General Anesthetics

1. What effects are used to achieve Balanced Anesthesis?

2. List the drugs used for these effects

• Balanced anesthesis

  • Hypnosis/amnesia + analgesia + immobility + autonomic control

• Hypnosis/amnesia

  • Propofol or volatile anesthetics

• Analgesia

  • opioids (fentanyl) ± adjuncts (ketamine)

• Immobility

  • Neuromuscular blockers (e.g., rocuronium) 

  • NOTE: paralysis; not unconsciousness

• Autonomic control

  • Blunt stress response 

  • (volatile + opioid ± dexmedetomidine/β-blocker)

Describe MAC

• What is it?

• Relationship to potency? Examples?

• Clinical Use

• Interpretation

What shifts MAC?

MAC

• What is it?

  • Minimum [] inhaled anesthetic -> prevents skeletal muscle movement in response to surgical incision in 50% 

• Relationship to Potency:

  • Inversely proportional

    • Nitrous oxide

      • Large MAC → low potency

    • Isoflurane

      • Small MAC → high potency

• Clinical Use:

  • Set vaporizer % 

  • Compare volatile anesthetics

• Interpretation:

  • MAC reflects immobility (spinal cord) more than amnesia/analgesia

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MAC SHIFTERS

• MAC ↓ (need less gas)

  • Elderly,

  • hypothermia,

  • pregnancy,

  • opioids/sedatives

• MAC ↑ (need more gas)

  • Hyperthermia,

  • chronic EtOH (classic)

Describe the Blood:gas partition

• What is it?

• What are the effects of High vs Low blood:gas partition

Blood:gas partition

• What is it?

  • How much dissolves in blood

• High vs Low blood:gas partition

  • High:

    • More soluble

    • Slower rise in alveolar [] → delayed induction/Wake-up 

  • Low:

    • Less soluble

    • Faster equilibration → rapid on/off (alveoli rise/fall quickly)

NOTE:

• Stuck in blood = slow; stays in gas = fast

List the UPTAKE DETERMINANTS and their relationships to induction. Why?

UPTAKE DETERMINANTS

• Ventilation ↑

  • Faster induction 

    • (alveolar partial pressure rises faster)

• Cardiac output ↑

  • Slower induction 

    • (blood “soaks up” more anesthetic)

• Solubility ↑

  • o Slower induction 

    • (more dissolved → less left in alveoli)

Describe the [] effect

• What is it?

• Ex?

Concentration effect: 

• What is it?

  • higher inspired % → FA (alveolar fraction)/FI (inspired fraction) rises faster

    • ***The more you increase the concentration of a drug, the faster the alveolar [] matches the [] and the faster the drug sets in***

• Ex:

  • N₂O ( often delivered at high %)

    • strong analgesic adjunct, weak anesthetic (needs partners)

  •  “fills fast” → quicker alveolar rise → faster onset

Note:

• High FI → fast FA

MEM TIP: Suck “HIS D, NO” (Highest → lowest Blood:Gas)

Describe the VOLATILE AGENTS

• Sevoflurane

  • Clinical Use? why

• Desflurane

  • Benefits? AE?

• Isoflurane

  • Clinical Use? Why?

• N2O

  • Uses? AE?

Describe the shared organ effects of volatiles:

• CV

• Resp

• CNS

VOLATILE AGENTS

• Sevoflurane

  • Smooth, non-pungent → best for mask induction (kids)

• Desflurane

  • Fastest on/off, 

    • airway irritant → coughing/laryngospasm risk

• Isoflurane

  • Pungent, “middle speed” → good for maintenance

    • not mask induction

• N₂O

  • Adjunct analgesic, weak anesthetic

    •  expands closed gas spaces + B₁₂ (methionine synthase) inhibition risk

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SHARED ORGAN EFFECTS

CV:

•  vasodilation → ↓SVR → ↓BP 

  • (dose dep).

Resp:

• ↓ ventilatory drive

  • Many: Bronchodilation

  • Pungent agents: cough/laryngospasm

CNS:

• ↓ CMRO₂ 

  • (cerebral metabolic rate of oxygen)

• ↑CBF/↑ICP at higher doses

  • (dose dep.)

Describe SEVOFLURANE

• Therapeutic use

• Pros

• AE

SEVOFLURANE

• Therapeutic Use

  • Inhalational (mask) induction 

  • maintenance (esp. pediatrics)

• Pros

  • Non-pungent → minimal airway irritation

  • Relatively fast on/off

• AE:

  • Dose-dependent hypotension 

  • respiratory depression

Describe DESFLURANE

• Pros

• AE

• Avoid

DESFLURANE

• Pros

  • Very rapid on/off → great for quick emergence

    • Fastest wake-up gas

• AE

  • Pungent

  • Airway irritant 

    • cough, bronchospasm, laryngospasm

  • sympathetic surge 

    • tachy/HTN

    • Esp w/ rapid increases

• Avoid:

  • Asthma/COPD or other reactive airway patients

  • Mask Induction

MEM TIP: HIS D, Stinky; Panic when inserted;

Describe ISOFLURANE

• Pros

• AE

• What is Coronary Steal Syndrome?

