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Anesthesia-phar > Induction Agents (Week 1) > Flashcards

Induction Agents (Week 1) Flashcards

1
Q

What are characteristics of the ideal IV Anesthetic?

A

1) Rapid, smooth onset of hypnosis
2) Stable in solution
3) Drug compatibility
4) Lack of CV or respiratory depression
5) Decreased cerebral metabolism and ICP
6) Low/no histamine release
7) Rapid metabolism to inactive metabolites
8) Steep dose/response curve
9) Rapid return to consciousness with analgesia
10) No adverse post-op effects

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2
Q

What is the chemical structure of propofol?

A

2,6 – diisopropylphenol

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3
Q

What drug class is Propofol? Uses?

A

Class: Hypnotic

Uses: May be used for the induction and maintenance of general anesthesia; and for monitored anesthesia care. Also, may be used as an anticonvulsant and antiemetic.

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4
Q

Mechanism of Action of Propofol

A

MOA: Mimics GABA at the receptor, directly activating chloride channels, which hyperpolarizes the postsynaptic membrane.

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5
Q

Dosing of Propofol… GA? Maintenance? Sedation?

A

Dosed adjusted to the individual: body weight, age and premedication

Induction of GA: 1-2.5 mg/kg

Maintenance of GA: 25-300 mcg/kg/min IV

Sedation: 25-100 mcg/kg/min

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6
Q

Dosing of Propofol for antiemetic purposes?

A

Antiemetic 10-20 mg can repeat every 5-10 minutes, or start infusion of 10 mcg/kg/min

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7
Q

Onset and duration of Propofol during induction?

A

Onset after induction dose: 30 seconds

Duration after induction dose: 5 – 15 minutes

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8
Q

Metabolism and Excretion of Propofol

A

Metabolized via hepatic and extrahepatic metabolism (mostly lungs), no active metabolite

Excreted by the kidney

*Propofol has the potential to change urine color (green or cloudy)

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9
Q

Discuss the progression of Propofol through the body from entry

A

Initially, all intravenously administered propofol resides in the blood

Then, there is a rapid redistribution to the vessel rich organs

­Peak concentration of propofol in the brain occurs in 1 minute

Then, there is a redistribution from vessel rich organs to muscle and fat

Then redistribution of propofol out of the brain results in patient awareness

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10
Q

CNS Effects of Propofol

A

Rapid onset and emergence

Raises seizure threshold

Reduces cerebral blood flow, CMRO2, ICP and IOP

No analgesia

Myoclonus may occur

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11
Q

Pulmonary Effects of Propofol

A

Dose dependent respiratory depression

Infusion will decrease TV and increase RR

Decrease reflexes

Shifts CO2 response curve to the right

Bronchodilation

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12
Q

Cardiovascular Effects of Propofol

A

Decreases BP r/t decrease SNS and vasodilation

Decrease myocardial contractility and SVR

Decrease venous tone - > lower preload

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13
Q

Metabolism & Elimination Effects of Propofol

A

Hepatic and extra hepatic metabolism

Renally excreted

Propofol has the potential to change urine color (green or cloudy)

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14
Q

Effects of Propofol on Muscles

A

Does not prolong neuromuscular blockade but can offer adequate intubation conditions

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15
Q

Additional Considerations with Propofol Usage

A

There is no evidence that propofol should be avoided in egg or soy allergic patients

Contains sulfites

Painful on injection

Thrombophlebitis

Bacterial infection risk

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16
Q

What is Propofol Infusion Syndrome?

A

Long-term high dose propofol infusions may result in metabolic derangements and organ system failures

Suggested etiology: Propofol inhibits oxidative phosphorylation

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17
Q

Risk Factors for Developing Propofol Infusion Syndrome

A

Risk factors include:

doses greater than 4 mg/kg/hour

duration greater than 48 hours

critical illness

concurrent catecholamine infusion

steroid administration

high-fat and low carbohydrate diet

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18
Q

Symptoms of Propofol Infusion Syndrome

A

metabolic acidosis, persistent bradycardia, cardiac failure, fever and severe hepatic and renal disturbances

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19
Q

What is Ketamine? Uses?

A

Chemical name: 2-(o-chlorophenyl)-2(methylamino) cyclohexanone hydrochloride

Class: phencyclidine derivative

Clinical Uses: May be used for GA induction and maintenance, and monitored anesthesia care

Used as an anesthetic, analgesic and antidepressant

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20
Q

Mechanism of Action of Ketamine

A

MOA: Non-competitive antagonist at NMDA receptor ion channels. Blocks the open channel, inhibiting the excitatory response to glutamate. It also binds with opioid, MAO, serotonin, NE, muscarinic and sodium channels

Provides amnesic and potent analgesia. DISSOCIATIVE STATE.

