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Induction Sequence Cheat Sheet by

This is a cheat sheet for Induction sequence for SRNAs & CRNAs.

Preadmit Holding Area

Talk to patient
Check name band (ident­ifier)
Check consents - ALWAYS - before sedation
Check if patient is marked
Check with holding are RN if patient is ready to go
Running IV?
Give pre-op sedation

Pre-op Sedation

Only give once consent is confirmed to have been signed
Admini­stered by TBW because of an increased central volume of distri­bution. Just about all books seem to agree with this. Dosing in this way will prolong the elimin­ation half-life and its duration of effect. In practice, it may cause over sedation in the obese pts who is sensitive to respir­atory depressant drugs
TBW = total body weight (obese patients could overdose due to larger body weight and thus larger dose)
GABA-A Agonist
change frequency of channel opening - neuronal hyperp­ola­riz­ation
most GABA-A agonists increase channel open time, benzos increase open frequency
30-60 seconds
20-60 min
Active Metabolite
Sedation dose
IV 0.01-0.1 mg/kg
Respir­atory Effects
minimal but synerg­istic respir­atory depression when combined with other sedatives
CV Effects
CNS Effects
antero­grade amnesia, antico­nvu­lsant proper­ties, anxiol­ysis, antisp­asmodic effects No analgesia
~anti spasmodic effects good for spinally mediated skeletal muscle relaxation (useful in CP patients)

Proceed to Operating Room

Transport patient to OR via stretcher or amulation
Move patient to OR table and ensure safety strap is secured
usually placed across thighs 2 inches above the knees over the cover
arms secured on padded arm boards or tucked
Apply Monitors
record vital signs at least every 5 minutes
-Pulse Ox

Preoxy­gen­ation aka Denitr­oge­nation

o 1948: Fowler and Comroe demons­trated that inhalation of 100% oxygen (O2) resulted in a very rapid increase of arterial oxyhem­oglobin saturation (Sao2) to between 98% and 99%, but that attainment of the last 1% to 2% was a much slower process
o 1950s: Rapid Sequence Induction (RSI) began being utilized in patients at risk for aspiration of gastric contents, preoxy­gen­ation became a component of the technique
Preoxy­gen­ation extends periods of safe apnea
• defined as the time until a patient reaches a saturation level of 88% - 90%, to allow for the placement of a definitive airway.
 Below this level, oxygen saturation can decrease to critical levels <70% within moments.
Goals of preoxy­gen­ation
 Achieve 100% oxygen­ation saturation prior to procedure
 Denitr­ogenate the residual capacity of the lungs, maximizing oxygen storage
 Denitr­ogenate and maximally oxygenate the bloods­tream.
Preoxy­gen­ation techniques
o Tidal volume breathing with 100% O2 for 3-5 minutes
o 8 deep breaths of 100% O2 for 60 seconds
o Sit up or reverse Trende­lenburg to increase FRC
Nasal oxygen @ 15L during intubation
 Preoxy­gen­ation and apneic oxygen­ation are partic­ularly beneficial if manual ventil­ation after induction of anesthesia is undesi­rable (eg during rapid sequence induction and intubation RSI), if difficulty with airway management is antici­pated and for pts who are expected to desat rapidly
• Obese
• Pregnant
• Pediatric
• Hyperm­eta­bolic pts

FRC Measur­ement

Functional Residual Capacity

Volume of air in lungs at end of expiration
o FRC is the reservoir of oxygen that prevents hypoxemia during apnea
o Diaphr­agmatic tone and position also effect FRC
o FRC cannot be measured with spirometry because the residual volume cannot be exhaled and RV is a component of FRC
Static equili­brium
At FRC the inward elastic recoil of the lungs is balanced by the outward elastic recoil of the chest wall
Normal FRC
35 ml/kg
Indirect FRC measur­ement
Nitrogen washout
Helium wash in
Body plethy­smo­graphy
How will FRC last during apnea?
o We can estimate how long a pt can remain apneic before desatu­ration if we know the patients FRC and oxygen consum­ption (VO2)
o Healthy adult breathing 100% O2 takes 6.9 minutes to desaturate to 90% on pulse oximetry
 1 minute if the patient was breathing room air
Desat formula
time until patient desats = FRC/VO2
Conditions that decrease FRC
• Decreased chest wall compliance
• Increased airway collap­sib­ility
• Diaphragm shifts cephalad due to gravid uterus
• First give O2!!!
• Decreased chest wall compliance
• Less alveoli
• Decreased lung compliance
• Cartil­aginous ribcage prone to collapse during inspir­ation
Postions that affect FRC
• Supine
• Trende­lenburg
• Lithotomy
• Prone
• Sitting
• Lateral- unchanged or increase

