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HSHD 2 Block 3 > General Anesthetics > Flashcards

General Anesthetics Flashcards

1
Q

What is anesthesia

A

Anesthesia IS a medication-induced, reversible depression of the central nervous system such that the perception of all senses is ablated

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2
Q

Desirable components of anesthesia

A

Amnesia

Hypnosis

Analgesia

Immobility

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3
Q

Brain areas targeted by general anesthesia

A

vSpecific brain areas affected by various anesthetics include the reticular activating system, cerebral cortex and hippocampus

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4
Q

Stages of anesthesia

A

Stage 1: Induction – analgesia and euphoria

Stage 2: Excitement – involuntary movement

Stage 3: Surgical anesthesia – unconsciousness and muscle relaxation

Stage 4: Medullary depression – apnea and cardiovascular depression

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5
Q

Characteristics of the Ideal Anesthetic

A

Smooth and rapid – ideal for induction and loss of consciousness

Physiologically stable – does not cause large variation in blood pressure, heart rate, etc.

Reversible and/or metabolized – allows for rapid return of cognitive function when discontinued

Safe – devoid of adverse effects and with a wide margin of safety

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6
Q

What is Context sensitive half-time

A

Time required for concentration of a drug to decrease by 50% after discontinuation of an infusion

The context-sensitive half-time cannot be predicted by the elimination half-life because it depends on distribution/redistribution

In general, drugs which are more lipid soluble have a longer context-sensitive half-time

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7
Q

Barbituates MOA and metabolism

A

GABA agonists

Produce rapid loss of consciousness – historically used as an induction agent

Hepatic metabolism to inactive metabolites

Relatively short elimination t1/2, unless repeat dosing or infusion

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8
Q

Barbituates effects on CNS, cardiovascular, resp

A

CNS effects

  • Cerebral vasoconstrictors therefore decrease CBF, ICP and CMRO2
  • Protective against focal ischemia
  • Anti-epileptic (except methohexital)
  • No associated analgesia or muscle relaxation

Cardiovascular effects

  • Peripheral vasodilation
  • Negative inotropic effect
  • Blunts baroreceptor response, transient hypotension

Respiratory effects

  • Decreases tidal volume and respiratory rate as well as decreased response to hypoxia and hypercarbia
  • Dose-dependent apnea
  • Does not depress airway reflexes (may have laryngospasm during use)
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9
Q

Barbituates examples

A

Sodium thiopental

vHistorically used as “truth serum”

vUsage declined with increasing use of propofol and etomidate

vNo longer manufactured or imported in the US due to association with lethal injection

Methohexital remains available

vActivates epileptic foci

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10
Q

Benzodiazapenes MOA

A

GABA Agonist

Produce anxiolysis and antegrade amnesia – often used as premedication prior to induction

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11
Q

Benzodiazapenes examples

A

Midazolam: most lipophilic, onset <5 minutes, half-life 2 hours

Lorazepam: onset <30 minutes, half-life 12-18 hours

Diazepam: onset 1-5 minutes, half-life extremely variable (20-100 hours) due to active metabolites

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12
Q

Benzodiazapenes metabolism

A

Liver metabolism, active metabolites (diazepam) and inactive metabolites (midazolam) excreted in urine

Reversal agent: flumazenil

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13
Q

Benzodiazapenes effects on CNS, cardiovasc, resp

A
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14
Q

Ketamine MOA and use

A

NDMA Antagonist

Functionally dissociates the thalamus from the limbic cortex; patients may appear conscious but are unable to process or respond to sensory input

Used for induction or in smaller doses as an adjunct anesthetic or analgesic

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15
Q

Ketamine metabolism

A

Midazolam mitigates unpleasant emergence hallucinations

Liver metabolism to minimally active metabolite, urine excretion

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16
Q

Ketamine effects on CNS, cardiovasc, resp

A
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17
Q

Propofol MOA and use

A

GABA Agonist

Also used as a continuous infusion for conscious sedation, general anesthesia or in the ICU

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18
Q

Propofol metabolism

A

Induction dose: 1-2.5mg/kg IV

Pain on injection

Liver and extrahepatic metabolism to inactive metabolites

Rapid induction and emergence

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19
Q

Propofol effects on CNS, cardiovasc, resp, GI

A
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20
Q

Propofol adverse effects

A

Anaphylaxis

Hypertriglyceridemia

Propofol Infusion Syndrome

Rare but serious syndrome that results after long-term, high-dose propofol infusion

More common in pediatric population

Critically ill patients receiving vasopressors and/or glucocorticoids seem to be at higher risk

Signs and symptoms:

