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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

Propofol français

Propofol français

Rapid sequence induction and intubation

Rapid Sequence Induction & Intubation (RSII): Indications & considerations “Full stomach”: ↑ risk of regurgitation, vomiting, aspiration Life-threatening injury or illness requiring immediate or rapid airway control ↓ Gastro- esophageal sphincter competence (elderly, pregnancy, hiatus hernia, obesity) ↑ Intragastric pressure (pregnancy, obesity, bowel obstruction, large abdominal tumors) Delayed gastric emptying (narcotics, anticholinergics, pregnancy, renal failure, diabetes) ↓ Level of consciousness (drug/alcohol overdose, head injury, trauma or shock state) Respiratory & ventilatory compromise (i.e., hypoxic or hypercapnic respiratory failure) Achalasia (esophageal motility disorder resulting in impaired swallowing) Dynamically deteriorating clinical situation (i.e., trauma) GI bleed Impaired airway reflexes ↓ Muscle tone of structures in the airway (i.e., tongue, pharyngeal walls, & soft palate) Patients who did not stop GLP-1 agonist preoperatively as advised Impaired clearance of secretions or vomitus ↓ Safe apnea time before hemodynamic decompensation Unprotected airway Need for rapidly securing airway while avoiding aspiration & hemodynamic compromise Rapid sequence intubation (RSI): Simultaneous administration of induction agent (unconsciousness) & neuromuscular blocking agent (paralysis) to achieve intubation conditions (~45-60 seconds after IV push) for rapid control of an emergency airway Preoxygenation Deranged physiologic conditions (i.e., hypotension, acidosis, hypoxemia) Reduced tolerance for apnea (period with no ventilation or oxygenation) Pre-oxygenate with high flow O2 (15L) to create a large pulmonary & tissue reservoir of oxygen ↓ Significant oxygen desaturation during apnea ↑ Oxygen saturation on pulse oximetry Induction Laryngoscopy & intubation are a potent sympathetic nervous system stimulus Airway manipulation causes a surge in catecholamines Paralysis Visualization & passage of endotracheal tube requires relaxation of vocal cords & surrounding muscles Neuromuscular blocking agents facilitate paralysis Rescue Some induction agents (i.e., propofol) are vasodilators Hemodynamically unstable or patients in shock Hypotension Tachycardia ↑ Intracranial pressure (ICP) Hypertension Suppress cough & gag reflex Prevent laryngospasm (involuntary closure of vocal cords to airway manipulation) Minimize movement during procedure Vasoactive agents (i.e., ephedrine, phenylephrine) ↑ systemic vascular resistance Atropine & glycopyrrolate ↑ heart rate Lidocaine (Na+ channel blocker) & opioids (μ receptor agonist) ↓ transmission of pain ↓ Sympathetic response, myocardial demand & physiologic stress Anesthetics (i.e., propofol) achieve unconsciousness for paralysis & intubation ↓ Airway trauma & damage to vocal cords Bag mask ventilation typically avoided in this step to ↓ gastric insufflation & risk of aspiration Cricoid pressure (Sellick maneuver): posterior displacement of cricoid ring to compress esophagus against C-spine to prevent passive regurgitation of gastric contents to airway. Applied from start of induction, released when placement of endotracheal tube is confirmed by capnography. Intubation ↑ Blood pressure and/or cardiac output Authors: Jen Guo Reviewers: Priyanka Grewa Luiza Radu Leyla Baghirzada* * MD at time of publication Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published November 18, 2024 on www.thecalgaryguide.com

Propofol

Propofol: Mechanism of Action & Side Effects Primary Process ↑ Allosteric binding affinity (binds to a site other than the active site on the receptor to induce conformational changes) of Gamma- aminobutyric acid (GABA) to GABAA receptor in brain (ionotropic receptor) GABA remains bound to GABAA receptor Prolonged opening of chloride channels in neuronal cell membrane Influx of negatively charged chloride into neuron Hyper- polarization of nerve cell membrane ↑ Difficulty reaching threshold for action potential ↓ Number of successful action potentials Inhibition of central nervous system Central Nervous System ↓ Neuronal activity ↓ Level of consciousness, achieving sedation or general anesthesia (dose-dependent effect) ↓ Cerebral metabolic activity ↓ Cerebral blood flow ↓ Intracranial pressure Respiratory System Inhibition of central respiratory centers in brainstem Relaxation of upper airway muscles ↓ Hypercapnic & hypoxic ventilatory drive Airway obstruction ↓ Respiratory rate ↓ Tidal volume Hypoxemia Hypercapnia Apnea Cardiovascular System Inhibition of sympathetic cardiovascular activity Inhibition of cardiac smooth & striated muscle activity ↓ Baroreceptor response to decrease in blood pressure Vasodilation ↓ Myocardial contractility ↓ Systemic (minor effect) vascular resistance Diminished reflex tachycardia Diminished vasoconstrictor response Hypotension Authors: Caitlin Bittman Ryden Armstrong Reviewers: Billy Sun, Joseph Tropiano Priyanka Grewal Luiza Radu Melinda Davis* * MD at time of publication Secondary Process Direct interaction with α1 subunit of L-type calcium channels Alteration of calcium channel conformation Inhibition of voltage-gated calcium channels ↓ Response to depolarization signals Smooth & striated muscle relaxation throughout body ↓ Calcium ion influx into smooth & striated muscle cells, & ↓ cell depolarization Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Mar 3, 2018; updated Aug 28, 2025 on www.thecalgaryguide.com