Rapid Sequence Intubation

Anthony G. Hillier, D.O.

EM Resident

St. John West Shore

Rapid Sequence Intubation

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 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

Rapid Sequence Intubation“6 P’s”

Preparation: T-10”– Positioning

Preoxygenation: T-5” Premedication: T-3”

Paralysis:T-0 Placement of tube: T+45 Post management: T+2”

Preparation

Preparation

Evaluate– LEMON

Equipment Check Positioning Drug Selection IV’s, monitor, oximetry Ancillary Staff Anticipate alternative airway maneuver

Preparation

LEMON– L-look– E-evaluate the 3-3-2 rule– M-Mallampati– O-Obstruction– N-Neck mobility

PREOXYGENATION

Preoxygenation

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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Preoxygenation

“nitrogen wash-out” Avoid bagging the patient if adequately

preoxygenated

PREMEDICATION

Premedication

Goal is to blunt the patient’s physiologic responses to intubation

Minimizes bradycardia, hypoxemia, cough/gag reflex, increases in intracranial, intraocular, and intragastric pressures

Premedication

Lidocaine Opioid Atropine Defasciculating doses “priming”

Lidocaine

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

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

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

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

Barbiturates/hypnotics Non-barbiturate Neuroleptics Opiates Benzodiazepines

Barbiturates/Hypnotics

Thiopental (Pentothal), Methohexital (Brevital) Short onset (10-20) seconds, duration 5-10

minutes May reduce intracranial pressure, cerebro-

protective Histamine release, hypotension, bronchospasm

Barbiturates/Hypnotics

Etomidate (Amidate) a nonbarbiturate hypnotic

Decreases ICP/IOP Rapid onset, short duration Minimal hemodynamic effects No histamine release Increases seizure threshold

Etomidate

No malignant hyperthermia reported Watch for myoclonus, vomiting May decrease cortisol synthesis (adrenal

insufficiency) Dose 0.3 mg/kg IV

Propofol

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

Ketamine-dissociative anesthetic Rapid onset, short duration Potent bronchodilator, useful in asthmatics Increases ICP, IOP, IGP Contraindicated in head injuries Increases bronchial secretions

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

Opiates

Fentanyl

Fentanyl Broad dose-response relationship Can be reversed with naloxone Fentanyl is rapid acting (<1 min), duration of

30 min– Does not release histamine

Fentanyl

May decrease tachycardia and hypertension associated with intubation

Seizures and chest wall rigidity have been reported

Dose: 2-10 mcg/kg IV

Morphine Sulfate

Longer onset (3-5) minutes and duration (4-6) 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

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

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

Moderate/long acting agents Longer onset time than midazolam May be more beneficial post-intubation for

sedation

Paralysis

Neuromuscular Blocking Agents

Chemical paralysis facilitates intubation by allowing visualization of the vocal cords and optimizing intubating condition

Only CONTRAINDICATION is anticipated difficult airway– Mallampati Class– Thyromental Distance

Depolarizing Agents

Exert their affect by binding with acetylcholine receptors at the neuromuscular junction, causing sustained depolarization of the muscle cell

Nondepolarizing

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

Depolarizing agents– Succinylcholine (Anectine)

Nondepolarizing Agents– Pancuronium (Pavulon)– Vecuronium (Norcuron)– Atracurium (Tracrium)– Rocuronium (Zemuron)– Mivacurium (Mivacron)

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

Succinylcholine cont

Prolonged paralysis seen with:– Pregnancy– Liver disease– Malignancies– Cytotoxic drugs– Certain antibiotics– Cholinesterase inhibitors– Organophosphate poisoning

Succinylcholine

Adverse reactions– Muscle fasiculations– Hyperkalemia– Bradycardia– Prolonged neuromuscular blockade– Trismus– Malignant hyperthermia

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

Depolarizing agents

Bradycardia– Most common in children <10 years due to higher

vagal tone– Also with repeated doses of succinylcholine– Premedicate with atropine

Depolarizing Agents

Malignant hyperthermia– From excessive calcium influx through open

channels– Genetic predisposition– Rapid temperature, rhabdomyolysis, muscle

rigidity, DIC– 60% mortality– Treatment: IV Dantrolene

Depolarizing Agents

Trismus (Masseter spasm)– Usually in children– Unknown cause– Treat with a nondepolarizing NMB

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

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

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

Placement of Endotracheal Tube

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

Post Intubation

Post Intubation Management

Secure tube Continuous pulse oximetry Reassess vital signs frequently Obtain chest x-ray, ABG Restrain patient Consider long term sedation

Questions??

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