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Surgery Clerkship > Anesthetic Pharmacology > Flashcards

Anesthetic Pharmacology Flashcards

1
Q

Propofol

A
  • Most commonly used intravenous anesthesia induction agent, given as an IV bolus of 1.5 to 2.5 mg/kg
  • Rapid loss of consciousness, short halflife, pleasant and rapid awakening, few residual effects on brain
  • May cause pain on injection, so local anesthesia prior to administration is best practice
  • Anesthetic of choice for malignant hyperthermia (given as continuous IV drip)
  • Side effects: Hypotension, apnea
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2
Q

Etomidate

A
  • IV general anesthetic distinguished from others by its paucity of effects on cardiovascular status
    • Agent of choice for patients with a risk of cardiovascular instability
  • Side effects: Adrenocortical suppression, myoclonus, activation of seizure foci
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3
Q

Thiopental (aka sodium pentothal)

A
  • Used as intravenous general anesthesia induction agent in those undergoing neurosurgery
  • Has a very long halflife and reduces the brain’s oxygen consumption, thus reducing ischemia-induced brain damage
  • May also be used for treatment of increased ICP intraoperatively
  • There is a myth that it is a “truth serum”. This is completely baseless.
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4
Q

Ketamine

A
  • Intravenous hypnotic drug which produces a dissociative state accompanied by analgesia, unawareness, and nystagmus
  • May be used for intravenous general anesthesia induction
  • Side effects: Bad dreams, , increased blood pressure, HR, and cardiac output, increased ICP, increased respiratory secretions, and emergence delirium
    • Emergent delirium is mitigated by pre-treatment with benzodiazepines
    • Pretreatment with an antisialogogue (specifically glycopyrrolate) can decrease respiratory secretions
  • Contraindicated in cases of intracranial pathology and/or increased ICP
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5
Q

Anesthetics good for ICP vs bad for ICP

A
  • Good for ICP: Thiopental
  • Bad for ICP: Ketamine
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6
Q

Minimum alveolar concentration

A

The alveolar concentration of an inhaled anesthetic that prevents movement in 50% of patients in response to a stimulus (such as surgical stimulation). It can also be considered an anesthetic’s ED50. The goal of an anesthetic is obviously not MAC, since 50% of patients move in response to a stimulus at this concentration.

Also indicates the potency of a gas anesthetic.

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7
Q

Blood/gas partition coefficient

A

Equilibrium constant of PPblood : PPalveolar gas for a given anesthetic

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8
Q

Blood/fat partition coefficient

A

Equilibrium constant of PPblood : PPfat for a given anesthetic

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9
Q

Desired properties of a gas anesthetic

A
  • Physical properties:
    • Lack of flammability (the fluranes are safe, N2O can combust)
    • Ease of vaporization at room temperature
    • Chemical stability
  • Properties involving lungs/ventilation:
    • Rapid induction and emergence
    • Lack of airway irritation
    • Bronchodilation
    • Lack of respiratory depression (no gas anesthetics meet this criterion)
  • Properties involving cardiovascular system:
    • Maintenance of MAP
    • Suppression of Sympathetic activity
    • Maintenance of heart rate
  • Properties involving other organ systems:
    • Low solubility in skeletal muscle and fat
    • Direct skeletal muscle relaxation
    • Not being a trigger for malignant hyperthermia (Only nitrous oxide)
    • Low hepatic metabolism
    • Lack of organ toxicity
  • Properties involving the CNS:
    • Analgesia
    • High potency/low off-target effects
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10
Q

Chemical reactions of gas anesthetics with CO2 and soda lime

A
  • Sevoflurane: A nephrotoxic vinyl compound
  • Desflurane: Carbon monoxide
  • Isoflurane: Also carbon monoxide
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11
Q

The more blood-soluble a gas anesthetic. . .

A

. . . the slower its rise in alveolar pressure, and thus the more of the gaseous form of the anesthetic is transmitted to organs like the brain

Conversely, the more insoluble the gas that’s inhaled, the quicker its alveolar and gaseous plasma concentrations rise, and the more rapid its action.

