Airway and Ventilator Questions in CRNA Interviews: RSI, ARDS, and Auto-PEEP
What changes after the tube goes in, and how to explain induction drugs, CO2 targets, and ventilator settings under follow-up.
Direct answer: Treat intubation as the start of a new hemodynamic problem: induction drops sympathetic tone, positive pressure cuts venous return, and your CO2 target changes cerebral blood flow and RV afterload at the same time.
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CRNA clinical questions: Practice clinical reasoning and follow-up questions across high-acuity ICU topics.
Key takeaways
- Succinylcholine’s potassium rise and lack of reversal follow directly from its depolarizing mechanism.
- Low CO2 is cold and tight; high CO2 is hot and swollen, and it raises PVR.
- ARDS ventilation protects the lung first: 6 mL/kg PBW, plateau ≤ 30, driving pressure under 15.
What happens after the tube goes in?
Airway questions test whether you see intubation as the end of the crisis or the start of a new hemodynamic problem. Propofol potentiates GABA-A receptors for fast hypnosis, then blunts sympathetic tone, depresses the myocardium, and vasodilates. Positive pressure then cuts venous return. In a patient who is already compensating, have a pressor ready before you push.
A strong answer names those shifts before the panel has to ask. Use the same order every time: mechanism, assessment finding, priority intervention with a number, first reassessment target.
What separates succinylcholine from rocuronium?
The potassium rise follows from the mechanism: sustained depolarization holds acetylcholine channels open and lets intracellular potassium leak out. A small IV dose of succinylcholine also breaks refractory laryngospasm.
Neuromuscular blockers at a glance
| Feature | Succinylcholine | Rocuronium | Vecuronium |
|---|---|---|---|
| Mechanism | Depolarizing; nicotinic ACh receptor agonist | Non-depolarizing; competitive antagonist | Non-depolarizing; competitive antagonist |
| Onset / duration | ~30–60 sec / 5–10 min | ~60 sec at RSI dose / 30–70 min | Slower onset / similar duration |
| Clearance | Plasma cholinesterase | Mostly hepatobiliary | Hepatic, with biliary and renal clearance |
| Reversal | None; wait it out | Sugammadex, or neostigmine | Sugammadex, or neostigmine |
| Watch for | K+ rises ~0.5 mEq/L; avoid in hyperkalemia, subacute burns, denervation, myopathy, MH history | Prolonged block in liver failure | Prolonged block in hepatic or renal failure |
How does CO2 change the brain and the lungs at the same time?
A simple model: low CO2 is cold and tight, high CO2 is hot and swollen. The second point is why permissive hypercapnia needs a caveat in a patient with RV failure or raised ICP.
- Hypocapnia: cerebral arterioles constrict, so cerebral blood flow and ICP fall. Alkalemia shifts the oxyhemoglobin curve left, so hemoglobin holds oxygen tighter and unloads less to tissue. Pulmonary vessels relax and PVR falls.
- Hypercapnia: cerebral vessels dilate, raising blood flow and ICP. Acidemia shifts the curve right and improves unloading. Pulmonary vessels constrict, PVR rises, and the right ventricle carries more afterload.
How do you ventilate ARDS without causing more lung injury?
ARDS starts with a direct or indirect insult (pneumonia, sepsis, aspiration, trauma, pancreatitis, TRALI) that inflames the alveolar-capillary membrane. Capillaries leak, alveoli flood with protein-rich fluid, and shunt drives hypoxemia that oxygen alone barely fixes.
One transport detail panels like: clamp the endotracheal tube at end-expiration when you switch ventilators. A disconnect drops PEEP to zero and derecruits the alveoli you spent hours opening.
- Tidal volume 6 mL/kg predicted body weight (range 4–8). PBW comes from height and sex.
- Plateau pressure ≤ 30 cmH2O; driving pressure (plateau minus PEEP) under 15.
- Permissive hypercapnia while pH stays at or above about 7.20.
- PEEP titrated to recruit, with conservative fluids.
- Refractory hypoxemia: early proning, neuromuscular blockade, ECMO evaluation.
How do you recognize and fix auto-PEEP?
Obstructive disease flips the problem. In a tachypneic COPD or asthma patient, the next breath arrives before the last one fully exhales, so volume stacks up. On the flow waveform, expiratory flow fails to return to zero before the next breath. That trapped pressure raises intrathoracic pressure, cuts venous return, and can cause hypotension or arrest.
Fix it by giving the patient time to exhale: lower the respiratory rate, lower tidal volume, shorten inspiratory time to lengthen expiration, treat bronchospasm, and treat the respiratory drive with analgesia or sedation. If the patient crashes, disconnect from the ventilator and let them exhale.
What do you do for acute stridor?
Stridor places the obstruction at or above the glottis: post-extubation edema, tumor, vocal cord paralysis, anaphylaxis. Call anesthesia or ENT early and bring the video laryngoscope, difficult airway cart, and cricothyrotomy tray to the bedside.
Keep the patient upright on high-flow oxygen. Give nebulized racemic epinephrine for mucosal vasoconstriction and IV dexamethasone for edema, plus IM epinephrine if anaphylaxis is possible. Move to controlled intubation by the most experienced operator if fatigue, desaturation, or confusion appears.
How do you practice the ventilator follow-up?
A first rep sounds like this: an ARDS patient has a PaO2 of 52 and PaCO2 of 54, and you raise tidal volume and rate to fix the gas. The follow-up asks what happens to the alveoli and right ventricle when plateau pressure hits 36.
A repaired answer sounds like this: I hold tidal volume at 6 mL/kg PBW and driving pressure under 15 to prevent barotrauma, accept the CO2 while pH stays above 7.20, titrate PEEP and FiO2 for oxygenation, and prone early to improve dorsal V/Q matching. I reassess plateau pressure, P/F ratio, and pH first.
Before your next rep, calculate it once: a 5’9” man has a PBW of about 70 kg, so 6 mL/kg is 420 mL. Then run two timed 60-second reps explaining how you would move that patient to a transport ventilator without losing PEEP, and test the follow-ups in the MoxPrep practice bank.
FAQ
Why is succinylcholine contraindicated in burns and denervation injuries?
Those injuries spread extra acetylcholine receptors across the muscle membrane. Succinylcholine opens all of them at once, and the potassium efflux can be large enough to cause a hyperkalemic arrest.
What tidal volume should I say for ARDS in a CRNA interview?
Say 6 mL/kg of predicted body weight, which comes from height and sex, with plateau pressure at or below 30 and driving pressure under 15.
CRNA prep hubs
- CRNA Interview Questions
- CRNA Behavioral Questions
- CRNA Clinical Questions
- CRNA EI Interview Questions
- CRNA Mock Interviews
- CRNA Interview Coach
- CRNA AI Coach
Last updated: 2026-10-20
Sources and claim scope
Clinical content comes from a CRNA applicant’s interview preparation sheet, checked against the sources below. Doses are typical starting points for interview discussion; follow your institution’s protocols at the bedside. Observations about how panels respond are Mox synthesis from interview practice, not a program’s published rubric.
- ARDS Network: Lower Tidal Volumes for ARDS (NEJM, 2000): The trial behind 6 mL/kg predicted body weight and plateau pressure limits.
- StatPearls: Succinylcholine Chloride: Depolarizing mechanism, potassium rise, and contraindications.
- StatPearls: Sugammadex: Encapsulation reversal of rocuronium and vecuronium.