Airway & Ventilator Management
From the decision to intubate through vent settings, oxygenation vs ventilation, troubleshooting, sedation, and weaning to extubation. Everything you need to manage the airway and the ventilator.
🔍 Overview -Airway Decision-Making
Indications for Intubation
- Airway protection -GCS ≤ 8, inability to handle secretions, impending obstruction
- Hypoxemic respiratory failure -SpO₂ < 90% despite high-flow O₂, P/F < 200
- Hypercapnic respiratory failure -rising PaCO₂ with acidosis (pH < 7.25), fatigue
- Impending respiratory failure -accessory muscle use, paradoxical breathing, rising work of breathing
Try NIV First (if appropriate): BiPAP/CPAP for COPD exacerbation, cardiogenic pulmonary edema, and mild-moderate hypoxemia. Avoid NIV in decreased consciousness, vomiting, hemodynamic instability, or inability to cooperate.
Key Vent Concepts
Pressure vs Volume
Volume Control (VC): You set the tidal volume -the vent delivers exactly that volume. Pressure varies. Preferred in ARDS (tight TV control).
Pressure Control (PC): You set the pressure -the volume varies depending on lung compliance. Preferred when you want to limit pressures.
Pressure Control (PC): You set the pressure -the volume varies depending on lung compliance. Preferred when you want to limit pressures.
Key Numbers to Know Every Morning
- Tidal volume (Vt) -actual delivered TV in mL/kg PBW
- Rate (RR) -set respiratory rate
- FiO₂ -fraction of inspired oxygen (0.21–1.0)
- PEEP -positive end-expiratory pressure in cmH₂O
- Peak pressure (Ppeak) -total pressure to deliver breath (airway resistance + alveolar)
- Plateau pressure (Pplat) -alveolar distension pressure (inspiratory hold). Target ≤ 30.
- Driving pressure = Pplat − PEEP. Target ≤ 15. Strong predictor of ARDS mortality.
- P/F ratio = PaO₂ ÷ FiO₂ -oxygenation index
- SpO₂ target -88–95% in ARDS; 94–98% otherwise
💨 Oxygen Delivery Devices
Escalation Ladder -Low Flow to High Flow
Rule of thumb: Each 1 L/min of nasal cannula adds ~4% FiO₂ above room air (21%). So 2L NC ≈ 28%, 4L ≈ 36%, 6L ≈ 44%. This breaks down above 6L.
| Device | Flow Rate | FiO₂ Delivered | Best For | ⚠️ Limitations |
|---|---|---|---|---|
| Nasal Cannula (NC) | 1–6 L/min | 24–44% | Mild hypoxemia. Stable patients. Most common starting point. | ⚠️ Uncomfortable > 6L (dries mucosa). Unreliable FiO₂ -depends on patient's minute ventilation and mouth breathing. |
| Simple Face Mask | 5–10 L/min | 35–55% | Moderate hypoxemia. Short-term use (ED, post-op). | ⚠️ Must run ≥ 5 L/min to prevent CO₂ rebreathing. Claustrophobic. Can't eat/talk well. |
| Venturi Mask | 4–12 L/min | Precise: 24%, 28%, 31%, 35%, 40%, 50% | COPD patients -need precise low FiO₂ (24–28%) to avoid suppressing hypoxic drive. Color-coded adapters. | ⚠️ Max 50% FiO₂. Bulky. Used mainly for COPD. |
| Non-Rebreather (NRB) | 10–15 L/min | 60–90% | Severe hypoxemia. Pre-oxygenation before intubation. CO poisoning. Trauma. | ⚠️ Reservoir bag must stay inflated. Not truly 100% -room air mixes around mask. If patient needs NRB → consider escalation. |
| High-Flow Nasal Cannula (HFNC) | 20–60 L/min | 21–100% (titratable) | Hypoxemic respiratory failure, post-extubation, immunocompromised (avoid intubation), pre-oxygenation. Delivers heated humidified O₂. | ⚠️ Generates ~1 cmH₂O PEEP per 10 L/min (so 60L ≈ 6 cmH₂O). Patient must breathe spontaneously. If still desatting on HFNC 60L/100% → intubate. |
When to Escalate
1
NC 1–6L -SpO₂ still < 92% → escalate
2
Simple mask / NRB 10–15L -SpO₂ still < 92% or work of breathing increasing → escalate
3
HFNC 40–60L -if SpO₂ < 92% on 60L/100% FiO₂, or RR > 30, or accessory muscle use → next step
4
NIV (BiPAP/CPAP) -if COPD exacerbation or cardiogenic pulmonary edema → try NIV before intubation
5
Intubation + Mechanical Ventilation -failing all above, declining mental status, unable to protect airway
⚠️ ROX Index (HFNC failure prediction): ROX = (SpO₂/FiO₂) ÷ RR. Check at 2, 6, 12 hours. ROX < 3.85 at 6h → high risk of HFNC failure → prepare for intubation. ROX > 4.88 → likely safe to continue HFNC.
🌬️ Non-Invasive Ventilation (NIV)
CPAP vs BiPAP
| CPAP | BiPAP | |
|---|---|---|
| What it does | Single continuous pressure (like PEEP) | Two pressures: IPAP (inhale) + EPAP (exhale) |
| Helps with | Oxygenation only -splints airways open, recruits alveoli | Both oxygenation AND ventilation -IPAP augments tidal volume (blows off CO₂), EPAP = PEEP |
| Best for | Cardiogenic pulmonary edema, OSA | COPD exacerbation (hypercapnic failure), obesity hypoventilation, neuromuscular weakness |
| Typical settings | CPAP 5–10 cmH₂O | IPAP 10–20 / EPAP 5–8 cmH₂O. Start IPAP 10, EPAP 5. Titrate IPAP up by 2 q15–30 min for CO₂. |
| Pressure support | None (single pressure) | PS = IPAP − EPAP. Higher PS = more ventilatory support. PS of 10 cmH₂O is moderate support. |
Indications for NIV
- COPD exacerbation with respiratory acidosis (pH < 7.35, PaCO₂ > 45) -strongest evidence, reduces intubation by 65% Brochard, 1995
- Cardiogenic pulmonary edema -CPAP or BiPAP both work. Reduces preload + afterload + recruits flooded alveoli. 3CPO, 2008
- Post-extubation -prophylactic NIV in high-risk patients reduces reintubation
- Immunocompromised with respiratory failure -try NIV/HFNC first to avoid vent-associated infections
- Palliative / DNI patients -ceiling of care when intubation is not desired
🚫 NIV Contraindications: Arrest · GCS ≤ 8 · Vomiting/aspiration risk · Shock · Facial trauma · Airway obstruction · Uncooperative
▶ How to Pick BiPAP Settings, Step by Step (tap to expand)
Understanding IPAP, EPAP & Pressure Support
The Key Concept: BiPAP delivers two pressures. IPAP (Inspiratory Positive Airway Pressure) is the pressure during inhale. EPAP (Expiratory Positive Airway Pressure) is the pressure during exhale (functionally identical to PEEP). The difference between them is Pressure Support (PS) = IPAP − EPAP. PS is what actually pushes air into the lungs and generates tidal volume.
