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Rapid Sequence Induction and Intubation (RSII): Clinical Approach

Rapid Sequence Induction and Intubation (RSII): Clinical Approach Authors: Sandy Ly Reviewers: Wendy Yao Melinda Davis* * MD at time of publication Reversible with Sugammadex (selective relaxant binding agent) Responds to acetylcholinesterase Reversible with acetylcholinesterase inhibitors Not immediately reversible due to high dose Classical RSII Modified RSII Induction Agent e.g. Ketamine or Propofol (2 mg/kg) Inhibitory effect on central nervous system Cricoid pressure (10 lbs pressure posteriorly) Esophagus at the level of the cricoid obstructed Reduced gastric regurgitation Succinylcholine (2 mg/kg) acts similar to Ach Depolarize end plate nicotinic receptors in skeletal muscle Non-competitive with no antagonist Rapid skeletal muscle paralysis (<30 seconds) with short duration (<10 minutes) Irreversible Preoxygenation with 100% O2 displaces nitrogen. Functional residual capacity (2.5L) is filled with O2 Oxygen consumption (250 mL/min) Extend time to desaturation (Ideal condition: 10 minutes) Gastric distension with use of bag valve mask ventilation (positive pressure) High dose Rocuronium (1 mg/kg) competitively antagonizes Ach Decreased Ach binding on nicotinic receptors in skeletal muscle Rapid skeletal muscle paralysis (<60 seconds) with long duration (>45 minutes) Quick Facts Induction of anesthesia Abbreviations Ach – acetylcholine See other pathways for more detailed pathophysiology • • • RSII is used in patients with increased risk of gastric aspiration. Cricoid pressure is NOT THE SAME as BURP (backward, upward, rightward pressure). Other induction agents possible (e.g. etomidate). Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published September 22, 2019 on www.thecalgaryguide.com

etomidate

Etomidate Ultrashort-acting carboxylated imidazole anesthetic administered intravenously to induce unconsciousness, usual dose 0.3 mg/kg IV Directly inhibits adrenal 11-beta- hydroxylase (enzyme responsible for cortisol biosynthesis) ↓ Adrenal cortisol production ↓ Serum cortisol available for stress response Transient adrenal steroid insufficiency ↑ Morbidity & mortality in trauma/critically ill patients (Contraindicated in sepsis) Inhibits nitric oxide signaling Transient cerebral vasoconstriction ↓ Cerebral blood flow ↓ Oxygen delivery to brain ↓ Cerebral metabolic rate Suppression of electrical activity in brain Flat electroencephalogram Binds to GABAA (inhibitory CNS neurotransmitter) receptor Authors: Cindy Chang Ran (Marissa) Zhang Reviewers: Melissa King Brooke Fallis Julia Haber* * MD at time of publication Abbreviations: • CNS - Central Nervous System • GABAA- Gamma- aminobutyric acid type A • TRPA1- Transient receptor potential type A1 Higher selectivity for specific GABAA receptor subtypes compared to other induction agents Positively modulates GABAA receptor (GABAA receptor activated at lower concentrations of GABA ) ↓ Cerebral blood volume Activation of fewer GABAA receptor subtypes in neurons and cardiovascular structures compared to other induction agents ↓ Intracranial pressure ↑ Hemodynamic stability (minimal changes in blood pressure or heart rate) Myoclonus (brief, involuntary, irregular muscle twitch) ↑ Spontaneous CNS neuron firing to skeletal muscle Prolonged opening of GABAA receptors (acts as ion channel for chloride) Inhibits activity of nerve cells in the reticular activating system Activation of peripheral nociceptor receptors ↑ Involuntary muscle contractions Influx of chlorideàHyperpolarization of nerve membranes in reticular activating system (brainstem neuronal network that regulates arousal and sleep- wake transitions) Depression of arousal & loss of consciousness Induction of general anesthesia (no analgesic effect) Direct activation of TRPA1 cation channels (key receptor in pain pathway) Stinging pain with injection (Treat with co-administration of local anesthetic) Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published July 9, 2022 on www.thecalgaryguide.com