Transcript Rapid Sequence Intubation

Rapid Sequence Intubation
Anthony G. Hillier, D.O.
EM Resident
St. John West Shore
Rapid Sequence Intubation
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The induction of a state of unconsciousness
with complete neuromuscular paralysis to
achieve intubation without interposed
mechanical ventilation in efforts to facilitate
the procedure and minimize risks of gastric
aspiration
Rapid Sequence Intubation
Indications
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Failure of airway maintenance/protection
- lost or diminished gag reflex
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Failure of oxygenation/ventilation
- pulmonary edema, COPD
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Anticipated clinical course
- multiple trauma, head injured
- intoxication, air transport
Rapid Sequence Intubation
“6 P’s”
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Preparation: T-10”
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Positioning
Preoxygenation: T-5”
Premedication: T-3”
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Paralysis:T-0
Placement of tube: T+45
Post management: T+2”
Preparation
Preparation
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Evaluate
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LEMON
Equipment Check
Positioning
Drug Selection
IV’s, monitor, oximetry
Ancillary Staff
Anticipate alternative airway maneuver
Preparation
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LEMON
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L-look
E-evaluate the 3-3-2 rule
M-Mallampati
O-Obstruction
N-Neck mobility
PREOXYGENATION
Preoxygenation
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100% O2 for 5 minutes of 5 vital capacity
breaths can theoretically permit 3-5 minutes
of apnea before desaturation to less than
90% occurs
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© 2005 Elsevier
Preoxygenation
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“nitrogen wash-out”
Avoid bagging the patient if adequately
preoxygenated
PREMEDICATION
Premedication
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Goal is to blunt the patient’s physiologic
responses to intubation
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Minimizes bradycardia, hypoxemia,
cough/gag reflex, increases in intracranial,
intraocular, and intragastric pressures
Premedication
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Lidocaine
Opioid
Atropine
Defasciculating doses “priming”
Lidocaine
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Thought to blunt the rise in intracranial
pressure associated with airway
manipulation and the use of depolarizing
neuromuscular blocking agents
1.5-3.0 mg/kg (average 100mg) three
minutes prior to intubation
Atropine
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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
Defasciculating doses
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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
Sedation
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Sedative agents administered at doses
capable of producing unconsciousness with
little or no cardiovascular effects
No ideal agent exists
Sedation should nearly always be used when
paralyzing the patient
Sedation
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Barbiturates/hypnotics
Non-barbiturate
Neuroleptics
Opiates
Benzodiazepines
Barbiturates/Hypnotics
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Thiopental (Pentothal), Methohexital (Brevital)
Short onset (10-20) seconds, duration 5-10
minutes
May reduce intracranial pressure, cerebroprotective
Histamine release, hypotension, bronchospasm
Barbiturates/Hypnotics
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Etomidate (Amidate) a nonbarbiturate
hypnotic
Decreases ICP/IOP
Rapid onset, short duration
Minimal hemodynamic effects
No histamine release
Increases seizure threshold
Etomidate
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No malignant hyperthermia reported
Watch for myoclonus, vomiting
May decrease cortisol synthesis (adrenal
insufficiency)
Dose 0.3 mg/kg IV
Propofol
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Propofol (Diprivan), sedative hypnotic
Extremely rapid onset (10 sec), duration of
10-15 minutes
Decreases ICP
Can cause profound hypotension
Dose 1-3 mg/kg IV for induction
Dose: 100-200 mcg/kg/min for maintenance
Ketamine
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Ketamine-dissociative anesthetic
Rapid onset, short duration
Potent bronchodilator, useful in asthmatics
Increases ICP, IOP, IGP
Contraindicated in head injuries
Increases bronchial secretions
Ketamine
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“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
Opiates
Fentanyl
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Fentanyl
Broad dose-response relationship
Can be reversed with naloxone
Fentanyl is rapid acting (<1 min), duration of
30 min
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Does not release histamine
Fentanyl
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May decrease tachycardia and hypertension
associated with intubation
Seizures and chest wall rigidity have been
reported
Dose: 2-10 mcg/kg IV
Morphine Sulfate
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Longer onset (3-5) minutes and duration (46) hours
May not blunt the rise in ICP, hypertension
and tachycardia as well as fentanyl
Dose 0.1-0.2 mg/kg IV
Histamine release
Benzodiazepines
Benzodiazepines
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Midazolam, Diazepam, Lorazepam
Provide excellent amnesia and sedation
Broad dose-response relationship
Reversed with Flumazenil (Romazicon)
Doses required are higher for RSI than for
general sedation
Midazolam
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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
Diazepam and Lorazepam
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Moderate/long acting agents
Longer onset time than midazolam
May be more beneficial post-intubation for
sedation
Paralysis
Neuromuscular Blocking Agents
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Chemical paralysis facilitates intubation by
allowing visualization of the vocal cords and
optimizing intubating condition
Only CONTRAINDICATION is anticipated
difficult airway
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Mallampati Class
Thyromental Distance
Depolarizing Agents
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Exert their affect by binding with
acetylcholine receptors at the neuromuscular
junction, causing sustained depolarization of
the muscle cell
Nondepolarizing
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Bind to acetylcholine receptors in a
competitive, non-stimulatory manner, no
receptor depolarization
Histamine release
Agents can be reversed with edrophonium or
neostigmine
Caution with myasthenia gravis
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Depolarizing agents
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Succinylcholine (Anectine)
Nondepolarizing Agents
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Pancuronium (Pavulon)
Vecuronium (Norcuron)
Atracurium (Tracrium)
Rocuronium (Zemuron)
Mivacurium (Mivacron)
Succinylcholine
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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
Succinylcholine cont
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Prolonged paralysis seen with:
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Pregnancy
Liver disease
Malignancies
Cytotoxic drugs
Certain antibiotics
Cholinesterase inhibitors
Organophosphate poisoning
Succinylcholine
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Adverse reactions
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Muscle fasiculations
Hyperkalemia
Bradycardia
Prolonged neuromuscular blockade
Trismus
Malignant hyperthermia
Depolarizing Agents
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Muscle fasiculations
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Thought to increase ICP/IOP/IGP
Causes muscle pain
Minimized by “priming” dose of NMB
Hyperkalemia
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Average increase in potassium of 0.5-1 mEq/L
Burns, crush injuries, spinal cord injuries,
neuromuscular disorders, chronic renal failure
Depolarizing agents
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Bradycardia
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Most common in children <10 years due to higher
vagal tone
Also with repeated doses of succinylcholine
Premedicate with atropine
Depolarizing Agents
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Malignant hyperthermia
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From excessive calcium influx through open
channels
Genetic predisposition
Rapid temperature, rhabdomyolysis, muscle
rigidity, DIC
60% mortality
Treatment: IV Dantrolene
Depolarizing Agents
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Trismus (Masseter spasm)
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Usually in children
Unknown cause
Treat with a nondepolarizing NMB
Pancuronium
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Long-acting agent (45-90 min)
Slow onset (1-5 min)
Renal excretion
Vagolytic tachyarrythmias common
Dose: 0.10-0.15 mg/kg IV
Vecuronium
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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
Rocuronium
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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
Placement of Endotracheal Tube
Placement of Tube
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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
Post Intubation
Post Intubation Management
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Secure tube
Continuous pulse oximetry
Reassess vital signs frequently
Obtain chest x-ray, ABG
Restrain patient
Consider long term sedation
Questions??
Thank You!