| Setting | What It Controls | How to Titrate | Think of It As |
|---|---|---|---|
| EPAP | Oxygenation (splints alveoli open, recruits collapsed lung) | Start 5 cmH₂O. ↑ by 2 if SpO₂ < 90% despite FiO₂. Max ~10-12. | = PEEP. Treats the O₂ problem. |
| IPAP | Ventilation (how much air is pushed in per breath) | Start 10 cmH₂O. ↑ by 2 q15-30 min if CO₂ still high. Max ~20-25. | = Tidal volume driver. Treats the CO₂ problem. |
| PS (= IPAP − EPAP) | Tidal volume per breath | Higher PS → bigger breaths → more CO₂ blown off. Target PS 5-15 cmH₂O for most patients. | PS is essentially your tidal volume knob. PS of 10 ≈ TV of ~400-500 mL in most adults. |
| FiO₂ | Oxygen concentration | Start 100%, wean to target SpO₂ 88-92% (COPD) or 92-96%. Always wean FiO₂ before weaning pressures. | Supplemental O₂. Independent of IPAP/EPAP. |
| Rate (backup) | Minimum breaths/min if patient doesn't trigger | Set 12-16. Usually not needed, patient triggers their own breaths. | Safety net for apnea. |
The Two Knobs: Fix O₂ vs Fix CO₂
| Problem | Which Knob to Turn | What to Do |
|---|---|---|
| SpO₂ low (oxygenation failure) | ↑ EPAP (or ↑ FiO₂) | EPAP recruits alveoli and improves V/Q matching. Think of it like adding PEEP on a vent. |
| CO₂ high (ventilation failure) | ↑ IPAP (keeping EPAP the same) | This increases PS, which increases tidal volume, which blows off more CO₂. ↑ IPAP by 2 cmH₂O every 15-30 min until pH improves. |
| Both | ↑ EPAP for O₂, ↑ IPAP for CO₂ | Always increase IPAP at least as much as EPAP to maintain the PS gap. If you raise EPAP by 2, raise IPAP by 2 also. |
⚠️ Critical Rule: If you increase EPAP without increasing IPAP, you decrease PS, which decreases tidal volume, which can worsen CO₂ retention. Always maintain or increase the PS gap when raising EPAP.
Example: IPAP 12 / EPAP 5 = PS 7. If you raise EPAP to 8 but keep IPAP at 12 → PS drops to 4 → patient gets smaller breaths → CO₂ rises. Fix: raise IPAP to 15 / EPAP 8 = PS 7 maintained.
Example: IPAP 12 / EPAP 5 = PS 7. If you raise EPAP to 8 but keep IPAP at 12 → PS drops to 4 → patient gets smaller breaths → CO₂ rises. Fix: raise IPAP to 15 / EPAP 8 = PS 7 maintained.
Starting Protocol & Titration
Step 1: Start BiPAP
- IPAP 10 / EPAP 5 (PS = 5) -safe starting point for most patients
- FiO₂ 100% (wean later based on SpO₂)
- Backup rate 12-16
- Fit mask snugly. Coach patient: "Breathe with the machine, let it push air in."
Step 2: Check ABG at 1 Hour
- CO₂ still elevated / pH still acidotic? → ↑ IPAP by 2 (e.g., IPAP 12 → 14 → 16). Recheck in 1h.
- SpO₂ still low? → ↑ EPAP by 2 (and raise IPAP by 2 to maintain PS). Or ↑ FiO₂.
- Both improving? → Hold current settings. Wean FiO₂ first.
Step 3: Reassess at 2 Hours
- pH improving and patient comfortable? → BiPAP is working. Continue. Recheck ABG q4-6h.
- No improvement or worsening? → NIV failure. Prepare for intubation. Do NOT delay.
Clinical Example: BiPAP Preventing Intubation in COPD
🏥 Scenario: 68M with severe COPD exacerbation
Presentation: Brought in by EMS, severe respiratory distress, accessory muscle use, speaking in 1-2 word sentences. RR 32, SpO₂ 84% on 6L NC, HR 115, BP 155/90.
ABG on arrival: pH 7.22, PaCO₂ 78, PaO₂ 52, HCO₃ 30 (acute-on-chronic hypercapnic respiratory failure).
Step 1 (Time 0): Start BiPAP IPAP 10 / EPAP 5 (PS = 5), FiO₂ 50%.
→ After 15 min: RR 28, SpO₂ 89%. Still distressed. CO₂ not moving.
Step 2 (Time 15 min): ↑ IPAP to 14 / EPAP 5 (PS = 9). Keep FiO₂ 50%.
→ After 30 min: RR 24, SpO₂ 91%. Patient visibly more comfortable. Able to speak in short sentences.
Step 3 (Time 1 hour): Repeat ABG: pH 7.28, PaCO₂ 62, PaO₂ 68. pH improving, CO₂ coming down. ↑ IPAP to 16 / EPAP 5 (PS = 11).
Step 4 (Time 2 hours): ABG: pH 7.32, PaCO₂ 55, PaO₂ 72. RR 20, SpO₂ 93%. BiPAP is working. Intubation avoided.
Overnight: Continue BiPAP. Wean FiO₂ to 35%. Give Ipratropium/Albuterol (DuoNeb) nebs q4h, Methylprednisolone (Solu-Medrol) 60 mg IV daily (= prednisone 40 mg PO; switch to PO when tolerating), Azithromycin (Zithromax) 500 mg IV. Next AM: ABG 7.38 / 48 / 78. Trial off BiPAP → tolerates nasal cannula. Extubation avoided.
→ After 15 min: RR 28, SpO₂ 89%. Still distressed. CO₂ not moving.
Step 2 (Time 15 min): ↑ IPAP to 14 / EPAP 5 (PS = 9). Keep FiO₂ 50%.
→ After 30 min: RR 24, SpO₂ 91%. Patient visibly more comfortable. Able to speak in short sentences.
Step 3 (Time 1 hour): Repeat ABG: pH 7.28, PaCO₂ 62, PaO₂ 68. pH improving, CO₂ coming down. ↑ IPAP to 16 / EPAP 5 (PS = 11).