Ketamine inhibits neuronal sodium channels (producing a modest local anesthetic action) and calcium channels (causing cerebral vasodilatation).

DOES NOT WORK ON GABA

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21
Q

What can be used to premedicate a patient before giving Ketamine?

A

*IF THE PATIENT CONDITION ALLOWS,

benzodiazepine and antisaligogue (e.g. glycopyrrolate)

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22
Q

Ketamine dosage for IV Induction

A

IV Induction 1-2 mg/kg

Onset: 2-5 minute

DOA: 10-20 minutes (may require an hour for full orientation)

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23
Q

Ketamine dosage for IM Induction

A

IM Induction 4-6 mg/kg

Onset: 20 minutes

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24
Q

Ketamine dosage for sedation and multimodal infusions

Also, what concentrations are available?

A

Sedation 1-3 mcg/kg/min or 0.5-1 mg/kg boluses as needed

Multimodal infusion – 3-5 mcg/kg/minute

Caution: 3 dilutions: 10, 50 or 100 mg/cc

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25
Q

________ is ­the least protein bound of induction agents

A

ketamine

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26
Q

How is ketamine metabolized and excreted?

A

­P450 enzymes in the liver

­Chronic ketamine use induces enzymes that metabolize it

­Active metabolite: norketamine is 1/3 as potent as ketamine and is renally excreted

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27
Q

Induction Agents and Protein Binding

A

Propofol – 98%

Diazepam – 98%

Midazolam – 94%

Dexmedetomidine – 94%

Lorazepam – 90%

Etomidate – 75%

Ketamine – 12%

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28
Q

Effects of Ketamine on the CNS

A

­Increased CMRO2 (cerebral metabolic rate of oxygen (CMRO2) is the rate of oxygen consumption by the brain), Increased CBF, Increased ICP

­Dissociative

­Analgesic

­Depression

­Associated with emergence delirium, nightmares and hallucinations

  • ­Benzodiazepines are an effective means of prevention
  • ­Risk factors: age > 15, female gender, personality disorder, dose > 2mg/kg
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29
Q

Cardiovascular Effects of Ketamine

A

­SNS stimulant

­Increased SVR, HR, myocardial O2 consumption, PVR

­Mild myocardial depression (in trauma patients)

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30
Q

Respiratory Effects of Ketamine

A

­Bronchodilator

­Maintains respiratory rate

­Preserves reflexes at low dose

­Increased secretions, often paired with an antisialagogue like glycopyrrolate

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31
Q

Occular Effects of Ketamine

A

­Nystagmus

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32
Q

Caution Ketamine Usage in patients with a history of which medical condition(s)?

A

Hypertension

Angina

CHF

Increased intracranial pressure

Increased ocular pressure

Auditory/Visual hallucinations

Airway problems d/t increase secretions

Emergence reactions – vivid dreams, hallucinations (lasts 1-3 hours) and can be reduced with propofol and/or benzodiazepines

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33
Q

What is Etomidate?

A

R-1-methyl-1-(a-methylbenzyl) imidazole-5-carboxylate

Carboxylated imidazole derivate

Class: Hypnotic

Uses: May be used for induction of anesthesia. Considered for CV stability and trauma

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34
Q

Mechanism of Action of Etomidate

A

Binds to the GABA-a receptor

Lower doses: potentiates GABA at its receptors

Higher doses: directly stimulates the GABA receptor

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35
Q

Etomidate dosing

A

Induction Dose: 0.3 mg/kg

Onset: 1 minute

Duration: 5 -15 minutes

36
Q

Metabolism & Excretion of Etomidate

A

Metabolism: Hepatic P450 enzymes and plasma esterases

Excreted by kidneys and in bile

No active metabolite

37
Q

CNS Effects of Etomidate

A

Reduces intracranial pressure, cerebral blood flow, CMO2

Myoclonia likely related to an imbalance of excitatory and inhibitory pathways in the thalamacortical tract and can induce EEG seizure foci

No analgesia

38
Q

Cardiovascular Effects of Etomidate

A

Hemodynamically stable

Minimal/no cardiac depression

Does not blunt sympathetic response to laryngoscopy

39
Q

Pulmonary Effects of Etomidate

A

Brief hyperventilation followed by apnea

Mild respiratory depression (less than propofol)

No histamine release

40
Q

Endocrine & GI Effects of Etomidate

A

Endocrine: inhibits cortisol; adrenal suppression via suppression of 11-beta hydroxylase

GI: N/V in 30-40% of patients

41
Q

Hematologic Effects of Etomidate

A

May induce acute intermittent porphyria

42
Q

What are porphyrias?

A

Porphyrias are a set of autosomally inherited metabolic disorders that are the result various defects in heme synthesis. Broadly, they can be classified into inducible, and non-inducible forms.

