Anesthetics Flashcards
nitrous oxide
Inhalable general anesthetic
MOA:
Increase GABAa receptor sensitivity–>enhanced inhibitory neurotransmission
Activation of K+ channels–>hyperpolarization–>attenuation of AP–>decrease release of neurotransmitters
Inhibit glutamate gated Na_ channels at NMDA receptors–>decreased excitatory synaptic responses–>decreased activation of post-synaptic neurons
Properties: blood/gas coeffecient=0.47 (low)–>rapid onset, MAC= 105% (high)–>not potent/not complete anesthesia
Pharmacological:
2nd gas effect= reduces induction time for primary agent and reduces dose needed for effect
Cardiovascular and respiratory centers intact
Not metabolized
MAC >100%–>lacks potency
Side effects: diffusion hypoxia (must administer 100% O2 after NO discontinued), bone marrow depression, miscarriage, depression of immune system
Indications: general anesthesia with other more toxic agent, analgesic for minor procedures (dentistry) or EMS
halothane (Fluothane)
Inhalable general anesthetic
Halogenated agent
MOA:
Increase GABAa receptor sensitivity–>enhanced inhibitory neurotransmission
Activation of K+ channels–>hyperpolarization–>attenuation of AP–>decrease release of neurotransmitters
Inhibit glutamate gated Na_ channels at NMDA receptors–>decreased excitatory synaptic responses–>decreased activation of post-synaptic neurons
Properties: potential induction use, medium rate of onset, relatively potent (MAC=0.76%)
Pharmacology:potent, complete anesthetic, poor analgesia and muscle relaxant, slow recovery (accumulates in fats)
Side effects: hypotension, respiratory depression, depression, decreased GFR, retention of fluids, hepatotoxicity, malignant hyperthermia
Indications: induction but mostly maintenance agent; not used that much anymore
enflurane (Ethrane)
Inhalable general anesthetic
Halogenated agent
MOA:
Increase GABAa receptor sensitivity–>enhanced inhibitory neurotransmission
Activation of K+ channels–>hyperpolarization–>attenuation of AP–>decrease release of neurotransmitters
Inhibit glutamate gated Na_ channels at NMDA receptors–>decreased excitatory synaptic responses–>decreased activation of post-synaptic neurons
Properties: MAC=1.68%, blood/gas coefficient=1.9
Pharmacology: less toxic, muscle relaxation, less metabolism
Disadvantages: CNS stimulation when given in high conc. or blood is alkaline
isoflurane (Forane)
Inhalable general anesthetic
Halogenated agent
MOA:
Increase GABAa receptor sensitivity–>enhanced inhibitory neurotransmission
Activation of K+ channels–>hyperpolarization–>attenuation of AP–>decrease release of neurotransmitters
Inhibit glutamate gated Na_ channels at NMDA receptors–>decreased excitatory synaptic responses–>decreased activation of post-synaptic neurons
Properties: MAC=1.4%, blood/gas coefficient=1.4, pungent–>used for maintenance
Pharmacology: rare hepatoxicity, muscle relaxation, respiratory deression, lacks CNS stimulation, low incidence of myocardial sensitization (use with pts w/ arrhythmia)
Used frequently as primary agent
desflurane (Suprane)
Inhalable general anesthetic
Halogenated agent
MOA:
Increase GABAa receptor sensitivity–>enhanced inhibitory neurotransmission
Activation of K+ channels–>hyperpolarization–>attenuation of AP–>decrease release of neurotransmitters
Inhibit glutamate gated Na_ channels at NMDA receptors–>decreased excitatory synaptic responses–>decreased activation of post-synaptic neurons
Properties: MAC=6.0% (less potent), blood gas coefficient=0.42 (very rapid onset), pungent (used for maintenance)
Pharmacology: very rapid induction and recovery due to low blood solubility, minute-to-minute control, potent myocardial and respiratory depression, potent vasodilator, irritating to respiratory passages
Often used due to rapid onset and recovery (outpatient surgery)
sevoflurane (Ultane)
Inhalable general anesthetic
Halogenated agent
MOA:
Increase GABAa receptor sensitivity–>enhanced inhibitory neurotransmission
Activation of K+ channels–>hyperpolarization–>attenuation of AP–>decrease release of neurotransmitters
Inhibit glutamate gated Na_ channels at NMDA receptors–>decreased excitatory synaptic responses–>decreased activation of post-synaptic neurons
Properties: MAC=2.0%, blood/gas coefficient=0.66, not irritating–>induction
Pharmacology: newest, commonly used due to rapid recovery
Disadvantages: metabolized to release fluoride ions, interactions with soda lime–>nephrotoxic material
Advantages: controllable (low blood tissue solubility and high potency), rapid induction and recovery, low incidence of airway irritation
Dose related cardiac depression, malignant hyperthermia
