Section 1
The 60-Second Resuscitation Card (First 5 Minutes)
The physiologically difficult airway—“HOP Killers” (Hypotension, Oxygenation/Hypoxemia, pH/Severe Metabolic Acidemia)— causes peri-intubation cardiovascular collapse even when glottic visualization is anatomically effortless [1,2]. Resuscitation before laryngoscopy is a Class I mandate [2,3].
0:00
Immediate Bedside Action & Exact Dosing
Calculate Shock Index (SI = HR/SBP) &
Screen LEMON/MOANS/RODS: If SI ≥ 0.8, SpO₂ < 93%, or pH < 7.20, declare a Physiologically Difficult Airway [1,2]. Call for 2nd airway operator and surgical cricothyrotomy tray at bedside.
Screen LEMON/MOANS/RODS: If SI ≥ 0.8, SpO₂ < 93%, or pH < 7.20, declare a Physiologically Difficult Airway [1,2]. Call for 2nd airway operator and surgical cricothyrotomy tray at bedside.
Equipment / Setup Specification
Dual large-bore (14–16 G) PIVs or IO access; Continuous waveform ETCO₂, 5-lead ECG, cycling NIBP q2min (or arterial line).
Physiological & Mechanical Objective
Identifies latent right/left ventricular preload dependency, depleted functional residual capacity (FRC), and respiratory compensation ceiling prior to apnea [1].
0:30
Immediate Bedside Action & Exact Dosing
Hemodynamic Pre-Loading (“Kill H”): Start Norepinephrine infusion at 0.05–0.3 mcg/kg/min [2,4]. Prepare Push-Dose Epinephrine (10 mcg/mL syringe: administer 10–20 mcg IV q2min PRN to keep MAP ≥ 65 mmHg or SBP ≥ 100 mmHg). Infuse 250–500 mL balanced crystalloid if volume-depleted [5].
Equipment / Setup Specification
Dedicated vasopressor lumen; 10 mL labeled push-dose Epinephrine syringe (10 mcg/mL) physically connected to a three-way stopcock.
Physiological & Mechanical Objective
Counteracts sedation-induced sympatholysis and positive-pressure mechanical ventilation reduction of right ventricular preload (ΔPpl surge) [1,4].
1:30
Immediate Bedside Action & Exact Dosing
Maximal Preoxygenation & Apneic
Oxygenation (“Kill O”): Elevate head of bed 20°–30° (ramped tragus-to-sternum). If SpO₂ ≥ 95%, apply non-rebreather mask at flush rate (40–60 L/min) + standard nasal cannula at 15 L/min. If SpO₂ < 93% (shunt physiology), apply NIPPV (CPAP/BiPAP) at IPAP 12–15 cmH₂O / EPAP 5–10 cmH₂O at FiO₂ 1.0 for 3 min [6].
Oxygenation (“Kill O”): Elevate head of bed 20°–30° (ramped tragus-to-sternum). If SpO₂ ≥ 95%, apply non-rebreather mask at flush rate (40–60 L/min) + standard nasal cannula at 15 L/min. If SpO₂ < 93% (shunt physiology), apply NIPPV (CPAP/BiPAP) at IPAP 12–15 cmH₂O / EPAP 5–10 cmH₂O at FiO₂ 1.0 for 3 min [6].
Equipment / Setup Specification
Video Laryngoscope (hyperangulated + standard Macintosh geometry blades tested), rigid stylet/bougie, suction (two DuCanto catheters connected to wall vacuum at −300 mmHg).
Physiological & Mechanical Objective
Replaces alveolar nitrogen with oxygen (denitrogenation of FRC) and recruits collapsed alveoli against intrapulmonary shunt via PEEP [6].
3:00
Immediate Bedside Action & Exact Dosing
Acidemia Protection & Buffering (“Kill
pH”): If severe metabolic acidemia (pH < 7.15, e.g., DKA, salicylates, lactic acidosis), maintain spontaneous tachypnea using Delayed Sequence Intubation (DSI) with Ketamine 0.5–1.0 mg/kg IV slow push [7]. During the apneic window, perform gentle mask ventilation using BVM with PEEP valve (5–10 cmH₂O) at 18–24 breaths/min [8].
pH”): If severe metabolic acidemia (pH < 7.15, e.g., DKA, salicylates, lactic acidosis), maintain spontaneous tachypnea using Delayed Sequence Intubation (DSI) with Ketamine 0.5–1.0 mg/kg IV slow push [7]. During the apneic window, perform gentle mask ventilation using BVM with PEEP valve (5–10 cmH₂O) at 18–24 breaths/min [8].
Equipment / Setup Specification
BVM fitted with an inline ETCO₂ sensor, manometer (keep peak pressure < 20 cmH₂O), and spring-loaded PEEP valve.
Physiological & Mechanical Objective
Prevents acute PaCO₂ rise during apnea, which otherwise crosses the blood-brain barrier and myocardium instantaneously, causing catastrophic intracellular acidosis [1,8].