Opioid Potency

Opioid Potency Least potent (left) Most Potent (Right)
Meperidine 100mg / 0.1 RP
Morphine 10mg / 1
Hydrom­orphone 1.4m / 7
Alfentanil 1000mcg / 10
Remife­ntanil 100mg / 100
Fentanyl 100mcg / 100
Sufentanil 10mcg / 1000

IV Induction Agents - General Anesthesia

Opioids - Fentanyl
mu receptor agonist
5 min
20-30 min
Active Metabolite
CYP3A4 (P450)
IV 1-2 mcg/kg
induction 10 mcg/kg (watch for chest wall or glottis rigidity)
Resp Effects
respir­atory depression
CV Effects
bradyc­ardia, vasodi­lation
CNS Effects
analgesia, N/V
Amine - Lidocaine
o Local anesth­etics bind to alpha-­subunit on inside of sodium channel
o When critical number of sodium channels are blocked cell can’t be depola­rized and action potential cant be propagated
Adverse Effects
 Mild CNS-re­lated symptoms
• Drowsiness
• dizziness
• metallic taste
• Headache
• blurred vision
• parest­hesia dysarthria
• euphoria
• Nausea
 Larger doses or if given rapidly

• Tinnitus
• Tremor
• Agitation
• Cardio­vas­cular changes are usually minimal with the usual doses
o 5% of patients have pain at propofol injection and of these, 1% of them have severe or excruc­iating pain
 40 mg Lidocaine prevents this
 Also can mix Lidocaine and Propofol
• Propofol and lidocaine= Magic
o Add 1 ml of 1 % or 2% lidocaine to a 10 ml syringe of propofol
 Place the IV in an antecu­bital vein (vs the hand).
 Pretreat with IV opioids.
 If the IV is in the hand, place a tourniquet proximally and pretreat with lidocaine
most common induction agent
GABA-A agonist (how long the channel stays open)
 GABA-A receptor stimul­ation hyperp­larizes neurons by increasing Cl- conduc­tance. More Cl- inside the cell makes the cell more negative. This reduces resting membrane potential (RMP moves further away from TP)
30-60 seconds
5-10 min
Liver and extra hepatic metabolism
Active Metabolite
Induction dose
1.5-2.5 mg/kg IV
Mainte­nance dose
25-200 mcg/kg/min
Resp Effects
decreased resp drive
CV Effects
decreased BP, SVR, preload, contra­ctility
CNS Effects
decreased ICP and IOP, no analgesia, +/- seizure activity
GABA-A agonist
30-60 seconds
5-15 min
Liver & plasma esterases
Active Metabolite
Induction dose
0.2-0.4 mg/kg IV
Resp Effects
Mild Resp Depression
CV Effects
CNS Effects
Decreased ICP, no analgesia
Side Effects
o Myoclonus (not a seizure)
o Does not cause seizures if the patient does not have a history of seizures
o Suppre­ssion of adreno­cor­tical function for up to 24 hrs. It should be avoided in sepsis and acute adrenal failure
o N&V (greater than any other induction agent)
o Acute interm­ittent porphyria
NMDA antagonist (creates dissoc­iated state)
MOA secondary
Many 2nd receptor targets including opioid, MAO, serotonin, NE, muscar­inic, and NA channels
Onset IV
30-60 seconds
Onset IM
2-4 minutes
Onset PO
10-20 minutes (can last 60-90 min to return to full orient­ation)
Active Metabolite
Induction Doses
IV 1-2 mg/kg
IM 4-8 mg/kg
PO 10mg/kg
Opioid Sparing Dose
0.1-0.5 mg/kg or 1-3 mcg/kg/min
Resp Effects
maintains resp drive, increased oral secretions (DROOL EVERYW­HERE, GIVE GLYCO)
CV Effects
Increased SNS tone, SVR, HR, and CO
CNS Effects
Increased ICP, IOP, nystagmus and analgesia
causes emergence delirium and lowers seizure threshold, can also treat severe depression

