Flashcards in E's intro to Anesthetics Deck (82):
what type of anesthesia provides numbness to a small area limited to where local anesthetic is injected?
What type of anesthesia provides numbness to a much larger areas, such as epidurals, spinals, and peripheral nerve blocks?
What type of anesthesia uses sedatives and other agents, but the patient is responsive and can breathe on their own?
MAC- monitored anesthesia care
What type of anesthesia is a deep state of sleep where the patient loses consciousness and sensation and usually (not always) requires assisted ventilation?
What type of anesthesia can be referred to as "IV sedation"?
Monitored anesthesia care
What is the major difference between monitored anesthesia care and general anesthesia?
MAC patient can still move (like for bronchoscopy and EGD; sedative)
General anesthesia the patient CANT MOVE/ no longer responds to stimulus
Distinguish the effects of Minimal sedation (vs moderate, deep, and general anesthesia)
(anxiolysis) patient can respond to verbal commands; cognitive function and coordination may be impaired; CV and Ventilatory functions are UNaffected
Distinguish the effects of moderate sedation/ analgesia (vs. minimal, deep, and general anesthesia)
(Conscious Sedation) patient responds purposefully to verbal commands, either alone or with tactile stimulation; adequate spontaneous ventilation; CV usually maintained. easily aroused
Distinguish the effects of deep sedation (vs. minimal, moderate, and general anesthesia)
NOT easily aroused; respond purposefully to repeated PAINFUL stimuli; ventilatory function and patent airway may be impaired; CV function usually maintained
Distinguish the effects of General anesthesia (vs. minimal, moderate, and deep sedation)
NOT arousable even with painful stimuli; IMPAIRED ventilatory function-->requires ventilatory assistance for patent airway; PPV may be required; CV function may be impaired (elderly may have CV issues, vasodilated...etc)
What is General Anesthesia?
generalized, reversible CNS depression
-NO sensory perception (all senses are gone)
-Loss of consciousness
-No recall of events
What are other potential effects of general anesthetics and adjuncts? (4)
-suppression of autonomic reflexes (good and bad: decreases the stress response, but knocks out ability to compensate BP etc.)
-Analgesia (NOT ALWAYS with general Anesth. ie. with EGD dont need pain relief)
What are the steps of General Anesthesia with an ETT template? (7)
- Pre-op medications/ sedation
- Induction Drug
- Neuromuscular blockade
- inhalation drug
- opioids/ local anesthetics etc.
- Neuromuscular Blockade reversal agent
What is the purpose of pre-op medication/sedation in the GA with an ETT template? (4)
patient comfort, reduce anxiety, prevent aspiration, antibiotics per surgeon request (usually benzos/versed)
What is the purpose of the induction drug in the GA with an ETT template?
to induce anesthesia (DUH!!!)--> can be IV (usually) or inhaled
What is the purpose of the neuromuscular blockade in the GA with ETT template?
to facilitate intubation and optimize surgical conditions (remember, you dont have to!! like you could give propofol)
What is the purpose of the inhalational drug in the GA with ETT template?
to maintain general anesthesia (can also be IVV gtt agent like propofol)
What is the purpose of opioids/local anesthetics etc. in the GA with ETT template?
to minimize physiological effects of pain and to promote comfort at emergence (ppl can feel pain on anesthetics! so give them the juice!)
What is the purpose of the antiemetic in the GA with ETT template?
to prevent nausea likely with opioids/inhalational agents "ain't nobody got time for that"
Whats the purpose of giving a neuromuscular blockade reversal agent?
to reverse the paralyzing effects of neuromuscular blockade (dont have to with the half-times of drugs....)
What are the 5 pharmacologic effects of Benzodiazepines?
-Anxiolysis**** especially with major surgeries like CV
-Anterograde Amnesia (From when you give it until its gone, so introduce yourself before!)
-Muscle Relaxation (Spinal Level)-- decreases muscle spasms
What is the prototype benzodiazepine?
What is the MOA of Benzodiazepines?
Potentiates binding of GABA to GABAa receptor; Increases GABA potency times 3 at the site
What happens due to the binding of GABA to GABAa receptors with respect to ions (3)....for benzodiazepines?
-increases chloride influx
-Decreased neuronal excitability
What are the uses of Benzodiazepines in anesthesia? (5)
-GA induction (rare)
-GA maintenance (rare)
What are the adverse effects and precautions of benzodiazepines?
-Dose dependent decrease in ventilation
-Hypoxemia and hypoventilation enhanced in presence of opioid
-decreases in SVR at induction dosage (only with large doses)
-BP consequently decreases especially with hypovolemia (BP generally stable except in large doses!)
