Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PR3136 PT IV > General Anaesthetics > Flashcards

General Anaesthetics Flashcards

1
Q

What are GA used for?

A
  • to produce unconsciousness and a lack of responsiveness to ALL PAINFUL STIMULI (inhibition of sensory and autonomic reflexes)
  • provide conditions for interventions - e.g. surgery to take place
  • skeletal muscle relaxation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the triad that GA provides? (triad of ___)

A

triad of hypnosis, amnesia, and analgesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the additional consideration that GA is used for?

A
  • used for control of physiology

–>Heart rate to go down, maintain a certain body temp, no reflexive manner

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the endpoint of using GA?

A
  • Keep patients SAFE and ALIVE upon GA reversal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the necessary steps a patient goes through to get GA?

A
  1. pre-assessment/ premed
  2. induction of anaesthesia
  3. airway management (incubation required)
  4. maintenance of anaesthesia (infuse more for deeper levels, also know how to reverse)
  5. reversal/ emergency
  6. post-op care
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What constitutes an ideal GA? What properties should an ideal anaesthetic drug have?

A
  • unconsciousness (but might still response to PAIN, thus requires analgesia)
  • analgesia
  • muscle relaxation
  • amnesia (dont remember the process)
  • brief & pleasant
  • depth of anaesthesia can be raised or lowered with ease
  • minimal adverse effects
  • margin of safety (LARGE)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is one thing to take note about the properties of GA?

A

NO single agent has ALL of these properties

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What constitutes in a BALANCED anaesthesia?

A
  • pain relief (analgesia)
  • unconsciousness (hypnosis and amnesia?)
  • inhibition of reflex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why should anaesthesia be balanced?

A

to ensure that induction is smooth and rapid, and that analgesia and muscle relaxation are adequate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What 2 types of anaesthetics are used in combi in GA?

A
  • Inhalation Anaesthetics

- IV anaesthetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What 3 types are the most commonly used GA?

A
  • short-acting barbiturates (For induction of anaesthesia) (unconsciousness)
  • neuromuscular blocking agents (for muscle relaxation) (inhibition of reflex)
  • opioids and nitrous oxide (for analgesia) (pain relief)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the properties of inhalant GA in tissue distribution?

A
  • solubility in blood
  • the higher the blood solubility –> the slower the onset

e.g. NO faster onset than halothane (BUT speed is NOT = efficacy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the names of the volatile liquids inhalant GA and how are they delivered?

A
  • Halothane, Enflurane, Desflurane, Isoflurane, Sevoflurane

- through aerosol nebuliser

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What gas is inhalant GA?

A

only nitrous oxide (NO) is a gas inhalant GA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the MOA of Inhalant GA?

A
  1. (ENHANCE INHIBITION) Enhance neurotransmission at inhibitory synapses via allosterically increasing GABA receptor sensitivity to action by GABA itself (positive allosteric modulator)
  2. (DEPRESS EXCITATION) also depressing neurotransmission at excitatory synapses via blocking glutamate neurotransmitter acting on NMDA receptor thus preventing NMDA receptor activation (negative allosteric modulator)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the minimum alveolar concentration (MAC) for inhalant GA volatile liquids?

A

MAC is an index of inhalation anaesthetics potency

low MAC = high anaesthetic potency

  • defined as the minimum conc of drug in the alveolar air that will produce immobility in 50% of patients exposed to a painful stimulus
  • MAC values alter with age, condition, concomitant administration of other drugs, etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the potency of NO?

A

110% (theoretical value)

onset of action is fast but potency is low

18
Q

What are the potencies of Isoflurane, sevoflurane, and desflurane (i think dont need to memorise the values but know how to compare potency)

A
  • isoflurane: 1.2% (You need 1.2% within alveolar –> knock out 50% of the people; more potent one)
  • sevoflurane: 2.2%
  • desflurane: 6.3% (less potent)
19
Q

What are the absorption factors we can look at for inhalant GA? (PK parameter - absorption)

A
  • inhalation anaesthetic must reach CNS conc sufficient to suppress neuronal excitability

Absorption:

  • conc of anaesthetic in inspired air
  • solubility of GA
  • blood flow through lungs

(if increase any of these absorption factors, it will increase rate of GA uptake into blood)

20
Q

What are the blood solubilities of the volatile liquids and NO?

A 
Halothane: 2.3 (high sol)
Isoflurane: 1.4
Enflurane: 1.8
Sevoflurane: 0.69 
volatile liquids are adm using agent specific-vaporiser

NO: 0.47 (low sol, thus onset of action fast to brain, doesnt require vaporiser)

21
Q

How is the distribution like for volatile liquids GA?

A

anaesthetic levels in brain, liver, lungs and heart tissues equilibrate with those in blood quickly after of administration (the organs here are highly perfused)

determined by regional blood flow –> which tissue(s) receive GA

22
Q

How are volatile liquids GA eliminated?

