Airway Supremacy: Principles of RSI Twitter, Instagram: @emboardbombs
Check out our podcasts and other cool study guides at www.emboardbombs.com
Author: Blake Briggs, MD
RSI: Quick administration of sedative and paralytic to achieve fast endotracheal intubation.
Why do we do it? One or more of the following:
1) patient’s inability to ventilate (hypercapnic respiratory failure)
2) inability to oxygenate (hypoxic respiratory failure)
3) inability to protect their own airway
4) for optimal control of the patient (i.e. to deliver care in which the patient would not tolerate or be uncooperative)
Goal: The point is to maximize chances of success on first attempt. In RSI we must assume the stomach has contents and therefore time
must be minimized till endotracheal intubation due to risks of respiratory failure and loss of airway protection, as well as aspiration
from prolonged BVM. Risks of aspiration, hypotension, esophageal intubation increase with number of attempts (also 15% à50%
increase in adverse events!).
Contraindications: all relative. Most important CI is difficult airway anticipation, of which rescue oxygenation is considered to be
impossible or hard to achieve.
If an anatomically difficult airway is anticipated, potential for rapid desaturation, or severe hemodynamic compromise, awake
intubation might be needed.
-Pros of awake intubation: avoids hemodynamic collapse, patient maintains spontaneous ventilation
-Cons: takes time, secretion control
When to delay RSI: There are key differences between “emergent” and “urgent” RSI. ABC’s is never 100% the correct order.
Sometimes it needs to be BAC or CAB. Some examples:
• Patient is apneic and unresponsive. This patient needs a definitive airway immediately = ABC
• Patient is in V tach and unresponsive. Still breathing spontaneously = CAB
• Patient is not responding and has no breath sounds on right side and is hypotensive = BAC
• Patient is in shock with BP 90/50 systolic = CAB
Steps to successful RSI- 6P’s of RSI: Prepare, Preoxygenate, Positioning, Paralysis, Proof of placement, Post-intubation
management
-Preparation: large bore wall suction, O2, tube, back-up plan x3, 2
large bore IVs
-Preoxygenate: high flow rate for minimum of 3 minutes. Replaces
mixed gases in the base of lung with oxygen-rich gas for optimal FRC
reservoir. 70 kg adult can maintain O2 saturation >90% for 8 minutes
during apnea. Children = 4 minutes. Obesity = 3 minutes. Use bag
mask for oxygen administration but no need to squeeze bag if patient
is cooperative and has adequate spontaneous ventilation. Maintain
nasal cannula flow during apneic period. For the very sick:
-if not able to spontaneously ventilate: positive pressure ventilation
with BVM and oxygen flow at max (15 L). Try to synchronize with patient’s respiratory MOANS Mnemonic for predicting difficult BVM
cycle. Do not ventilate >20 cm H2O due to risk of gastric insufflation. Mask Seal: any beards, coarse facial features,
blood present
-if not cooperative, NRB is used with flush oxygen. Obesity
Age >55
Positioning: sniffing position with alignment of vertical axes. Jaw thrust forward and No teeth: leave dentures in but take them out
immediately prior to intubating
upward, patient’s head more anterior with slight upward extension. Sleep apnea
-Pre-intubation optimization: recognize and address obvious or potential pathologies
and problems before RSI. Most common issue is hypotension. Causes are multifactorial LEMON assessing difficult intubation
and include pre-intubation drugs, bleeding, dehydration, patient’s clinical condition Look externally
Evaluate for 3-3-2 rule
(e.g. shock). Must consider giving IV fluids and/or vasopressors if significant concern. -Incisor distance <3 fingerbreadths
-Hyoid/mental distance <3 fingerbreadths
-Paralysis with induction: in the ideal situation, 2 drugs are needed for RSI: a sedative -Thyroid-to-mouth distance <2 fingerbreadths
and a paralytic. Both are virtually given within 1 minute apart, with the sedative given Mallampati Score >3
first. All the induction agents below work as allosteric agonists of the GABA pathway Obstruction: any blockage of airway- recent neck
surgery, tumor, prior radiation/chemo, epiglottitis
in the brain. Ketamine is the exception and is primarily an NMDA antagonist.