Step 4 (Time 2 hours): ABG: pH 7.32, PaCO₂ 55, PaO₂ 72. RR 20, SpO₂ 93%. BiPAP is working. Intubation avoided.
Overnight: Continue BiPAP. Wean FiO₂ to 35%. Give Ipratropium/Albuterol (DuoNeb) nebs q4h, Methylprednisolone (Solu-Medrol) 60 mg IV daily (= prednisone 40 mg PO; switch to PO when tolerating), Azithromycin (Zithromax) 500 mg IV. Next AM: ABG 7.38 / 48 / 78. Trial off BiPAP → tolerates nasal cannula. Extubation avoided.
✅ Why this worked: Each time we raised IPAP (while keeping EPAP the same), we increased PS → bigger tidal volumes → more CO₂ blown off per breath → pH corrected. The key was titrating IPAP up aggressively every 15-30 minutes until the ABG improved. If by 1-2 hours the pH hadn't improved, this patient would have needed intubation.
Quick Reference: Common BiPAP Settings by Scenario
| Scenario | Starting IPAP / EPAP | PS | Goal | Titration Target |
|---|---|---|---|---|
| COPD exacerbation | 10-12 / 5 | 5-7 | ↓ CO₂, ↑ pH | ↑ IPAP q15-30 min → max 20-25. Target pH > 7.30. |
| Cardiogenic pulmonary edema | 10-12 / 8-10 | 2-4 | ↑ O₂, ↓ preload | Higher EPAP for recruitment. CPAP 10-12 is often enough. |
| Obesity hypoventilation | 14-18 / 8-10 | 6-10 | ↓ CO₂ | Need higher pressures due to chest wall compliance. ↑ IPAP aggressively. |
| Neuromuscular weakness | 10-14 / 5 | 5-9 | Augment weak inspiratory muscles | ↑ IPAP if NIF declining. Low threshold for intubation (GBS, MG crisis). |
| Post-extubation (prophylactic) | 8-10 / 5 | 3-5 | Prevent reintubation | Low support. Alternate with HFNC. Wean over 24-48h. |
| DNI / comfort care | 10-15 / 5-8 | 5-7 | Symptom relief | Titrate to comfort + dyspnea relief. No ABG targets. |
Special Consideration: The Obese Patient
Obesity makes BiPAP harder. Abdominal and chest wall fat reduces lung compliance, compresses the diaphragm (especially supine), and causes baseline hypoventilation. These patients need more aggressive settings than normal-weight patients.
| Challenge | Why It Happens | What to Do |
|---|---|---|
| Higher IPAP needed | Chest wall is stiff → needs more pressure to generate the same tidal volume | Start IPAP 14-18 (not 10). May need IPAP 20-25 in BMI > 50. Don't be afraid to go higher. |
| Higher EPAP needed | Abdominal mass compresses diaphragm → atelectasis → V/Q mismatch → hypoxemia | Start EPAP 8-10 (not 5). Acts like higher PEEP to recruit collapsed bases. |
| Positioning matters hugely | Supine = diaphragm splinted by abdomen. Functional residual capacity drops. | Sit patient upright at 30-45° or reverse Trendelenburg. This alone can improve oxygenation dramatically. |
| Chronic CO₂ retention | Obesity hypoventilation syndrome (OHS), chronic hypercapnia with elevated bicarb | Don't normalize CO₂. Target their baseline PaCO₂ (often 50-60). Check HCO₃, if elevated, it's chronic. Over-ventilating → alkalosis → arrhythmias. |
| Mask leak | Facial fat makes mask seal harder | Use a full-face mask (oronasal). May need a larger size. Check for beard. Tighten straps but avoid skin breakdown. |
💡 Practical Example, BMI 48 with OHS Exacerbation:
Patient arrives with pH 7.18, PaCO₂ 95, HCO₃ 34 (chronic + acute). SpO₂ 82%.
• Start: IPAP 18 / EPAP 10 (PS = 8), FiO₂ 40%, upright positioning
• 15 min: SpO₂ 88%, still tachypneic → ↑ IPAP to 22 (PS = 12)
• 1 hour ABG: pH 7.25, PaCO₂ 75. Improving. Hold settings.
• Target: pH > 7.30 and PaCO₂ toward their baseline (~55-60). Do NOT target PaCO₂ 40, that's over-ventilation for this patient.
Patient arrives with pH 7.18, PaCO₂ 95, HCO₃ 34 (chronic + acute). SpO₂ 82%.
• Start: IPAP 18 / EPAP 10 (PS = 8), FiO₂ 40%, upright positioning
• 15 min: SpO₂ 88%, still tachypneic → ↑ IPAP to 22 (PS = 12)
• 1 hour ABG: pH 7.25, PaCO₂ 75. Improving. Hold settings.
• Target: pH > 7.30 and PaCO₂ toward their baseline (~55-60). Do NOT target PaCO₂ 40, that's over-ventilation for this patient.
When NIV is Failing -Escalate to Intubation
⚠️ Signs of NIV failure (reassess within 1–2 hours):
• No improvement in pH or PaCO₂ after 1–2h of BiPAP
• Worsening tachypnea (RR > 30 despite NIV)
• SpO₂ < 90% despite FiO₂ escalation
• Declining mental status (somnolence, confusion)
• Hemodynamic instability
• Patient intolerance / non-compliance with mask
Do NOT delay intubation if NIV is failing. Late intubation = worse outcomes.
• No improvement in pH or PaCO₂ after 1–2h of BiPAP
• Worsening tachypnea (RR > 30 despite NIV)
• SpO₂ < 90% despite FiO₂ escalation
• Declining mental status (somnolence, confusion)
• Hemodynamic instability
• Patient intolerance / non-compliance with mask
Do NOT delay intubation if NIV is failing. Late intubation = worse outcomes.
🚨 Rapid Sequence Intubation (RSI)
The 7 P's of RSI
1
Preparation
Equipment: ETT (7.0–7.5 women, 7.5–8.0 men), laryngoscope (video preferred), bougie, BVM, suction, end-tidal CO₂, backup airway (LMA). Two IV lines. Monitors on. Confirm code status.
Equipment: ETT (7.0–7.5 women, 7.5–8.0 men), laryngoscope (video preferred), bougie, BVM, suction, end-tidal CO₂, backup airway (LMA). Two IV lines. Monitors on. Confirm code status.
2
Pre-oxygenation
3–5 minutes of 100% O₂ via NRB or HFNC 60L/min (builds O₂ reserve in FRC). Goal: SpO₂ 100%. In obese or critically ill → apneic oxygenation: leave NC at 15L under the NRB or continue HFNC during intubation attempt.