Metabolic acidosis and hyperkalemia

Rhabdomyolysis leading to renal failure

Lipemia

Cardiac failure

Green urine may be a herald sign

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21
Q

MOA of etomidate

A

GABA Agonist

vRapid induction and emergence

vPain on injection and myoclonus frequently observed

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22
Q

Etomidate effects on CNS, cardiovasc, resp, endocrine

A
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23
Q

Dexmedetomidine MOA and use

A

Selective CNS α2 adrenergic agonist, Related to clonidine

Often used as a continuous infusion for conscious sedation in OR/ICU, or as an adjunct to general anesthesia

Prevents memory formation

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24
Q

Dexmedetomidine metabolism

A

Liver metabolism, long context specific half life

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25
Dexmedetomidine effects on CNS, cardiovasc, resp
26
Major opioid receptors and fucntion
μ –analgesia, respiratory depression, dependence, constipation, urinary retention, euphoria κ – analgesia, sedation, dysphoria, miosis δ –analgesia, dependence, respiratory depression, urinary retention
27
Opioid effects on CNS, cardiovasc, resp, GI
28
How do vaporizers work
29
What is the partition coefficient
The ratio of concentration of anesthetic in blood vs in the lung when steady state is reached: **Pblood / Palveolar**
30
How is solubility measured
**blood:gas partition coefficient** Less soluble agents have faster onset/offset
31
What is Minimum Alveolar Concentration (MAC):
Avalveolar concentration (at equilibrium) which prevents movement in response to a standard surgical stimulus in 50% of patients
32
Process of inhalatation uptake
Once inhaled, the anesthetic **begins to cross the alveolar membrane and enters pulmonary (and then systemic) circulation** The blood concentration of the anesthetic gradually increases with each pass of circulation, until it is equal to the inspired concentration in the upper airway The solubility of the gas in tissues affects the speed at which equilibration occurs Inhaled anesthetics with low tissue solubility reach equilibrium more quickly and have more rapid onset/offset **Induction is faster with: high minute ventilation, low FRC, high fresh gas flow** **Induction is slower with: high cardiac output and high lipid solubility**
33
Inhalational anesthetics – mechanism theories
**Meyer-Overton Correlation**: noted in 1847, anesthetic potency is positively correlated with lipid solubility **Modern Lipid Hypothesis**: solubilization of an anesthetic in the lipid bilayer causes a redistribution of the membrane’s lateral pressure [based on statistical thermodynamics] **Membrane Protein Hypothesis**: general anesthetics bind to an as-yet-unidentified target ion channel, causing a conformational change that leads to membrane disruption
34
Groups that need an increase MAC
35
Groups that need decreased MAC
36
Is MAC additive
Yes ## Footnote MAC is additive. If you mix 2 gases (in practice this is only N2O + one of the halogenated gases), you can add them together.
37
Process of inhaled anesthetics elimination
Modern inhalational anesthetics undergo minimal metabolism; **virtually all of the of the elimination is by ventilation** Agents with low solubility typically exit the body faster and provide for faster emergence Other ways **to increase speed** of “wash out”: **Increased the flow of fresh gas entering the circuit Increasing the patient’s minute ventilation** (respiratory rate and/or tidal volume)
38
Examples of inhaled anesthetics
visoflurane, sevoflurane, and desflurane, as well as nitrous oxide
39
Isoflurane characteristics
MAC 1.2% Relatively soluble --\> slower onset/offset Relatively inexpensive Pungent; not suitable for inhalational induction
40
Isoflurane effect on CNS, cardiovasc, resp
41
Sevoflurane characteristics
MAC 2% Mid-range solubility Relatively inexpensive Non-pungent; **agent of choice for inhalational induction**
42
Sevoflurane effects on CNS, cardiovasc, resp
43
Desflurane characteristics
MAC 6% Very low solubility Relatively expensive Greenhouse gas, environment-unfriendly Very pungent; airway irritant Has unusually high vapor pressure – requires special heated vaporizer for use
44
Desflurane effects on CNS, cardiovasc, resp
45
Nitrous Oxide characteristics
MAC 105% Non-volatile: exists as a gas at room temperature Supplied via hospital pipeline Colorless/odorless Diffuses very rapidly Diffuses into air-containing spaces and **may worsen pneumothorax, pneumocephaly, intraocular air, air embolism** Diffuses out of alveoli faster than O2 diffuses in – phenomenon known as “diffusion hypoxia” Avoid by using 100% O2 after discontinuation of N2O
