Induction Flashcards
Routine induction vs RSI
- 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)
Transfusion infection risks for HIV, Hep C, Hep B, HTLV, Symptomatic bacterial sepsis, West Nile virus per 1 unit pRBCs
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
Equipment preparation routine vs RSI
Same
Check equipment, drugs, suction, and monitors; prepare an alternative laryngoscope blade and a second ETT tube one size smaller, suction on
pre-oxygenation/denitrogenation routine vs rsi
same
100% O2 for 3 mins or 4-8 vital capacity breaths
pre-treatment agents routine vs rsi
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
Induction agents routine vs rsi
routine - use iv or inhalation induction agent of choice
rsi - use pre-determined dose of fast acting induction agent of choice
muscle relaxants routine vs rsi
routine - choice given after onset of induction agent
rsi - pre-determined dose of fast acting (ex. SCh) given IMMEDIATELY after induction agent
Ventilation routine vs RSI
Routine - bag mask ventilation
rsi - DO NOT bag ventilate - can increase risk of aspiration
cricoid pressure routine vs rsi
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)
Intubation routine vs rsi
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
Secure machines routine vs rsi
same
secure ETT, and begin manual/machine ventilation
order of induction
- equipment preparation
- pre-oxygenation/denitrogenation
- pre-treatment agents
- induction agents
- muscle relaxants
- ventilation
- cricoid pressure
- intubation
- secure machines
Solubility of volatile anesthetics in blood from least to most soluble
Nitrous oxide < desflurane < sevoflurane < isoflurane < halothane
What are intravenous induction agents, their purpose and examples
- 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
Propofol (Diprivan) class, action, indications, caution, dosing, special considerations
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
Ketamine (Ketalar, Ketaject) class, action, indications, caution, dosing, special considerations
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
Benzodiazepines (midazolam [Vesed], diazepam [Valium], lorazepam [Ativan]) class, action, indications, caution, dosing, special considerations
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
Etomidate class, action, indications, caution, dosing, special considerations
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
Physiology of the neuromuscular junction
- action potential arrives
- release of ach into cleft
- ach binds to ach receptor, ion channels open
- change in membrane permeability
- achE hydrolyzes ach
- action potential spreads across muscle membrane
Type of muscle relaxants
- depolarizing (non-competitive) (succinylcholine SCh)
2. non depolarizing (rocuronium, mivicurium, vecuronium, cistarcurium, pancuronium)
Muscle relaxants mechanism
Block nicotinic cholinergic receptors in nmj
What muscles do muscle relaxants affect
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
muscle relaxation produces which desired effects
- facilitates intubation
- assists with mechanical ventilation
- prevents muscle stretch reflex and decreases muscle tone
- allows access to the surgical field (intracavitary surgery)
how to assess degree of nerve block intraoperatively
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
What is plasma cholinesterase and what does it do
Plasma cholinesterase is produced by the liver and metabolizes SCh, ester local anesthetics, and mivacurium.
a prolonged duration of blockade by sch occurs with
(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
Depolarizing muscle relaxants moa
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
Depolarizing muscle relaxants intubating dose
1-1.5 mg/kg
Depolarizing muscle relaxants onset
30-60 s – rapid (fastest of all muscle relaxants)
Depolarizing muscle relaxants duration
3-5 min – short (no reversing agent for SCh)
Depolarizing muscle relaxants metabolism
SCh is hydrolyzed by plasma cholinesterase (pseudocholinesterase), found only in plasma and not at the NMJ
Depolarizing muscle relaxants indications
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
Depolarizing muscle relaxants side effects
- 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)
- 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
- Can trigger MH (see Malignant Hyperthermia, A28)
- Increased ICP/intraocular pressure/intragastric pressure (no increased risk of aspiration if competent lower esophageal sphincter)
- Fasciculations, post-operative myalgia – may be minimized if small dose of non-depolarizing agent given before SCh administration
Depolarizing muscle relaxants contraindications
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
Non-depolarizing muscle relaxants MOA
competitive blockade of postsynaptic ACh receptors preventing depolarization
Non-depolarizing muscle relaxants indications
Assist intubation, assist mechanical ventilation in some ICU patients, reduce fasciculations and post-operative myalgias secondary to SCh
Muscle relaxant reversing agents
- 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)
Reversal agents for non-depolarizing relaxants mechanism of action
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
Onset of pyridostigmine
slow
onset of neostigmine
intermediate
onset of edrophonium
intermediate
onset of sugammadex
fast
Recommended anticholinergic with pyridostigmine
glycopyrolate
Recommended anticholinergic with neostigmine
glycopyrolate
Recommended anticholinergic with edrophonium
atropine
Recommended anticholinergic with sugammadex
N/A
General anesthesia maintenance using what
volatile inhalation agents and/or IV agents (ie propofol infusion)
Extubation criteria
criteria: patient must no longer have intubation requirements
■ patency: airway must be patent
■ protection: airway reflexes intact
■ patient must be oxygenating and ventilating spontaneously
Extubation general guidelines
• 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)
Complications of extubation
- early extubation: aspiration, laryngospasm
* late extubation: transient vocal cord incompetence, edema (glottic, subglottic), pharyngitis, tracheitis
What is laryngospasm
- 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
in who is laryngospasm more likely to occur
more likely to occur in semi-conscious patients
laryngospasm prevention
extubate while patient is still deeply under anesthesia or fully awake
laryngospasm treatment
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
