General Anesthesia Flashcards
(30 cards)
1
Q
What is anesthesia?
A
- a combo of amnesia, analgesia and muscle relaxation to allow the performance of surgery or other procedures
2
Q
3 phases of general anesthesia?
A
- induction
- maintenance
- emergence
3
Q
What are the agents used in induction?
A
- “putting to sleep”
- most commonly used induction agent is propofol
which causes:
drop in BP and CO, antiemetic properties
other agents: - etomidate:
doesn’t cause vasodilation, higher rate of post op nausea, inhibits the biosynthesis of cortisol, use is limited due to increase risk of death by 2.5x - ketamine:
used in pts w/ hemodynamic instabilility, cardiac stimulant, significant analgesia, bronchodilation, hallucinations
4
Q
What are the agents used in maintenance?
A
- use inhaled (volatile) or IV
- anesthetics inhalation anesthetic agents:
- volatile anesthetic agents: sevoflurane and desflurane
- nitrous oxide: can be used in combo w/ volatile gases
- IV anesthetic agents: propofol and remifentanil
5
Q
Emergence phase? What can this result in? What can blunt this autonomic response?
A
- waking up
can result in autonomic hyper-responsiveness: - tachycardia, HTN, bronchospasm, laryngospasm
- short acting narcotics, BBs or lidocaine can blunt this autonomic response
6
Q
What is propofol (Diprivan)?
When is it used? Onset of action? Duration? Effects?
A
- non-barbiturate hypnotic agent
- rapidly metabolized in liver and excreted in urine, so it can be used for long durations of anesthesia
- used for general surgery, cardiac surgery, neurosurgery, and ped surgery
- rapid onset of action (distribution 2-4 minutes), rapid clearance, and reversibility of effect once the drip is shut off
- onset 40 sec
- duration: 1-3 hrs
- some anti-emetic effect so less nausea and vomiting assoc w/ use
- weaker amnestic effect thanmidazolam (Versed)
- no analgesic effect
- milky looking soln (emulsion)
- clear-headedness during recovery
7
Q
Adverse effects of propofol?
A
- can support rapid growth of microorganisms
- hypotensive (administer slowly)
- may cause hypertonia and movement
- respiratory depression
8
Q
Use of ketamine (ketalar)? affects what? Duration?
A
- affects senses, produces a dissociative anesthesia (catatonia, amnesia, analgesia) in which the pt may appear awake and reactive, but can’t respond to sensory stimuli
- frequently used in ped pts b/c anesthesia and analgesia can be achieved w/ an intramuscualr injection
- also used in high-risk geri pts and in shock cases, b/c it also provides cardiac stimulation
- rapid onset: 30sec
- short duration: 5-10 min
9
Q
What are the anesthestic gases used in surgery?
A
- isolflurane (Forane)
- desfluorane (Suprane)
- sevofluorane (Ultane)
- nitrous oxide
10
Q
What is an impt property of anesthetics?
A
- reversibility
- once anesthetic gas is turned off, blood stream brings the gas back to lungs where it is eliminated: more soluble the gas is in blood, the longer it takes to eliminate
- nitrous oxide and desflurane are the shortest acting anesthetic gases b/c they are the least soluble in blood
11
Q
How do inhaled anesthetics work?
A
- inhaled anesthetics act in different ways at level of CNS
- disrupt normal synaptic transmission by:
interfering w/ release of neurotransmitters from presynaptic nerve terminal (enhance or depress excitatory or inhibitory transmission).
Alter re-uptake of neurotransmitters, and changes binding of NTs to post-synaptic receptor sites
12
Q
MAC of inhaled agents?
A
- Minimum alveolar concentration: inhaled anesthetic concentration (steady state) at which 50% of pts move in response to a std midline abdominal incision (37C, 30-55yo, 1 atm) - nitrous oxide: 105% - isoflurane: 1.15% - sevoflurane: 1.8% - desflurane: 6.2%
13
Q
Characteristics of isoflurane? What can it cause?
A
- higher blood-gas solubility so takes longer for onset and longer for emergence
- causes tachycardia
- causes peripheral vasodilation
- airway irritation, coughing
14
Q
What does Desflurane require? What can it cause?
