Induction Flashcards

1
Q

Routine induction vs RSI

A
  • routine induction is the standard in general anesthesia, however a RSI is indicated in patients at risk of regurgitation/aspiration (see Aspiration, A5)
  • RSI uses pre-determined doses of induction drugs given in rapid succession to minimize the time patient is at risk for aspiration (i.e. from the time when they are asleep without an ETT until the time when the ETT is in and the cuff inflated)
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2
Q

Transfusion infection risks for HIV, Hep C, Hep B, HTLV, Symptomatic bacterial sepsis, West Nile virus per 1 unit pRBCs

A

HIV 1 in 21 million

Hep C 1 in 13 million

Hep B 1 in 7.5 million

HTLV 1 in 1-1.3 million

Sepsis 1 in 40 000 from platelets and 1 in 250 000 from RBC

WNV no cases since 2003

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3
Q

Equipment preparation routine vs RSI

A

Same

Check equipment, drugs, suction, and monitors; prepare an alternative laryngoscope blade and a second ETT tube one size smaller, suction on

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4
Q

pre-oxygenation/denitrogenation routine vs rsi

A

same

100% O2 for 3 mins or 4-8 vital capacity breaths

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5
Q

pre-treatment agents routine vs rsi

A

routine - Use agent of choice to blunt physiologic responses to airway manipulation 3 min prior to laryngoscopy

rsi - same but can skip this step in an emergent situation

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6
Q

Induction agents routine vs rsi

A

routine - use iv or inhalation induction agent of choice

rsi - use pre-determined dose of fast acting induction agent of choice

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7
Q

muscle relaxants routine vs rsi

A

routine - choice given after onset of induction agent

rsi - pre-determined dose of fast acting (ex. SCh) given IMMEDIATELY after induction agent

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8
Q

Ventilation routine vs RSI

A

Routine - bag mask ventilation

rsi - DO NOT bag ventilate - can increase risk of aspiration

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9
Q

cricoid pressure routine vs rsi

A

routien - posterior pressure on thyroid cartilage to improve view of vocal cords as indicated

rsi - Sellick maneuver, also known as cricoid pressure, to prevent regurgitation and assist in visualization (2 kg pressure with drowsiness, 3 kg with loss of consciousness)

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10
Q

Intubation routine vs rsi

A

routine - Intubate, inflate cuff, confirm ETT position

rsi - Intubate once paralyzed (~45 s after SCh given), inflate cuff, confirm ETT position; cricoid pressure maintained until ETT cuff inflated and placement confirmed

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11
Q

Secure machines routine vs rsi

A

same

secure ETT, and begin manual/machine ventilation

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12
Q

order of induction

A
  1. equipment preparation
  2. pre-oxygenation/denitrogenation
  3. pre-treatment agents
  4. induction agents
  5. muscle relaxants
  6. ventilation
  7. cricoid pressure
  8. intubation
  9. secure machines
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13
Q

Solubility of volatile anesthetics in blood from least to most soluble

A

Nitrous oxide < desflurane < sevoflurane < isoflurane < halothane

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14
Q

What are intravenous induction agents, their purpose and examples

A
  • IV induction agents are non-opioid drugs used to provide hypnosis, amnesia and blunt reflexes
  • these are initially used to draw the patient into the maintenance phase of general anesthesia rapidly, smoothly and with minimal adverse effects

■ examples include propofol, sodium thiopental (not available in North America), or ketamine

■ a continuous propofol infusion may also be used for the maintenance phase of GA

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15
Q

Propofol (Diprivan) class, action, indications, caution, dosing, special considerations

A

class - alkylphenol (hypnotic)

action - Inhibitory at GABA synapse Decreased cerebral metabolic rate and blood flow, decreased ICP, decreased SVR, decreased BP, and decreased SV

indications - Induction Maintenance Total intravenous anesthesia (TIVA)

caution - Patients who cannot tolerate sudden decreased BP (e.g fixed cardiac output or shock)

dosing - IV induction: 2.5-3.0 mg/kg (less with opioids) Unconscious <1 min Lasts 4-6 min t1/2 = 55 min Decreased postoperative sedation, recovery time, N/V

special considerations - 0-30% decreased BP due to vasodilation Reduce burning at IV site by mixing with lidocaine

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16
Q

Ketamine (Ketalar, Ketaject) class, action, indications, caution, dosing, special considerations

A

class - Phencyclidine (PCP) derivative – dissociative

action - May act on NMDA (antagonistically), opiate, and other receptors Increased HR, increased BP, increased SVR, increased coronary flow, increased myocardial O2 uptake CNS and respiratory depression, bronchial smooth muscle relaxation

indications - Major trauma, hypovolemia, obstetric bleeding, severe asthma because sympathomimetic

caution - Ketamine allergy TCA medication (interaction causes HTN and dysrhythmias) History of psychosis Patients who cannot tolerate HTN (e.g. CHF, increased ICP, aneurysm)

dosing - IV induction 1-2 mg/kg Dissociation in 15 s, analgesia amnesia, and unconsciousness in 45-60 s Unconscious for 10-15 min, analgesia for 40 min, amnesia for 1-2 h t1/2 = ~3 h

special considerations - high incidence of emergence reactions (vivid dreaming, out-ofbody sensation, illusions) Pretreat with glycopyrrolate to decrease salivation

