rapid sequence in tub at ion
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Rapid Sequence Intubation
Anthony G. Hillier, D.O.
EM Resident
St. John West Shore
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Rapid Sequence Intubation
The induction of a state of unconsciousness
with complete neuromuscular paralysis toachieve intubation without interposed
mechanical ventilation in efforts to facilitate
the procedure and minimize risks of gastric
aspiration
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Rapid Sequence IntubationIndications
Failure of airway maintenance/protection
- lost or diminished gag reflex
Failure of oxygenation/ventilation
- pulmonary edema, COPD
Anticipated clinical course
- multiple trauma, head injured
- intoxication, air transport
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Rapid Sequence Intubation6 Ps
Preparation: T-10 Positioning
Preoxygenation: T-5
Premedication:T
-3
Paralysis:T-0
Placement of tube: T+45
Post management: T+2
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Preparation
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Preparation
Evaluate
LEMON
Equipment Check
Positioning
Drug Selection IVs, monitor, oximetry
Ancillary Staff
Anticipate alternative airway maneuver
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Preparation
LEMON
L-look E-evaluate the 3-3-2 rule
M-Mallampati
O-Obstruction
N-Neck mobility
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PREOXYGENATION
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Preoxygenation
100% O2 for 5 minutes of 5 vital capacity
breaths can theoretically permit 3-5 minutesof apnea before desaturation to less than
90% occurs
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Downloaded from: Rosen's Emergency Medicine (on 6 August 2006 02:03 PM)
2005 Elsevier
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Preoxygenation
nitrogen wash-out
Avoid bagging the patient if adequatelypreoxygenated
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PREMEDICATION
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Premedication
Goal is to blunt the patients physiologic
responses to intubation
Minimizes bradycardia, hypoxemia,
cough/gag reflex, increases in intracranial,
intraocular, and intragastric pressures
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Premedication
Lidocaine
Opioid Atropine
Defasciculating doses priming
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Lidocaine
Thought to blunt the rise in intracranial
pressure associated with airwaymanipulation and the use of depolarizing
neuromuscular blocking agents
1.5-3.0 mg/kg (average 100mg) three
minutes prior to intubation
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Atropine
0.02 mg/kg, minimum 0.1 mg IV, max 1 mg,
three minutes prior to intubation Can minimize vagal effects, bradycardia and
secretions
Infants and children < 8 years may develop
profound bradycardia during intubation
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Defasciculating doses
Decreases muscle fasiculations caused by
the depolarizing agents (succinylcholine) Attenuates rise in intracranial pressure
Agents used are the non-depolarizing
blocking agents (vecuronium, pancuronium
etc.) usually 1/10 of standard dose
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Sedation
Sedative agents administered at doses
capable of producing unconsciousness withlittle or no cardiovascular effects
No ideal agent exists
Sedation should nearly always be used when
paralyzing the patient
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Sedation
Barbiturates/hypnotics
Non-barbiturate Neuroleptics
Opiates
Benzodiazepines
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Barbiturates/Hypnotics
Thiopental (Pentothal), Methohexital (Brevital)
Short onset (10-20) seconds, duration 5-10minutes
May reduce intracranial pressure, cerebro-
protective
Histamine release, hypotension, bronchospasm
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Barbiturates/Hypnotics
Etomidate (Amidate) a nonbarbiturate
hypnotic Decreases ICP/IOP
Rapid onset, short duration
Minimal hemodynamic effects
No histamine release
Increases seizure threshold
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Etomidate
No malignant hyperthermia reported
Watch for myoclonus, vomiting May decrease cortisol synthesis (adrenal
insufficiency)
Dose 0.3 mg/kg IV
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Propofol
Propofol (Diprivan), sedative hypnotic
Extremely rapid onset (10 sec), duration of10-15 minutes
Decreases ICP
Can cause profound hypotension
Dose 1-3 mg/kg IV for induction
Dose: 100-200 mcg/kg/min for maintenance
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Ketamine
Ketamine-dissociative anesthetic
Rapid onset, short duration Potent bronchodilator, useful in asthmatics
Increases ICP, IOP, IGP
Contraindicated in head injuries Increases bronchial secretions
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Ketamine
Emergence phenomenon can occur though
rarely in children less than 10 years Emergence reactions occur in up to 50% of