A
  • export in expired breath
    ~ inhalation anaesthetics eliminated almost entirely via lungs
    ~ minimal hepatic metabolism
    ~ factors that determine uptake also determine elimination (since blood flow to brain is the highest, anaesthetic levels drop rapidly when administration is stopped)
23
Q

What are the concerns of volatile liquids GA metabolites?

A
  • some metabolites can be toxic
  • e.g. inorganic fluorides of isoflurane and enflurane are NEPHROTOXIC, halothane is HEPATOTOXIC

(when induce too much anaesthesia)

24
Q

What are the key points to take note of for halothane?

A
  • 1st modern inhaled anaesthetic, standard for comparison

~ volatile liquid, non-flammable and non-irritating

  • potent (MAC 0.75%)
  • medium rate of onset and recovery

~ little to no analgesia UNTIL unconsciousness supervenes
- causes respiratory depression dose-dependently

~ dec BP due to depression of cardiac output; Bradycardia and arrhythmia may also occur leading to hypotension and dysrhythmia
- relaxes skeletal muscle and potentiates skeletal muscle relaxants (neuromuscular blocker + halothane)

~ may lead to halothane-associated hepatitis

25
Q

What are the key points to take note of for isoflurane?

A
  • pungent smell
    ~ potent (MAC 1.4%)
    ~ Medium rate of onset and recovery
  • similar to halothane w less hypotension and arrhythmia (all inhalant GA decreases BP)
  • decreases BP mainly due to decrease in systemic vascular resistance
26
Q

What are the key points to take note of for sevoflurane?

A
  • potent (MAC 2%) (poorer blood solubility, get to brain faster)
  • More rapid rate of onset and recovery
    ~ metabolised in liver to release inorganic fluoride –> NEPHROTOXIC
  • unstable when exposed to CO2 absorbents in anaesthetics machines, degrading to a compound that is potentially NEPHROTOXIC
27
Q

What are the key points to take note of for NO gas?

A
  • odourless, non-flammable
  • rapid onset and recovery but LACK POTENCY (MAC 105-110%)
  • NO alone gives analgesia and amnesia but NOT COMPLETE UNCONSCIOUSNESS or surgical anaesthesia
  • pts undergoing GA receive NO to supplement the analgesic effects of primary anaesthetic
    E.g. Take some time for halothane to work; thus NO to give some analgesic effect in case if the primary anaesthetic dont have analgesic pprty
  • when used alone: as analgesic agent (e.g. dentistry, during deliver obstetric use)
  • major concern: Post-op NV
28
Q

What are Intravenous GA?

A
  • induction agent that induces unconsciousness
  • does not necessarily keep you asleep for very long (short acting)
  • most agents depress respiration; need to take over ventilation of patients
  • may be used alone or to supplement the effects of inhalation agents
29
Q

What are some examples of IV GA?

A
  • Thiopentone
  • etomidate
  • propofol
  • ketamine (reduce excitation)
  • midazolam (anxiolytic, benzodiazepam)
30
Q

What are the 2 advantages of Inhaled combi w IV GA?

A
  • permit dosage of the inhalation agent to be reduced
  • produce effects that cannot be achieved with an inhalation alone

Synergistic, after a while IV will wear off, the gaseous low dose and maintain anaesthesia
Sometimes dont have anxiolytic/ analgesic effect, thus combi impt

31
Q

What is the MOA of thiopentone (sodium thiopental)?

A
  • cause CNS depression by potentiating the action of the neurotransmitter GABA on the GABA(A) receptor-gated CL ion channels (excite inhibition)

Memb potential –> hyperpolarised (prevents depolarisation)–> whole neuron is inhibited

32
Q

What are some points/PK parameters to take note for thiopentone?

A
  • Barbiturate w extremely high lipid solubility: enters brain easily and rapidly - rapid onset of action, unconscious within 10-20sec after IV
  • Single dose: redistributes to less vascularised tissues - ultra-short duration of action (low blood solubility); injected alone and w/o inhale agents, pts will wake up in ~10min
  • Multiple doses/infusions: duration of action depends on CLEARANCE
  • Slow elimination, large Vd (stay in brain), active metabolite (pentobarbital), metabolised in liver with liver cirrhosis –> can result in prolongation of clinical action
  • (KIV) extensively bound to plasma protein: small amt of free drug can be excreted by glomerular filtration + reabsorption in tubules
  • (KIV) less than 1% excreted unchanged
33
Q

What are some points/PK parameters to take note for propofol?

A
  • most common IV anaesthetic used in SG (ready-made in injectable form, no need to reconstitute, unlike thiopentone)
  • induction rate is similar to thiopentone, and recovery is more rapid (pts move sooner and feel better)
  • used both for induction and maintenance
  • rapid onset (unconsciousness develops within ~60sec)
  • short duration of action (~3-5min following single injection) because rapid redistribution from brain to other tissues
  • extensively used in “day surgery”
  • needs continuous, low-dose infusion for extended effects
  • reduced post-op vomiting (may be related to an anti-emetic action)
  • significant cardiovascular effect during induction (Dec BP and negative inotropic) - hypotension
  • to be used with caution in elderly patients, patients with compromised cardiac function, hypovolemic patients
34
Q

What are some points/PK parameters to take note for ketamine?

