Basic Pharm of Anesthetics Flashcards
Benzodiazepines 5 pharm effects and prototype
1 Anxiolysis 2 Sedation 3 Anterograde Amnesia (from the min drug given until drug is gone) 4 Anticonvulsant Actions 5 Muscle Relaxation (Spinal Level, not muscle) -Prototype: Diazepam(valium) fyi: midazolam(versed) lorazepam(ativan) 
Benzodiazepines Mechanism of Action
enhances the affinity for GABA to bind to GABAa receptor
increases GABAs potencyX3
Causes greater frequency of channels to open:
-Increases chloride influx
-Hyperpolarization
-Decreased neuronal excitability (when AP comes along nothing happens)
Benzodiazepines uses in anesthesia
-Pre-medication
-IV sedation
-General Anesthetic induction (rare)
-General Anesthetic maintenance (rare)
-Post-op anxiolysis (rare)

Benzo adverse effects and precautions
-Dose dependent decrease in ventilation
-Hypoxemia and hypoventilation enhanced in presence of opioid (synergistic)
-Decreases SVR at induction dosage
-BP consequently decreases especially with hypovolemia
*Contraindicated in pregnancy

Opioids effect and prototype
Supra spinal(brain) and SpinalAnalgesia – activation of endogenous pain suppression system
- analgesia without loss of touch or consciousness.
- Prototype: Morphine
Opioid MOA
- Acts at brainstem, spinal cord, and peripheral tissues-Agonist at stereospecific opioid receptors – activates pain-modulating systems
- Binding at opioid receptor = decreased neurotransmission
- Immediate decrease in neurotransmitter release
- Acts at pre and post synaptic sites
- -Increased K conductance – hyperpolarization
- -Ca channel inactivation
Opioid uses
-Pre-medication
-Intra-op pain management (IV, epidural, spinal)
-General anesthesia (high doses)
-Post-op pain management

Opioid Adverse effect and Precautions (7)
- Bradycardia (in cardiac surg, this is a good thing)
- Respiratory Depression (decreased RR, increased tidal volume, but volume won’t off set slow rate)
- Miosis
- Urinary retention
- Constipation
- Physical dependence
- Sedation (in higher doses, synergistic w/other drugs)
Barbiturates MOA
- Decreases the rate at which GABA dissociates from its receptor→ increases duration of GABA activated Cl- channel opening (enhances GABA activity!)
- Mimics GABA at the receptor (direct activation of Cl- channels)
- Produces functional inhibition of the post- synaptic neuron
- Depresses Reticular Activating System → Sleep
(basically: activates GABA and mimics GABA)
Barb uses and prototype
-Sedation and Hypnosis
-Cerebral Protection
-Anti–seizure (benzos > effective)
-Anesthetic Uses
—Induction of general anesthesia (useful in patients with increased intracranial pressure and/or focal brain ischemia)
* Thuiopental (no longer used)
Barbs Adverse effects (cardiac, and resp) and Precautions
- “Hang-over”effect–elimination 1/2life is so long
- Depression of medullary vasomotor center & decreased SNS outflow from CNS → peripheral vasodilation→ preload decreases→
- SBP decreases, compensatory HR increase
- If SNS not intact OR hypovolemia OR large doses given to reduce ICP, will see significant decreases in BP and myocardial depression
- Ventilatory Depression
Barbs adverse effects and precautions
-Intraarterial injection (can result in gangrene/nerve damage)–drug has high pH so if in artery precipitates fast
-Hepatic enzyme induction with chronic use–phenobarb most potent inducer
-Increases the metabolism of oral anticoagulants, phenytoin, TCAs, corticosteroids and Vit. K
-Accelerated production of heme by stimulation of enzyme: D-aminolevulinic acid synthetase- Avoid in patients with porphyria
-Allergy 1:30,000, high mortality
-Readily crosses placenta!

Propofol/Diprivan class, how it’s stored
-Classification: Nonbarbiturate IV anesthetic
-Supplied as: 1% Solution in egg, soy, glycerol
-Infection Control- EDTA (ethylenediamine tetraacetic acid)
• Preservatives-Sodium metabisulfite (caution use asthma) vs EDTA
*dont spike twice
Propofol MOA
-Enhances binding of GABA to GABAa receptor (B1 subunit)
-Decrease the rate of disassociation of GABA from receptor (increase how long GABA interacts with receptor)
• Increases chloride influx
• Hyperpolarization
• Decreased neuronal excitability