Neck Mobility: presence of C-collar, history of neck
surgery/fusion, short neck.
Airway Supremacy: Principles of RSI Twitter, Instagram: @emboardbombs
Sedative Onset Benefits Adverse effects Dose
Etomidate <30 seconds Least likely to cause hypotension. Been documented to suppress adrenal cortisol 0.3 mg/kg
production.* Can cause myoclonus (not significant but
mistaken as seizure).
Ketamine <1 minute; Catecholaminergic stimulation leading to Very small, but scary, risk of laryngospasm (<0.4%), can 1-2
lasts for 20 increased cerebral blood flow, MAP, cause paradoxical hypotension in those in shock mg/kg
minutes cardiac output, and bronchodilation. ("catechol-depleted"). Avoid in those with high MAP
Analgesic! and ICP elevation.
Hypersalivation- no need to tx.
Hallucinations- 2% clinically significant. Occurs <10% in
kids, 20% in adults.
Should not be used in <3m/o.
Propofol <30 seconds Bronchodilation, great for those with Dose-related hypotension 1.5-2
seizures/ epilepsy. Anticonvulsant effects mg/kg
Midazolam <1 minute Benzo effects- anxiolytic and amnesic Dose-related hypotension and myocardial depression. 0.3 mg/kg
properties. Can be used in seizures/ Not typically used anymore unless above options not
epilepsy. Anticonvulsant. available.
*This risk of adrenal suppression is due to etomidate inhibition of 11-B-hydroxylase, but this should NOT stop its usage during sepsis if patient has
significant hypotension precluding the use of other hypotensive-producing induction agents. If worsening hypotension that is refractory to vasopressors and
fluids develops after etomidate usage in the first 24 hours, give glucocorticoids.
Paralytic- none provide any anesthesia or sedation. Neither of the below medications have any difference in clinical outcomes with
regards to successful intubation. The only important differences are related to adverse effects and time of onset/offset.
Paralytic Onset/Offset Benefit Contraindications Dose Antidote
Succinylcholine <1 minute; Rapid onset and Malignant Hyperthermia*. 1.5 mg/kg (better No direct antidote
offset in 10 offset. Hyperkalemia (raises K by about to overestimate!)
Blocks Ach in minutes May be used in 0.5, so this is only a problem in Dantrolene if
skeletal muscle Myasthenia Gravis those already hyperkalemic). (2-2.5 mg/kg for Malignant
cells by binding to (MG) except an Rhabdomyolysis, stroke >72 hours MG) Hyperthermia is
and turning on Ach increased dose is old, burn >72 hours old, muscular suspected
receptors on post- needed. dystrophy, ESRD with unknown If IM is only
synaptic cleft. last dialysis session.** option: 4 mg/kg
So, it depolarizes (combine with
them but does not Trismus occurs in <0.1%. If present, Ketamine 4 mg)
allow for give rocuronium. Trismus might be "Hit ‘em with
repolarization a sign of MH. 4/4"
Bradycardia is not uncommon. If
severe it responds well with
atropine.
Rocuronium 1 min/offset in Less side effects No absolute contraindications 1 mg/kg Sugammadex- binds
~45 min than Relative contraindications include (0.6 mg/kg for and reverses agent.
Reversible Succinylcholine. possibility of difficult airway MG) -associated with
competitive May be used in arrhythmias
inhibitor of the Myasthenia Gravis
Ach receptor but at a lower dose Neostigmine- works as
an acetylcholine-sterase
inhibitor
*Succinylcholine is absolutely contraindicated in patients with a personal or family history of malignant hyperthermia.