-contraindicated in pregnancy
What are the pharmacological effects of opioids in supraspinal and spinal analgesia?
activation of endogenous pain suppression system
What are the opioid receptors and where does it act at the synapse?
agonist acts at the mu receptors- activates pain modulating systems
-acts at pre and post synaptic sites
What happens with neurotransmission when opioids bind to the receptor?
-increased K conductance-- hyperpolarization
-Ca2+ channel inactivation
-Immediate decrease in neurotransmitter release (Substance P)
What are the uses of opioids in anesthesia? (4)
- pre-medication (unless in the OR, dont premedicate with versed/fentanyl b/c synergistic and will stop breathing!)
- Intra-operative pain management (IV, epidural, spinal)
- General anesthesia (at very high doses)
- Post-op pain management
What is the prototype for opioids?
How do opioids affect the CV system?
VERY CARDIAC STABLE!
What are the adverse effects and precautions of opioids? (7)
- respiratory depression
- urinary retention
- physical dependence
- sedation (in higher doses, synergistic with other drugs)
What happens in respiratory depression with opioids regarding respiratory rate and tidal volume?
decreased respiratory rate and increased tidal volume (breathe deep and slow)
What is the MOA of Barbiturates? (4)
-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 site (direct activation of Cl- channels)
-produces function inhibition of the post-synaptic neuron
- Depresses RAS--> sleep
Where in the synapse do barbiturates work?
POST synaptic neuron
What is the prototype drug for barbiturates?
What are the uses of barbiturates? (4)
- sedation and hypnosis
- Cerebral protection (decreases cerebral blood flow and CMrO2)
- Anti-seizure (better effects than benzos)
- Anesthetic Uses
What are the anesthetic uses of barbiturates?
- induction of general anesthesia (useful in patients with increased ICP and/or focal brain ischemia
What are the adverse effects and precautions of Thiopental (barbiturates?) (6)
-"hang-over" effect (distrib. quickly but hangs out in the plasma for a long time)
-depression of medullary vasomotor center & decreases SNS outflow from CNS (peripheral vasodilation-> preload decreases->
- SBP decreases, compensatory HR increases
- if SNS not intact OR hypovolemia OR large doses given to reduce ICP, will see significant decreases in BP and myocardial depression
- Ventilatory depression
- Intraarterial injection (can result in gangrene/ nerve damage)
~MASSIVE decrease in BP (but propfol is worse)
What can result from intraarterial injection of barbiturates?
gangrene/ nerve damage
What are the adverse effects and precautions of barbiturates? (5)
- Hepatic enzyme induction with chronic use (phenobarb is MOST potent inducer!)
-increases 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!
What is the classification of Propofol/Diprivan?
Nonbarbiturate Intravenous Anesthetic
What is propofol supplied as?
1% soln in egg, soy, glycerol base (causes pain when administered!)
What is added to propofol as a preservative to decrease bacterial growth?
Sodium metabisulfite vs. EDTA
What is the MOA of Propofol?
-Potentiates binding of GABA to GABAa receptor (B1 subunit)
-Decreases the rate of disassociation of GABA from the receptor
What happens at the cellular level when propofol decreases the rate of disassociation of GABA from receptor? (3) hint....it has to do with an ion
-increases chloride influx
-decreased neuronal excitability
What are the pharmacological effects of propofol? (5)
-dose dependent sedation and hypnosis
-attenuation of bronchoCONSTRICTION
What is the attentuation of bronchospasm usually related to with regards to propofol?
- usually related to the patient not being deep enough under anesthesia (ie. for asthmatics maintain a very deep level of sedation
What are the anesthetic uses of propofol? (5)
-induction of general anesthesia
-maintenance of general anesthesia
-part of balanced technique for maintenance of anesthesia
-antiemetic (small doses)
What are the adverse effects and precautions of propofol? (6)
-dose dependent ventilatory depressant
-dose dependent myocardial depression and vasodilation (similar decreases in SV, CO, and SVR)
-Myoclonus (jerky movements that are not purposeful)
-pain on injection
-Lipidemia with long term infusion
-Bronchospasm (b/c some of the sulphite preservatives in it can cause bronchoconstriction)
What happens to heart rate when propofol is in use?
(not good, more so because propofol is blocking baroreceptors from being able to compensate)
What does action potential mean?
depolarization of nerve terminal
What are the Pre-synaptic events at the NMJ? (4)
-Ca channels open
-Ca diffuses down gradient to nerve terminal
-Ach spills out into synaptic cleft
What are the post-synaptic events at the NMJ? (5)
- Ach combines with nicotinic receptors
-after both nicotinic receptors occupied. Channels open Na+, Ca diffuse into cell and K+ diffuses out
-motor end plate depolarizes
-action potential created
-skeletal muscle contracts
Name 4 things regarding the acetylcholine receptor.