thiopental (Pentothal)
Intravenous general anesthetic
Barbiturate
MOA:
Increase GABAa receptor sensitivity–>enhanced inhibitory neurotransmission
Activation of K+ channels–>hyperpolarization–>attenuation of AP–>decrease release of neurotransmitters
Inhibit glutamate gated Na_ channels at NMDA receptors–>decreased excitatory synaptic responses–>decreased activation of post-synaptic neurons
Properties: not stable (must be prepared fresh each day), repeated doses accumulate, used for initial induction
Pharmacology: rapid onset, sequestered in fat, bind plasma proteins, metabolized by liver, eliminated by kidney, acute tolerance, antalgesic
Effects: myocardial depression; decrease BP, CO, and SV; dysrhythmias, increased O2 consumption and HR, respiratory depression, decreased cerebral flow
Indications: commonly used induction agent, not mono anesthetic, pts must have good veins and no respiratory problems (caution with bronchial asthma)
Complications: improper injection–>necrosis; cough, depression of temperature regulation
propofol (Diprivan)
Intravenous general anesthetic
“milk of amnesia”
MOA:
Increase GABAa receptor sensitivity–>enhanced inhibitory neurotransmission
Activation of K+ channels–>hyperpolarization–>attenuation of AP–>decrease release of neurotransmitters
Inhibit glutamate gated Na_ channels at NMDA receptors–>decreased excitatory synaptic responses–>decreased activation of post-synaptic neurons
Properties: rapid induction and recovery, hepatic metabolism, break apnea, cardiovascular depression
Side effects: pain at injection site, involuntary movements, cough, hiccough, nausea, vomiting, post anesthetic dreaming
Use: widely used induction
ketamine (Ketalar, Ketaject)
Intravenous general anesthetic
Dissociative anesthesia–>pt is immobilized but appears awake
MOA:
Interrupts cerebral association pathways, depresses thalamoneocortical systme, spares limbic system
Properties:
No muscle relaxation, muscle rigidity, movements, ventilation maintained, stimulates cardiovascular system, sensory function hypersensitive, salivary secretion, vocalizations, eyes fixed and open, recovery difficult, onset slower
Use: diagnostic procedures (superficial but not visceral pain), poor risk patients, children and infants, possibly to treat depression
Contraindications: increased intracranial or intraoccular pressure, hypertension, psychiatric history, procedures of mouth or larynx
etomidate (Amidate, Hypromidate)
Intravenous general anesthetic
Primary induction agent in Europe
MOA:
Increase GABAa receptor sensitivity–>enhanced inhibitory neurotransmission
Activation of K+ channels–>hyperpolarization–>attenuation of AP–>decrease release of neurotransmitters
Inhibit glutamate gated Na_ channels at NMDA receptors–>decreased excitatory synaptic responses–>decreased activation of post-synaptic neurons
Properties: potent hypnotic, no analgesia, rapid induction, rapid transformation in kidney and liver, minimal cardiovascular and respiratory depression
Disadvantages: involuntary muscular contractions, pain at injection site with thrombophlebitis, depletes adrenal steroids
Use: alternative to thiopental
Mechanism of action of local anestheics
block transient increase in Na+ permeability–>raises excitability threshold
4 sites of action:
1) external surface of Na+ channels (no drugs but toxins)
2) internal side of membrane affecting gates for Na+ and K+ (drug must be uncharged to cross phospholipid barrier and charged for binding to receptor)
3) nonspecific site within phospholipid membrane–>distortion of proteins that form Na+ channel
4) combination of 2 and 3
lidocaine articaine mepivacaine etidocaine prilocaine bupivacaine ropivaaine levobupivacaine
Local anesthetic amides
Destruction of drug: active until metabolized
Metabolized by liver via P450s
Remain active until reach liver–>potential systemic toxicity
CAUTION with liver disease
Eliminate via kidneys
Side effects: hypersensitivity (rare), systemic toxicity (active during circulation)
High conc. promote absorption across BBB–>depression, anxiety, fear
Hypotension, block/suppress pacemaker activity
procaine cocaine chloroprocaine tetracaine benzocaine
Local anesthetic esters
Destruction of drug: metabolized by plasma pseudocholinesterases
Plasma pseudocholinesterase inactivates to PABA moiety
Eliminate via kidneys
Side effects: hypersensitivity (from PABA), systemic toxicity (rare)
High conc. promote absorption across BBB–>depression, anxiety, fear
Hypotension, block/suppress pacemaker activity
Alternative: antihistamines (diphenhydramine) used when can’t receive ester or amide