5:00
Immediate Bedside Action & Exact Dosing
First-Pass Execution & Immediate
Post-Intubation Vent Coupling: Administer Ketamine 1.0 mg/kg IV (or Etomidate 0.15–0.2 mg/kg IV reduced dose in shock) + Rocuronium 1.2–1.5 mg/kg IV [2,9]. Intubate via Video Laryngoscopy [10]. Immediately connect to ventilator matching pre-intubation minute ventilation (VE = RR × VT, up to 25–30 breaths/min in severe acidemia).
Post-Intubation Vent Coupling: Administer Ketamine 1.0 mg/kg IV (or Etomidate 0.15–0.2 mg/kg IV reduced dose in shock) + Rocuronium 1.2–1.5 mg/kg IV [2,9]. Intubate via Video Laryngoscopy [10]. Immediately connect to ventilator matching pre-intubation minute ventilation (VE = RR × VT, up to 25–30 breaths/min in severe acidemia).
Equipment / Setup Specification
Endotracheal tube (7.5–8.0 mm ID) loaded on bougie or rigid stylet; syringe cuff manometer (20–30 cmH₂O).
Physiological & Mechanical Objective
High-dose Rocuronium ensures rapid 45–60 sec paralysis in low-cardiac-output states without fasciculation-induced O₂ consumption or hyperkalemia [1,2].
| Time | Immediate Bedside Action & Exact Dosing | Equipment / Setup Specification | Physiological & Mechanical Objective |
|---|---|---|---|
| 0:00 | Calculate Shock Index (SI = HR/SBP) & Screen LEMON/MOANS/RODS: If SI ≥ 0.8, SpO₂ < 93%, or pH < 7.20, declare a Physiologically Difficult Airway [1,2]. Call for 2nd airway operator and surgical cricothyrotomy tray at bedside. | Dual large-bore (14–16 G) PIVs or IO access; Continuous waveform ETCO₂, 5-lead ECG, cycling NIBP q2min (or arterial line). | Identifies latent right/left ventricular preload dependency, depleted functional residual capacity (FRC), and respiratory compensation ceiling prior to apnea [1]. |
| 0:30 | Hemodynamic Pre-Loading (“Kill H”): Start Norepinephrine infusion at 0.05–0.3 mcg/kg/min [2,4]. Prepare Push-Dose Epinephrine (10 mcg/mL syringe: administer 10–20 mcg IV q2min PRN to keep MAP ≥ 65 mmHg or SBP ≥ 100 mmHg). Infuse 250–500 mL balanced crystalloid if volume-depleted [5]. | Dedicated vasopressor lumen; 10 mL labeled push-dose Epinephrine syringe (10 mcg/mL) physically connected to a three-way stopcock. | Counteracts sedation-induced sympatholysis and positive-pressure mechanical ventilation reduction of right ventricular preload (ΔPpl surge) [1,4]. |
| 1:30 | Maximal Preoxygenation & Apneic Oxygenation (“Kill O”): Elevate head of bed 20°–30° (ramped tragus-to-sternum). If SpO₂ ≥ 95%, apply non-rebreather mask at flush rate (40–60 L/min) + standard nasal cannula at 15 L/min. If SpO₂ < 93% (shunt physiology), apply NIPPV (CPAP/BiPAP) at IPAP 12–15 cmH₂O / EPAP 5–10 cmH₂O at FiO₂ 1.0 for 3 min [6]. | Video Laryngoscope (hyperangulated + standard Macintosh geometry blades tested), rigid stylet/bougie, suction (two DuCanto catheters connected to wall vacuum at −300 mmHg). | Replaces alveolar nitrogen with oxygen (denitrogenation of FRC) and recruits collapsed alveoli against intrapulmonary shunt via PEEP [6]. |
| 3:00 | Acidemia Protection & Buffering (“Kill pH”): If severe metabolic acidemia (pH < 7.15, e.g., DKA, salicylates, lactic acidosis), maintain spontaneous tachypnea using Delayed Sequence Intubation (DSI) with Ketamine 0.5–1.0 mg/kg IV slow push [7]. During the apneic window, perform gentle mask ventilation using BVM with PEEP valve (5–10 cmH₂O) at 18–24 breaths/min [8]. | BVM fitted with an inline ETCO₂ sensor, manometer (keep peak pressure < 20 cmH₂O), and spring-loaded PEEP valve. | Prevents acute PaCO₂ rise during apnea, which otherwise crosses the blood-brain barrier and myocardium instantaneously, causing catastrophic intracellular acidosis [1,8]. |
| 5:00 | First-Pass Execution & Immediate Post-Intubation Vent Coupling: Administer Ketamine 1.0 mg/kg IV (or Etomidate 0.15–0.2 mg/kg IV reduced dose in shock) + Rocuronium 1.2–1.5 mg/kg IV [2,9]. Intubate via Video Laryngoscopy [10]. Immediately connect to ventilator matching pre-intubation minute ventilation (VE = RR × VT, up to 25–30 breaths/min in severe acidemia). | Endotracheal tube (7.5–8.0 mm ID) loaded on bougie or rigid stylet; syringe cuff manometer (20–30 cmH₂O). | High-dose Rocuronium ensures rapid 45–60 sec paralysis in low-cardiac-output states without fasciculation-induced O₂ consumption or hyperkalemia [1,2]. |
Keep reading with Pro
9 more sections, images and the original PDF are included in Pro.