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12
Q

Most blood insoluble gas anesthetics

A
  • Nitrous oxide
  • Desflurane
  • Thus, these have the most rapid onset/offset of any gas anesthetics
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13
Q

Most blood soluble gas anesthetic

A
  • Isoflurane
  • Thus, its onset/offset are delayed when compared to other gas anesthetics used for induction
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14
Q

The more lipid-soluble a gas anesthetic, . . .

A

. . . the more ease with which it crosses the blood-brain barrier.

Isoflurane and sevoflurane are quite lipid soluble, while nitrous oxide and desflurane are not.

Note: This also means it dissolves in fat, and so anesthetic may accumulate in fat during the operation, resulting in a prolonged emergence period.

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15
Q

Gas anesthetics that irritate the airway

A
  • Isoflurane and desflurane have an unpleasant, pungent odor
  • May cause coughing, laryngeal spasms
  • For this reason, desflurane in particular is only used for maintenance anesthesia
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16
Q

Gas anesthetics that also bronchodilate

A

Great for patients w/ reactive airway disease or asthma

Sevoflurane, isoflurane

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17
Q

Desflurane’s effects on bronchi

A

No effect in non-smokers, but produces bronchoconstriciton in smokers

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18
Q

Only gas anesthetic that does not drop the MAP

A

Nitrous oxide

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19
Q

Effects of gas anesthetics on sympathetic nervous activity

A

None decrease SNS activity, and in fact nitrous oxide, isoflurane, and desflurane all increase SNS activity.

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20
Q

Inhaled anesthetics and heart rate

A

They all increase the heart rate!

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21
Q

Gas anesthetics and muscle relaxation

A
  • Best muscle relaxants — worst muscle relaxants:
  • Desflurane + Sevoflurane > Isoflurane >> Nitrous oxide
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22
Q

“Rule of 2’s” for hepatic metabolism of gas anesthetics

A

Halothane is roughly 20% metabolized, enflurane 2%, isoflurane 0.2%, desflurane 0.02%, and sevoflurane roughly 4% (2% × 2).

Nitrous oxide is not metabolized by the liver in any meaningful way.

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23
Q

Organ toxicities of gas anesthetics

A
  • Hepatic: Isoflurane + desflurane
  • Renal: Sevoflurane
  • Bone marrow: Nitrous oxide
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24
Q

In a patient with a history of inhaled gas anesthetic-induced hepatitis, it is advisable to avoid. . .

A

. . . the volatile inhaled anesthetics: isoflurane, sevoflurane, AND desflurane

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25
Q

Pros and cons of nitrous oxide as a gas anesthetic

A
26
Q

Pros and cons of isoflurane as a gas anesthetic

A
27
Q

Pros and cons of desflurane as a gas anesthetic

A
28
Q

Pros and cons of sevoflurane as a gas anesthetic

A
29
Q

Only gas anesthetic that doesn’t trigger malignant hyperthermia

A

Nitrous oxide

30
Q

Contraindication to nitrous oxide for gas anesthesia

A

pulmonary hypertension

It increases PVR in these patients

31
Q

Presentation of malignant hyperthermia

A
  • There will be fever and generalized muscle contraction/rigidity, including respiratory muscles with increasing end-tidal CO2
  • Intraoperative or immediately following surgery
  • Late signs: myoglobinuria, oliguria, DIC, complex arrhythmias
32
Q

Adverse effects of succinylcholine

A
  • The post-junctional membrane depolarization induced by succinylcholine results in efflux of K+ from muscle cells. The risk of hyperkalemia is significantly increased when succinylcholine is administered to patients with other risk factors for hyperkalemia (e.g., burns, trauma, kidney failure).
    • Non-depolarizing neuromuscular blockers such as rocuronium are used to facilitate intubation under these circumstances to avoid hyperkalemia.
33
Q

WHO analgesic ladder

A
34
Q

Adverse effects of halothane

A
  • Halothane hepatitis: Presents 2 days to 3 weeks following surgery in which inhaled halothane is used for anesthesia. Leads to elevated serum aminotransferases, elevated bilirubin, eosinophilia, and slightly elevated alkaline phosphatase. Liver biopsy is not necessary for diagnosis but typically shows massive centrilobular hepatic necrosis.
35
Q

If someone is presenting in severe pain (8-10 out of 10), just let them have. . .

