rapid sequence in tub at ion

8/6/2019 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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