adults
Dose: 1-2 mg/kg
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Opiates
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Fentanyl
Fentanyl
Broad dose-response relationship Can be reversed with naloxone
Fentanyl is rapid acting (
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Fentanyl
May decrease tachycardia and hypertension
associated with intubation Seizures and chest wall rigidity have been
reported
Dose: 2-10 mcg/kg IV
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Benzodiazepines
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Benzodiazepines
Midazolam, Diazepam, Lorazepam
Provide excellent amnesia and sedation Broad dose-response relationship
Reversed with Flumazenil (Romazicon)
Doses required are higher for RSI than forgeneral sedation
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Midazolam
Slower onset (3-5) min than the
barbiturate/hypnotic agents Considered short-acting (30-60 min)
Does not increase ICP
Causes respiratory and cardiovascular
depression
Dose: 0.1-0.4mg/kg IV
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Diazepam and Lorazepam
Moderate/long acting agents
Longer onset time than midazolam May be more beneficial post-intubation for
sedation
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Paralysis
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NeuromuscularBlocking Agents
Chemical paralysis facilitates intubation by
allowing visualization of the vocal cords andoptimizing intubating condition
Only CONTRAINDICATION is anticipated
difficult airway
Mallampati Class
Thyromental Distance
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Depolarizing Agents
Exert their affect by binding with
acetylcholine receptors at the neuromuscularjunction, causing sustained depolarization of
the muscle cell
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Nondepolarizing
Bind to acetylcholine receptors in a
competitive, non-stimulatory manner, noreceptor depolarization
Histamine release
Agents can be reversed with edrophonium or
neostigmine
Caution with myasthenia gravis
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Depolarizing agents
Succinylcholine (Anectine) Nondepolarizing Agents
Pancuronium (Pavulon)
Vecuronium (Norcuron)
Atracurium (Tracrium)
Rocuronium (Zemuron)
Mivacurium (Mivacron)
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Succinylcholine
Stimulates nicotinic/muscarinic cholinergic
receptors Gold standard for 50 years
Onset 45 seconds, duration 8-10 minutes
Dose: (adults 1.5 mg/kg IV)
Children 2.0 mg/kg IV
Inactivated by pseudocholinesterase
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Succinylcholine cont
Prolonged paralysis seen with:
Pregnancy Liver disease
Malignancies
Cytotoxic drugs
Certain antibiotics Cholinesterase inhibitors
Organophosphate poisoning
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Succinylcholine
Adverse reactions
Muscle fasiculations Hyperkalemia
Bradycardia
Prolonged neuromuscular blockade
Trismus Malignant hyperthermia
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Depolarizing Agents
Muscle fasiculations
Thought to increase ICP/IOP/IGP Causes muscle pain
Minimized by priming dose of NMB
Hyperkalemia
Average increase in potassium of 0.5-1 mEq/L
Burns, crush injuries, spinal cord injuries,
neuromuscular disorders, chronic renal failure
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Depolarizing agents
Bradycardia
Most common in children
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Depolarizing Agents
Malignant hyperthermia
From excessive calcium influx through openchannels
Genetic predisposition
Rapid temperature, rhabdomyolysis, muscle
rigidity, DIC 60% mortality
Treatment: IV Dantrolene
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Depolarizing Agents
Trismus (Masseter spasm)
Usually in children Unknown cause
Treat with a nondepolarizing NMB
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Pancuronium
Long-acting agent (45-90 min)
Slow onset (1-5 min) Renal excretion
Vagolytic tachyarrythmias common
Dose: 0.10-0.15 mg/kg IV
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Vecuronium
Duration of 30-60 min
Onset of 1-4 min Hypotension may occur from loss of venous
return and sympathetic blockade
Mostly biliary excretion
Dose 0.1 mg/kg
priming dose 0.01 mg/kg
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Rocuronium
Has the shortest onset of the
nondepolarizing agents (1-3 min) Duration 30-45 min
Tachycardia can occur
Dose: 0.6-1.2 mg/kg
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Placement of Endotracheal Tube
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Placement of Tube
Allow medications to work and assure complete
neuromuscular blockade of the patient
Maintain Sellick maneuver until cuff inflated
Ventilate with bag-valve mask if unsuccessful
Additional doses of sedatives/NMB may be
necessary
Confirm tube placement
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Post Intubation
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Questions??
Thank You!
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