Induction Agents (Week 1) Flashcards

Question

\_\_\_\_\_\_\_\_ is the least protein bound of induction agents

Answer 1

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

Answer 2

Propofol – 98% Diazepam – 98% Midazolam – 94% Dexmedetomidine – 94% Lorazepam – 90% Etomidate – 75% Ketamine – 12%

Answer 3

**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

Answer 4

SNS stimulant Increased SVR, HR, myocardial O2 consumption, PVR **Mild myocardial depression (in trauma patients)**

Answer 5

**Bronchodilator** Maintains respiratory rate Preserves reflexes at low dose **Increased secretions, often paired with an antisialagogue like glycopyrrolate**

Answer 6

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

Answer 7

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

Answer 8

Binds to the GABA-a receptor Lower doses: potentiates GABA at its receptors Higher doses: directly stimulates the GABA receptor

Answer 9

**Induction** Dose: **0.3 mg/kg** Onset: **1 minute** Duration: **5 -15 minutes**

Answer 10

**Metabolism**: **Hepatic P450 enzymes and plasma esterases** **Excreted by kidneys and in bile** No active metabolite

Answer 11

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

Answer 12

Hemodynamically stable Minimal/no cardiac depression Does not blunt sympathetic response to laryngoscopy

Answer 13

Brief hyperventilation followed by apnea Mild respiratory depression (less than propofol) No histamine release

Answer 14

**Endocrine**: inhibits cortisol; adrenal suppression via suppression of 11-beta hydroxylase **GI:** N/V in 30-40% of patients

Answer 15

May induce acute intermittent porphyria

Answer 16

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.

Answer 17

(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**.

Answer 18

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

Answer 19

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**.

Answer 20

Class: Selective alpha2 adrenergic agonist Use: May be used for monitored anesthesia care, induction, analgesia and prevention of emergence delirium

Answer 21

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**.

Answer 22

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

Answer 23

Cardiovascular: Hypotension and bradycardia Respiratory: Minimal respiratory depression

Answer 24

Pain: Analgesic properties, Enhance neuraxial blockade Other: Reduces emergence delirium in pediatric patients, reduces inhalational agent requirements

Answer 25

Metabolized by the P450 system in the liver Cleared by the liver Inactive metabolites

Answer 26

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

Answer 27

**Enhances the response to the GABA A receptor** **Provides anterograde amnesia**, not retrograde amnesia

Answer 28

**Propylene glycol** \*Propylene glycol can cause venous irritation **Midazolam does not require propylene glycol , because it contains an imidazole ring**

Answer 29

**Absorption**: Oral, IV, IM, intranasal **Distribution** **DOA**: midazolam \< lorazepam \< diazepam Determined by redistribution Potency: Lorazepam \> midazolam \> diazepam **Highly protein bound**

Answer 30

Metabolized by the liver Excreted by the kidneys

Answer 31

**Premed**: titrated 0.5-2 mg IV (adult) or .2-.6 mg/kg PO (pedi) **Induction dose**: 0.1 - 0.3 mg/kg

Answer 32

Onset: **1 minute** Peak: **2 – 5 minutes** DOA of induction dose: **6-15 minutes** Highly protein bound (95%)

Answer 33

**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

Answer 34

Sedation dose: Minimal effects **Induction dose**: **decrease BP and decrease SVR**

Answer 35

Reduce muscular tone in upper airway Decrease CO2 and hypoxia response Patients with COPD are more sensitive depressant effects

Answer 36

Anterograde amnesia Anticonvulsant Anxiolysis Antispasmodic No analgesia

Answer 37

Premed: **2 - 4 mg PO or 0.25 – 1 mg IV** Risk for **venous irritation and thrombophlebiti**s Metabolized in the liver to an inactive metabolite Excreted by the kidneys

Answer 38

Acts on GABA receptors like midazolam and has organ-independent metabolism (plasma esterases) like remifentanil In preliminary phase II trial

Answer 39

Competitive antagonist for benzodiazepines (reversal agent) Short half life – risk for rebound effect

Answer 40

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**

Answer 41

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

Answer 42

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

Answer 43

Absorption: IV, rectal methohexital Distribution: Onset ~ 1 minute DOA ~ 20 minutes and is determined by redistribution

Answer 44

Metabolism: Most barbiturates are **metabolized in the liver** Excretion: Most barbiturates are **excreted by the kidneys** Methohexital is excreted in feces

Answer 45

**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

Answer 46

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

Answer 47

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

Answer 48

**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**

Answer 49

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**

Answer 50

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.

Answer 51

Oxybarbiturate Induction 1-2 mg/kg Shorter half life than thiopental CNS excitation

Answer 52

PO, IM, PR, IV Oxybarbiturate Sometimes used for procedural sedation Brain protection; induced coma

Answer 53

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

Answer 54

Etomidate Ketamine Alfentanil + Propofol (?together) Aminophylline

Answer 55

Propofol Midazolam Lorazepam Fentanyl Lidocaine

Answer 56

Methohexital Dexmedetomidine Clonidine Esmolol

Answer 57

Hypoventilation, Hypercarbia, Hypoxia

Answer 58

Hyperventilation & Hypocapnia

Answer 59

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