Propofol effects
- Dose Dependent Sedation & Hypnosis
- Antiemetic
- Antipruritic
- Anticonvulsant
- decreases the effect of Bronchoconstriction (except with metabisulfite)
Propofol uses
- Intravenous sedation
- Induction of general anesthesia
- Maintenance of general anesthesia (TIVA)
- Part of balanced technique for maintenance of anesthesia
- Antiemetic (small doses)
Propofol adverse effects and precautions
Dose dependent ventilatory depressant, myocardial depression and vasodilation
- Similar decreases in SV, C.O. and SVR
- HR unchanged (? baroreceptor inhibition)
- Bradycardia related death – 1.4/100,000 patients
- Myoclonus (twitching)
- Pain on injection (lido first, or give fast)
- Lipidemia with long term infusion
- Infection and bronchospasm
Succinylcholine class, MOA
Classification: Depolarizing Neuromuscular Blockade
Mechanism of action:
-binds to nicotinic receptors
-channel opens, motor endplate depolarizes
-Single contraction occurs
-Sch not metabolized by true acetylcholinesterases
-Channels stay open until Sch diffuses back into the circulation
-Further action potentials cannot be initiated
Succinylcholine effect and uses
- Neuromuscular Blockade
- Optimize intubating conditions–Rapid sequence induction
- Treatment of life-threatening laryngospasm
Succinylcholine adverse effects and precautions
- Cardiacdysrhythmias
- Hyperkalemia (increased susceptibility seen with burns, trauma, nerve damage, neuromuscular diseases, renal failure)
- Muscle Pains (fasciculations)
- Increased ICP (avoid with head injuries)
- Increased IOP
- Potent Malignant Hyperthermia triggering agent
- Avoid in patients with atypical acetylcholinesterase
Vecuronium class and MOA
Classification: Non-depolarizing Muscle Relaxant; Monoquaternary aminosteroid
- Mechanism of Action: Competitive antagonist at pre and post neuromuscular junction nACH receptors (prevent Ach from binding to receptor site—no AP)
- Occupies alpha subunits of ACH receptor without inducing a conformational change
- Action Potential can not be initiated
Vecuronium effect and used
- Muscle Relaxation/Paralysis
- Facilitate endotracheal intubation (must test vent before giving muscle relaxant)
- Optimize surgical conditions
Vecuronium adverse effects and precautions
- Prolonged/ unpredictable effect with:
- -Liver and kidney disease
- -Neuromuscular disease
- -Hypothermia, electrolyte imbalances
- -Antibiotics: aminoglycosides
- Resistance in burn patients
- Be on the look out for residual neuromuscular blockade in all patients (make sure completely recovered ex. all 4 of TOF)
- In theory, at higher risk for recall if inadequate general anesthesia given
Isoflurane class and MOA
Class: Inhalational Anesthetic; Halogenated methyl ethyl ether
Mechanism of Action:
**Lipid solubility very important (determines onset, duration, etc.)
-These agents eliminated almost entirely via the lungs, contemporary inhaled agents minimally metabolized by the liver or eliminated via kidney
Isoflurane effects and use
- Bronchodilator
- General Anesthesia (sedation, hypnosis, partial muscle relaxation)
- Induction (usually Sevoflurane only)
- Maintenance
Isoflurane adverse effects and precautions
Respiratory effects: --Depression: higher rates, lower volumes. Cardiac effects: --Depression: ↓C/O, and BP, cause vasodilation Malignant Hyperthermia --Ca++channelinterference --Muscle rigidity --↑ temperature --↑ CO2 Aspiration --Airway reflexes are abolished (NPO) OR pollution
MAC (not monitored…)
Mean Alveolar Concentration = MAC (of a volatile anesthetic to which a 50% of patients do not move to a noxious stimulus)
- Describes potency (similar ED50)
- Tells us how much of a specific gas to administer
Isoflurance: MAC
MAC of isoflurane is 1.2%
-So, if I had the patient on 100% Oxygen and dialed my isoflurane vaporizer to 1.2%. The patient would be breathing the following gas mixture:
• 98.8% Oxygen molecules
• 1.2% Isoflurane molecules
Nitrous Oxide MAC
Nitrous oxide is the only inhaled agent that will not by itself provide 100% anesthesia – its MAC is 104%
Local Anesthetics MOA and prototype
-Local anesthetics block impulse conduction during the depolarization phase of the action potential
-Blockade is caused by the inhibition of the influx of sodium ions (sodium channel blockade)
-Blockade only occurs when Na channels are in the inactivated closed state
Prototype: Lidocaine
LA effect
- Block afferent nerve transmission to produce analgesia and anesthesia without loss of consciousness
- Autonomic blockade
- Somatic sensory blockade
- Somatic motor blockade
Lidocaine class
Amide
molecule consist od lipophilic head (aromatic ring), and intermediate chain either an amide or ester and a Hydrophilic Tail
-the tail
the lipophilic head is what it can cross the BBB (CNS toxicity)
LA adverse effects and precautions
CNS toxicity
- Circumoral /tongue numbness, tinnitus, vision changes, dizziness, slurred speech, restlessness
- Seizure followed by CNS depression, apnea, hypotension
- pt must be awake to assess for this
- will see CNS effects before cardiac
LA adverse effects and precautions cardiac
More resistant to toxic effects than CNS!
- Hypotension, myocardial depression, reduced SVR and C.O
- Bupivacaine- Arrhythmias, AV heart block, hypotension and arrest may occur
- Cocaine overdose manifests as massive sympathetic outflow, coronary vasospasm, MI, dysrhythmias including V-fib
