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Brain and Behavior 2 > Anesthesia > Flashcards

Anesthesia Flashcards

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1
Q

What are the three forms of early inhaled anesthesia?

A
  • Diethyl ether
  • Nitrous oxide
  • Chloroform
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2
Q

What element has been added to modern inhaled anesthesia and why? What type of chemical compound are they? What are the clinically relevant differences between agents?

A

Fluorine has been added to prevent explosions of ether. All modern inhaled anesthetics are ether derivatives. Halogenated volatile agents can provide complete general anesthesia at high doses.

Relevant differences include: anesthetic potency, solubility in fat and blood, degree of noxious character/pungency, and cost per mL

Examples: isoflurane, desflurane, sevoflurane

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3
Q

What does a good general anesthetic induce in a patient?

A
  • Hypnosis (sleep)
  • Amnesia (forgetfulness)
  • Analgesia (comfort)
  • Immobility, muscle relaxation, akinesia
  • Blunting of autonomic relfexes like tachycardia, hypertension, and bradycardia (unresponsive)
  • Readily induced and reversible
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4
Q

How is anesthesia similar to coma and sleep?

A
  • Loss of consciousness
  • Synchrony in brain activity
  • Change in local patterns of activation
  • Decrease metabolism
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5
Q

How is anesthetic gas delivered, taken up, and eliminated?

A

Liquid anesthetic agent is vaporized and inhaled via a breathing circuit. It is taken up in the blood and distributed in the brain, liver, and kidney, as well as fat and muscle. It is eliminated by pulmonary ventilation. There is almost no metabolic breakdown of inhaled agents.

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6
Q

Describe the relevance of solubility.

A

Anesthesia is moderately soluble in muscle, less soluble in the brain, and very soluble in fat. Less soluble means less potent, faster onset/offset, and less accumulation in fat/tissue. Desflurane is the least soluble in fat so it is the fastest for recovery

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7
Q

What are the CNS effects of inhaled anesthetics?

A
  • Produce unconsciousness
  • Decrease cerebral metabolic activity
  • Increase cerebral blood flow
  • Impair cerebral autoregulation
  • Impair memory formation
  • Block movement in response to stimulus
  • Dose dependent changes in EEG
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8
Q

What are the respiratory effects of inhaled anesthetics?

A
  • Bronchodilation
  • Increased respiratory rate
  • Decreased tidal volume
  • Decreased reflexes to maintain ventilation and oxygenation
  • Decreased ventilatory response to low blood oxygen and high blood CO2
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9
Q

What are the cardiovascular effects of inhaled anesthetics?

A
  • Vasodilation: decreased blood pressure and redistribution of blood from core to periphery
  • Impaired autonomic reflexes to maintain blood pressure
  • Impaired contractile strength of heart muscle
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10
Q

What is MAC? What affects the dose of anesthetic gas for complete anesthesia?

A

The minimum alveolar concentration is the concentration at which 50% of patients will not move in response to surgical incision. It is different for each inhaled agent and is not a physical property of the anesthetic agent–it is influenced by many factors. The MAC is an approximate dose–the dose of anesthetic is affected by:

  • Intensity and type of surgical stimulus
  • Age and medical condition of patient
  • Concurrent use of other anesthetics in addition to anesthetic gas

The right dose is determined by BP, HR, and RR during the surgery, patient responsiveness, and dose of other medications used.

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11
Q

What are some problems associated with inhaled anesthetics?

A
  • Nausea/vomiting
  • Respiratory depression
  • Cardiovascular collapse
  • Inhibition of uterine contraction
  • Rarely: malignant hyperthermia syndrome and liver toxicity
  • Controversial: neurotoxicity
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12
Q

Describe the mechanisms of inhaled anesthetics.

A

There is no well defined mechanism. They act on the brain and spinal cord, likely through multiple different mechanisms. They disrupt the patterns of neuronal transmission involved in consciousness.

Initial theory: insertion of agent into lipid membrane modifies potentials and structure.

Current theory: allosteric binding to specific binding sites alters function of complex. Relevant receptors include GABA-A, NMDA, glycine, voltage gated Na/K/Ca channels, and nicotinic ACh receptors.

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13
Q

What is sedation and what are sedatives and hypnotics used for?

A

Sedation is the blunting of consciousness. Sedatives and hypnotics are used for induction and maintenance of general anesthesia as well as ICU sedation, procedural sedation, seizure treatment, generalized anxiety disorder and panic disorder, ethanol withdrawal, insomnia, and muscle spasms.

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14
Q

What is the difference between pharmacokinetics and pharmacodynamics? What is the relevance of drug distribution and elimination?