ISOFLURANE

• Pros

  • Stable, predictable maintenance anesthesia

• AE

  • Dose-dependent ↓SVR → hypotension

  • Pungent → not great for mask induction

• Coronary steal syndrome

  • Vasodilation -> redistribute flow away from ischemic regions

MEM TIP: I Steal

Describe Nitrous Oxide

• Clinical Use

• AE

N₂O (NITROUS OXIDE)

• Clinical Use:

  • Fast adjunct analgesic

  • Not a stand alone anesthetic

• AE:

  • Air-space rule

    • Diffuses into closed spaces faster than N₂ leaves -> expands bubbles

      • Avoid when air can’t escape

        • Pneumothorax, bowel obstruction, middle ear surgery

  • Chronic Exposure:

    • B₁₂ inactivation (↓ methionine synthase)

      • neuropathy + megaloblastic anemia.

Describe IV Induction:

• Clinical Usage

• Pros

• Ideal induction drug Characteristics

IV INDUCTION

• Clinical usage:

  • Fastest way to “turn off consciousness”

    • Maintain w/ volatile anesthetic or TIVA (infusion)

• Pros:

  • Quick, predictable onset for airway control + smooth transition to maintenance

• Ideal induction drug Characteristics

  • Rapid onset, short duration, hemodynamically tolerable

Describe PROPOFOL

• Clinical Usage

• MOA

• Pros

• AE

PROPOFOL

• Clinical Usage:

  • IV induction “workhorse”

• MOA

  • Potentiates GABAA → hypnosis/amnesia.

• Pros

  • Rapid on/off + antiemetic (smooth wake-up)

•  Adverse Effects

  • ↓ BP (vasodilation/↓inotropy), 

  • resp depression/apnea, 

  • Injection pain

  • Propofol infusion syndrome  (w/ prolonged/high-dose)

    • metabolic acidosis + rhabdo + cardiac failure

      • “ARC”

Describe ETOMIDATE

• Clinical Usage

• MOA

• AE

ETOMIDATE

• Clinical Usage:

  • Induction choice when BP = fragile

    • Best for Hemodynamic instability 

      • (minimal BP drop vs propofol)

• MOA

  • Potentiates GABAA → hypnosis

• AE:

  • Adrenal suppression

    • (↓ 11β-hydroxylase → ↓cortisol/aldosterone)

  • Myoclonus

  • PON/V (postoperative nausea & vomiting)

MEM TIP:MI DATE, Fragile (BP) Men (low adrenal)

Describe Katamine:

• Clinical Usage

• MOA

• AE

KETAMINE

• Clinical Usage:

  • anesthesia + analgesia (strong)

  • Asthma/bronchospasm, trauma, hypotension

• MOA

  • NMDA antagonist

• AE:

  • ↑ sympathetic tone (↑HR/↑BP)

  • Bronchodilation

  • Emergence reactions 

    • (vivid dreams/hallucinations) + ↑secretions → cough/laryngospasm risk

MEM TIP: AE very similar to DESflurane

Describe Midazolam

• Class

• Clinical usage

• AE

• Reversal

Midazolam

• Class:

  • BENZODIAZEPINES

• Clinical Usage:

  • Rapid anxiolysis + anterograde amnesia

    • (adjunct, not analgesic)

    • MEM TIP: AAAA, NA; (anxiolysis, anteriograde amnesia, adjunct, not analgesic)

• AE:

  • Sedation 

  • Seizures

  • respiratory depression

  • Withdrawal in benzo-dependent pts

• Reversal

  • Flumazenil 

    • (competitive antagonist)

  • MEM TIP: the FLU Stopped ME DAZO (dazzling)

Describe Barbiturates 

• Class

• Members

• MOA

• AE

• Classic CI

Barbiturates 

• Class:

  • Induction drugs 

• Members:

  • Thiopental

  • methohexital

• MOA:

  • GABAA → ↑ duration of Cl⁻ channel opening

    • ***vs benzos ↑ frequency***

• AE:

  • ↓CMRO₂ → ↓CBF/↓ICP

  • Hypotension + respiratory depression

• Classic CI:

  • Acute intermittent porphyria (trigger/worsen attacks)

Describe CONTEXT-SENSITIVE HALF-LIFE

• What is it?

• Clinical Usage

• Classic comparison

CONTEXT-SENSITIVE HALF-LIFE

• What is it?