3–5 minutes of 100% O₂ via NRB or HFNC 60L/min (builds O₂ reserve in FRC). Goal: SpO₂ 100%. In obese or critically ill → apneic oxygenation: leave NC at 15L under the NRB or continue HFNC during intubation attempt.
3
Pre-treatment (optional)
Fentanyl 1–3 mcg/kg IV (blunts sympathetic surge -useful in elevated ICP, aortic dissection). Lidocaine 1.5 mg/kg IV (for elevated ICP -controversial). Most patients skip this step.
Fentanyl 1–3 mcg/kg IV (blunts sympathetic surge -useful in elevated ICP, aortic dissection). Lidocaine 1.5 mg/kg IV (for elevated ICP -controversial). Most patients skip this step.
4
Paralysis with Induction (push simultaneously)
See drug table below. Induction agent → wait 20–30 seconds → paralytic.
See drug table below. Induction agent → wait 20–30 seconds → paralytic.
5
Protection & Positioning
Sniffing position: neck flexed, head extended (aligns oral-pharyngeal-laryngeal axes). Elevate head of bed 20–30° in obese. Apply cricoid pressure (Sellick maneuver -controversial but still used).
Sniffing position: neck flexed, head extended (aligns oral-pharyngeal-laryngeal axes). Elevate head of bed 20–30° in obese. Apply cricoid pressure (Sellick maneuver -controversial but still used).
6
Placement
Direct or video laryngoscopy → visualize cords → pass tube through cords → inflate cuff → confirm placement: (1) End-tidal CO₂ waveform (gold standard), (2) bilateral breath sounds, (3) misting in tube, (4) CXR for depth (2–4 cm above carina).
Direct or video laryngoscopy → visualize cords → pass tube through cords → inflate cuff → confirm placement: (1) End-tidal CO₂ waveform (gold standard), (2) bilateral breath sounds, (3) misting in tube, (4) CXR for depth (2–4 cm above carina).
7
Post-intubation Management
Start sedation (propofol or midazolam + fentanyl). Set initial vent settings. Secure tube (tape or holder). NG/OG tube. Arterial line if not already placed. ABG in 30 min. CXR to confirm ETT position.
Start sedation (propofol or midazolam + fentanyl). Set initial vent settings. Secure tube (tape or holder). NG/OG tube. Arterial line if not already placed. ABG in 30 min. CXR to confirm ETT position.
RSI Drug Table
| Drug | MOA | Dose | Onset | Duration | Best For | ⚠️ Avoid If |
|---|---|---|---|---|---|---|
| INDUCTION AGENTS | ||||||
| Etomidate | GABA-A agonist | 0.3 mg/kg IV push | 15–30 sec | 5–15 min | Hemodynamically unstable -most neutral on BP. Most common RSI induction agent. | ⚠️ Adrenal suppression (single dose is clinically insignificant). Avoid in septic shock? -debated. |
| Ketamine (Ketalar) | NMDA antagonist | 1–2 mg/kg IV push | 30–60 sec | 10–20 min | Asthma/bronchospasm (bronchodilator), hypotension (preserves BP via sympathetic stimulation), elevated ICP (old teaching said avoid -now considered safe). | ⚠️ Psychosis/schizophrenia (emergence reactions). Increases secretions -give glycopyrrolate. |
| Propofol (Diprivan) | GABA-A agonist | 1.5–2.5 mg/kg IV push | 15–30 sec | 5–10 min | Status epilepticus (anticonvulsant), elevated ICP (lowers ICP). | ⚠️ Causes significant hypotension -avoid in shock, hypovolemia. Egg/soy allergy (controversial). |
| Midazolam (Versed) | GABA-A agonist (benzo) | 0.1–0.3 mg/kg IV push | 1–2 min | 15–30 min | Rarely used for RSI (slower onset). Backup option. Provides amnesia. | ⚠️ Hypotension. Slower onset than etomidate/ketamine. Can reverse with flumazenil. |
| PARALYTICS (NEUROMUSCULAR BLOCKERS) | ||||||
| Succinylcholine (Anectine) | Depolarizing NMB -mimics ACh, sustained depolarization → paralysis | 1–1.5 mg/kg IV push | 30–45 sec | 6–10 min | Fastest onset + shortest duration. Good when you need to quickly reassess neuro status (e.g., stroke). | ⚠️ Hyperkalemia (burns > 48h, crush injury, denervation, renal failure with K⁺ > 5.5). Malignant hyperthermia (personal/family history). Myasthenia gravis. |
| Rocuronium (Zemuron) | Non-depolarizing NMB -competitive ACh blocker at nicotinic receptor | 1.2 mg/kg IV push (RSI dose) | 45–60 sec | 45–70 min | When succinylcholine is contraindicated. Reversible with sugammadex (16 mg/kg for immediate reversal). Becoming first-line at many centers. | ⚠️ Long duration -if can't intubate AND can't ventilate, patient is paralyzed for 45+ min (unless sugammadex available). |
⚠️ Cannot Intubate, Cannot Oxygenate (CICO) -Surgical Airway
If 2 intubation attempts fail AND cannot bag-mask ventilate AND LMA fails → cricothyrotomy. Palpate cricothyroid membrane (between thyroid and cricoid cartilage) → vertical skin incision → horizontal stab through membrane → insert bougie → railroad 6.0 ETT or cric tube. This is the final rescue. Do not delay.
If 2 intubation attempts fail AND cannot bag-mask ventilate AND LMA fails → cricothyrotomy. Palpate cricothyroid membrane (between thyroid and cricoid cartilage) → vertical skin incision → horizontal stab through membrane → insert bougie → railroad 6.0 ETT or cric tube. This is the final rescue. Do not delay.
