12.1 Rapid Sequence Induction (RSI), Cricoid Pressure & Intubation Protocols

12.1 Rapid Sequence Induction (RSI), Cricoid Pressure & Intubation Protocols

Rapid sequence induction (RSI) is a specialized airway management technique engineered to achieve rapid endotracheal intubation while minimizing the critical time interval between loss of protective airway reflexes and inflation of the endotracheal tube (ETT) cuff. Mastery of aspiration risk stratification, preoxygenation physiology, cricoid force dynamics, pharmacologic timing, and verification standards is vital for safe CRNA practice.

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1. Pulmonary Aspiration Pathophysiology & Clinical Indications for RSI

Pulmonary aspiration of gastric contents remains a leading contributor to anesthesia-related morbidity and mortality. When acidic gastric contents enter the tracheobronchial tree, they trigger an acute chemical pneumonitis known historically as Mendelson's Syndrome.

+-------------------------------------------------------------------------+
|                   MENDELSON'S SYNDROME CLASSICAL CRITERIA               |
+------------------------------------+------------------------------------+
| Critical Gastric Fluid Volume      | Critical Gastric Fluid pH          |
+------------------------------------+------------------------------------+
| • Gastric volume > 0.4 mL/kg       | • Gastric pH < 2.5                 |
|   (or > 25 mL in a 70 kg adult)    | • Severe chemical burn of alveolar-|
| • Particulate matter worsens       |   capillary membranes leading to   |
|   atelectasis and inflammatory     |   intense bronchospasm, exudation, |
|   exudative response               |   and severe hypoxemia             |
+------------------------------------+------------------------------------+

Clinical Indications & Aspiration Risk Factors

Any condition that delays gastric emptying, increases intragastric pressure, or impairs the competence of the lower esophageal sphincter (LES) warrants an RSI protocol:

+-------------------------------------------------------------------------+
|                    CLINICAL RISK FACTORS REQUIRING RSI                  |
+-----------------------+-------------------------------------------------+
| Clinical Category     | Pathophysiologic Mechanism                      |
+-----------------------+-------------------------------------------------+
| **Non-Fasted State**  | Solid intake < 6-8 hours or clear liquids < 2   |
|                       | hours; residual solid and acidic liquid volume  |
| **Emergency Surgery / | Pain, anxiety, and sympathetic activation halt  |
|   Acute Trauma**      | normal gastric motility immediately upon injury |
| **Gastrointestinal    | Mechanical obstruction, paralytic ileus, active |
|   Pathology**         | peritonitis, acute appendicitis, bowel ischemia |
| **Symptomatic GERD /  | Incompetent lower esophageal sphincter, loss of |
|   Hiatal Hernia**     | normal anatomical barrier at gastroesophageal jn|
| **Pregnancy (≥14 wk)**| Progesterone reduces LES tone; gravid uterus    |
|                       | mechanically elevates intragastric pressure     |
| **Gastroparesis**     | Autonomic neuropathy (diabetes mellitus), chronic|
|                       | uremia, systemic sclerosis, Parkinson's disease |
| **Opioid Use**        | Profound inhibition of gastric emptying and     |
|                       | coordinated gastrointestinal peristalsis        |
| **Morbid Obesity**    | Elevated baseline intra-abdominal pressure and  |
|                       | increased incidence of hiatal hernia/GERD       |
| **Elevated ICP**      | Brain injury disrupting central vagal control   |
+-----------------------+-------------------------------------------------+

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2. Preoxygenation & Denitrogenation Kinetics

Preoxygenation (denitrogenation) replaces the nitrogen residing in the patient's Functional Residual Capacity (FRC) with pure oxygen, creating an intrapulmonary oxygen reservoir that sustains cellular respiration during apnea.

