L38→↑↓ Drugs Used in Anesthesia Flashcards
Nitrous Oxide (N2O)
Prolonged use interferes with vitamin B12
Analgesia and sedation
Isoflurane
Color code: purple →Anesthesia but NOT analgesia → Decreases BP and increases HR → Decreases respiratory volume but increases rate → Moderate respiratory irritant → Increases bronchial secretions
Desflurane
Color code: blue
→ Anesthesia but NOT analgesia
→ Dose-dependent cardiovascular depression
→ May get tachycardia at higher concentrations
→ Dose dependent respiratory depression
→ Respiratory irritant
→ Increases bronchial secretions
Sevaflurane
Color code: yellow → Anesthesia but NOT analgesia → Decreases BP and HR → Dose-dependent depression of respiratory rate →NOT irritant to airways →→ Suitable for inhalational induction → Eliminated predominantly via the lungs; 5% metabolized by cytochrome P450
Types and name of I.V. Induction Agents
Rapidly acting
Barbiturates
→thiopental
Phenols
→propofol
Imidazoles
→etomidate
Slow acting Phencyclidine derivatives → ketamine Benzodiazepines →midazolam
Drugs Used in TIVA
Hypnotics
Propofol, etomidate,
Analgesics (opioid class)
Fentanyl, remifentanil,
Muscle relaxation
→ Atracurium, vecuronium
Drug combination for TIVA
Propofol and remifentanil
Propofol and fentanyl
Mechanism, Contraindication, S/E of Propofol
A free radical scavenging agent
MoA
→ It decreases the rate of dissociation of the GABA from the receptor, thereby increasing the duration of the GABA-activated opening of the chloride channel with resulting hyperpolarization of cell
membranes.
Adverse (side) effects:
→ Pain on injection
→ Bacterial growth
Mechanism, Contraindication, S/E of Etomidate
MoA
It binds at a distinct binding site associated with a Cl- ionophore at
the GABAA receptor, increasing the duration of time for which the
Cl- ionophore is opened
Maintains a good cardiopulmonary function
Adverse (side) effects:
→ Suppresses the production of cortisol
→ High concentration of propylene glycol in etomidate preparation causes hemolysis resulting in hemoglobinuria
Mechanism, Contraindication, S/E of Ketamine
Non-competitive antagonism at the NMDA receptor Ca2+ channel
pore
→ It reduces the presynaptic release of glutamate
→ Interaction with opioid receptors (Mu and Kappa), but NOT antagonized
by naloxone
→ Antagonistic interaction with monoaminergic, muscarinic and
nicotinic receptors
Adverse (side) effects: → Blurred vision → Dizziness → Drowsiness → Nausea and vomiting → Loss of appetite
MOA of Local Anesthetics
→Blockade of voltage-gated sodium channel conductance
→→ Prevents the initiation and propagation of the nerve impulse by
reducing the passage of Na+ ions through voltage-gated Na+ channels
Mechanism, Contraindication, S/E of
Lidocaine
used multipurpose LA
combination with epinephrine (adrenaline) – why?
→ Epinephrine binds to q1 receptors located on the blood vessels, which causes vasoconstriction
→→prolongs the duration of local anesthesia several-fold and may improve the frequency of successful nerve block
→→minimizes systemic toxicity of the local
anesthetic by reducing the peak blood concentration of the local anesthetic agent
→→When local anesthetic solutions are given by infiltration, epinephrine tends to reduce blood loss associated with
surgical procedures
→ In combination with an opioid in intrathecal or epidural
anesthesia
At normal therapeutic doses
→Dizziness
→ Paraesthesia – a burning or prickling sensation
→ Euphoria
At higher doses
→ Confusion
→ Vertigo
→ Tinnitus
Severe toxicity may precipitate seizures
Overdose toxicity → Cardiac arrhythmias → Lowering blood pressure → Coma → Respiratory arrest
Classification of Local anesthetics
Amide group
Lidocaine
Prilocaine
Ester group
cocaine
procaine
Systemic Toxicity
→LAs absorbed into systemic circulation
→Most effects are dose-dependent
Methemoglobinemia →Hepatic metabolism of prilocaine →Can also be induced by →→ Benzocaine (ester type) Central nervous system toxicity → seizures → initially light headedness and dizziness
→ Cardiovascular system toxicity
→→cause vasodilation in area
of injection
Drug interaction
→Local anesthetics potentiate nondepolarizing muscle relaxant
blockade
→Succinylcholine and ester group local anesthetics depend on
pseudocholinesterase for metabolism
→ Pseudocholinesterase inhibitors can prolong the metabolism
of ester local anesthetics
→ Histamine (H2) receptor antagonists (blockers) and non-
selective receptor antagonists (blockers)(e.g. propranolol) decrease hepatic blood flow and lidocaine clearance
→a2-Adrenergic agonists (e.g. clonidine) potentiate local
anesthetic analgesia produced after peripheral nerve block injection