Test 1: Ketamine Flashcards

1
Q

What is Ketamine a derivative of?

A

Phencyclidine (PCP)
-1/10th as potent as PCP

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2
Q

What is the MOA of Ketamine?

A

-NMDA Receptor antagonist in the spinal cord and brain, which results in a selective depressant effect on the medial thalamic nuclei that is responsible for blocking afferent signals of pain perception to the thalamus and cortex (Thalamic nuclei = functional dissociation of the cerebral cortex and the thalamus).

-Non-competitive binding with the ion channel pore
-Inhibits nicotinic Ach receptors (analgesia)
-Also inhibits TNF-alpha and IL-6 (anti-inflammatory effects)

New evidence of binding: (causes local anesthetic properties)
-Na+ Channels
-ĸ and μ – opioid receptors

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3
Q

What is Dissociative Anesthesia?

A

A unique, catatonic state in which the patient feels separated from the environment and has profound analgesia and amnesia yet retains most protective reflexes.
-Hypnosis + analgesia
-Psychological SEs like hallucination and emergence delirium limit its use
-Evidence showing subanesthetic doses can be used for tx of acute/chronic pain

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4
Q

What are the Pharmacokinetics associated with Ketamine?

A

-Onset = 1-2 minutes
-Low protein binding = 12%
-Highly lipid soluble
-Metabolism: Hepatic CYP = demethylation to form an active metabolite = Norketamine (1/3 - 1/5 as potent as Ketamine)
-DOA = 5-15 minutes
1/2 life = 2.5 -3 hours (dependent on liver blood flow)

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5
Q

What is the Induction dose of Ketamine?

A

1-2 mg/kg IV or 4-6 mg/kg IM

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6
Q

What are the maintenance doses for Ketamine?

A

-30 - 90 mcg/kg/min
OR
-15-45 mg/kg/min + 50-70% N2O

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7
Q

What are the CNS effects of Ketamine?

A

-Profound analgesia
-Cataleptic state = eyes open, pupils reactive to light, corneal reflexes intact, lacrimation, blinking, involuntary muscle mvmt (nystagmus)
-Salivary glands increased
-CBF increased 60-80%
-Increased CMRO2, CBF, and ICP and IOP
-Being studied in Germany for neuro surgery due to improved cerebral perfusion, but impedes patient’s ability to follow commands postop.

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8
Q

What are the Respiratory effects of Ketamine?

A

-Bronchodilation
-Maintenance of Respiratory muscle tone and respiratory drive
-Increased salivation (counter with glycopyrrolate but beware of tachycardia)
-Airway reflexes intact (potential for laryngospasm)
-Potential for silent aspiration
-Respiratory depression can occur at high doses or when used with opioids

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9
Q

What are the CV effects of Ketamine?

A

-A useful induction agent for patients with hypovolemia
-Increased SNS tone = Increased CO (if normal catechol stores)
-Direct myocardial depressant effect (bad for patients in shock with depleted catecholamine stores)
-Increases BP, CO, HR, CVP, myocardial contractility, and myocardial O2 consumption

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10
Q

What are the Misc. effects of Ketamine?

A

-Aqueous solution = NO pain on injection
-Tracheal, bronchial, and salivary muscle gland secretions are increased with ketamine, which may require the use of an antisialagogue (risk for laryngospasm).
-Ketamine usually increases IOP, but the effect appears dose dependent.
-Ketamine causes nystagmus, increased muscle tone, and muscle spasms, which may not be appropriate for some ophthalmic procedures.
-Moderate analgesia
-Crosses into placenta (highly lipid soluble)
-Onset of effect is relatively slow compared to other induction drugs (2–5 min).

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11
Q

How does Ketamine have such a rapid onset?

A

-Depressed consciousness + increased sympathetic tone
-Increased SNS tone leads to an increased in CO (if normal catechol stores)
-More lipid soluble and less protein bound than other IV induction agents
-Inc CO + inc CBF = rapid cerebral uptake and then redistribution to peripheral compartments

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12
Q

What is Norketamine?

A

The active metabolite of Ketamine.
-1/3 to 1/5 as potent as Ketamine
-Has the potential to contribute to clinical effects with long infusions or chronic use

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13
Q

What are the anesthetic uses for Ketamine?

A

Enhances opioid-induced analgesia and prevents hyperalgesia
-Used as an adjunct at low doses to augment RA for C/S when block is inadequate for delivery
-Induction agent for patients with asthma or hypovolemia
-Adjunct bronchodilator in status asthmaticus (relaxes bronchial smooth muscle)
-Analgesic for burn therapy dressing changes
-Generally avoided in neuroanesthesia
-Aids in fiberoptic intubation, both awake and asleep

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14
Q

What conditions is Ketamine C/I in?

A

-CHF
-CAD
-Uncontrolled HTN
-Neuro & cerebral aneurysms

Requires caution in patients with hypertension, angina, congestive heart failure, increased intracranial pressure, increased intraocular pressure, psychiatric disease, and airway problems

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15
Q

Explain how Ketamine works on the NMDA Receptor.

A

The NMDA receptor is a ligand-gated ion channel where anions Ca 2+ and Na + are voltage dependent. L-glutamate, an amino acid, is probably the most important excitatory neurotransmitter in the CNS. At the NMDA receptor, it causes the opening of the ion channel. A rapid influx of Na + , Ca 2+ , and K + results in the depolarization of the normally negative postsynaptic membrane that initiates the action potential. Ketamine is a noncompetitive antagonist at this receptor.

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16
Q

How do you measure depth of anesthesia with Ketamine?

A

Because the usual signs of anesthesia are not evident with ketamine, movement in response to painful stimuli is often required for judgments of adequate anesthesia.
-BIS can be unchanged or ever increased, even when patients are unconscious

17
Q

What is important to know regarding Ketamine and emergence?

A

Emergence is associated with psychic disturbances (vivid illusions, sensations of drunkenness, delirium, restlessness, altered states of consciousness, extracorporeal sensations, and combativeness. Usually resolves within a few hours). The benzodiazepines diazepam, lorazepam, and midazolam were found to significantly decrease the incidence of these reactions.

18
Q

How does Ketamine cause increased SNS tone?

A

Ketamine is an indirect sympathomimetic, releasing catecholamines. This action accounts for the cardiac stimulation and bronchodilation.

Makes you release endogenous catechol stores. If patient already has low SNS tone (ex: trauma), ketamine can cause them to worsen even further.
-Can have decrease in BP, but balances out with increased SNS response. However, in patient with low SNS stores already, this will cause a severe drop in BP and be very bad.

19
Q

What is the induction dose of Ketamine (Katzung)?

A

1-2 mg/kg IV

20
Q

What is the DOA of Ketamine (Katzung)?

A

5-10 min

21
Q

What is the dose of Ketamine used to augment RA when additional analgesia is needed (ex: C/s under neuraxial with insufficient block)?

A

0.2 - 0.8 mg/kg IV

22
Q

What is the dose of Ketamine given during GA and postop to augment opioid analgesia and reduce opioid tolerance/opioid-induced hyperalgesia?

A

3 - 5 mcg/kg/min