Post on 22-Oct-2015
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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
Evaluate– LEMON
Equipment Check Positioning Drug Selection IV’s, monitor, oximetry Ancillary Staff Anticipate alternative airway maneuver
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
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
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
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
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
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
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 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 Management
Secure tube Continuous pulse oximetry Reassess vital signs frequently Obtain chest x-ray, ABG Restrain patient Consider long term sedation