GENERAL ANESTHESIA Flashcards
anesthesia is the combination of
combo of amnesia + analgesia + muscle relaxation to allow the performance of surgery or other procedures
amnesia + analgesia + muscle relaxation
3 phases of general anesthesia
1) Induction
2) Maintenance
3) Emergence
most commonly used induction agent
Propofol (Diprivan)
Propofol causes a drop in
BP & CO
also has antiemetic properties
INDUCTION AGENTS
Propofol
etomidate
ketamine
Etomidate
⦁ Doesn’t cause vasodilation
⦁ higher rate of post-op nausea
⦁ inhibits the biosynthesis of cortisol
⦁ use is limited due to increased risk of death by 2.5x
higher rate of post op nausea
use is limited due to increased risk of death by 2.5x
ETOMIDATE
used in pts with hemodynamic instability
hallucinations
often used in kids
significant analgesic
ketamine
KETAMINE
⦁ Used in patients with hemodynamic instability
⦁ is a cardiac stimulant
⦁ significant analgesia, bronchodilation, and hallucinations
⦁ can cause severe hallucinations to where patient may not want to ever have surgery again…used more in children, pain management & treatment resistant depression
INDUCTION PHASE
- “putting to sleep”
- most commonly used induction agent = PROPOFOL
PROPOFOL CAUSES
- a drop in BP & cardiac output, antiemetic properties
OTHER AGENTS o Etomidate ⦁ Doesn't cause vasodilation ⦁ higher rate of post-op nausea ⦁ inhibits the biosynthesis of cortisol ⦁ use is limited due to increased risk of death by 2.5x
o Ketamine
⦁ Used in patients with hemodynamic instability
⦁ is a cardiac stimulant
⦁ significant analgesia, bronchodilation, and hallucinations
⦁ can cause severe hallucinations to where patient may not want to ever have surgery again…used more in children, pain management & treatment resistant depression
MAINTENANCE PHASE
- use of inhaled (volatile) or IV anesthetics
- Inhalation Anesthetic Agents
⦁ Volatile Anesthetic Agents = Sevoflurane & Desflurane
⦁ Nitrous Oxide: can be used in combo with volatile gases - IV anesthetic agents
⦁ Propofol and Remifentanil
EMERGENCE
“WAKING UP”
last phase of general anesthesia
- can result in autonomic hyper-responsiveness
⦁ tachycardia, hypertension, bronchospasm, laryngospasm
to blunt these responses = can give
- short acting Narcotics
- Beta blockers
- Lidocaine
emergence autonomic hyper-responsiveness can cause
- tachycardia
- hypertension
- bronchospasm
- laryngospasm
to help blunt autonomic hyper-responsiveness in emergence
- short acting narcotics
- beta blockers
- lidocaine
PROPOFOL (DIPRIVAN)
- Non-barbiturate hypnotic agent
- rapidly metabolized in liver & excreted in the urine - so can be used for long durations of anesthesia
- used for general surgery, cardiac surgery, neurosurgery & pediatric surgery
- rapid onset of action (distribution = 2-4 minutes)
- rapid clearance
- reversibility of effect once the drip is shut off
- duration of action = 1-3 hours, onset = 40 seconds
- Has some anti-emetic effect - so less Nausea / vomiting associated with use
- weaker amnestic effect than Midazolam (versed)
- no analgesic effect
- milky looking solution (emulsion) - so called “milk of amnesia”
- clear-headedness during recovery (rapidly clears, so don’t have much of a hangover during recovery period)
adverse effects of Propofol (diprivan)
⦁ can support rapid growth of microorganisms
⦁ hypotensive (so administer slowly)
⦁ may cause hypertonia & movement
⦁ respiratory depression
is a cardiac stimulant
KETAMINE (KETALAR)
KETAMINE
- affects the senses
- produces a dissociative anesthesia (catatonia, amnesia, analgesia) in which the patient may appear awake and reactive, but cannot respond to sensory stimuli
- frequently used in pediatric patients because anesthesia and analgesia can be achieved with an IM injection
- also used in high-risk geriatric patients and in shock cases - because it also provides cardiac stimulation
- rapid onset (30 seconds)
- short duration (5-10 minutes)
ANESTHETIC GASES
⦁ Isoflurane (Forane)
⦁ Desflurane (Suprane)
⦁ Sevoflurane (Ultane)
⦁ Nitrous Oxide
the more soluble the anesthetic gas is in the blood =
the longer it takes to eliminate
which anesthetic gases are the shortest acting