The FRC Oxygen Reservoir

In a standard $70 \text{ kg}$ adult breathing room air ($21\% \text{ O}_2$):

• $FRC \approx 30 \text{ mL/kg} \approx 2100 - 2500 \text{ mL}$
• At $21\% \text{ O}_2$, total FRC oxygen content is only $\approx 450 \text{ mL}$.
• Basal metabolic oxygen consumption ($VO_2$) is $\approx 3.5 \text{ mL/kg/min} \approx 250 \text{ mL/min}$.
• Without denitrogenation, arterial desaturation ($SpO_2 < 90\%$) occurs within $1.5 - 2 \text{ minutes}$ of apnea.

Following maximal denitrogenation with $100\% \text{ O}_2$:

• Alveolar nitrogen ($79\%$) is washed out, lifting alveolar oxygen concentration to $>90\%$.
• FRC oxygen reservoir expands to $>2000 - 2200 \text{ mL}$.
• Safe apnea time (time until $SpO_2$ drops below $90\%$) extends to $6 - 8 \text{ minutes}$ in healthy adults.

+-------------------------------------------------------------------------+
|                     STANDARD PREOXYGENATION PROTOCOLS                   |
+------------------------------------+------------------------------------+
| 1. Tidal Volume Breathing Method   | 2. Deep Vital Capacity Method      |
+------------------------------------+------------------------------------+
| • 100% FiO₂ via tight mask seal    | • 8 deep vital capacity breaths    |
| • 3 minutes of normal tidal        |   over 60 seconds (or 4 breaths    |
|   breathing at FGF ≥ 10 L/min      |   over 30 seconds if emergency)    |
| • Endpoint: End-Tidal O₂ (EtO₂)    | • Comparable denitrogenation to    |
|   reaches ≥ 0.90 (90%)             |   3-minute tidal method            |
+------------------------------------+------------------------------------+

Clinical Factors Accelerating Desaturation

Safe apnea time is drastically shortened in populations with reduced FRC, elevated $VO_2$, or ventilation-perfusion ($V/Q$) mismatching:

• Morbid Obesity: Reduced chest wall compliance and elevated abdominal pressure compress FRC; increased metabolic mass raises $VO_2$ (safe apnea drops to $<2.5-3 \text{ minutes}$). Use ramped positioning (head elevated above clavicles) to expand FRC.
• Pregnancy (3rd Trimester): Elevated diaphragm shrinks FRC by $20-30\%$; fetal-placental unit elevates $VO_2$ by $35-50\%$.
• Pediatric Patients: High metabolic rate ($VO_2 \approx 6-8 \text{ mL/kg/min}$) and highly compliant chest wall lead to rapid desaturation within $<1-2 \text{ minutes}$.
• Sepsis / Hypermetabolic States / ARDS: Extreme $VO_2$ consumption combined with intrapulmonary shunt.

Apneic Oxygenation (THRIVE / High-Flow Nasal Cannula)

Applying nasal cannula oxygen at $10 - 15 \text{ L/min}$ during induction and subsequent laryngoscopy generates continuous mass flow. Because alveolar oxygen uptake ($250 \text{ mL/min}$) far exceeds carbon dioxide excretion into the alveoli ($20 \text{ mL/min}$ while the remaining $CO_2$ dissolves in blood), a negative subatmospheric pressure gradient develops in the alveoli, drawing fresh oxygen passively down the tracheobronchial tree (apneic diffusion oxygenation) and substantially prolonging safe apnea.

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3. Cricoid Pressure (Sellick Maneuver): Anatomy, Force & Protocols

Introduced by Brian Sellick in 1961, cricoid pressure is designed to occlude the upper esophagus and hypopharynx to prevent passive regurgitation of gastric contents into the pharynx during induction.

                    [SELLICK MANEUVER ANATOMICAL CROSS-SECTION]

                                Anterior Neck
                                      |
                             [Thyroid Cartilage]
                                      |
                             (Cricovocal Membrane)
                                      |
                       >>>  [CRICOID CARTILAGE]  <<< (Only complete cartilaginous
                                      |               ring; signet-ring shape)
                                      v
                         [Upper Esophageal Lumen]    (Post-cricoid hypopharynx
                                      |               compressed shut)
                                      v
                           [C6 VERTEBRAL BODY]       (Rigid posterior bony
                                                      counter-support)

