidine
- Sedation
- Anxiolysis
- Analgesia
- Antihypertensive
Ketamine
- Induction GA
- Conscious sedation
- Analgesia
- Severe asthma
Route
Dexmedetomidine
IV – load then infusion
Ketamine
IV
Onset
Dexmedetomidine
15 mins
Ketamine
30-60sec IV
MoA
Dexmedetomidine
Activates pre-synaptic α2 adrenoreceptors in CNS → ↓NA release
∴ ↓symp outflow
α2 agonism in CNS → sedation & anxiolysis
α2 agonism in AS/C fibres → analgesia
α2 agonism in CNS/SC → ↓symp outflow → ↓HR, VD
Ketamine
NMDA Antagonism
Voltage sensitive Ca2+ channel inhibition
Muscarinic antagonist
Facilitates descending inhibitory monoaminergic pathways → inhibits reuptake of CA → INDIRECT SYMPATHOMIMETIC
Weak opioid receptor agonism
PD
Dexmedetomidine
CNS
- Sedation
- Anxiolysis
- But does not cause Resp D
- Gives sedation in a cooperative & semi-rousable state
Resp – none
CVS – ↓MAP, ↓HR
Ketamine
CNS
- Dissociative anaesthesia
- Amnesia (anterograde)
- Analgesia
- Emergence delirium → visual, auditory, illusion & delirium
- ↑CMRO2 & ↑CBF
(Directly dilates cerebral arteries)
RESP
- ↑airway secretions → anticholinergic
- Preserves laryngeal reflexes
- Bronchodilation → ↑symp & Ca2+ channel inhibition
- ↑PAP → ↑symp NS
CVS
- ↑MAP, PAP, CVP, HR, CO, myocardial O2 requirements
GI
- Salivation = antimuscarinic
↑BSL = ↑symp
Both sedate but Dex has more anxiolysis and co-operativity.
Increase CBF with ketamine
Both do not cause respiratory depression however Ketamine has more adverse resp side effects
Dex lowers BP & HR whereas Ketamine sustains despite being a direct -ve inotrope
PK
Dexmedetomidine
A
IV only
D
High PPB 94%
Low VD 1.3L/kg
M
Hepatic
E
Metabolites in urine
Ketamine
A
D
PPB small 12%
Large → 5L/kg
M
High hepatic ER
Norketamine = active
E
H2O soluble metabolites excreted by kidney
<5% unchanged
Both heptically metabolised. Ketamine much more sensitive to altered hepatic BF which will reduce clearance
Ketamine has active metabolites
Adverse Effects
Dexmedetomidine
Hypotension
Bradycardia
Dry Mouth
Nausea
Ketamine
Tolerance (enzyme induction
IHD/HTN/CCF = Increases myocardial work
Increases ICP, CBF and CMRO2
Pregnancy = reduces uterine BF
Prolongs SUX activity
Unmasks myocardial depression when given w sympatholutic
Enhances NDMR block
Ketamine has abuse potential
Dex expensive
- Author: Krisoula Zahariou