nitrous oxide
desflurane (suprane)
because they are the LEAST SOLUBLE in the blood
ANESTHETIC GASES
- an important property of anesthetics = reversibility
- once the anesthetic gas is turned off, the blood stream brings the gas back to the lungs, where it is eliminated; the more soluble the gas in the blood, the longer it takes to eliminate
- Nitrous oxide & Desflurane = shortest acting anesthetic gases because they are the least soluble in the blood
how do inhaled anesthetics work
- Inhaled anesthetics act in different ways at the level of the CNS
- They disrupt normal synaptic transmission by:
⦁ interfering with the release of neurotransmitters from presynaptic nerve terminals (enhance or depress excitatory or inhibitory transmission)
⦁ alter the re-uptake of neurotransmitters
⦁ change the binding of neurotransmitters to the post-synaptic receptor sites
DOSING OF INHALED AGENTS
MAC
o MAC = Minimum Alveolar Concentration = the inhaled anesthetic concentration (steady state) at which 50% of patients move in response to a standard midline abdominal incision
⦁ Nitrous Oxide = 105%
⦁ Isoflurane = 1.15%
⦁ Sevoflurane = 1.8%
⦁ Desflurane = 6.2%
inhaled agent with highest MAC
nitrous oxide
then desflurane
(these are the shortest acting agents…are the least soluble in blood)
inhaled agent with the lowest MAC
isoflurane
then Sevoflurane
MAC & AGE
- the MAC required for adequate anesthesia decreases with age, due to alterations in metabolism (need lower dose with age)
ISOFLURANE = inhaled agent
- Higher blood-gas solubility => so it takes longer for onset, and longer for emergence
- causes tachycardia
- causes peripheral vasodilation (hypotension)
- airway irritation & coughing (bronchospasm)
fastest onset & offset inhaled agent
desflurane
has highest airway irritation
least well tolerated on the airway (can cause coughing / bronchospasm)
desflurane
DESFLURANE
- requires a heated-pressurized vaporizer for delivery
- causes tachycardia (just like isoflurane)
- causes peripheral vasodilation (hypotension - just like isoflurane)
- least well-tolerated on the airway - can cause coughing, bronchospasm
- not used for mask induction
- fastest onset & offset
which inhaled agent does NOT cause tachycardia
sevoflurane
still causes peripheral vasodilation though
not used for mask induction
well-tolerated for mask induction
desflurane
sevoflurane
SEVOFLURANE
- does NOT cause tachycardia
- causes peripheral vasodilation
- well tolerated for mask induction
- fast onset & quick awakening
NITROUS OXIDE
MAC = 104 - therefore, nitrous oxide alone cannot provide anesthesia
- nitrous oxide diffuses into air-containing cavities 34x faster than nitrogen can leave the space
- so bowel, middle ear, pneumothorax, pneumocranium, pneumo-peritoneum, or cuffs of endotracheal tubes can all increase in size when nitrous oxide is being used
- Increases post-op nausea
- has analgesic properties (nice for dental procedures)
alone cannot provide anesthesia
nitrous oxide
increased post op nausea (2)
decreased nausea (1)
etomidate & nitrous oxide
propofol
no analgesic effect
analgesic effect
Propofol
nitrous oxide
advantages of nitrous oxide
Inexpensive Readily available Odorless/slightly sweet Limited effect No special equipment Sympathomimetic Will not cause malignant hyperthermia
will not cause malignant hyperthermia
nitrous oxide
inexpensive & readily available
disadvantages to nitrous oxide
High MAC/Limits FIO2
Sympathomimetic
Methionine synthetase inhibitor
Expands air-filled spaces
expands air filled spaces
nitrous oxide
PHARMACOKINETICS OF INHALED AGENTS
uptake time: Isoflurane > Sevoflurane > Desflurane > Nitrous Oxide
elimination time: Isoflurane > Sevoflurane > Desflurane > Nitrous Oxide
physiologic responses to inhaled anesthetic agents
- Tachycardia (except Sevoflurane)
- Hypotension (vasodilation)
- decreased cardiac output
- respiratory depression (decreased ventilation)
CONTRAINDICATIONS TO INHALED ANESTHETIC AGENTS
⦁ inability to tolerate the physiologic alterations produced (can pt tolerate decreased CO, hypotension, tachycardia, decreased ventilation?)
⦁ Malignant hyperthermia (does pt have a hx of MH?)