A

Pharmacokinetics: how drugs get to the site of action (route of administration, elimination, metabolism, and distribution)

Pharmacodynamics: drug effect as a result of receptor binding (agonists/antagonists, genetic variability, dose response, efficacy, potency, and toxicity)

Distribution: IV drugs go to the central compartment first (brain, heart, kidney, etc.) and then move into rapidly equilibrating compartments (muscle) and then slowly equilibrating compartments (fat). The effect of the drug terminates as it is redistributed because the clinical effect is due to concentration in the central compartment.

Elimination is the process of metabolizing the drug. The longer you infuse a drug, the longer it takes to eliminate it (context-sensitive half time).

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15
Q

What are the major clinical uses of propofol? Describe its pharmacokinetics, pharmacodynamics, and metabolism.

A

Propofol is used for induction and maintenance of general anesthesia, procedural sedation, ICU sedation, and off label uses (anti-epileptic, anti-emetic, chronic headache therapy, drug withdrawal)

Redistribution half life is 2-8 minutes; elimination half-life is 4-23.5 hours.

Propofol potentiates the effects of GABA.

Metabolized in the liver, kidney, and possibly lungs and intestines.

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16
Q

Describe the physiologic effects of propfol and its adverse effects and contraindications.

A
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17
Q

Is propofol a drug of abuse? If so, why?

A

Yes–rapid onset/offset, potent hypnotic, increases dopamine concentration in nucleus accumbens (euphoria), sexual dreams

Not schedule by DEA

18
Q

What are the major clinical uses of etomidate? Describe its pharmacokinetics, pharmacodynamics, and metabolism.

A
19
Q

What are the physiologic effects of etomidate as well as it’s adverse effects and contraindications?

A

Physiologic effects:

  • Cardiovascular: few, minimal to moderate hypotension
  • Respiratory: few, minimal to moderate respiratory depression
  • Neurologic: decreased cerebral metabolic rate (burst suppression), decreased cerebral blood flow, can cause seizures

Adverse effects: adrenal suppression in critically ill patients, increased post-operative nausea/vomiting

Absolute contraindications: allergy

Relative contraindications: adrenal insufficiency, critical illness (septic shock), history of post-operative nausea or vomiting

20
Q

Is etomidate a drug of abuse? If so, why?

A

No

21
Q

What are the major clinical uses of thiopental? Describe its pharmacokinetic, pharmacodynamic, and metabolism?

A

The major clinical use of thiopental is the induction of general anesthesia but it has been largely replaced by propofol. Thiopental is a barbiturate used in lethal injections in some states.

The redistribution half life is 5-10 minutes; the elimination half life is 7-17 hours.

Thiopental is metabolized by hepatic biotransformation and renal excretion (exhibits zero order kinetics at supratherapeutic doses).

22
Q

What are the physiologic effects of thiopental as well as its adverse effects and contraindications?

A

Physiologic effects (similar to propofol)

  • Cardiovascular: hypotension
  • Respiratory: hypoapnea/apnea, decreased response to hypercarbia
  • Neurologic effects: decreased cerebral metabolic rate (burst suppression), decreased cerebral blood flow
  • Exception: methohexitoal decreases the seizure threshold relative to other induction agents

Adverse effects: garlic/onion taste, tissue irritation or necrosis, stimulation of formation, anti-analgesic effect

Absolute contraindications: allergy, acute intermittent porphyria

Relative contraindications: hemodynamic instability, questionable IV access

23
Q

What are the major clinical uses of ketamine? Describe its pharmacokinetics, pharmacodynamics, and metabolism.

A

Ketamine is a phencyclidine derivative which causes dissociative hypnosis. It is used in veterinary anesthesia and pediatric anesthesia.

The redistribution half life is 11-16 minutes; the elimination half life is 2-3 hours.

Ketamine is an NMDA receptor antagonist but it also affects GABA, nAChR, 5HT-3, and opiate receptors in the brain and spinal cord.

Ketamine undergoes hepatic degradation and excretion in the urine. It’s primary metabolite has some clinical activity.

24
Q

What are the desirable and undesirable properties of ketamine? What are it’s adverse effects and contraindications?

A

Desirable properties:

  • Can be given IV, PO, IM, intranasal
  • Hypnotic, amnesic
  • Maintains sympathetic tone
  • Potent bronchodilator, preserves respiration
  • Potent analgesic with opioid sparing effect

Undesirable properties: dysporia, increased salivation and lacrimation, sympathetic stimulation, increased intracranial pressure

Adverse effects: salivation, dysphoria, dissociation, tachycardia, hypertension

Absolute contradindications: allergy

Relative contraindications: psychosis, compromised myocardial function, inability to tolerate tachycardia or hypertension, intracranial hypertension

25
Q

What are some other sedatives and hypnotics?