A
  • racemic (potency S- > R+); I/M, oral, rectal routes
  • produces dissociative anaesthesia (patient feels dissociated from env)
  • can cause sedation, immobility, analgesia and amnesia
  • rapid induction: responsiveness to pain is lost
  • metabolised in liver to less active metabolite, excreted in urine and bile
  • large Vd, rapid clearance –> suitable for continuous infusion w/o the lengthening in duration of action
  • unpleasant psychologic reactions (hallucination, disturbing dreams, delirium) may occur during recovery from ketamine
  • risks of psychologic adverse reactions may be reduced with premedication of diazepam/ midazolam (reduces the dose of ketamine)
  • ONLY IV anaesthetic that possess ANALGESIC property –> popular in 3rd world countries as the only anaesthetic, due to lack of other anaesthetic agents
35
Q

How can anaesthetic adjuncts help GA? (kiv)

A
  • augment GA

- Lower GA doses used –> reduce GA side effects

36
Q

What are some anaesthetic adjuncts/ post-op care?

A
  • benzodiazepines (midazolam): anxiolytics, amnesia, sedation PRIOR to induction of anesthesia (perioperative period) or used for sedation during procedures not requiring GA
  • a2 adrenergic agonists: sedation PRIOR to and/or during procedures in non-intubated patients
  • analgesics: typically administered WITH GA to reduce anaesthetic requirement
  • Neuromuscular blocking agents: induction of anaesthesia to relax muscles (jaw, neck, airway) to facilitate laryngoscopy and endotracheal intubation (e.g. prevent gag reflex when doing a scope)
37
Q

What are the key points for midazolam (benzodiazepine)? (kiv)

A
  • perioperative period: anxiolysis, amnesia, sedation
  • use for sedation during procedures not requiring GA
  • rapid onset when used for induction (unconsciousness develops in 80sec; peak ~2min); sedates ~30min when used by itself

Metabolised in liver (elderly tend to be more sensitive, slower recovery)

Midazolam high TI –> lesser cardiovascular and respiratory depressing effects VS other IV anaesthetics

SE: compounded by concurrent usage of other agents

Adverse effects minimised by injecting midazolam slowly (over 2 or more min) and by waiting another 2 or more mins for full effects to develop before dosing again

38
Q

What are the key points for dexmedetomidine IV (a2 adrenergics)? (kiv)

A
  • highly selective a2 adrenergic receptor agonist
  • short term sedation (<24h)
  • sedation and analgesic effects (doesnt produce reliable GA even at max doses)
  • little respiratory depression
  • tolerable dec in BP and HR
  • Undesirable SE: Nausea, dry mouth, hypotension bradycardia
39
Q

What are the key points for NSAIDs (analgesics)? (kiv)

A
  • for minor surgical procedures, use COX-2 inhibitors and paracetamol
  • opioids (fentanyl, morphine) - for perioperative period
  • agonist activity at mu-opioid receptors
  • relative potency to morphine (duration of action)
    • sufentanil (1000x) (intermediate 15min)
    • remifentanil (300x) (ultra-short ~10min)
    • fentanyl (80x) (intermediate ~30min)
    • alfentanil (15x) (intermediate~20min)

choice is based primarily on DOA

Metabolised in liver except remifentanil is hydrolysed by tissue and plasma esterases

Excretion: urine, bile

40
Q

What are the key points for succinylcholine/ vecuronium (neuromuscular blockers)? (kiv)

A
  • depolarising succinylcholine
  • non-depolarising (e.g. vecuronium)
  • administered during induction of anaesthesia to relax muscles of jaw, neck, airway –> facilitate laryngoscopy and endotracheal intubation
  • aids many surgical procedures and provide additional insurance of immobility
  • note: barbiturates will precipitate when mixed with muscles relaxants –> should be allowed to clear form IV line prior to injection of muscle relaxant (Need to clear barbiturates first then succinylcholine added)
41
Q

WHAT ARE THE KEY TAKEAWAYS?

A
  • GA produce unconsciousness and insensitivity to painful stimuli
  • Balance anaesthesia
  • MAC lower –> higher potency
  • MOA by inhalation anaesthetics
  • Inh anaesthetics eliminated through expired air
  • principal adverse effects of GA: depression of respiratory and cardiac performance
  • NO differs from other - GAs; very high MAC, cant be used alone to produce GA; high analgesic potency (not the same as the MAC potency) ; low blood solubility, reach brain faster; frequently combined with other GAs to supplement their analgesic effect
  • Induction of anaesthesia usually accomplished with short-acting barbiturate (thiopentone, sodium thiopental)
  • IV Ketamine: dissociative anaesthesia
  • ability of an adequate GA includes the ability to suppress “recall”/awareness in addition to “unconsciousness”

PR3136 PT IV (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions