AIRWAY MANAGEMENT (Clinical Anaesthesiology 5th ed.

by M & M)

ANATOMY
*innervation to anterior nasal mucous membrane: anterior
ethmoidal n-> ophthalmic div (V1)->CNV

*sense of smell, nasal mucosa: CNI

*innervation to post. nasal mucous membrane; superior and

inferior surfaces of hard and soft palate: sphenopalatine n -
>maxillary div (V2)-> CNV

*general sensation ant. 2/3 of tongue:lingual n-> madibular

div (V3)-> CNV

taste: CNVII (facial n)

*CNIX--> general sensation and posterior 2/3 of tongue; roof

of pharynx, tonsils, and under surface of soft palate

*motor innervation to larynx between glottis and vocal cords:

external br. of sup laryngeal n ->CNX

sensory innervation to larynx between glottis and vocal cords:

internal br. of sup. laryngeal n -> CNX

*innervation of larynx below vocal cords and trachea; all

muscles of larynx: recurrent laryngeal-> CNX

****except CRICOTHYROID muscle-> external (motor) sup.

laryngeal n->CNX
*ROUTINE AIRWAY MANAGEMENT*

• Airway assessment

• Preparation and equipment check

• Patient positioning

• Preoxygenation

• Bag and mask ventilation (BMV)

• Intubation (if indicated)

• Confirmation of ETT placement

• Intraop management and troubleshooting

• Extubation

❖ AIRWAY ASSESSMENT

o Mouth opening: an incisor distance of >/= 3 cm desirable in adult

o Upper lip bite test: lower teeth brought in front of the upper teeth; degree of which this
can be done estimates range of motion of TMJ

o Mallampati classifaction: examines size of tongue in relation to oral cavity; greater

tongue obstructs view of the pharyngeal structures, more difficult intubation

o Thyromental distance: distance between mentum and the superior thyroid notch; >3
fingerbreadths is desirable

o Neck circumference >27 inches suggestive of difficulties in visualization of the glottis

opening
 **Mallampati Classification**

Class I: entire palatal arch, including bilateral faucial pillars, visible down to bases

Class II: upper part of faucial pillars and most of the uvula visible

Class III: only the soft and hard palates are visible

Class IV: only hard palate visible

❖ EQUIPMENT

o O2 source

o BMV capability

o Laryngoscopes

o Several ETT of different sizes

 o Other airway devices (oral, nasal)

▪ Oral: sizes- small( 80mm/Guedel No.3), med (90mm/Guedel No.4),

large(100mm/Guedel No.5)

▪ Nasal: length-distance from nares to meatus of ear; 2-4 cm longer than oral
airways (b/c risk of epistaxis, less desirable in anticoagulated/thrombocytopenic
pts); use with caution in pts w/ basilar skull #s

o Suction

o Oximetry and CO2 detection

o Stethoscope

o Tape

o BP and ECG monitors

o IV access

**FACE MASK AND VENTILATION TECHNIQUE**

-Effective mas ventilation requires both a gas tight mask fit and patent airway
-Improper technique-> no sign of equal bilateral rise of chest, no misting of mask, deflation of
anaesthesia reservoir bag (indicative of leak around mask); improper reading on capnograph/no
end-tidal CO2 detected (if you’re comfortable in your positioning, your’re probably doing it
incorrectly)

*E-C placement of fingers of left hand

1. Most important maneuver to allow proper ventilation to pt is Jaw Thrust

2. Little finger of left hand placed under the angle of mandible and used to thrust the jaw
anteriorly, lifting base of tongue away from posterior pharynx opening the airway

3. The middle and ring finger grasp the mandible to facilitate extension of the atlantooccipital
joint (finger pressure should be placed on the bony mandible & not on soft tissues which may
obstruct airway)

4. The left thumb and index finger holds the mask against the face by downward pressure
 5. The right hand is used to generate positive-pressure ventilation by squeezing the
reservoir/breathing bag

**NB: eyes should be taped shut to avoid corneal abrasions and to avoid injury to pt during intubation**

❖ POSITIONING

o “Sniffing the morning air” position to achieve alignment of the oral and pharyngeal axes

▪ Cervical spine pathology keep head in neutral position during all airway
manipulations; until C-spine has been cleared

▪ Morbidly obese pts- 30° upward ramp (functional residual capacity- FRC
deteriorates in supine position)

❖ PREOXYGENATION

o Face mask oxygenation should precede all airway management interventions

o O2 delivered via face mask for several minutes prior to anaesthetic induction

▪ FRC (pt’s O2 reserve) is purged of nitrogen

▪ 90% of normal FRC of 2 L following preoxygenation is filled with O2

▪ Normal oxygen demad 200-250 ml/min; preoxygenated pt may have 5-8 min O2
reserve
 o Conditions increase O2 demand

▪ Sepsis, pregnancy,

o Conditions decrease FRC

▪ Morbid obesity

▪ Pregnancy

❖ BAG AND MASK VENTILATION (BMV)

o Usually first step in airway management in most situations; except with patients
undergoing rapid sequence induction (RSI)

▪ RSI avoid BMV to avoid stomach inflation and to reduce potential for aspiration
of gastric contents in nonfasted pts/ delayed gastric emptying

❖ SUPRAGLOTTIC AIRWAY DEVICES (SADs)

o Used with both spontaneously and ventilated pts during anaesthesia

o Conduits to aid in ET intubation when BMV and ET intubation have failed

o SADs consist of a tube that is connected to respiratory circuit or breathing bag, attached
to a hypopharyngeal device that seals and directs airflow to glottis, trachea and lungs

**LARYNGEAL MASK AIRWAY (LMA)

o Wide bore tube; proximal end connects to a breathing circuit w/ a standard 15mm connector
and distal end is atraumatic and attached to an elliptical cuff that can be inflated thru a
pilot tube

o Deflated cuff is lubricated and inserted blindly into hypopharynx, once inflated, cuff forms
low pressure seal around entrance of larynx

o Requires anaesthetic depth and relaxation greater than that of oral airway

o Ideal placement-cuff bordered superiorly by base of tongue, pyriform sinuses laterally and
inferiorly by upper oesophageal sphincter

o Protects airway from pharyngeal secretions but not gastric regurg

o Remains in place until pt regains airway reflexes; alternative ventilation thru face mask or
ETT
**ENDOTRACHEAL INTUBATION

o Employed both for general anaesthesia and to facilitate the ventilator management of the
critically ill

o Made from polyvinyl chloride

o Distal end is beveled and atraumatic to aid in visualization and insertion thru vocal cords; Murphy
tubes have a hole (Murphy eye) to decrease the risk of occlusion if the distal end was to obstruct
the trachea/carina

o Proximal end has 15mm connector and cuff inflating system (valve, pilot balloon, inflating tube
and cuff ; stylet is used to alter the shape and rigidity

o Valve prevents air loss after cuff inflation

o Pilot balloon provides indication of cuff inflation

o Inflating tube connects valve to the cuff and is incorporated into tube’s wall

o Cuff provides positive pressure ventilation and reduce likelihood of aspiration

 7P's of RSI:
1.PREPARATION (2
mnemonics your
preference)

*'SOAP ME'*
--Suction
--Oxygen (100% non
rebreather/ bag mask vent)
--Airways (laryngoscope &
blades, ETT, oral and nasal
--Pharmacology (IV set up &
meds drawn)
--Monitor
--Equipment

*SAMMM*
--Suction
--Airways
--Machine (connected,
functioning and pressures
ok)
--Monitors (available
connected and working)
--Medications (iv fluids and
kit ready, emergency meds
correct location and
accesssible)

2.PREOXYGENATION
(100% O2)
3.PREMEDICATE
4.PARALYSIS WITH
INDUCTION
5.PROTECTION AND
PASSAGE OF ETT (Sellick
manoeuvre)

*Sellick's Manoeuvre
RSI- simultaneous administration (Cricoid pressure) -
of a sedative and a technique applied during
neuromuscular blocking endotracheal intubation
(paralytic) agent to render a used to either prevent
patient rapidly unconscious and regurgitation or assist with
flaccid in order to facilitate visualization of the glottis by
emergent endotracheal a practitioner attempting
intubation and minimize risk of intubation
aspiration
6.PLACEMENT OF PROOF
INDICATIONS: 7.POST INTUBATION
>unable to protect airway MANAGEMENT
(GCS<8)
>airway trauma
>inadequate oxygenation with
spontaneous respiration (O2 sat
<90% with 100% O2 or rising
pCO2)
>profound shock
>patients at risk for regurgitation
 APPROACH TO BURN PATIENTS

I. ATLS GUIDELINES- ABCDE (AIRWAY, BREATHING, CIRCULATION,

DISABILITY, ENVIRONMENT)
II. SECURE THE AIRWAY IN ANY BURNS PATIENT DUE TO
SUSPECTED/EXPECTED LOSS OF AIRWAY . ALWAYS SUSPECT INHALATION
INJURY IN THESE PATIENTS.

REMEMBER RAPID SEQUENCE INDUCTION

7Ps -

Prepare -SOAPME- <Suction, Oxygenate, Airway, Pharm., Monitor,

Equipment

Suction
Oxygenate- 100% O2
Airway- ET tube (check cuff), BVM
Pharm.- IV meds drawn
Monitor- cardiac. pulse ox.
Equipment- laryngoscope, blades etc.

Pre-oxygenate- 100% O2 for 2-3 minutes

Pre medicate-lidocaine, opioids
Paralyse with induction- depolarising vs. nondepolarising agents
Protect & Pass tube- Sellick maneuver
Placement Proof- capnography, 5-point auscultation
Post intubation mangement

NOTE: In paralysing for tube placement remember that succ. should be avoided. This is due to
its ability to increase potassium concentration in the extracellular compartment by 0.5mEq, thus
can lead to arrhythmia and eventually death.

Instead of using succ. a non-depolarising agent such as cisatracrium can be used. Cisatracrium
is not associated with histamine release is an intermediately acting non-depolarizing agent
especially if the renal or hepatic status of the patient is unknown. Cisatracrium is eliminated vis
Hoffman elimination. Another non-depolarizing agent that can be mentioned is Rocuronium,
since its onset of action approaches that of succ. (90-120 s. However, its duration is 40-90
minutes (dose dependent) and if HYPERKALEMIA is suspected in the patient this would be the
drug of choice according to some texts given at a dose of 1mg/kg IV.
Along with the non-depolarizing agent a benzo. should be used. The most widely accepted
bento used in this case would be midiazalam, which is a short acting agent which causes
amnestic properties (0.1mg/kg IV).

Once the paralytic agents have been passed then the endotracheal tube should be passed
immediately following paralysis. The size of the endotracheal tube is :

males 8/9
females 7/8
paeds: (age/ 4+4)

III. FLUID MANGEMENT -

Once the airway is secured then fluid management should occur.

For an adult the TBSA of the burn should be calculated using the “RULE OF NINES” in order to
deliver
adequate
quantities of
fluid.
 head & neck (face NOT included)———9%
EACH upper limb—————————————9%
Torso (chest + abdomen) ———————ANTERIOR CHEST—————9%
ANTERIOR ABD——————-9%
POSTEROIR CHEST————-9%
POSTERIOR ABD——————9%
EACH lower limb——————————-9%
Perinum——————————————-1%
Hand———————————————-1%

The “RULE OF NINES” does not apply to children instead the following diagram is used to
calculated the TBSA % of the burn:

The most commonly used formulas for estimating fluid loss are the Parkland formula and the
Modified Brooke formula. The Parkland formula used the TBSA5
 Volume = TBSA% * 4mg/mL *kg

Parkland formula recommends 4mL of LACTATED RINGERS’s per kg for the first 24hours. The
first half administered during the first 8 hours post burn, and the rest is administered during the
subsequent 16 hours.

The modified Brooke formula is similar to the Parkland formula exceptt that the 2mL is used
instead of the 4ml. NO COLLOIDS ARE INFUSED WITHIN THE FIRST 24hrs.

Parkland Formula:
 Classical Fluid
Management
would include the
following:

IV. PAIN MANGEMENT

Criteria to admit the patient:

• >20% TBSA involved

• >20% TBSA (<10years old; >40 years old)
• >10% TBSA full thickness burns
• Burn involves eyes, ears, face, feet, perineum
• High voltage burns
• Brain injuries complicated by major trauma

LARGE BURNS —- IV OPOIDS——small doses of morphine (2-4mg) or fentanyl (0.05-0.1mg)

continuous infusion is preferred to the administration of a
bolus.

SMALL BURNS-ORAL OPIODS—-hydromorphine (4mg twice daily) or,

oxycodone (10mg twice daily or 20 mg/daily)
In addition an anxiolytic drug such as a bento can be added due to the psychological stress that
can be associated with the trauma and the burn. Preferred are miadiazolam or lorazepam along
with stomach mucosa-protecting agents such as Pepcid.

Lidocaine
Lidocaine (XYLOCAINE, others), an aminoethylamide, is the prototypical amide local
anesthetic.

MOA:

Local anesthetics act at the cell membrane to prevent the generation and the conduc- tion
of nerve impulses. Local anesthetics block conduction by decreasing or preventing the
+
large transient increase in the permeability of excitable membranes to Na that normally
is produced by a slight depolarization of the membrane. This action of local anesthetics is
+
due to their direct interaction with voltage-gated Na channels. As the anesthetic action
progressively develops in a nerve, the threshold for electrical excitability gradually
increases, the rate of rise of the action potential declines, impulse conduction slows, and
the safety factor for conduction decreases. These factors decrease the probability of
propagation of the action potential, and nerve conduction eventually fails.
+
Local anesthetics can bind to other membrane proteins. In particular, they can block K
+
channels. However, since the interaction of local anesthetics with K channels requires
higher concentrations of drug, blockade of conduction is not accompanied by any large or
consistent change in resting membrane potential.

NOTE: Lidocaine produces faster, more intense, longer-lasting, and more

extensive anesthesia than does an equal concentration of procaine. Lidocaine is an
alternative choice for individuals sensitive to ester-type local anesthetic.
When a local anesthetic is injected into tissues it established an equilibrium
between two forms- (BH+ and B) which depends on the local pH. In order for the
local anesthetic to move through the tissues and the nerve sheath it must be in its
uncharged, base form. Thus, the lower the pKa the higher the concentration the
base form and the faster the onset of action. Thus, in humanss injecting a LA into
an infected area with a low pH, the LA is ineffective because this cause the
dissociation of the LA into its charged form rendering it unable to penetrate the
nerve membrane
Undesired Effects of Local Anesthetics. In addition to blocking conduction in
nerve axons in the peripheral nervous system, local anesthetics interfere with the
function of all organs in which conduction or transmission of impulses occurs.
Thus, they have important effects on the CNS, the autonomic ganglia, the
neuromuscular junction, and all forms of muscle .The danger of such adverse
reactions is proportional to the concentration of local anesthetic achieved in the
circulation. In general, in local anesthetics with chiral centers, the S-enantiomer is
less toxic than the R-enantiomer.

• Central Nervous System. Following absorption, local anesthetics may

cause CNS stimulation, producing restlessness and tremor that may
progress to clonic convulsions. In general, the more potent the
anesthetic, the more readily convulsions may be produced. Alterations
of CNS activity are thus predictable from the local anesthetic agent in
question and the blood concentration achieved. Central stimulation is
followed by depression; death usually is caused by respiratory failure.
 i) Cardiovascular System. Following systemic absorption,
local anesthetics act on the cardiovascular system. The primary site of
action is the myocardium, where decreases in electrical excitability,
conduction rate, and force of contraction occur. In addition, most local
anesthetics cause arteriolar dilation. 571 Untoward cardiovascular
effects usually are seen only
after high systemic concentrations are attained and effects on the CNS
are produced. However, on rare occasions, lower doses of some local
anesthetics will cause cardiovascular collapse and death, probably due
to either an action on the pacemaker or the sudden onset of ventricular
fibrillation. Ventricular tachycardia and fibrillation are relatively
uncommon consequences of local anesthetics other than bupivacaine.
The effects of local anesthetics such as lidocaine and procainamide, is
used as antiarrhythmic drugs. Finally, it should be stressed that
untoward cardiovascular effects of local anesthetic agents may result
from their inadvertent intravascular administration, especially if
epinephrine also is present.

Smooth Muscle. Local anesthetics depress contractions in the intact

bowel and in strips of isolated intestine. They also relax vascular and
bronchial smooth muscle, although low concentrations initially may
produce contraction . Spinal and epidural anesthesia, as well as
instillation of local anesthetics into the peritoneal cavity, cause
sympathetic nervous system paralysis, which can result in increased tone
of GI musculature. Local anesthetics may increase the resting tone and
decrease the contractions of isolated human uterine muscle; however,
uterine contractions are seldom depressed directly during intrapartum
regional anesthesia.

Neuromuscular Junction and Ganglionic Synapse. Local

anesthetics also affect transmission at the neuromuscular junction.
Procaine, e.g., can block the response of skeletal muscle to maximal
motor-nerve volleys and to ACh at concentrations at which the muscle
responds normally to direct electrical stimulation. Similar effects occur at
autonomic ganglia. These effects are due to block of nicotinic ACh
receptors by high concentrations of the local anesthetic.

Hypersensitivity to Local Anesthetics. Rare individuals are hyper-

sensitive to local anesthetics. The reaction may manifest itself as an allergic
dermatitis or a typical asthmatic attack. It is important to distinguish
 allergic reactions from toxic side effects and from the effects of co-
administered vasoconstrictors. Hypersensitivity seems to occur more
frequently with local anesthetics of the ester type and frequently extends to
chemically related compounds. For example, individuals sensitive to
procaine also may react to structurally similar compounds (e.g., tetracaine)
through reaction to a common metabolite. Although allergic responses to
agents of the amide type are uncommon, solutions of such agents may
contain preservatives

Pharmacokinetics:

Lidocaine is absorbed rapidly after parenteral administration and from the GI and
respiratory tracts. Although it is effective when used without any vasoconstrictor,
epinephrine decreases the rate of absorption, such that the toxicity is decreased and
the duration of action usually is prolonged. In addition to preparations for
injection, lidocaine is formulated for topical, opthalmic, mucosal, and transdermal
use.
Lidocaine is dealkylated in the liver by CYPs to monoethylglycine xylidide and glycine
xylidide, which can be metabolized further to monoethylglycine and xylidide. Both
monoethylglycine xylidide and glycine xylidide retain local anesthetic activity. In
humans, ~75% of the xylidide is excreted in the urine as the further metabolite 4-
hydroxy-2, 6-dimethylaniline.
Toxicity. The side effects of lidocaine seen with increasing dose include drowsiness,
tinnitus, dysgeusia, dizziness, and twitching. As the dose increases, seizures, coma, and
respiratory depression and arrest will occur. Clinically significant cardiovascular
depression usually occurs at serum lidocaine levels that produce marked CNS effects.
The metabolites monoethylglycine xylidide and glycine xylidide may contribute to some
of these side effects.
Toxic dose of lidocaine:

• 3 mg/kg IV

• 5mg/kg when injected without epinephrine within the young margin

• 7mg/kg when injected with epinephrine into young margin

Clinical Uses. Lidocaine has a wide range of clinical uses as a local anesthetic; it has
utility in almost any application where a local anesthetic of intermediate duration is
needed. Lidocaine also is used as an antiarrhythmic agent .
 Thiopental vs. Propofol
Thiopental Propofol

The HER is equal to about 0.15, therefore slow Propofol has an HER ~1, which means it has a
extraction and responsible for residual anesthetic faster recovery from anesthesia
affects. (Not suitable for continuous infusion) *this
is the biggest difference

Thiopental is considered an anti-analgesic Propofol is not an anti-analgesic

Induction dose of thiopental causes hypotension to Induction dose of propofol causes a larger decline
a lesser degree in BP

Contraindicated in asthmatic patients, causing Not contraindicated in asthmatic patients

bronchospasm

Fall in cerebral metabolic rate for O2, which can Smaller fall in cerebral metabolic rate for O2
protect the brain from ischemic and hypoxic
attacks *used to induce Barbiturate coma

These were five concrete differences that I found between the two but I’m not sure what else to
really include.

Thiopental has a faster onset of action (30s) vs Proposal (< 1min)

*if you guys, know anymore differences feel free to make note of it