A
  • Benzodiazepines
  • Opioids
  • Alpha-2 adrenoreceptor antagonists
  • Dopamine antagonists
  • Antihistamines
  • Melatonin agonists
  • General anesthetics
  • Recreational use: alcohol, GHB
26
Q

What are the most important aspects of propofol?

A

Rapid onset and offset

Used for anesthetic induction, TIVA, and ICU sedation

Partially metabolized in extrahepatic tissues

27
Q

What are the most important aspects of etomidate?

A

Drug of choice in hemodynamically compromised patients

Causes adrenocortical suppression

28
Q

What are the most important aspects of thiopental?

A

Very similar to propofol in pharmacokinetic properties

Contraindicated of porphyria

29
Q

What are the most important aspects of ketamine?

A

Causes sympathetic stimulation

Potent analgesic

Causes dissociative anesthesia and dysphoria

Does not require IV access

30
Q

Describe the basic features of local anesthetics.

A
  • Reversibly block nerve conduction
  • Act on every nerve fiber including sensory, motor, and sympathetic fibers
  • Act on cardiac muscle, skeletal muscle, and the brain
  • No structural damage to the nerve cell
31
Q

What are the goals and ideal features of local anesthetics?

A

Goals: operate on awake patients without pain, ability to suture without pain, the ability to do painful procedures without pain

Ideally: nonirritating to tissue, short onset, long enough duration but not too long to entail prolonged recovery

32
Q

Describe the chemical structure of local anesthetics.

A

Local anesthetics are weakly basic in nature and comprised of a lipophilic aromatic ring, an intermediate group (amide or ester), and a hydrophilic carbon chain with an amino group. Some local anesthetics are chiral (the S form is less cardiotoxic)

33
Q

How do local anesthetics work?

A

Local anesthetics block the sodium channel by binding to the internal membrane of the alpha subunit of the sodium channel in the open and inactive states.

In its basic form, the local anesthetic crosses the nerve membrane, gets protonated, and binds the internal side of the sodium channel–if injected into an acidic environment it will not be effective because it will be protonated before entering the nerve.

Local anesthetics decrease the amplitude of the action potential, slow the rate of depolarization, increase the firing threshold, slow impulse conduction, and prolong the refractory period

34
Q

Describe the pharmacokinetics of local anesthetics, including distribution and mechanisms.

A

Local anesthetics bind alpha-1-glycoprotein and albumin in the blood. There is considerable first pass uptake by the lung.

Distribution

  • Alpha phase: rapidly redistributed to well perfused tissue
  • Beta phase: less perfused or slowly equilibraing tissue
  • Gamma phase: clearance representing metabolism and excretion

Mechanisms

  • Esters: hydrolyzed in the plasma by pseudocholinesterase
  • Amides: occurs in the endoplasmic reticulum of hepatocytes
35
Q

Describe the relevance of lipid solubility and anesthetic potency and duration?

A

Lipid solubility is correlated with anesthetic potency because the anesthetic must cross the nerve lipid bilayer. The more lipid soluble an anesthetic is, the lower the dose necessary.

Greater lipid solubility also means longer duration because lipid soluble molecules are less readily removed by the blood stream (relevant to toxicity)

36
Q

Describe how rapidity of onset is related to pKa?

A

The closer it is to the body’s pH, the quicker the onset

37
Q

What kinds of allergic reactions are seen with local anesthetics?

A

Ester local anesthetics are metabolized to para-aminobenzoid acid which is a potential allergen. Allergy to amide local anesthetics are extremely rare.

Ester local anesthetics are metabolized in the plasma quickly so there is less toxicity risk.

38
Q

Describe CNS toxicity of local anesthetics.

A

Toxic effects: numbness of tongue, lightheadedness, visual disturbances, muscular twitching, unconsciousness, convulsions, and coma (occurs before respiratory effects and CVS depression)

Inhibitory neurons are much more sensitive to local anesthetics than excitatory neurons so there are unopposed excitatory responses.

Treatment: stop injection, give benzodiazepine or thiopental, hyperventalate if seizures occur

39
Q

Describe cardiovascular toxicity of local anesthetics.

A

Contractility: negative ionotropic effects

Automaticity: negative chronotropic effects

Rhythmicity and conductivity: ventricular arrhythmias

Exception: cardiac dysrhythmias are seen at subconvulsant doses of bupivicaine

Treatment: local anesthetics are lipid soluble so lipid emulsions reverse toxicity

At low doses they cause vasoconstriction, at high doses they cause vasodilation

40
Q

What is the most widely used local anesthetic?

A

Lidocaine

Brain and Behavior 2 (9 decks)

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