A
- reqrs a heated-pressurized vaporizer for delivery
- causes tachycardia
- causes peripheral vasodilation
- least well-tolerated on the airway - can cause coughing, bronchospasm
- not used for mask induction
- fastest onset and off-set of volatiles
15
Q
What does sevoflurane cause? Onset?
A
- doesn’t cause tachycardia
- causes peripheral vasodilation
- well-tolerated for mask induction
- fast onset and quick awakening
16
Q
Effects of nitrous oxide?
A
- MAC is 105%: therefore alone, can’t provide anesthesia
- nitrous oxide diffuses into air containing cavities 34x faster than nitrogen can leave that 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
17
Q
Advantages of Nitrous oxide?
A
- inexpensive
- readily available
- odorless/slightly sweet
- limited effect
- no special equipment
- sympathomimetic
- will not cause malignant hyperthermia
18
Q
Disadvantages of nitrous oxide?
A
- high MAC/FIO2
- sympathomimetic
- methionine synthetase inhibitor
- expands air-filled spaces
19
Q
CI to potent inhaled anesthetic agents?
A
- inability to tolerate the physiologic alterations produced
- malignant hyperthermia
20
Q
What are the NMBD drugs used?
A
- succinylcholine (Anectine)
- Rocuronium (Zemuron)
- Vecuronium (Norcuron)
- Pancuronium (Pavulon)
- Cisatracurium (Nimbex)
21
Q
NMBDs produce what?
A
immobility needed for:
- endotracheal intubation
- surgical immobility/relaxation (Abdominal)
- mechanical ventilation
22
Q
Action of ACh?
A
- released into synaptic cleft and binds to nicotinic cholinergic receptors
- then opens ion channel which causes depolarization along the muscle - and then contraction
23
Q
2 types of NMBDs?
A
- depolarizing: succinylcholine (Anectine)
- nondepolarizing:
rocuronium
vecuronium
pancuronium
cisatracurium
24
Q
MOA of depolarizing agents (NMBDs)?
A
- causes 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 b/c the membrane is depolarized
25
MOA of Succinylcholine (Anectine)? When is it used? Onset, duration?
- causes depolarization at motor endplate
- in contrast to ACh, succinylcholine slowly dissociates from ACh receptors, resultign in an inactive state
- broken down by butyrylcholinesterase to choline and succinylmonocholine
- often agent of choice when rapid control of airway is necessary
- rapid onset: less than 1 min
- short duration: 6-10 min
26
Disadvantages of Succinylcholine?
- cardiac dysrhythmias (tachyarrhythmias)
- sinus bradycardia
- myalgias
- myoglobinuria
- hyperkalemia
- pt restrictions (kids)
- masseter spasm (not good for intubation)
- malignant hyperthermia trigger
- possible increases in intraocular, gastric, and intracranial pressures
- dependent upon normal (rare genotype that doesn't metabolize properly)
27
MOA of nondepolarizing NMBDs?
- reversible competition b/t drug and ACh binding site
- no fasciculations
- nerve stimulation exhibits a fade in train-of four or tetany
- best clinical marker of strength is sustained head-lift
28
Nondepolarizing agents?
- long acting: Pancurounium (onset: 1-1.5 min, duration 60 min, met: renal, SE: vagolytic)
- intermediate acting:
Vecuronium (1.5-2 min, duration: 40 min, hepatic, no SE)
Rocuronium (1-1.5 min, 35 min, hepatic, none)
Cisatracurium (2.5-3 min, 25 min, other metabolism, no SE)
- short acting:
Mivacurium
29
What is the train of 4?
way you can measure concentration of NMBDs
- when 4 twitches seen: 0-75% of receptors blocked
- 3 twitches: at least 75% blocked
- 2 twitches: 80% blocked
- 1 twitch: 90% blocked
- no twitches: 100% of receptors are blocked
30
Reversal for NMBDs?
Acetylcholine esterase inhibitors:
- neostigmine, edrophonium result in accumulation of Ach at neuromuscular jxn
- sugammadex: no anticholinergic effects like those above, reverses vecuronium and rocuronium
