Non barbiturate induction agent.
Structure- Phencyclidene derivative that produces “Dissociate anaesthesia”
Dissociation between thalamus and limbic system – catalyptic state in which eyes remain open with a slow nystagmic gaze, noncommunication although wakefulness present.
Hypertonic and purposeful skeletal muscle movement often occur independently.
Chemical properties- Water soluble phencyclidine derivative ‘s’ isomer – intense analgesia,rapid metabolism and emergence reactions.
Action on N-methyl – D-aspartate receptors ,opioid receptors,monoaminogenic receptors, muscarinic and voltage sensitive Calcium channel.
Noncompetative antagonist of NMDA receptor.
It also act on Mu,delta and kappa receptors.
Antinociceptive action through monoaminergic receptors.
Bronchodilatation and emergence delirium through muscarinic receptors.
RAPID ONSET OF ACTION-Within one min of IV and 5 min.of IM. Injection.
Large volume of distribution
Elimination half life 2-3 hrs.
Hepatic microzomal enzymes cytochrome P450 .
- Analgesia-0.2 to 0.5 mg/kg
- Induction of anaesthesia 1-2 mg/kg IV or 4-8 mg/kg IM.-
Action in30-60 sec.
Maintain pharangyeal and laryngeal reflexes.
Dressings of Burn patients – commonly used.
Induction agent in asthamatic patients as it causes bronchodilation,
Cath lab procedures in paediatric pt.
- Neuraxial analgesia-intradurally [preservative free prepration]
CNS-cerebral vasodilation-increase in 60%cerebral blood flow.
EEG- abolish alpha rhythm and dominance of theta activity.increase excitatory activity.unlikely to precipitate convulsion in pts with seizure disorder.
- Heart Rate- increases by 0-59%
- MAP- increases by 40 %
SVR- Increases by 33%
Pulmonary artery pressure – increases by 44-47%
PVR-increases by 33%.
LVEDP /PAOP – unchanged .
RA pressure -15 to 33%
Cardiac INDEX- 0 to 42%
Stroke volume – decreases by 0-21%
Dp/Dt – unchanged.
Myocardium- 1.positive ionotropic effect.increase in calcium influx.
- Sympathadrenal release of norepinephrine.
Actions or not dose related.second dose has opposite effect of first dose.
Increase heart rate – can have problem with pts.of coronary artery disease and valvular heart disease.
Ventilation and airway
- No depression of ventilation
- Upper airway reflexes,skeletal muscle toneis maintained.
Bronchomotor tone- Bronchodilation
Mechanism- increase catecholamine concentration.
Inhibition of catecholamine uptake.
Voltage sensitive Ca Channel block
Inhibition of post synaptic nicotinic and muscarinic receptors.
- Induction agents in 1.Hypovolemic patients
- Burn patient.
- Children with cyanotic congenital heart disease.
- Constrictive pericarditis
- Cardiac tamponade.
Interaction with Inhalational agents- no increase in symathoadrenal activity of ketamine.
Benzodiazepines- Decreases cardiovascular actions.
Verapamil- Hypertensive effect of Ketamine attenuated.
Emergence Delirium- Visual,Auditory,proprioceptive and confusional illusions progress to delirium.
Cortical blindness – transient effect
Dreams and hallucinations-up to 24 hrs.
Mechanism of emergence delirium – Ketamine induced inhibition of inferior colliculus and medial geniculate nucleus as leading to misinterpretation of auditory and visual stimuli.
Loss of skin and musculoskeletal sensation result in decrease ability to perceive gravity.
Increased risk of emergence delirium present in->15 yrs pt.
Doses>2 mg /kg
H/o personality problem.