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17
Q

Benzodiazepines (midazolam [Vesed], diazepam [Valium], lorazepam [Ativan]) class, action, indications, caution, dosing, special considerations

A

Class - benzodiazepines (anxiolytic)

action - Inhibitory at GABA synapse Produces antianxiety and skeletal muscle relaxant effects Minimal cardiac depression

indications - Used for sedation, amnesia, and anxiolysis

caution - Marked respiratory depression

dosing - Onset less than 5 min if given IV Duration of action long but variable/somewhat unpredictable

special considerations - Antagonist: flumazenil (Anexate®) competitive inhibitor, 0.2 mg IV over 15 s, repeat with 0.1 mg/mn (max of 2 mg), t1/2 of 60 min Midazolam also has amnestic (antegrade) effect and decreased risk of thrombophlebitis

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18
Q

Etomidate class, action, indications, caution, dosing, special considerations

A

Class - imadazole derivative (hypnotic)

action - Decreases concentration of GABA required to activate receptor CNS depression Minimal cardiac or respiratory depression

indications - induction Poor cardiac function, severe valve lesions, uncontrolled hypertension

caution - Post-operative nausea and vomiting Venous irritation

dosing - IV induction 0.3 mg/kg Onset 30-60 seconds Lasts 4-8 minutes

special considerations - Adrenal suppression after first dose, cannot repeat dose or use as infusion Myoclonic movements during induction

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19
Q

Physiology of the neuromuscular junction

A
  1. action potential arrives
  2. release of ach into cleft
  3. ach binds to ach receptor, ion channels open
  4. change in membrane permeability
  5. achE hydrolyzes ach
  6. action potential spreads across muscle membrane
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20
Q

Type of muscle relaxants

A
  1. depolarizing (non-competitive) (succinylcholine SCh)

2. non depolarizing (rocuronium, mivicurium, vecuronium, cistarcurium, pancuronium)

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21
Q

Muscle relaxants mechanism

A

Block nicotinic cholinergic receptors in nmj

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22
Q

What muscles do muscle relaxants affect

A

provides skeletal muscle paralysis, including the diaphragm, but spares involuntary muscles such as the heart and smooth muscle

never use muscle relaxants without adequate preparation and equipment to maintain airway and ventilation

23
Q

muscle relaxation produces which desired effects

A
  1. facilitates intubation
  2. assists with mechanical ventilation
  3. prevents muscle stretch reflex and decreases muscle tone
  4. allows access to the surgical field (intracavitary surgery)
24
Q

how to assess degree of nerve block intraoperatively

A

nerve stimulator (i.e. train of four) is used intraoperatively to assess the degree of nerve block; no twitch response seen with complete neuromuscular blockade

25
Q

What is plasma cholinesterase and what does it do

A

Plasma cholinesterase is produced by the liver and metabolizes SCh, ester local anesthetics, and mivacurium.

26
Q

a prolonged duration of blockade by sch occurs with

A

(a) decreased quantity of plasma cholinesterase, e.g. liver disease, pregnancy, malignancy, malnutrition collagen vascular disease, hypothyroidism
(b) abnormal quality of plasma cholinesterase, e.g. normal levels but impaired activity of enzymes, genetically inherited

27
Q

Depolarizing muscle relaxants moa

A

Action
Mimics ACh and binds to ACh receptors causing prolonged depolarization; initial fasciculation may be seen, followed by temporary paralysis secondary to blocked ACh receptors by SCh

28
Q

Depolarizing muscle relaxants intubating dose

A

1-1.5 mg/kg

29
Q

Depolarizing muscle relaxants onset

A

30-60 s – rapid (fastest of all muscle relaxants)

30
Q

Depolarizing muscle relaxants duration

A

3-5 min – short (no reversing agent for SCh)

31
Q

Depolarizing muscle relaxants metabolism

A

SCh is hydrolyzed by plasma cholinesterase (pseudocholinesterase), found only in plasma and not at the NMJ

32
Q

Depolarizing muscle relaxants indications

A

Assist intubation

Increased risk of aspiration (need rapid paralysis and airway control (e.g. full stomach), hiatus hernia, obesity, pregnancy, trauma)

Short procedures

Electroconvulsive therapy (ECT)