43
Q

Inducible porphyrias

A

(i.e. Acute Intermittent Porphyria) can present with acute neurological and/or GI symptoms.

Patients may have anxiety, confusion, autonomic instability (manifested as hypertension or tachycardia), emesis, and severe abdominal pain.

44
Q

Acute attacks of porphria can be precipitated by _______

A

stress, fasting, dehydration, sepsis, and certain medications, including some meds commonly used in the perioperative period.

45
Q

What are examples of triggering agents for porphyria? What drugs are safe to use?

A

potential triggering agents = barbiturates, etomidate, diazepam, ketorolac, phenytoin and sulfonamides.

Drugs that are safe to use in the perioperative period include propofol, ketamine, succinylcholine, atropine, neostigmine, nitrous oxide, fentanyl and morphine.

46
Q

What is dexmedetomidine?

A

Class: Selective alpha2 adrenergic agonist

Use: May be used for monitored anesthesia care, induction, analgesia and prevention of emergence delirium

47
Q

Mechanism of Action for Dexmedetomidine?

A

Centrally and peripherally alpha 2 adrenergic receptor agonist. Acts on alpha 2 receptors thereby producing sedation by decreasing sympathetic nervous system activity and the level of arousal.

How does it regulate the cardiac system? by inhibiting norepinephrine release.

How does it regulate HR & BP? by decreasing the tonic levels of sympathetic outflow from the CNS and augmenting cardiac vagal activity.

48
Q

Dosing for Dexmedetomidine

A

For procedural sedation: start at 1 mcg/kg over 10 minutes, followed by a maintenance infusion from 0.2 to 1 mcg/kg/hr.

49
Q

Cardiac & Respiratory Effects of Dexmedetomidate

A

Cardiovascular: Hypotension and bradycardia

Respiratory: Minimal respiratory depression

50
Q

Pain Effects of Dexmedetomidine and Miscellaneous

A

Pain: Analgesic properties, Enhance neuraxial blockade

Other: Reduces emergence delirium in pediatric patients, reduces inhalational agent requirements

51
Q

Pharmacokinetics of Dexmedetomidine

A

Metabolized by the P450 system in the liver

Cleared by the liver

Inactive metabolites

52
Q

Medication class & use of benzodiazepines

A

Class: Hypnotic

Clinical Use: Sedative, anxiolytic, amnestic, anticonvulsant (increases seizure threshold), muscle relaxant

53
Q

MOA of Benzodiazepines

A

Enhances the response to the GABA A receptor

Provides anterograde amnesia, not retrograde amnesia

54
Q

_______ is added to diazepam and lorazepam to enhance water solubility.

A

Propylene glycol

*­Propylene glycol can cause venous irritation

Midazolam does not require propylene glycol , because it contains an imidazole ring

55
Q

Absorption & Distribution of Benzodiazepines

A

Absorption: Oral, IV, IM, intranasal

Distribution

­DOA: midazolam < lorazepam < diazepam

­Determined by redistribution

­Potency: Lorazepam > midazolam > diazepam

­Highly protein bound

56
Q

Metabolism and Excretion of Benzodiazepines

A

Metabolized by the liver

­Excreted by the kidneys

57
Q

Midazolam Dosing

A

Premed: titrated 0.5-2 mg IV (adult) or .2-.6 mg/kg PO (pedi)

Induction dose: 0.1 - 0.3 mg/kg

58
Q

Onset, Peak and DOA of Midazolam

A

Onset: 1 minute

Peak: 2 – 5 minutes

DOA of induction dose: 6-15 minutes

Highly protein bound (95%)

59
Q

Metabolism & Excretion of Midazolam

A

Metabolized by the CYP 450 system in the liver

Active metabolite: 1-hydroxymidazolam

Excreted by the kidneys

* Caution: May be related to post operative delirium in the elderly

60
Q

Cardiovsacular Effects of Midazolam

A

­Sedation dose: Minimal effects

­Induction dose: decrease BP and decrease SVR

61
Q

Respiratory Effects of Midazolam

A

­Reduce muscular tone in upper airway

­Decrease CO2 and hypoxia response

­Patients with COPD are more sensitive depressant effects

62
Q

CNS Effects of Midazolam

A

­Anterograde amnesia

­Anticonvulsant

­Anxiolysis

­Antispasmodic

­No analgesia

63
Q

Lorazepam… premedication dosing and metab/excretion

A

Premed: 2 - 4 mg PO or 0.25 – 1 mg IV

Risk for venous irritation and thrombophlebitis

Metabolized in the liver to an inactive metabolite

Excreted by the kidneys

64
Q

Remimazolam

A

Acts on GABA receptors like midazolam and has organ-independent metabolism (plasma esterases) like remifentanil

In preliminary phase II trial

65
Q

What is Flumazenil?