-5 protein subunits
-central core for cation channeling
-Ach must bind to both "a" subunits to open the core
-"A" subunits are the site of agonism and antagonism
What is the classification for succinylcholine?
Depolarizing neuromuscular blockade
What is the MOA of succinylcholine?
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
What is the pharmacologic effect/anesthetic use of Succinylcholine?
Trauma setting/ Neuromuscular Blockade
-optimize intubating conditions****
-rapid sequence induction
-treatment of life-threatening laryngospasm
What are the adverse effects and precautions of succinylcholine? (7)
-CARDIAC DYSRHYTHMIAS**** esp. in kids
-Hyperkalemia (increased susceptibility seen with burns, trauma, nerve damage, neuromuscular diseases, renal failure)
-Muscle Pains (fasciculations)
-*******POTENT MALIGNANT HYPERTHERMIA TRIGGERING AGENT
-Avoid in patients with atypical acetylcholinesterase
What is the drug classification for Vecuronium?
Non-depolarizing muscle relaxant; monoquaternary aminosteroid
What is the MOA of Vecuronium?
Competitive antagonist at PRE and POST neuromuscular junction nicotinic AcH receptors
-occupies alpha subunits of ACH receptor without inducing a conformational change
-AP can not be initiated
(BLOCKS ACTION POTENTIALS)
What are the pharmacological effects/anesthetic uses of Vecuronium?
-facilitate endotracheal intubation
-optimize surgical condictions*****
~for us and the surgeons, not for the patient
What are the adverse effects and precautions of Vecuronium? (7)
-Prolonged/ unpredictable effects with: liver and kidney disease, neuromuscular disease, hypothermia and electrolyte imbalances, antibiotics: aminoglycosides (metabolized similarly so it can prolong the action of vecuronium)
-resistance in burn patients
-be on the look out for residual neuromuscular blockade in all patients
-in theory, at higher risk for recall if inadequate general anesthesia given
What is the drug class of Isoflurane?
Inhalational anesthetic; halogenated methyl ethyl ether
What determines onset, duration, etc. for isoflurane?
Lipid solubility!!! (potency and how long it lasts)
How are inhalational agents, Isoflurane, eliminated?
almost entirely by the lungs, contemporary inhaled agents minimally metabolized by the liver or eliminated via kidney
What are the pharmacological effects and anesthetic uses of isoflurane (inhaled anesthetics)? (2)
-general anesthesia (sedation, hypnosis, partial muscle relaxation)--> induction (usually sevo only) and maintenance of anesthsia
What are the adverse effects and precautions of isoflurane (inhaled anesthetics)? (5)
- Respiratory effects: higher rates, lower volumes
-cardiac effects: depression- dcreased CO, and BP and causes vasodilation
-**Malignant Hyperthermia (1st sign is increasing CO2): Ca2+ channel interference, muscle rigidity, increased temp, and increased CO2
-Aspiration (RISK; airway reflexes are abolished)
What is MAC: Mean Alveolar Concentration?
of a volatile anesthetic to which a 50% of patients do not move to noxious stimulus (ie. dose at which 50% of people will not move)
-tells us how much of a specific gas to administer
What is the minimum alveolar concentration of Isoflurane?
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 and 1.2% isoflurane molecules
What is the only inhaled agent that will not by itself provide 100% anesthesia, and what is its MAC?
Nitrous oxide, and its MAC is 104%
What is the MOA of local anesthetics? (3)
-local anesthetics block impulse conduction during the depolarization phase of the action potential
What causes the blockade by local anesthetics?
-blockade is caused by the inhibition of the influx of SODIUM ions
What condition regarding sodium channels must occur for local anesthetics to cause blockade?
blockade ONLY occurs when Na channels are in the INACTIVATED closed state
What is the drug prototype for local anesthetics?
What are the pharmacologic effects of local anesthetics?
Blocks afferent nerve transmission to produce analgesia and anesthesia without loss of consciousness
What 3 types of blockade occur from local anesthesia?
-somatic sensory blockade
-somatic motor blockade
What is the drug classification of lidocaine?
AMIDE local anesthetics
What does the typical local anesthetic molecule consist of ?
-lipophilic head (an aromatic ring)
-intermediate chain (containing either an amide (NH) or an ester (COO-)
-hydrophilic tail (a tertiary amine)
What are the CNS adverse effects and precautions of local anesthetics?
-circumoral/tongue numbness, tinnitus, vision changes, dizziness, slurred speech, restlessness
-seizure followed by CNS depression, apnea, hypotension