Laryngospasm

33
Q

Depolarizing muscle relaxants side effects

A
  1. SCh also stimulates muscarinic cholinergic autonomic receptors (in addition to nicotinic receptors; may cause bradycardia, dysrhythmias, sinus arrest, increased secretions of salivary glands (especially in children)
  2. Hyperkalemia Disruption of motor nerve activity causes proliferation of extrajunctional (outside NMJ) cholinergic receptors Depolarization of an increased number of receptors by SCh may lead to massive release of potassium out of muscle cells Patients at risk 3rd degree burns 24 h-6 mo after injury Traumatic paralysis or neuromuscular diseases (e.g. muscular dystrophy) Severe intra-abdominal infections Severe closed head injury Upper motor neuron lesions
  3. Can trigger MH (see Malignant Hyperthermia, A28)
  4. Increased ICP/intraocular pressure/intragastric pressure (no increased risk of aspiration if competent lower esophageal sphincter)
  5. Fasciculations, post-operative myalgia – may be minimized if small dose of non-depolarizing agent given before SCh administration
34
Q

Depolarizing muscle relaxants contraindications

A

Absolute - Known hypersensitivity or allergy, positive history of malignant hyperthermia, myotonia (m congenita, m. dystrophica, paramyotonia congenital), high risk for hyperkalemic response

Relative - Known history of plasma cholinesterase deficiency, myasthenia gravis, myasthenic syndrome, familial periodic paralysis, open eye injury

35
Q

Non-depolarizing muscle relaxants MOA

A

competitive blockade of postsynaptic ACh receptors preventing depolarization

36
Q

Non-depolarizing muscle relaxants indications

A

Assist intubation, assist mechanical ventilation in some ICU patients, reduce fasciculations and post-operative myalgias secondary to SCh

37
Q

Muscle relaxant reversing agents

A
  • sugammadex is a selective relaxant binding agent
  • neostigmine, pyridostigmine, edrophonium are acetylcholinesterase inhibitors
  • administer reversal agents when there has been some recovery of blockade (ie. muscle twitch)
  • can only reverse the effect of non-depolarizing muscle relaxants
  • anticholinergic agents (e.g. atropine, gylcopyrrolate) are simultaneously administered to minimize muscarinic effect of reversal agents (i.e. bradycardia, salivation, increased peristalsis and bronchoconstriction)
38
Q

Reversal agents for non-depolarizing relaxants mechanism of action

A

Pyridostigmine, neostigmine, edrophonium - (acetylcholineste ase inhibitors) Inhibits enzymatic degradation of ACh, increases ACh at nicotinic and muscarinic receptors, displaces non-depolarizing muscle relaxants Muscarinic effects of reversing agents include unwanted bradycardia, salivation, and increased bowel peristalsis*

Sugammadex - encapsulates and inactivates rocuronium and vecurionium, which decreases amount of agent available to bind to receptors in NMJ

39
Q

Onset of pyridostigmine

A

slow

40
Q

onset of neostigmine

A

intermediate

41
Q

onset of edrophonium

A

intermediate

42
Q

onset of sugammadex

A

fast

43
Q

Recommended anticholinergic with pyridostigmine

A

glycopyrolate

44
Q

Recommended anticholinergic with neostigmine

A

glycopyrolate

45
Q

Recommended anticholinergic with edrophonium

A

atropine

46
Q

Recommended anticholinergic with sugammadex

A

N/A

47
Q

General anesthesia maintenance using what

A

volatile inhalation agents and/or IV agents (ie propofol infusion)

48
Q

Extubation criteria

A

criteria: patient must no longer have intubation requirements

■ patency: airway must be patent

■ protection: airway reflexes intact

■ patient must be oxygenating and ventilating spontaneously

49
Q

Extubation general guidelines

A

• general guidelines

■ ensure patient has normal neuromuscular function (peripheral nerve stimulator monitoring) and hemodynamic status

■ ensure patient is breathing spontaneously with adequate rate and tidal volume

■ allow ventilation (spontaneous or controlled) with 100% O2 for 3-5 min

■ suction secretions from pharynx, deflate cuff, remove ETT on inspiration (vocal cords abducted)

■ ensure patient is breathing adequately after extubation

■ ensure face mask for O2 delivery available

■ proper positioning of patient during transfer to recovery room (supine, head elevated)

50
Q

Complications of extubation

A
  • early extubation: aspiration, laryngospasm

* late extubation: transient vocal cord incompetence, edema (glottic, subglottic), pharyngitis, tracheitis

51
Q

What is laryngospasm

A
  • defined as forceful involuntary spasm of laryngeal muscles caused by stimulation of superior laryngeal nerve (by oropharyngeal secretions, blood, extubation)
  • causes partial or total airway obstruction
52
Q

in who is laryngospasm more likely to occur

A

more likely to occur in semi-conscious patients

53
Q

laryngospasm prevention

A

extubate while patient is still deeply under anesthesia or fully awake

54
Q

laryngospasm treatment

A

apply sustained positive pressure with bag-mask ventilation with 100% oxygen, lowdose propofol (0.5-1.0 mg/kg) optional, low-dose succinylcholine (approximately 0.25 mg/kg) and reintubation if hypoxia develops