Inhaled anesthetics properties

Inhaled anesthetics properties

Gas blood solubility / blood gas Gas lipid solubility / Oil/gas

partition coe cient partition coe cient
Check the e ectiveness of the To determine potency
anesthetics How much is the dose / determine
potency

Gas blood solubility / blood gas partition coe cient

High solubility Lowe solubility

Longer time to saturate blood Quickly saturate blood
Slower induction time Quick induction time
Slower washout Quick washout

- [blood]1.4>[alveoli]
The higher the number =
dissolve well in blood = slow
induction
Gas blood solubility: after blood saturated
here gas start being in it’s gas form because
it can’t dissolve anymore = measured by
partial pressure = more gas not dissolved the
higher the partial pressure
• Molecules dissolved in blood: No
anesthetic e ect
• Molecules NOT dissolved: Anesthetic e ect
• Need to saturate blood to generate
partial pressure
• So MORE solubility in blood = LONGER to
take e ect

Gas lipid solubility / oil/gas partition coe cient

↑lipid a nity = more potent (Meyer-Overton rule)
MAC / minimum alveolar concentration low = need small dose concentration of anesthetic to prevents
movement in 50% ( 1 MAC = 50% e cacy )
= high potency ( less dose ) and high lipid solubility

Bene t of MAC is drug combination: use multiple

drugs small doses and avoid side e ect

Determine multiple drugs potency: by adding the

MAC up

Take home points:

- ↑blood solubility = ↑blood / gas partition coe cient = slower induction
- ↓MAC = ↑oil / gas partition coe cient = ↑potent / low dose
- MAC = dose = lower MAC mean we need low dose of the drug to be e ective
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Special Side E ects of inhaled anesthesia
Halothane – Hepatotoxicity & malignant hyperthermia
• Liver tox: Rare, life-threatening
• Massive necrosis, increased AST/ALT

Methoxy urane – Nephrotoxicity

• Renal-toxic metabolite

En urane – Seizures
• Lowers seizure threshold

GABA Receptor Intravenous Anesthetics

• Etomidate
• Propofol
• Benzodiazepines
• Barbiturates ( thiopental / pentothal )
• GABA is largely inhibitory
• These drugs activate receptor→sedation

Clinical use scenarios of anesthesia:

Induction ( mostly IV drug ): Put patient to sleep
• Propofol
• Etomidate
• Ketamine
Maintenance – Keep patient asleep ( usually use inhaled
anesthesia )
• Propofol
• sevo urane
• des urane

Typical Open Heart Case

Induction
• Propofol, Midazolam ( give some amnesia)

Paralysis
• Rocuronium

Maintenance
• Sevo urane( to put the patient to sleep but don’t stop the
pain ), fentanyl ( to block pain )

Example of opioid overdose

Pharma equations
1. blood gas partition coe cient: [blood]1.4>[alveoli]

2. Lipid solubility or potency equation

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 Intravenous anesthesia drugs:

Mechanism Uses and Potency Side e ect

Barbiturates Binding to GABA High potency from high lipid Myocardial / respiratory depression
( thiopental / receptor solubility easily cross BBB ↓ cerebral blood ow
Pentothal ) Ultra short acting because the drug
will redistribute / stored into muscle
and fat but is take long time to
washout
Rapid - onset short - acting

Benzodiazepines • Bind to GABA Orally they are anti-anxiety and IV • Cause cardio-respiratory depression
Midazolam, receptors = increase they are anesthesia =↓BP
Lorazepam, frequency of GABA ion • Overdose: treated by Flumazenil
Diazepam, channel opening = • Low dose: anti-anxiety (anxiolytic) • Midazolam (Versed): Short
Alprazolam Increase level of CI • High dose: sedation, amnesia, procedures (endoscopy)
make muscle less anticonvulsant
likely to depolarize

Opioids Act on opioid (mu) Orally for chronic pain and high dose Side e ects:
Morphine,Fentan receptors in brain IV for anesthesia • ↓respiratory drive
yl, • opioids bind to Mu People who take them for chronic • ↓BP
Hydromorphone receptors pain over long term develop tolerance • Nausea/vomiting
• G-protein linked and decrease e ectiveness = major • Ileus
• 2nd messengers not problem with cancer pain • Urinary retention
clearly understood • No amnesia
• Increase K e ux Decreased e ect on
from cells causing • Pain Overdose:
HYPERpolarizes→l • Sedation Cause life threatening respiratory
ess pain • Nausea, vomiting depression treated by naloxone
transmission • Respiratory depression Opioid antidote / Mu antagonist
• Cough suppression Reverses e ects within minutes
Important to give drug • Urinary retention
Must be given IV/nasal→ because it’s
cause amnesia inactivated by liver if it given orally
because opioids are • No tolerance to constipation or
analgesics but have miosis
no amnesia e ect

Ketamine PCP / phencyclidine / It’s dissociative drug mean cause Good thing about ketamine it have few
angel dust derivative ( analgesia and amnesia ( they will not respiratory and cardiovascular side
abused by people but remember anything ) e ect
important side e ect
hallucination and Can cause ↑BP ↑HR
being violent ) When it’s abused as street drug it cause
hallucination and violent behaviors
Antagonist of NMDA
receptor ( NMDA are If ketamine used alone when the patient
receptor activated by wake up will have “Emergence
glutamate) Reactions” can stay for few hours
• Disorientation
• Dreams, hallucinations
•Can be frightening to patients
• Co-administer midazolam
( Benzodiazepines )
to help

Etomidate Modulates GABA Relatively hemodynamically neutral Blocks cortisol synthesis = cause acute
receptors / Blocks • Good for hypotensive patients adrenal insu ciency
neuro excitation
Used for Rapid sequence intubation Etomidate and succinglcholine both
Anesthesia but not for patient in severe respiratory washout very fast
analgesia = mean the distress and need emergency placed
patient can be sleep on a ventilator
but still feel pain Usually in this case it’s co-
administrated with succinglcholine

Propofol GABA modulator Used mostly for patient of ventilator Myocardial depression
Quick induction Sedation, amnesia Hypotension
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