A

. . . a PCA pump, to avoid undertitration

36
Q

Ester and Amide group local anesthetics

A
  • Ester group:
    • Procaine, chloroprocaine, benzocaine, tetracaine
    • Metabolized in the serum by esterases
    • Have a higher risk of causing allergic reactions or systemic toxicity
  • Amide group:
    • Lidocaine, prilocaine, mepivacaine, bupivacaine, etidocaine, ropivicaine
    • Metabolized in the liver
    • Generally safe than esters and should be used when patients are allergic to esters
37
Q

Features of local anesthetic toxicity

A
  • CNS:
    • Tinnitus, metallic taste, perioral paresthesias, seizures, CNS depression
  • Cardiovascular system: (especially bupivacaine)
    • Bradycardia, AV block, ventricular arrhythmia, either hypertension or hypotension
  • Hematologic: (especially benzocaine)
    • Methemoglobinemia
38
Q

Most common allergy to local anesthetics

A

Itchy rash 3 days post-administration

39
Q

Anesthetics effective when given topically

A
  • Lidocaine
  • Prilocaine
  • Tetracaine
40
Q

Overdose or inadvertent injection of an LA into a blood vessel can cause. . .

A
  • CNS symptoms:
    • Tinnitus
    • Seizures
    • Metallic taste*
  • CVS symptoms:
    • Arrhythmias
    • Bradycardia
    • Vasovagal syncope
41
Q

Short vs Long amide and ester local anesthetics

A
  • Amide:
    • Short:
      • Lidocaine
      • Prilocaine
      • Mepivacaine
    • Long:
      • Bupivacaine
      • Etidocaine
      • Ropivacaine
  • Ester:
    • Short:
      • Procaine
      • Chloroprocaine
      • Benzocaine
    • Long:
      • Tetracaine
42
Q

Differentiating amide and ester local anesthetics by spelling

A

Amide LAs (e.g., lidocaine, bupivacaine) contain an “i” in their name preceding “-caine.” Ester LAs do not.

43
Q

Bupivicaine is often injected along with ___

A

Bupivicaine is often injected along with epinephrine (in order to prolong its action, alpha-2 mediated) and sodium bicarbonate (in order to increase the anionic fraction and speed up onset of action)

44
Q

Relevance of chemical properties of local anesthetics to their therapeutic utility

A

They are weak bases that must enter the cell in order to act, and they must be deprotonated in order to enter the cell

Therefore, they do not work well when injected into acidic environments, such as an abscess.

45
Q

Since local anesthetics can only bind the Na channel in its open state, they disproportionately act upon. . .

A

. . . rapidly firing neurons

This property is called “state-dependent blockade”, and it is in part why they work so well as ventricular anti-arrhythmics

46
Q

Order of local anesthetic fiber blockade and its etiology

A
  • Etiology: Local anesthetics work best on the less myelinated neurons. Therefore, their order of decreasing effectiveness is that of increasing degrees of myelination:
    1. Sympathetic fibers
    2. Pain and temperature fibers
    3. Proprioception fibers
    4. Touch and pressure fibers
    5. Motor transmission fibers
47
Q

How to remember which local anesthetic family is more likely to cause allergy

A

Esters get IgE

48
Q

Physiochemical properties and clinical effect of anesthetics

A
  • pKa: Determines onset of action (closer to 7.4, greater anionic fraction, faster diffusion, faster action)
  • Lipid solubility: Determines potency
  • Protein binding: Determines duration of action and plasma halflife
49
Q

Site of injection and effect of local anesthetic

A

The more vascular the site of injection, the higher the peak plasma level of the local anesthetic

Also, the higher the potential for toxicity and the shorter the duration of blockade

50
Q

Epinephrine-containing test dose

A

Test dose is administered prior to the full injection in order to ensure that local anesthetic is not being injected directly into the circulation

Since the test dose also contains epinephrine, the readout is heart rate and blood pressure, which will rapidly increase by ~10-20% if the material is injected into an artery or vein. Since epinephrine also locally vasoconstricts, it will also result in less spread of toxicity even if you do inject into vasculature!