Food Allergies & Propofol

Overseen by the American Academy of Allergy, Asthma and Immuno­logy. They state:
o Propofol can cause anaphy­lactic reactions, the cause of these reactions is unclear and appears not to be related to soy or egg allergy.
o Egg allergy
 Patients with soy, peanut allergy or egg allergy can receive propofol without any special precau­tions. – Probably safe
 Most people with egg allergies are allergic to the albumin egg whites. Egg lecithin found in propofol is derived from the YOLK
o Soy
 Any soy proteins that are capable of producing an immune response are removed during the refining process
 Prop is safe to use in pts with soy allergy
o Peanut
 Like soy peanuts are a type of legume. Some have speculated the potential of cross sensit­ivity between peanuts and soy (and thus propofol) although there is no evidence to support this
 Prop is safe to use in pts with a peanut allergy
o Increased Risk of Bacterial Contam­ination
 Propofol syringes must be discarded within 6 hrs
 Infusions (and the tubing) must be discarded within 12 hrs


Total body weight Mainte­nence
• Weight when individual steps on scale
Describes the BMI associated with the lowest risk of body weight related comorb­idi­ties. We can estimate the ideal body weight with the following formulas:
o Men (kg)= height (cm) – 100
o Women (Kg)= Height (cm) - 105
Lean body weight
 LBW = 1.3 X IBW
Fentanyl ((nl))­Suf­entanil
Loading (not preop)
Epidural Local
75% of normal dose

Guedel's Stages of Anesthesia

Stage 1 - Analgesia or Disori­ent­ation
o Can be initiated in a preope­rative holding area
o Patient is given medication and may begin to feel its effects but has not yet become uncons­cious
o Induction stage
 Patients are sedated but conver­sat­ional
 Breathing is slow and regular
 Patient progresses from analgesia free of amnesia to analgesia with concurrent amnesia
 This stage comes to an end with the loss of consci­ous­ness.
o Loss of Consci­ousness
 Count backwards from 100, the patient typically loses consci­ousness between 80 to 90, i.e. stops counting – the old way
 Blinking increases, and nystagmus may appear
 Eyes eventually fix in the midline as the lids close • GENTLE
 Patient becomes unresp­onsive, atonic, apneic, and the oculoc­ephalic (or more precisely vestib­ula­r-o­cul­oce­phalic) and corneal reflexes are lost
 Call patients name
 Eyelash reflex
 Tape eyes- as soon as you lose consci­ousness
• If you struggle to ventilate they you could hurt their eyes
• Not on sedation cases
• Don’t tape in endo watch the L eye
o Eye Protection after Loss of Consci­ousness
 Tape eyes horizo­ntally after loss of consci­ousness
 Eyes should be protected before instru­menting the air way
Stage 2 - Excitement
o There is a higher risk of laryng­ospasm (invol­untary tonic closure of vocal cords) at this stage, which may be aggravated by any airway manipu­lation
o The combin­ation of spastic movements, vomiting, and rapid, irregular respir­ations can compromise the patient's airway.]
o Fast-a­cting agents help reduce the time spent in stage 2 as much as possible and facilitate entry to stage 3.
o If you are using gas induction no muscle relaxa­tion- you can really see this
 Its really short with IV induction
• Laryngospasm
• Don’t touch them too soon
Stage 3 - Deep
o Surgical Anesthesia targeted anesthetic level for procedures requiring general anesthesia
o Ceased eye movements and respir­atory depression are the hallmarks of this stage.
o Airway manipu­lation is safe at this level
4 planes in stage
Plane 1, there is still regular sponta­neous breathing, constr­icted pupils, and central gaze
• eyelid, conjun­ctival, and swallow reflexes usually disappear in this plane
• Just gazing
Plane 2, there are interm­ittent cessations of respir­ation along with the loss of corneal and laryngeal reflexes. Halted ocular movements and increased lacrim­ation may also occur.
Plane 3 is marked by complete relaxation of the interc­ostal and abdominal muscles and loss of the pupillary light reflex. This plane is referred to as "true surgical anesth­esi­a" because it is ideal for most surgeries.
Plane 4 is marked by irregular respir­ation, parado­xical rib cage movement, and full diaphragm paralysis resulting in apnea.

Mask Ventil­ation

One hand
o C
o E
o If you are struggling put in oral airway
Two hands
o Get it less than 20
o Two people approach
Non- Invasive Airway Maneuvers
• Chin lift
• Not usually in induction
• Jaw Thrust
Placement of LMA if unable to ventilate
• Difficult suprag­lottic airway placement
o Restricted mouth opening
o Obstru­ction
o Distorted airway
o Stiff lungs or C spine
Upper Airway Patency
• Pharynx
• Collap­sible tube inside box
• Box is formed:
o Tongue
o Soft palate
o Pharyngeal tissue
o Cervical spine
During inspir­ation a negative gradient draws air into lungs
• Tendency to make airway collapse
• In awake state
o Counte­racted by three sets of dilator muscle
If able to ventilate give muscle Relaxant
• Upper airway consists of the cartil­aginous and bony structures of the nose and mouth, followed by the soft tissue of the oropharynx and laryng­oph­arynx, and ending in the rigid trachea
• Soft tissue of the pharynx is prone to collapse in the uncons­cious, or anesth­etized, patient and may be further compro­mised by obesity, a large tongue, airway edema, large neck circum­fer­ence, external compre­ssion, and many other factors
• When placing an endotr­acheal tube after induction o Histor­ically been instructed to refrain from admini­stering muscle relaxation until adequate mask ventil­ation in the anesth­etized patient was confirmed in order to both avoid
 Critical hypoxemic event
 Ensure an attempt at an escape wake up.
o There is little published evidence to support this practice, and the admini­str­ation of muscle relaxation before ensuring adequate BVM ventil­ation remains contro­versial
o Neurom­uscular Blockade and the Airway
 Regarding Mask Ventilate- There is evidence that paralysis of the upper airway muscul­ature improves ability to ventilate
 A recent study published data indicating that NMB using rocuronium facili­tated bag-mask ventil­ation in anesth­etized patients

Oral Airways

Airway Obstru­ction

Difficult Ventil­ation Mnemonic

Ventilate Patient with mask after loss of consci­ousness

Upper Airway Patency

Mneumonic for Difficult LMA Placement

Why Neurom­uscular Blockades (NMB)?

• They allow for easy airway and operative field manipu­lation
o Good for specific types of surgery
o No single agent is ideal for every situation
• What is the Neurom­uscular Junction? (NMJ)
o The neurom­uscular junction is a synapse that develops between a motor neuron and a muscle fiber o Made up of several compon­ents: the presyn­aptic nerve terminal, the postsy­naptic muscle membrane, and the interv­ening cleft (or gap)
o End Plate
 Acetyl­choline is hydrolyzed rapidly by the enzyme acetyl­cho­lin­est­erase in the synaptic cleft
 Not all acetyl­choline that is released reaches the endplate, some is hydrolyzed en route.
• Muscle Relaxants
o Disrupts the physio­logical sequence of neurom­uscular transm­ission.
o Used to optimize surgical condition and facilitate intuba­tions.
o Mechanism of action occurs at the neurom­uscular junction (NMJ)
o Post junction nicotinic receptors are composed of five subunits
o Lined up circum­fer­ent­ially around ion conducting core
o Two alpha subunits

Neurom­uscular junction

Muscle Relaxants

End Plate

Post Junction Nicotinic Receptors

o Post junction nicotinic receptors are composed of five subunits
o Lined up circum­fer­ent­ially around ion conducting core
o Two alpha subunits

Depola­rizing NMB

Succin­ylc­holine chloride (Anectine, Quelicin)
o Depola­rizing neurom­uscular blockers act as agonists at postsy­naptic nicotinic acetyl­choline receptors and cause prolonged membrane depola­riz­ation resulting in neurom­uscular blockade.
• Resemble ACH bind to ACH receptors
• generating an action potential ....depola­riz­ation.
• Sodium channels are open as a result of depola­riz­ation, then close in a resting state and muscle relaxation occurs.
• Ach binds to subuni­t-a­llows channel to open -depola­riz­ation occurs
• Depola­rizing neuro muscular blockers
– Bind to alpha subunits
– Cause Channel to remain open- mimics Ach
– Prolonged depola­riz­ation occurs
Chemical formula: C14H30N2O4
agonists at postsy­naptic nicotinic acetyl­choline receptors and cause prolonged membrane depola­riz­ation resulting in neurom­uscular blockade
IV 60-90 sec
IM 2-3 min
5 min
IV 0.5-1.5 mg/kg
Ped IV 4-5 mg/kg
Laryngospasm: 1-.5 mg/kg/IV or 4-6mg/kg IM
Adverse Effects
 Hyperk­alemia
 Malignant Hypert­hermia
 Apnea

Non-De­pol­arizing NMB

o NDMR compete with acetyl­choline for the active binding sites at the postsy­naptic nicotinic acetyl­choline receptor
o Resemble ACH enough to bind to the ACH receptor, but fail to activate the receptor, thus blocking its action (paral­yzing the muscle transm­ission)
o “The key fits but won’t open the door.”
o Compet­itive Antagonist – compete with ACH

o The bond is very tight depending upon the drug, it will last from 20 to 90 minutes.
o Compet­itive Antagonist
 Two alpha subunits are binding sites for Ach
 Sites occupied by nondep­ola­rizing neuro muscular blockers
 Cause channel to remain closed
 Ion flow to produce depola­riz­ation can’t occur
 Rocuronium is the most widely used nondep­ola­rizing relaxant in the United States.
 Can be used for rapid sequence induction (RSI) when succin­ylc­holine is contra­ind­icated.
o Resemble ACH enough to bind to the ACH receptor, but fail to activate the receptor, thus blocking its action (paral­yzing the muscle transmission)
o Compet­itive Antagonist – compete with ACH
1-2 min
20-35 min
IV 0.6 - 1.2 mg/kg
Infusion 5-12 mcg/kg/min
Pretreatment 5mg
no recons­tit­ution
Neostigmine (less effective)
some de-ace­tyl­ation
3-5 min
20-35 min
IV: .08 - .12 mg/kg
Infusion: 1-2 mcg/kg/min
• To shorten the onset time, the priming principle involves the admini­str­ation of a small dose of rocuronium usually 3 minutes prior to induction
• The optimal priming dose which is the largest dose that it is given that will not produce weakness in an awake patient is very small
• Priming dose is given prior to succin­ylc­holine rapid sequence induction to decrease the myalgias (5 mg)

Rapid Sequence Induction

o Patient at risk for regurg­itation and aspiration who require GA History of
o Recent vomiting or recent meal
o Pregnancy
 Over 18 weeks
 Full stomach
 Loose spincter
o Increased intra-­abd­ominal pressure
o Abdominal distension
o Poorly controlled GE reflux
o Decreased level of consci­ousness
o Gastro­paresis
o Bowel Obstru­ction
 GOP1
Rapid Sequence Induction Method
o Preoxy­gen­ation is critical
o Suction and airway altern­atives available
o Use adjuvant drugs to control BP, HR response: midazolam, narcotics, lidocaine, ketamine, etc
o Explain and rehearse use of cricoid pressure with the patient.
o Optimize position of upper airway.
o Identify person to do cricoid pressure
o Apply Cricoid while patient is awake
 Conscious 20N (2 kg)
 If you cant see they are pushing too hard
 Tell them to keep holding pressure until you them to let go
o Propofol 1.5-2.5 mg/kg
o asleep 40N (4 kg) of pressure
o Succin­ylc­holine 0.5 to 1.5 mg/kg or Rocuronium 1.2 mg/kg
o Loss of consciousness-fasciculations
o Eye Protection
o Intubate
o Hold cricoid until endotr­acheal tube cuff is inflated and placement is confirmed
Modified Rapid Sequence
o Same steps but with ventil­ation
o Gentle IPPV (Paw 10-15 cm H2O) with 100% O2 until relaxant has peak effect.
o If you cant see vent until glide scope

General Anesthesia - Inhalation Induction

 Difficult IV access
 Develo­pme­ntally delayed adult
 Pediatrics
 Potential airway obstru­ction e.g. epiglo­ttitis
 Kids or special need,
 Sevo dilates vein- if you cant get IV
 Aspiration risk
 Active bleeding in airway (risk of cough, laryng­ospasm)
Inhalation Induction Technique
 Prime circuit with anesthesia agent from vaporizer at maximum setting
 Oxygen at 8L/min
 Pop off valve open and patient end of circuit occluded.
 Have patient exhale maximally, then apply face mask to patient and inhale maximally from primed circuit.
 Expect prompt onset of sleep (60 seconds) followed by transient apnea, then pattern of rapid shallow respir­ations.
 They are crying then go dominate
 Then you put the IV in and tube them
 Need the pop up valve OPEN
Inhalation Induction Technique #2
 Prime circuit with N2O 70%,
 FGF at 8L/min
 Pop off valve open and patient end of circuit occluded.
 When patient is comfor­table with situation, begin volatile agent increasing vaporizer setting by 0.5% every 3 or 4 breaths
 Reassure patient with calm voice encour­aging a regular smooth breathing pattern.
 Use of a deep breathing pattern here may lead to premature onset of apnea with prolonged phase.
 Expect several minutes to fall asleep. Assist ventil­ation
 Don’t use N2O if you are trying to get pregnant- spont miscar­riage
 For adults or special needs

General Anesthesia - LMA Induction Sequence

 Pre-Ox­ygenate
 Lidocaine
 Propofol
 Loss of consci­ousness
 Eye protection
 Usually don’t ventilate
 Open mouth insert LMA
 When you take it out don’t deflate cough- all the secretions go right in the airway
Fentanyl LMA
 Many anesthesia providers do not give fentanyl on induction
 Wait for return of sponta­neous respir­ation
 Others give small dose


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