Difficult Airway Predictors (LEMON):
L ook externally (short neck, obesity, facial trauma, beard)
E valuate 3-3-2 (3 fingers mouth opening, 3 fingers hyoid-to-chin, 2 fingers thyroid notch-to-floor of mouth)
M allampati score (III/IV = harder)
O bstruction (epiglottitis, angioedema, tumor, hematoma)
N eck mobility (c-spine collar, ankylosing spondylitis, rheumatoid arthritis)
L ook externally (short neck, obesity, facial trauma, beard)
E valuate 3-3-2 (3 fingers mouth opening, 3 fingers hyoid-to-chin, 2 fingers thyroid notch-to-floor of mouth)
M allampati score (III/IV = harder)
O bstruction (epiglottitis, angioedema, tumor, hematoma)
N eck mobility (c-spine collar, ankylosing spondylitis, rheumatoid arthritis)
⚙️ Ventilator Modes Explained
▶ Ventilator Modes Explained, AC, PC, SIMV, PSV, APRV (tap to expand)
Every vent mode answers two questions: (1) What triggers a breath? (patient or machine), (2) What's guaranteed -volume or pressure?
| Mode | How It Works | You Set | What Varies | Best For | ⚠️ Watch For |
|---|---|---|---|---|---|
| AC/VC Assist Control / Volume Control | Every breath (patient-triggered or machine-triggered) delivers a set tidal volume. | TV, RR, FiO₂, PEEP, flow rate | Pressure (Ppeak varies with compliance/resistance) | Most common mode. Default for most intubations. ARDS (guarantees 6 mL/kg TV). | ⚠️ If compliance drops → pressures rise → barotrauma. Watch Pplat. |
| AC/PC Assist Control / Pressure Control | Every breath delivers a set pressure for a set inspiratory time. | Pressure, I-time, RR, FiO₂, PEEP | Tidal volume (varies with compliance) | When you want to limit pressures strictly. Neonatal/pediatric. Some ARDS protocols. | ⚠️ If compliance worsens → TV drops → hypoventilation. Must monitor TV closely. |
| SIMV Synchronized Intermittent Mandatory Ventilation | Delivers set number of mandatory breaths. Patient can take extra breaths on their own (unsupported or with PS). | TV, RR, FiO₂, PEEP, PS level | Patient's spontaneous breaths are variable | Weaning mode -gradually reduce mandatory rate as patient takes over. | ⚠️ Increases work of breathing if PS too low on spontaneous breaths. Largely fallen out of favor -SBT preferred for weaning. |
| PSV Pressure Support Ventilation | Patient triggers every breath. Vent augments each breath with set pressure support. | PS level, FiO₂, PEEP | TV and RR (entirely patient-driven) | SBT (PS 5–8 cmH₂O), weaning assessment, awake cooperative patients. | ⚠️ No backup rate -if patient becomes apneic, no breaths are delivered. Need apnea backup alarm. |
| APRV Airway Pressure Release Ventilation | Sustained high pressure (P-high) with brief releases to low pressure (P-low) for CO₂ clearance. Essentially inverse-ratio CPAP. | P-high, T-high, P-low, T-low | TV during releases | Refractory ARDS -keeps alveoli open with sustained high pressure. Allows spontaneous breathing. | ⚠️ Complex to manage. Requires experience. Not proven superior to standard lung-protective ventilation. Hemodynamic effects from sustained high intrathoracic pressure. |
Quick Decision: Which Mode?
| Scenario | Mode | Why |
|---|---|---|
| Fresh intubation (default) | AC/VC | Guarantees tidal volume. Simple. Predictable. |
| ARDS | AC/VC (6 mL/kg PBW) | Must control TV tightly for lung protection. |
| COPD / asthma | AC/VC (low rate, long I:E) | Need guaranteed TV with long expiratory time to avoid air trapping. |
| High peak pressures | Switch AC/VC → AC/PC | Limits pressure delivery. But monitor TV -may drop. |
| Ready to wean / SBT | PSV 5–8 / PEEP 5 | Minimal support. Tests if patient can breathe independently. |
| Refractory ARDS | APRV (by experienced team) | Last resort before ECMO. Keeps alveoli recruited. |
🫁 Oxygenation vs Ventilation
The Most Important Concept on the Vent
Oxygenation and ventilation are two completely separate physiologic processes. They are fixed by different vent settings. Confusing them is the #1 mistake interns make in the ICU. If you learn nothing else about the vent, learn this table.
| 🔵 Oxygenation (O₂) | 🔴 Ventilation (CO₂) | |
|---|---|---|
| What is it? | Getting oxygen INTO the blood | Getting CO₂ OUT of the blood |
| Measured by | PaO₂ (ABG) or SpO₂ (pulse ox) | PaCO₂ (ABG) or EtCO₂ (capnography) |
| Normal values | PaO₂ 80–100 mmHg, SpO₂ 94–98% | PaCO₂ 35–45 mmHg |
| Problem | Hypoxemia -O₂ too low | Hypercapnia -CO₂ too high Hypocapnia -CO₂ too low |
| Vent settings that fix it | FiO₂ (↑ = more O₂ delivered) PEEP (↑ = recruits collapsed alveoli, improves gas exchange surface area) | Respiratory Rate (↑ RR = blow off more CO₂) Tidal Volume (↑ TV = each breath removes more CO₂) Together = Minute Ventilation (MV = RR × TV) |
| Think of it as | How much oxygen you're putting IN the lungs | How much air you're moving THROUGH the lungs |
Quick Decision Framework
🔵 Patient is HYPOXEMIC (SpO₂ low)
Step 1: ↑ FiO₂ (quick fix -increase the O₂ concentration)
Step 2: ↑ PEEP (recruit alveoli -increases surface area for gas exchange)
Step 3: Prone positioning -flip patient face-down ≥ 16h/day. Redistributes ventilation to dorsal lung (where perfusion is greatest) → improves V/Q matching. Mortality benefit in severe ARDS (P/F < 150) PROSEVA, 2013
Step 4: Inhaled nitric oxide (iNO) 5–40 ppm or inhaled epoprostenol -selective pulmonary vasodilators. Dilate vessels ONLY in ventilated alveoli → redirects blood flow to functioning lung units → improves V/Q matching + oxygenation. ⚠️ No proven mortality benefit -used as rescue/bridge therapy.
Step 5: ECMO (VV-ECMO) -when all above fail. Blood is oxygenated externally. Consider if P/F < 80 despite optimal vent + prone + iNO.
⚠️ Do NOT increase RR or TV -these do not fix oxygenation. Breathing faster doesn't put more O₂ in the blood if the alveoli can't exchange gas.
Step 2: ↑ PEEP (recruit alveoli -increases surface area for gas exchange)
Step 3: Prone positioning -flip patient face-down ≥ 16h/day. Redistributes ventilation to dorsal lung (where perfusion is greatest) → improves V/Q matching. Mortality benefit in severe ARDS (P/F < 150) PROSEVA, 2013
Step 4: Inhaled nitric oxide (iNO) 5–40 ppm or inhaled epoprostenol -selective pulmonary vasodilators. Dilate vessels ONLY in ventilated alveoli → redirects blood flow to functioning lung units → improves V/Q matching + oxygenation. ⚠️ No proven mortality benefit -used as rescue/bridge therapy.
Step 5: ECMO (VV-ECMO) -when all above fail. Blood is oxygenated externally. Consider if P/F < 80 despite optimal vent + prone + iNO.
⚠️ Do NOT increase RR or TV -these do not fix oxygenation. Breathing faster doesn't put more O₂ in the blood if the alveoli can't exchange gas.