  • Time for plasma level to drop 50% after stopping an infusion

    • ***Context = how long is the injusion***

    • ***longer infusion = longer half life

      • tissue redistribution → drug leaks back ***

    • ***NOTE, CONTEXT IS NOT LINEAR***

• Clinical Usage:

  • Predicts wake-up time better than elimination t½ after prolonged drips

• Classic Comparison:

  • Remifentanil & propofol stays short

  • Fentanyl & midazolam get longer as infusion time increases

Describe Opioids

• Clinical Usage

• AE

• Monitor Closely

OPIOIDS

• Clinical Usage:

  • analgesia + “stress response blocker”

  • blunt sympathetic surges (↓HR/↓BP)

    • laryngoscopy/intubation

    • incisions 

• AE:

  • respiratory depression

    • Dose dependent

    • Sedatives synergy

  • Fentanyl

    • chest wall rigidity → difficult ventilation

• Monitor Closely:

  • Pain off + RR down

What are the clinical usages of Neuromuscular blockers

NEUROMUSCULAR BLOCKERS

• Clinical Usage:

  • Paralysis only

    • must still sedate + treat pain

  • Intubation & surgical relaxation

NOTE:

• Always confirm adequate sedation before/while paralyzed

Describe Succinylcholine

• Class

• Clinical Usage

• MOA

• AE

Succinylcholine

• Class: 

  • DEPOLARIZER

• Clinical Usage:

  • Fastest paralytic (rapid onset, short duration)

• MOA:

  • Persistent end-plate depolarization → paralysis

• AE

  • HyperK⁺, bradycardia, ↑IOP

  • Malignant hyperthermia 

    • w/ volatile agents

Describe the NONDEPOLARIZERS

• Clinical Usage

• Members

• Reversal Strats

NONDEPOLARIZERS

• Clinical Usage:

  • Paralysis only (no sleep/pain relief)

• Members:

  • Cisatracurium

  • Rocuronium

  • Vecuronium

• Reversal:

  • Neostigmine (↑ACh) + glycopyrrolate (blocks muscarinic AEs)

  • Sugammadex 

    • rocuronium & vecuronium

Describe Dexmedetomidine (Precedex) 

• MOA

• Clinical Usage

• Pros

• AE

Dexmedetomidine (Precedex) 

• MOA:

  • α₂-agonist → “cooperative” sedation + sympatholysis + opioid- sparing.

• Clinical Usage:

  • smooths induction/emergence; 

  • Blunts tachy/HTN; 

  • lowers volatile + opioid needs.

• Pros:

  • minimal respiratory depression 

    • (unlike opioids/benzos).

• AE:

  • bradycardia + hypotension 

    • (watch preload/AV block).

Describe MALIGNANT HYPERTHERMIA

• Trigger

• Signs

• Labs

• Tx

Describe Dantrolene

• MOA

• Clinical Usage

MALIGNANT HYPERTHERMIA

• Trigger

  • Volatile anesthetics + succinylcholine

• Sign:

  • Rapid rise in end-tidal CO₂ (↑ ETCO₂) (despite ventilation) → 

    • muscle rigidity + tachycardia → fever

• Labs

  • Acidosis

  • HyperK

  • Rhabdomyolysis/↑CK

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Tx

• Stop triggers

  • Volatile agents + succinylcholine OFF

• 100% O₂ + hyperventilate (flush anesthetic, blow off CO₂)

• Dantrolene

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Dantrolene:

• MOA:

  • blocks RyR1 → ↓ SR Ca²⁺ release → ↓ rigidity + ↓heat/CO₂ production

• Clinical Usage:

  • Active cooling

  • Treat hyperK + acidosis

  • Manage rhabdo/arrhythmias

Describe Awareness 

• What is it?

• High risk Settings

• Prevention?

Awareness 

• What is it?

  • explicit recall during anesthesia

    • (rare, high-stakes)

• High-risk settings: 

  • trauma + OB + hemodynamic instability 

    • (dose often “light”)

  • TIVA (Total Intravenous Anesthesia )

    • no end-tidal agent → dosing/IV failure can be missed

• Prevention:

  •  end-tidal anesthetic concentration monitoring 

    • (when using volatiles)

  • depth monitoring when appropriate/high risk

    • (e.g., BIS)

Describe PONV & EMERGENCE DELIRIUM

• PON/V risk Factor

• Prophylaxis

• How to reduce triggers?

• What causes Emergence delirium

• Management

PONV & EMERGENCE DELIRIUM

• PON/V risk factor:

  • Female + nonsmoker + opioids + motion sickness

• Prophylaxis

  • Ondansetron ± dexamethasone

• Reduce triggers:

  • Minimize volatiles + opioid-sparing analgesia

• Emergence delirium

  • Due to sevoflurane/desflurane in some settings 

• Management

  • Reassure, reorient, treat pain/hypoxia

  • Stay calm