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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 to achieve intubation without interposed mechanical ventilation in efforts to facilitate the procedure and minimize risks of gastric aspiration
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Rapid Sequence Intubation Indications 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 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”
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Preparation
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Evaluate – LEMON Equipment Check Positioning Drug Selection IV’s, 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 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
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PREMEDICATION
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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
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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 airway manipulation 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 with little 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 5-10 minutes 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 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
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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 Broad dose-response relationship Can be reversed with naloxone Fentanyl is rapid acting (<1 min), duration of 30 min – Does not release histamine
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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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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
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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
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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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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
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Depolarizing Agents Exert their affect by binding with acetylcholine receptors at the neuromuscular junction, causing sustained depolarization of the muscle cell
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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
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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 <10 years due to higher vagal tone – Also with repeated doses of succinylcholine – Premedicate with atropine
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Depolarizing Agents Malignant hyperthermia – From excessive calcium influx through open channels – 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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Post Intubation Management Secure tube Continuous pulse oximetry Reassess vital signs frequently Obtain chest x-ray, ABG Restrain patient Consider long term sedation
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Questions?? Thank You!
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