🔴 Patient is HYPERCAPNIC (CO₂ high)
Step 1: ↑ Respiratory Rate (blow off more CO₂ per minute)
Step 2: ↑ Tidal Volume (each breath removes more CO₂)
Minute Ventilation = RR × TV → this is what determines CO₂ clearance
Step 3 (if bronchospasm): Heliox (70–80% helium / 20–30% O₂) -helium is less dense than nitrogen → reduces turbulent airflow resistance → gas flows past the obstruction more easily → improves ventilation in severe bronchospasm/upper airway obstruction refractory to bronchodilators. ⚠️ Limitation: Max FiO₂ is 30% (rest is helium), so don't use if patient needs high FiO₂.
⚠️ Do NOT increase FiO₂ or PEEP -these do not remove CO₂. Giving more oxygen doesn't help ventilation.
⚠️ Watch for auto-PEEP: If RR too high (especially in COPD), patient may not fully exhale → air trapping → hemodynamic collapse.
Step 2: ↑ Tidal Volume (each breath removes more CO₂)
Minute Ventilation = RR × TV → this is what determines CO₂ clearance
Step 3 (if bronchospasm): Heliox (70–80% helium / 20–30% O₂) -helium is less dense than nitrogen → reduces turbulent airflow resistance → gas flows past the obstruction more easily → improves ventilation in severe bronchospasm/upper airway obstruction refractory to bronchodilators. ⚠️ Limitation: Max FiO₂ is 30% (rest is helium), so don't use if patient needs high FiO₂.
⚠️ Do NOT increase FiO₂ or PEEP -these do not remove CO₂. Giving more oxygen doesn't help ventilation.
⚠️ Watch for auto-PEEP: If RR too high (especially in COPD), patient may not fully exhale → air trapping → hemodynamic collapse.
Common Scenarios -What to Adjust
| ABG Shows | Problem | Adjust | ⚠️ Watch For |
|---|---|---|---|
| PaO₂ 55, SpO₂ 88% | Hypoxemia | ↑ FiO₂ and/or ↑ PEEP | FiO₂ > 0.6 for > 24h → O₂ toxicity. Wean FiO₂ first, then PEEP. |
| PaCO₂ 65, pH 7.22 | Respiratory acidosis (hypoventilating) | ↑ RR or ↑ TV (↑ minute ventilation) | Auto-PEEP in COPD. Pplat > 30 if TV too high. Max RR ~35 before ineffective. |
| PaCO₂ 25, pH 7.55 | Respiratory alkalosis (overventilating) | ↓ RR or ↓ TV (↓ minute ventilation) | Patient may be anxious/in pain → treat the cause. Don't just sedate to fix CO₂. |
| PaO₂ 55 AND PaCO₂ 60 | Both hypoxemic + hypercapnic | ↑ FiO₂/PEEP (for O₂) AND ↑ RR/TV (for CO₂). If refractory → prone + iNO + ECMO. | Suggests severe disease (ARDS + dead space). Consider prone, paralytics, iNO, ECMO. |
| PaO₂ 120, FiO₂ 1.0 | Over-oxygenating | ↓ FiO₂ (wean to target SpO₂ 92–96%) | Hyperoxia harms: ↑ mortality in cardiac arrest, stroke, MI. Wean FiO₂ aggressively. |
The Memory Trick
🔵
O₂ = FiO₂ + PEEP
Escalation: FiO₂ → PEEP → Prone → iNO → ECMO
🔴
CO₂ = RR × TV
"How much air am I moving?"
⚠️ Permissive hypercapnia: In ARDS, it's OK to let CO₂ run high (up to 60–70) and pH drop to ~7.20 -as long as oxygenation is maintained. The priority is lung-protective ventilation (TV 6 mL/kg, Pplat ≤ 30). Don't sacrifice lung protection to normalize a CO₂ number. Same principle applies in status asthmaticus (accept PaCO₂ 60–80 with pH > 7.20 to avoid breath stacking and auto-PEEP).
Oxygen Dissociation Curve (40-50-60 / 70-80-90 Rule)
The relationship between PaO₂ (the partial pressure of dissolved O₂) and SpO₂ (% of hemoglobin saturated) is sigmoid, not linear. Memorizing three points on the curve lets you mentally convert between the two at the bedside.
| PaO₂ (mmHg) | SpO₂ (%) | What it means |
|---|---|---|
| 40 | 70 | Mixed venous blood. Severe hypoxemia if arterial. |
| 50 | 80 | Critically low. On the steepest part of the cliff. |
| 60 | 90 | The "knee." Above this you're on the safe plateau; below, on a cliff. |
| ~95-100 | 97-100 | Normal arterial. Far up the plateau. |
Bedside shortcut: on the steep part of the curve (SpO₂ 70-90), SpO₂ minus 30 ≈ PaO₂. So an SpO₂ of 88 ≈ PaO₂ ~58. Above SpO₂ 90 the plateau is too flat for this trick to work, small SpO₂ changes hide much larger PaO₂ swings.
Why the curve has a knee at SpO₂ 90 / PaO₂ 60
- Above the knee (PaO₂ > 60, SpO₂ > 90): flat plateau. Big PaO₂ changes produce only small SpO₂ changes. PaO₂ 100 vs PaO₂ 80 both look like 96-97% on the pulse ox.
- Below the knee (PaO₂ < 60, SpO₂ < 90): steep cliff. Small PaO₂ drops produce massive SpO₂ drops. Crashes look sudden because the curve falls off fast here.
- Why this matters for targets: aim for SpO₂ ≥ 92% (general) or 88-92% (COPD CO₂ retainers, permissive hypoxemia in ARDS). Sitting at 92% is at the edge, small drops can plummet quickly.
Curve shifts (the Bohr effect and friends)
| Direction | Effect | Caused by |
|---|---|---|
| RIGHT shift | Hgb releases O₂ more easily (higher P50). Good for tissues, bad for lungs at low PaO₂. | CADET, face Right: ↑ CO₂, Acidosis, 2,3-DPG (BPG), Exercise, Temperature. |
| LEFT shift | Hgb holds O₂ tighter (lower P50). Hgb saturates well in the lungs but unloads poorly to tissues. | Hypothermia, alkalosis, ↓ CO₂, ↓ 2,3-BPG (stored blood), CO poisoning, methemoglobin, fetal hemoglobin. |
Two states where the pulse ox lies:
- CO poisoning: SpO₂ reads ~100% even though tissues are profoundly hypoxic. The pulse ox can't distinguish HbCO from HbO₂. Use co-oximetry (carboxyhemoglobin level) on a venous or arterial sample. Treat with 100% O₂ via NRB; hyperbaric for severe cases.