This is done in order to reduce likelihood of toxicity, including seizures and arrhythmias.

51
Q

Indications for neuromuscular blocking agents

A
  • To facilitate tracheal intubation
  • To optimize surgical conditions
  • To optimize ventilation in a patient who requires controlled mechanical ventilation
52
Q

The only depolarizing neuromuscular blocker

A

Succinylcholine

It binds at the nicotinic receptor to produce initial depolarization (manifested as fasciculation) followed by paralysis

53
Q

Succinylcholine in patients with hyperkalemia

A

Since succinylcholine depolarizes, it causes massive release of potassium, typically elevating serum potassium by 0.5-1 mEq

Thus, in someone with pre-existing hyperkalemia, it may trigger a fatal arrhythmia. It is therefore contraindicated in these patients. It is okay to use in ESRD as long as the patient has potassium < 5.5 mEq/dL

For the same reason, it often is associated with post-sedation myalgias (from locally high potassium)

54
Q

Succinylcholine metabolism

A

It is metabolized by plasma pseudocholinesterase.

Thus, in patients with familial deficiency or enzymatic alteration in pseudocholinesterase, the halflife of succinylcholine is greatly prolonged.

55
Q

Ideal muscle relaxant for intubation

A

Succinylcholine

Due to its rapid onset and short duration of action

56
Q

Non-depolarizing muscle relaxants

A
  • Intermediate acting:
    • Rocuronium: Rapid onset of action. Hepatobiliary excretion (prolonged in liver disease).
    • Vecuronium: Hepatobiliary excretion (prolonged in liver disease). Down-stream metabolite is also active and excreted by kidney (prolonged in kidney disease).
    • Cisatracurium: Cleared by the Hoffman equation (physiologic pH and temp). Ideal for patients with kidney or liver disease.
  • Long acting:
    • Pancuronium: Also affects pre-synaptic neurons. Primarily renal clearance (prolonged in kidney disease). Also has vagolytic effects that increase heart rate.
57
Q

Train of Fours

A
  • Nerve simulation of adductor pollicus longus four times over 2 seconds
    • 4 twitches felt: Less than 75% paralyzed
    • 3 twitches felt: 75-85% paralyzed
    • 2 twitches felt: 85-95%
    • 1 twitch: 95-99%
    • 0 twitches: fully paralyzed
  • Generally the presence of 1-3 twitches is adequate for surgical exploration. Only within 1-3 twitches do you know roughly how much leway you have (if 4, somewhere <75%, if 0, who knows how long they will be paralyzed).
58
Q

Emergence from paralysis

A
  • Usually achieved with neostigmine
  • Patient should have at least one twitch on the train of four for emergence to be attempted
  • Due to the cholinergic effects of cholinesterase inhibitors, glycopyrrholate is usually administered concomittantly to focus the effect on nicotinic receptors.
  • Clinical signs of adequate reversal:
    • Patient able to lift head for 5 seconds
    • Able to protrude tongue
    • Able to maintain inspiratory pressure >-21 cm H2O
59
Q

Which is more common in the general population: Pseudocholinesterase deficiency, or atypical pseudocholinesterase enzyme activity?

A

Atypical enzyme activity is more common than true deficiency

If you encounter a patient with delayed recovery from succinylcholine, prior probability states that this is the more likely diagnosis

60
Q

Methohexital

A
  • Ultra-short acting barbiturate
  • Increases ictal activity and can produce suppression of the EEG spike
    • Produces longer siezures than propofol, but not too long (like etomidate). Less likely to need restimulation with methohexital than propofol.
    • Induction agent of choice for ECT

Surgery Clerkship (42 decks)

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