Please enable JavaScript.
Coggle requires JavaScript to display documents.
Anesthetics (Pharmacology) - Coggle Diagram
Anesthetics (Pharmacology)
General Anesthetics
Intravenous anesthetics
Dissociative
Drugs
Ketamine
Possible Mechanism
Blocks excitation by glutamate at NMDA receptors
Pharmacologic Effects
Analgesia, amnesia
and catatonia but consciousness retained, cardiovascular (CV)
stimulation!
Pharmacokinetics
Moderate duration of action-hepatic metabolism
Toxicities and Interactions
Increased intracranial pressure,
emergence reactions
Imidazole
Possible Mechanism
-
Pharmacologic Effects
Minimal effects on CV and respiratory functions
Drugs
Etomidate
Pharmacokinetics
Short duration due to redistribution
Toxicities and Interactions
No analgesia, pain on injection (may need opioid), myoclonus,nausea, and vomiting
Benzodiazepines
Pharmacologic Effects
Less depressant than barbiturates Slower onset, but longer duration than barbiturates
Pharmacokinetics
Slower onset, but longer duration than barbiturates
Possible Mechanism
-
Toxicities and Interactions
Postoperative respiratory depression reversed by flumazenil
Drugs
Midazolam
Opioids
Pharmacologic Effects
Marked analgesia,respiratory depression
Pharmacokinetics
Alfentanil and remifentanil fast onset (induction)
Possible Mechanism
Interact with µ, κ, and δ opioid receptors
Toxicities and Interactions
Respiratory depression reversed by naloxone
Drugs
Fentanyl
Alfentanil
Remifentanil
Morphine
Barbiturates
Pharmacologic Effects
Circulatory and respiratory depression decrease intracranial pressure
Pharmacokinetics
High lipid solubility-fast onset and short duration due to redistribution
Possible Mechanism
Barbiturates, benzodiazepines, etomidate, and propofol facilitate GABA mediated inhibition at GABAA receptors
Toxicities and Interactions
Extensions of CNS depressant actions additive CNS depression with many drugs.
Drugs
Thiopental
Thioamylal
Methohexita
Phenols
Pharmacologic Effects
Vasodilation and hypotension,negative
inotropy.Fospropofol
water-soluble
Pharmacokinetics
Fast onset and fast recovery due to inactivation
Possible Mechanism
Uncertain
Toxicities and Interactions
Hypotension (during
induction),cardiovascular
depression
Drugs
Propofol
,Fospropofol
Inhaled anesthetics
Pharmacologic Effects
Increase cerebral blood
flow enflurane and halothane decrease cardiac
output. Others cause vasodilation all decrease
respiratory functions lung irritation (desflurane)
Pharmacokinetics
Rate of onset and recovery vary by blood:gas partition coefficient
recovery mainly due to redistribution from brain
to other tissues
Possible Mechanism
Facilitate GABA-mediated inhibition block brain NMDA and
ACh-N receptors
Toxicities and Interactions
Toxicity: extensions of effects
on brain, heart/vasculature, lungs
Drug interactions: additive
CNS depression with many agents, especially opioids and
sedative-hypnotics
Drugs
Desflurane
Enflurane
Halothane
Isoflurane
Sevoflurane
Nitrous oxide
Local Anesthetics
Amides
Pharmacokinetics
Hepatic metabolism via
CYP450 in part ,Half lives ; Lidocaine ,Prilocaine < 2 hr, others 3-4 hrs
Clinical uses
Analgesia via topical use,or injection (perineural, epidural, subarachnoid)
Mechanism of Action
Blockade of Na+ channels slows,then prevents actionpotential propagation
Toxicities
CNS: excitation, seizure CV: vasodilation,hypotension, arrhythmias(bupivacaine)
Drugs
Articaine
Bupivacaine
Levobupivacaine
Lidocainea
Mepivacaine
Prilocaine
Ropivacaine
Esters
Pharmacokinetics
Rapid metabolism via plasma esterases. short half-lives
Clinical uses
Analgesia, topical only for cocaine and benzocaine
Mechanism of Action
As above, plus cocaine has intrinsic sympathomimetic actions
Toxicities
As above re CNS actions
Cocaine vasoconstrictsAnalgesia, topical only for
cocaine and benzocaine
When abused cocaine has caused hypertension,seizures, and cardiac arrhythmias
Drugs
Benzocaine a
Cocaine a
Procaine
Tetracaine a