- Methemoglobinemia: SpO₂ stuck around 85% regardless of true saturation. Suspect with cyanosis unresponsive to O₂, "chocolate brown" blood, history of dapsone, benzocaine, nitrites, or aniline dyes. Treat with methylene blue 1-2 mg/kg IV (avoid in G6PD deficiency).
P/F ratio = PaO₂ ÷ FiO₂ -the single best number to assess oxygenation on a vent.
> 300: Normal
200–300: Mild ARDS
100–200: Moderate ARDS
< 100: Severe ARDS → consider prone, paralytics, ECMO
> 300: Normal
200–300: Mild ARDS
100–200: Moderate ARDS
< 100: Severe ARDS → consider prone, paralytics, ECMO
Types of Respiratory Failure
| Type | Name | Mechanism | ABG Pattern | Common Causes | Treatment Focus |
|---|---|---|---|---|---|
| Type 1 | Hypoxemic | Failure of gas exchange -O₂ can't cross alveolar membrane into blood. V/Q mismatch, shunt, diffusion impairment. | PaO₂ < 60 PaCO₂ normal or low | Pneumonia, ARDS, pulmonary edema, PE, pulmonary fibrosis, atelectasis | 🔵 FiO₂ + PEEP → prone → iNO → ECMO |
| Type 2 | Hypercapnic | Failure of ventilation -can't move enough air to clear CO₂. Pump failure (muscles, drive, mechanics). | PaCO₂ > 50 pH < 7.35 PaO₂ may be low too | COPD, asthma, obesity hypoventilation, neuromuscular disease (GBS, MG, ALS), drug overdose (opioids), chest wall deformity | 🔴 RR × TV (↑ minute ventilation). BiPAP first if possible. |
| Type 3 | Perioperative | Atelectasis from anesthesia, supine positioning, diaphragm splinting (pain, abdominal distension). | PaO₂ low PaCO₂ usually normal | Post-surgical (especially abdominal/thoracic), obesity, poor pain control limiting deep breathing | Incentive spirometry, early mobilization, pain control, CPAP if needed |
| Type 4 | Shock | Hypoperfusion → insufficient O₂ delivery to tissues despite adequate lung function. Respiratory muscles fatigue from hypoperfusion. | Lactic acidosis Mixed picture | Cardiogenic shock, septic shock, hypovolemic shock, Category E PE | Treat the shock first (fluids, vasopressors, inotropes). Intubate to reduce O₂ consumption by respiratory muscles. |
Why does this matter? Knowing the type tells you what to fix. Type 1 → fix oxygenation (FiO₂/PEEP). Type 2 → fix ventilation (RR/TV or BiPAP). Type 3 → prevent/reverse atelectasis. Type 4 → fix the circulation, not just the lungs.
📌 Settings
Initial Vent Settings
| Parameter | Standard | ARDS | COPD/Obstructive |
|---|---|---|---|
| Mode | AC/VC or AC/PC | AC/VC | AC/VC or SIMV |
| Tidal Volume | 8 mL/kg PBW | 6 mL/kg PBW | 6–8 mL/kg PBW |
| Rate | 14–16 /min | 18–22 /min | 10–14 /min (avoid stacking) |
| FiO₂ | Start 1.0, wean | Wean to keep SpO₂ 88–95% | Target SpO₂ 88–92% |
| PEEP | 5 cmH₂O | 8–16 (ARDSnet table) | Auto-PEEP concern -keep low |
| I:E Ratio | 1:2 | 1:2 to 1:3 | 1:3 to 1:4 (more time to exhale) |
📌 Trouble
Acute Deterioration on the Vent -DOPE
Patient suddenly desaturating or high pressures alarm → Call for help + use DOPE mnemonic immediately
D -Displacement
- ETT displaced (too deep → right mainstem, or dislodged)
- Check: confirm with laryngoscope, CXR, ETCO₂, auscultation
- Fix: reposition or replace tube
O -Obstruction
- Mucus plug, biting tube, kinked circuit
- Check: suction catheter passes easily? Pass suction first
- Fix: suction, reposition head, bite block
P -Pneumothorax
- Tension pneumothorax: absent breath sounds + tracheal deviation + hypotension
- Fix: needle decompression NOW (2nd ICS, MCL or 4th ICS, anterior axillary line) then chest tube. Do NOT wait for CXR if hemodynamically unstable.
E -Equipment
- Vent malfunction, circuit disconnect, O₂ supply failure
- Fix: disconnect from vent → manually bag the patient → troubleshoot equipment
High Peak, Normal Plateau
Peak – Plateau > 10 cmH₂O → airway resistance problem (mucus plug, bronchospasm, kinked tube). Treat: suction, bronchodilators, reposition.
High Peak AND High Plateau
Both elevated → decreased compliance problem (worsening ARDS, pneumothorax, pulmonary edema, pneumonia). Check CXR, assess clinically.
🧪 Workup
Workup
- ABG pre/post intubation
- CXR -ETT 2-4cm above carina
- Plateau pressure -goal <30
- Driving pressure -Pplat−PEEP, goal <15
- Auto-PEEP -expiratory hold
- Peak vs Plateau -high peak + normal plat = airway resistance; both high = compliance problem
🚨 Management
Management
- Lung-protective: TV 6–8 mL/kg PBW, Pplat < 30, driving pressure < 15
- ARDS: TV 6 mL/kg PBW ARDSNet, 2000, PEEP per ARDSNet table, prone if P/F < 150 PROSEVA, 2013
- Daily SBT: FiO₂ ≤ 40%, PEEP ≤ 8, following commands → PSV 5/5 × 30 min
- Sedation: RASS 0 to −2. Daily SAT before SBT.
💊 Medications
Medications
| Drug | Dose | Route | Notes |
|---|---|---|---|
| Propofol (Diprivan) | 5–50 mcg/kg/min | IV | First-line sedation. ⚠️ Propofol infusion syndrome (PRIS) risk if > 48h or > 80 mcg/kg/min (check CK, triglycerides, lactate). |
| Fentanyl (Sublimaze) | 25–200 mcg/hr | IV | Analgesia-first approach. Preferred analgesic in ICU. Lipophilic -accumulates > 72h. |
| Cisatracurium | 1–3 mcg/kg/min | IV | Neuromuscular blockade for severe ARDS × 48h. Must have adequate sedation first -paralyzed + aware = torture. ACURASYS, 2010 |
| Dexmedetomidine | 0.2–1.5 mcg/kg/hr | IV | Less delirium than benzos MENDS, 2007. SEDCOM, 2009. DEXCOM, 2016: reduced delirium and shorter time to extubation vs midazolam. ⚠️ Bradycardia, hypotension. No respiratory depression -can use during SBT. |
NONSEDA, 2020: No sedation vs light sedation in mechanically ventilated patients showed similar outcomes, though no-sedation had more agitation episodes. Supports minimizing sedation depth when feasible.