A

Competitive antagonist for benzodiazepines (reversal agent)

Short half life – risk for rebound effect

66
Q

Flumazenil Dosing

A

Initial dose is 0.2 mg IV and titrated in 0.1 mg increments to prevent rebound effect

Onset: 1-3 minutes

DOA: 3 – 30 minutes

Caution for those on chronic benzodiazepines, may cause acute withdrawal

67
Q

Chemical Composition of Barbituates

A

Urea + malonic acid -> barbituric acid

Your 2nd carbon is replaced by either oxygen or sulfa.

If its oxygen… = oxy barb

If its Sulfa = Thio barb – increases solubility

68
Q

Clinical Use and MOA of Barbituates

A

Clinical Use: Phenobarbital is an anticonvulsant

Thiopental and Methohexital are anesthetic agents

MOA: Binds to the GABA A receptor resulting in increase Cl- conduction into the cell causing hyperpolarization

­Lower doses – enhances GABA effect

­Higher doses – directly stimulates GABA receptors

69
Q

Absorption & Distribution of Barbituates

A

­Absorption: ­IV, rectal methohexital

­Distribution:

­Onset ~ 1 minute

­DOA ~ 20 minutes and is determined by redistribution

70
Q

Metabolism & Excretion of Barbituates

A

­Metabolism: Most barbiturates are metabolized in the liver

­Excretion: ­Most barbiturates are excreted by the kidneys

­Methohexital is excreted in feces

71
Q

Cardiac Effects of Barbituates

A

Tachycardia r/t central vagolytic effect and decrease BP

CO is maintained r/t baroreceptor reflex (resulting in increase HR and contractility)

This process may be inhibited in the setting of hypovolemia, CHF & beta-adrenergic blockade

72
Q

Respiratory Effects of Barbituates

A

Depression of the medullar ventilatory center decreases ventilatory response to hypercapnia and hypoxia

Induction doses often result in apnea

Airway reflexes are not completely depressed

73
Q

CNS Effects of Barbiturates

A

Constriction of cerebral vasculature may result in decrease cerebral blood flow, cerebral blood volume, and intracranial pressure

Cerebral perfusion pressure increases Decreased CBF (vasoconstriction)

Decreased cerebral oxygen consumption

74
Q

Renal & Hepatic Effects of Barbiturates

A

Renal: Reduction in renal blood flow and glomerular filtration, both in proportion to decrease systemic BP

Hepatic: Hepatic blood flow is decreased

Chronic barbiturate use often results in an increased metabolism of the CYP450

Stimulates the formation of porphyrin and should be avoided in individuals with porphyria

75
Q

Thiopental

A

rapid-onset short-acting barbiturate general anesthetic

Thio barbiturate

Alkaline; pH ~10

Ultra short acting because of redistribution

Elimination half life: >11 hours

Onset: 30 seconds

Dose: Induction 3-6 mg/kg

76
Q

Special considerations for Thiopental

A

Rapid onset

Painful injection

Highly alkaline making infiltration or inadvertent arterial injection serious.

Long half life means residual sedation post op

Cumulative with repeat doses as storage depots get filled.

Not currently available in US but used worldwide.

77
Q

Methohexital: Brevital

A

Oxybarbiturate

Induction 1-2 mg/kg

Shorter half life than thiopental

CNS excitation

78
Q

Phenobarbital

A

PO, IM, PR, IV

Oxybarbiturate

Sometimes used for procedural sedation

Brain protection; induced coma

79
Q

ECT therapy

A

ECT is a treatment option for medication-resistant depression, mania, catatonia, suicidal ideation and forms of schizophrenia

Initial response: Increased PNS activity during the tonic phase

decreased heart rate (r/f asystole) and hypotension

Secondary response: Increased SNS activity during the clonic phase

increased heart rate (r/f SVT and atrial fibrillation) and hypertension

80
Q

Drugs that increase seizure duration = _____

A

Etomidate

Ketamine

Alfentanil + Propofol (?together)

Aminophylline

81
Q

Drugs that decrease seizure duration = _____

A

Propofol

Midazolam

Lorazepam

Fentanyl

Lidocaine

82
Q

Drugs that have no effect on seizue duration = ______

A

Methohexital

Dexmedetomidine

Clonidine

Esmolol

83
Q

Conditions that decrease seizure duration = _____

A

Hypoventilation, Hypercarbia, Hypoxia

84
Q

Conditions that increase seizure duration = _____

A

Hyperventilation & Hypocapnia

85
Q

Describe HOW Ketamine produces a dissociative state?

A

by depressing the cerebral cortex and thalamus and stimulating the hippocampus.

Anesthesia-phar (18 decks)

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