46
Nitrous oxide effects on CNS, cardiovasc, resp, GI
47
Process of muscle contraction
48
Use of Nueromuscular Blockers (NMB)
Blockade of the neuromuscular junction f**acilitates tracheal intubation** and may be useful for some types of surgical procedures
49
Depolarizing vs nondepolarizing NMBs
**Depolarizing NMBs structurally resemble ACh** - Bind to ACh receptors and depolarize the motor end plate à muscle fasciculations - The period of relaxation is short and effectively represents the refractory period while the end plate repolarizes. - The only depolarizing NMB in clinical use is succinylcholine **Nondepolarizing NMBs are larger molecules that occupy ACh receptor at the motor end plate but do not activate it** -Competitive inhibition – prevents ACh from reaching the receptor to depolarize the end plate.
50
Succinylcholine MOA and characteristics
Structurally similar to ACh – **depolarizing NMB** Dose: 0.5mg/kg IV vs 1mg/kg IV (RSI) **Quick onset (30-60 seconds), short duration (5-8 minutes)** **Metabolized by pseudocholinesterase** in the plasma Muscle contraction releases potassium and increases serum K by ~0.5mEq/L
51
Succinylcholine effects on CNS, cardiovasc, resp
52
Complications of succinylcholine
**Fasciculations** may cause postoperative myalgias **Prolonged duration** of action in patients with genetically **abnormal pseudocholinesterase** Life-threatening **hyperkalemia in patients with extrajunctional ACh receptors** [burns, denervating injuries such as stroke or spinal cord injury, myopathies such as Muscular Dystrophy] May trigger malignant **hyperthermia**
53
Rocuronium MOA and characteristics
54
Rocuronium effects on CNS, cardiovasc, resp
55
Vecuronium MOA and characteristics
**Nondepolarizng NMB** vIntubating dose 0.1mg/kg IV vOnset 2-3 minutes vNot approved for RSI vDuration 45-60 minutes vElimination hepatobiliary + renal vDuration prolonged in patients with hepatic or renal failure
56
Vecuronium effects on CNS, cardio, resp
57
cisatracurium MOA and characteristics
**Nondepolarizng NMB** vIntubating dose 0.15mg/kg IV vOnset 2-5 minutes vNot appropriate for RSI vDuration 20-35 minutes vDegradation by Hofmann elimination
58
Cisatracurium effects on CNS, cardio, resp
59
Reversal of NMB
Blockade of the neuromuscular junction will continue until ACh can out-compete the NDMB **Decrease NDMB concentration**: diffuses away from the cleft and is metabolized at some predictable rate **Increase ACh concentration**: inhibition of acetylcholinesterase prevents breakdown of ACh
60
Neostigmine MOA and characteristics
**Most commonly-used anticholinesterase** Dose 0.04-0.08 mg/kg IV (max 5mg) **Typically given with glycopyrrolate** vPeak effect 5-8 minutes vDoes not cross blood brain barrier vMay cause nausea
61
Neostigmine effects on CNS, resp, card, GI
62
Glycopyrrolate MOA and characteristics
**Anticholinergic medication used to offset muscarinic effects of neostigmine** vRapid onset: \<1 minute (IV) vDose 0.005-0.01mg/kg IV
63
Glycopyrrolate effects on CNS, cardio, resp, GI
64
Atropine MOA and characteristics
**Anticholinergic used to offset muscarinic side effects** Other uses: vSymptomatic bradycardia vOrganophosphate poisoning vDose 0.01mg/kg IV for reversal vOnset 5-15 minutes
65
Atropine effects on CNS, cards, resp, GI
66
Sugammadex MOA and characteristics
67
Sugammadex effects on CNS, cardio, resp
68
Signs/SX of malignant hyperthermia
Muscle rigidity Hypercarbia Tachycardia Hyperkalemia Arrhythmia – ectopy, ventricular tachycardia, ventricular fibrillation Rhybdomyolysis, myoglobinuria Coagulopathy Hyperthermia
69
Genetics and malignant hyperthermia
**Autosomal dominant mutation in RYR-1 with variable penetrance** Ryanodine receptor Calcium channel in skeletal muscle Associated conditions: King Denborough, Central Core Syndrome
70
Drugs that can cause malignant hyperthermia
All volatile anesthetics Succinylcholine
71
DX of malignant hyperthermia
Definitive diagnosis is by muscle biopsy --\> caffeine-halothane contracture test
72
TX of malignant hyperthermia
Treatment is **primarily supportive** Discontinue triggering agents Optimize ventilation – hyperventilate with 100% O2 Monitor potassium, bicarbonate and treat as indicated Cool the patient ACLS if needed **Definitive therapy is dantrolene**
73
MOA of dantrolene and use
Definitive therapy for malignant hyperthermia 2.5mg/kg IV with repeated dosing as needed **Calcium channel blocker that specifically targets RYR** Comes with mannitol and sodium bicarbonate mixed in

HSHD 2 Block 3 (15 decks)

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