NEUROMUSCULAR BLOCKING DRUGS (NMBDs)
⦁ Succinylcholine (Anectine) ⦁ Rocuronium (Zemuron) ⦁ Vecuronium (Norcuron) ⦁ Pancuronium (Pavulon) ⦁ Cisatracurium (Nimbex)
function of NMBDs
- Produce the immobility that is needed for:
⦁ endotracheal intubation (if pt isn’t tolerating mechanical ventilation)
⦁ surgical immobility / relaxation (ex: abdominal)
⦁ mechanical ventilation
depolarizing NMBD
succinylcholine (anectine)
nondepolarizing NMBDs
⦁ Rocuronium (Zemuron)
⦁ Vecuronium (Norcuron)
⦁ Pancuronium (Pavulon)
⦁ Cisatracurium (Nimbex)
ACh is rapidly inactivated by
acetylcholinesterase
DEPOLARIZING AGENT MOA
Depolarizing agents cause brief twitches or fasciculations, followed by flaccid paralysis
- Paralysis is due to depolarization of the nerve terminal, and the nerve being in a refractory state, because the membrane is depolarized; In a refractory state = cannot receive another impulse
ex: Succinylcholine (Anectine)
SUCCINYLCHOLINE (ANECTINE)
- causes depolarization at the motor endplate
- in contrast to ACh, succinylcholine SLOWLY dissociates from the ACh receptors, resulting in an inactive state. as it dissociates, the effects wear off
- broken down by Butyrylcholinesterase to Choline + Succinylmonocholine
- Succinylcholine is often the agent of choice when rapid control of the airway is necessary
- rapid onset (< 1 minute) & short duration (6 - 10 minutes)
- the go to paralytic for rapid sequence intubation
SUCCINYLCHOLINE is broken down by
butyrylcholinesterase
into choline + succinylmonocholine
go to paralytic for rapid sequence intubation
succinylcholine
because of rapid onset (< 1 minute) and short duration (6-10 minutes)
DISADVANTAGES TO SUCCINYLCHOLINE
⦁ cardiac dysrhythmias
⦁ sinus bradycardia
⦁ myalgias (muscle pain = common complaint)
⦁ myoglobinuria
⦁ hyperkalemia
⦁ patient restrictions (ex: children)
⦁ masseter spasm = one of the first signs of malignant hyperthermia
⦁ malignant hyperthermia trigger
⦁ possible increases in intraocular, gastric and intracranial pressures
⦁ dependent upon normal butyrylcholinesterase (breaks down succinylcholine)
⦁ can have inappropriately prolonged response to medication with certain genotype (heterozygous or homozygous atypical)
non-depolarizing NMBD
best clinical marker of strength
sustained head-lift
non-reversible NMBDs
- reversible competition between drug & ACh binding site
- no fasciculations (unlike succinylcholine - depolarizing)
- nerve stimulation exhibits a fade in train-of-four or tetany
- best clinical marker of strength = sustained head-lift
long acting non-depolarizing NMBD
intermediate acting
short acting
Pancuronium
Vecuronium, Rocuronium, Cisatracurium
Mivacurium
shortest onset, shortest duration = rocuronium
longer onset, longest duration = pancuronium
longest onset, shortest duration = cisatracurium
which non-depolarizing NMBD has vagolytic side effects
PANCURONIUM
Vecuronium, Rocuronium, Cisatracurium = no SE
metabolism of 4 non-depolarizing NMBD
pancuronium = renal
rocuronium & vecuronium = hepatic
cisatracurium = other…spontaneously degenerates
TRAIN OF FOUR (non-depolarizing NMBDs)
⦁ When 4 twitches are seen, 0-75% of the receptors are blocked.
⦁ When 3 twitches are seen, at least 75% of the receptors are blocked.
⦁ When 2 twitches are seen, 80% of the receptors are blocked.
⦁ When 1 twitch is seen, 90% of the receptors are blocked.
⦁ When no twitches are seen, 100% of receptors are blocked.
reverses vecuronium & rocuronium
Sugammadex
REVERSAL OF NMBDs
- Acetylcholinesterase Inhibitors*
⦁ Neostigmine, Edrophonium = result in the accumulation of ACh at NMJ
⦁ Sugammadex = no anticholinergic effects like the 2 above…reverses Vecuronium and Rocuronium
MALIGNANT HYPERTHEMIA
- An uncommon and sometimes life-threatening reaction to some anesthetic agents
- autosomal dominant condition of skeletal muscle; disruption of intracellular calcium metabolism
- the build up of calcium causes violent sustained muscle contraction & rigidity, heat production, acidosis, muscle necrosis & rhabdomyolysis (myoglobinuria)
TRIGGERS = Inhaled halogenated anesthetic agents & Succinylcholine
- quick rise in CO2 (hypercarbia)
- masseter muscle rigidity
- increase in body temp (1-2 degrees q5 minutes)
- tachycardia
- cyanosis
- muscle rigidity
- compartment syndrome
- rhabdomyolysis
- Hyperkalemia
TREATMENT = IV Dantrolene - rapid IV push
- can give oral dantrolene for 1-2 days prior to surgery, and up to 3 days after for prophylaxis
- cooling blankets
- Mannitol or Sodium Bicarb for renal support
- Treat Hyperkalemia & Compartment Syndrome