**Think of the stroke, burn, and rhabdomyolysis risks lumped together as "prolonged downtime", meaning we do not know how long
the patient was unconsciousness or if a stroke occurred. Also, the longer they are down, the more risk of cell death and hyperkalemia.
-Placement with proof: There are many steps to ensure adequate tube placement- 1) direct glottis visualization with ETT passing
through, 2) ETCO2 via monitor and color change on color-change capnographer. The CXR and listening for breath sounds as well as
gastric insufflation is NOT reliable alone but should be done after color change capnography. BELIEVE the End-Tidal! It is more
reliable and faster to respond to changes than Pulse Ox (this lags behind by several seconds up to 1 minute in some cases).
-Postintubation management: 1) secure the tube, 2) CXR to confirm tube positioning, 3) address any lingering preintubation problems
(hypotension, shock, etc), 4) optimize the patient’s respiratory status via ventilator settings, 5) address sedation/analgesia as needed.
What if hypotension does not improve after initial recovery from apnea? Think about pneumothorax, tracheal tube cuff rupture, mucus
plugging, esophageal intubation.
References
1. Li J, Murphy-Lavoie H, Bugas C, et al. Complications of emergency intubation with and without paralysis. Am J Emerg Med 1999; 17:141.
2. Cicala R, Westbrook L. An alternative method of paralysis for rapid-sequence induction. Anesthesiology 1988; 69:983.
3. Bozeman WP, Kleiner DM, Huggett V. A comparison of rapid-sequence intubation and etomidate-only intubation in the prehospital air medical setting. Prehosp Emerg Care 2006; 10:8.
4. Lundstrøm LH, Duez CH, Nørskov AK, et al. Avoidance versus use of neuromuscular blocking agents for improving conditions during tracheal intubation or direct laryngoscopy in adults and adolescents. Cochrane Database Syst Rev
2017; 5:CD009237.
5. Topulos GP, Lansing RW, Banzett RB. The experience of complete neuromuscular blockade in awake humans. J Clin Anesth 1993; 5:369.
6. Naguib M, Samarkandi AH, El-Din ME, et al. The dose of succinylcholine required for excellent endotracheal intubating conditions. Anesth Analg 2006; 102:151.
7. Lemmens HJ, Brodsky JB. The dose of succinylcholine in morbid obesity. Anesth Analg 2006; 102:438.
Airway Supremacy: Principles of RSI Twitter, Instagram: @emboardbombs
8. Levitan R. Safety of succinylcholine in myasthenia gravis. Ann Emerg Med 2005; 45:225.
9. Gronert GA. Cardiac arrest after succinylcholine: mortality greater with rhabdomyolysis than receptor upregulation. Anesthesiology 2001; 94:523.
10. Martyn JA, Richtsfeld M. Succinylcholine-induced hyperkalemia in acquired pathologic states: etiologic factors and molecular mechanisms. Anesthesiology 2006; 104:158.
11. Magee DA, Gallagher EG. "Self-taming" of suxamethonium and serum potassium concentration. Br J Anaesth 1984; 56:977.
12. Carroll JB. Increased incidence of masseter spasm in children with strabismus anesthetized with halothane and succinylcholine. Anesthesiology 1987; 67:559.
13. Sims C. Masseter spasm after suxamethonium in children. Br J Hosp Med 1992; 47:139.
14. Perry JJ, Lee J, Wells G. Are intubation conditions using rocuronium equivalent to those using succinylcholine? Acad Emerg Med 2002; 9:813.
15. Nava-Ocampo AA, Velázquez-Armenta Y, Moyao-García D, Salmerón J. Meta-analysis of the differences in the time to onset of action between rocuronium and vecuronium. Clin Exp Pharmacol Physiol 2006; 33:125.
16. Blichfeldt-Lauridsen L, Hansen BD. Anesthesia and myasthenia gravis. Acta Anaesthesiol Scand 2012; 56:17.