Application Force & Technique

1. Landmark Identification: Palpate the thyroid prominence, move inferiorly across the cricothyroid membrane to locate the prominent cricoid ring (located at the level of the sixth cervical vertebra, C6).
2. Applied Force Progression:
   • Awake / Conscious State: Apply $10 \text{ Newtons (N)}$ of force ($\approx 1 \text{ kg}$ or $2.2 \text{ lbs}$ of pressure) using the thumb and index/middle finger. This prevents patient discomfort, retching, or airway occlusion.
   • Loss of Consciousness (Unconscious): Increase force to $30 \text{ Newtons (N)}$ ($\approx 3 \text{ kg}$ or $6.7 \text{ lbs}$ of pressure) as the hypnotic takes effect, maintaining steady posterior pressure until endotracheal intubation is confirmed and the cuff is fully inflated.

+-------------------------------------------------------------------------+
|                    SELLICK vs BURP MANEUVER DISTINCTION                 |
+------------------------------------+------------------------------------+
| Sellick Maneuver (Cricoid Pressure)| BURP Maneuver                      |
+------------------------------------+------------------------------------+
| • Target: Cricoid Cartilage (C6)   | • Target: Thyroid Cartilage        |
| • Direction: Purely Posterior      | • Direction: Backward, Upward,     |
| • Purpose: Esophageal occlusion    |   Rightward, Pressure              |
|   to prevent passive regurgitation | • Purpose: Improves glottic visual |
| • Maintained until ETT cuff up     |   alignment during laryngoscopy    |
+------------------------------------+------------------------------------+

Critical Safety Rules & Contraindications

• Active Vomiting (ABSOLUTE RELEASE MANDATE): If the patient begins active vomiting or retching, cricoid pressure MUST BE RELEASED IMMEDIATELY. Active retching against an occluded upper esophagus generates immense intragastric and intraluminal pressure, risking catastrophic esophageal rupture (Boerhaave's Syndrome). Suction the oropharynx and tilt the bed into Trendelenburg.
• Unstable Cervical Spine Fracture: Cricoid pressure can displace unstable vertebral fractures at C6.
• Direct Laryngeal / Cricotracheal Trauma: Risk of complete airway collapse.
• Impaired Laryngoscopic Visualization: If cricoid pressure distorts laryngeal anatomy or impedes tube passage, it should be adjusted, relaxed, or released.

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4. RSI Pharmacologic Agents & Dosing Strategies

Classic RSI avoids positive-pressure bag-mask ventilation prior to intubation to prevent introducing air into the stomach (which reduces LES pressure and provokes regurgitation). In a "modified RSI", gentle bag-mask ventilation with peak inspiratory pressures $<15 - 20 \text{ cmH}_2\text{O}$ may be utilized if the patient desaturates rapidly or cannot tolerate apnea.

+-------------------------------------------------------------------------+
|                       RSI PHARMACOTHERAPY COMPARISON                    |
+--------------------+------------------------+---------------------------+
| Drug & Class       | RSI Dosage             | Key Clinical Highlights   |
+--------------------+------------------------+---------------------------+
| **Propofol**       | 1.5 - 2.5 mg/kg IV     | Rapid onset (30-40s);     |
| (Hypnotic)         |                        | profound vasodilation;    |
|                    |                        | suppresses airway reflexes|
| **Etomidate**      | 0.2 - 0.3 mg/kg IV     | Hemodynamic stability;    |
| (Hypnotic)         |                        | transient adrenal cortical|
|                    |                        | suppression; myoclonus    |
| **Ketamine**       | 1.5 - 2.0 mg/kg IV     | Sympathetic stimulation;  |
| (Hypnotic/NMDA)    |                        | bronchodilation; ideal for|
|                    |                        | shock, trauma, & asthma   |
| **Succinylcholine**| 1.0 - 1.5 mg/kg IV     | Gold standard NMBA onset  |
| (Depolarizing NMBA)|                        | (30-60s); duration 5-10m; |
|                    |                        | hyperkalemia risk         |
| **Rocuronium**     | 1.0 - 1.2 mg/kg IV     | High-dose onset (60s);    |
| (Non-depolarizing) | (Standard is 0.6)      | duration 60-90m; reverse  |
|                    |                        | with Sugammadex 16 mg/kg  |
+--------------------+------------------------+---------------------------+

Succinylcholine vs. High-Dose Rocuronium in RSI

1. Succinylcholine ($1.0 - 1.5 \text{ mg/kg}$ IV):
   • Provides complete vocal cord paralysis within $30 - 60 \text{ seconds}$ with rapid spontaneous recovery in $5 - 10 \text{ minutes}$.
   • Absolute Contraindications: Malignant Hyperthermia susceptibility, hyperkalemia ($K^+ > 5.5 \text{ mEq/L}$), denervation injuries (spinal cord injury, stroke $>24-48 \text{ hours}$ old), severe burn injury ($>24-48 \text{ hours}$ old), muscular dystrophies (Duchenne/Becker), severe intra-abdominal sepsis ($>24 \text{ hours}$ old), and plasma cholinesterase (pseudocholinesterase) deficiency.
2. Rocuronium ($1.0 - 1.2 \text{ mg/kg}$ IV):
   • Administering twice the standard intubating dose ($2 \times ED_{95} = 0.6 \text{ mg/kg} \rightarrow 1.0 - 1.2 \text{ mg/kg}$) accelerates onset to $\approx 60 \text{ seconds}$, achieving intubating conditions comparable to succinylcholine.
   • Duration Caveat: Neuromuscular blockade lasts $60 - 90 \text{ minutes}$.
   • Immediate Rescue Reversal: In a "cannot intubate, cannot ventilate" scenario following high-dose rocuronium, Sugammadex $16 \text{ mg/kg}$ IV provides rapid encapsulation and full reversal within $2 - 3 \text{ minutes}$, outperforming spontaneous recovery from succinylcholine.

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5. Tracheal Intubation Verification & Troubleshooting Protocols

Proper confirmation of endotracheal tube placement is mandatory immediately following intubation to prevent unheralded esophageal intubation and catastrophic hypoxic brain injury.

+-------------------------------------------------------------------------+
|                  INTUBATION CONFIRMATION STANDARDS                      |
+------------------------------------+------------------------------------+
| Primary / Gold Standard Monitor    | Secondary Clinical Assessments     |
+------------------------------------+------------------------------------+
| • **Continuous Quantitative        | • Direct visualization of ETT cuff |
|   Waveform Capnography**           |   passing through vocal cords      |
| • Demonstration of ≥ 3 to 5        | • Bilateral equal chest expansion  |
|   consecutive breaths with normal  | • Bilateral equal breath sounds in |
|   alveolar plateau and stable      |   mid-axillary and apical fields   |
|   ETCO₂ amplitude (>30 mmHg)       | • Absence of gastric gurgling      |
| • Sustained, repeatable waveforms  | • Condensation/fogging in tube     |
+------------------------------------+------------------------------------+

Capnographic Esophageal Intubation Recognition

When an ETT is erroneously placed into the esophagus:

• Ingestion of carbonated beverages or prior bag-mask ventilation may force residual $CO_2$ gas into the stomach.
• The capnograph may display $1 - 2$ small, irregular, rapidly attenuating $CO_2$ waves.
• By breath $3 - 5$, the measured $CO_2$ exponentially decays to zero (flatline).
• Rule: Failure to sustain $\ge 5$ consistent, rectangular capnogram waveforms mandates immediate ETT removal and re-oxygenation via mask.

                       [CAPNOGRAM WAVEFORM DECAY PATTERNS]

   Tracheal Placement (Sustained Waves)       Esophageal Placement (Rapid Decay)
   CO₂ (mmHg)                                 CO₂ (mmHg)
    40 |  /-----\  /-----\  /-----\            40 |  /--\
    20 | /       \/       \/       \           20 | /    \   /\
     0 +---------------------------->           0 +--------\/---\__________->
         Breath 1  Breath 2  Breath 3               Breath 1  2    3   4 (Flatline)