🔓 Weaning & Extubation
Ventilator Weaning & Extubation
Step 1: Daily Spontaneous Awakening Trial (SAT)
- Stop sedation infusions daily (unless contraindicated: active seizures, alcohol withdrawal, paralytics, elevated ICP)
- Assess: Is patient following commands? Opening eyes? Breathing comfortably?
- Restart sedation at half dose if patient fails (agitation, RR > 35, SpO₂ < 88%, distress)
Step 2: Spontaneous Breathing Trial (SBT)
Perform if SAT passes. Place on minimal vent support (CPAP 5 / PS 5–8) for 30–120 minutes.
SBT readiness criteria: FiO₂ ≤ 40%, PEEP ≤ 8, hemodynamically stable (no/low vasopressors), adequate mental status, intact cough reflex.
Pass criteria -ALL of the following:
- RR < 30, SpO₂ > 90%, TV > 5 mL/kg PBW
- RSBI (Rapid Shallow Breathing Index) = RR ÷ Vt (in L) < 105 -most validated weaning predictor
- No distress, paradoxical breathing, or diaphoresis
- HR and BP within 20% of baseline
Step 3: Extubation Checklist
- Passed SBT ✓
- Airway reflexes intact -strong cough, follows commands
- Cuff leak test: deflate cuff → listen for air leak around tube. No leak suggests laryngeal edema → post-extubation stridor risk → give dexamethasone and delay extubation
- Secretion burden manageable (not suctioning > q2h)
- Consider dexamethasone 8 mg IV q8h × 4 doses starting 12h before extubation if intubated > 7 days or failed cuff leak
- Anesthesia or airway team notified if anticipated difficult reintubation
⚠️ Failed Extubation: Need to reintubate within 48–72 hours -associated with significantly higher mortality (up to 25–50%). Better to wait one more day than to extubate prematurely. Risk factors for failure: age > 65, COPD, HF, weak cough, excessive secretions, high RSBI.
Post-extubation: Apply supplemental O₂ (nasal cannula or HFNC). Monitor closely for 24–48h. If high-risk for reintubation → prophylactic HFNC or NIV (BiPAP) post-extubation reduces reintubation rates.
🗣️ Tracheostomy Speaking Valve (Passy-Muir)
⚠️ THE ONE RULE THAT CAN KILL: deflate the cuff first. The Passy-Muir Valve (PMV* (Passy-Muir Valve, the speaking valve)) is a one-way valve -air enters through the trach on inhalation, but the only exit on exhalation is up around the tube and out through the larynx, mouth, and nose. If the cuff is still inflated it blocks that exit, so air stacks with every breath → rising intrathoracic pressure → barotrauma and potentially fatal respiratory arrest. The cuff must be 100% deflated and a leak around the tube confirmed before the valve goes on. Never place a PMV on an inflated cuff.
How It Works
The PMV is a bias-closed, no-leak one-way valve that snaps onto the trach hub (with a quarter-turn) or sits in-line on the ventilator circuit. It is the only speaking valve that stays closed at rest: it opens on inhalation to let air in through the trach, then closes on exhalation and forces the exhaled breath up through the vocal folds and upper airway. That redirected, continuous column of air is what restores voice and subglottic pressure -the physiologic basis for nearly all of its benefits.
Other speaking valves are bias-open (open at rest). The PMV's closed-at-rest design is what re-establishes a continuous subglottic air column, which is why it tends to outperform on phonation and swallowing.
Indications & Benefits
| Indication | Why it works |
|---|---|
| Restore voice / phonation | Exhaled air is forced through the larynx instead of out the trach, giving audible speech. The primary reason it is placed and the biggest quality-of-life and delirium-reducing win. |
| Improve swallowing, reduce aspiration | Closing on exhalation restores subglottic pressure and normal aerodigestive pressures, improving laryngeal sensation, cough strength, and airway protection. |
| Better secretion clearance & cough | Restored subglottic pressure produces a more effective, productive cough so secretions clear through the mouth rather than needing trach suction. |
| Restore smell & taste | Re-establishing nasal and oral airflow returns olfaction, and with it taste and appetite. |
| Facilitate weaning & decannulation | Reintroduces upper-airway airflow and reconditions a more physiologic breathing pattern, a step toward capping and tube removal. |
| Restore physiologic PEEP | The closed exhalation phase recreates the native end-expiratory pressure that is lost when the upper airway is bypassed. |
Contraindications
| Type | Contraindication | Why |
|---|---|---|
| ABSOLUTE | Inflated cuff | Blocks the only exhalation route → air stacking → barotrauma / fatal arrest. Must be fully deflated first. |
| ABSOLUTE | Foam-filled cuff (e.g., Bivona Fome-Cuf) | Self-inflates and cannot be reliably kept deflated, so the exhalation path can re-occlude. Same trapping risk. |
| ABSOLUTE | Total laryngectomy | No patent connection from trachea to upper airway -exhaled air has nowhere to go. |
| ABSOLUTE | Unconscious / comatose / unstable | Cannot protect the airway or signal distress, so the valve cannot be safely trialed. |
| CAUTION | Severe upper-airway obstruction (tracheal/subglottic stenosis, bilateral vocal-fold paralysis, large granulation, or trach tube too big for the airway) | Not enough room to exhale around the tube. Always do the leak check first; no leak means do not place. |
| CAUTION | Severe aspiration risk | Redirecting airflow does not fix a grossly unsafe swallow; assess before trialing. |
| CAUTION | Thick, copious, unmanageable secretions | Secretions can occlude the valve membrane. |
| CAUTION | Severely reduced lung elasticity (end-stage obstructive disease) | Exhaling through the upper airway adds work of breathing the patient may not tolerate. |
Not for endotracheal tubes. The PMV is a tracheostomy device only; it is never placed on an ETT.
Bedside Placement & Safety
1
Confirm candidacy -awake, stable, none of the absolute contraindications above.
2
Suction the trach and oral secretions (have suction ready -deflation often triggers a cough).
3
Deflate the cuff fully and slowly. 100% down, no exceptions. This is the step that prevents the lethal complication.
4
Confirm a leak around the tube -feel/listen for exhaled air at the mouth and nose, or watch the returned tidal volume drop on the vent. No leak = airway too obstructed → do NOT place.
5
Apply the valve (quarter-turn for a friction-tight fit). Coach: breathe in through the valve, voice on exhalation.
6
Monitor SpO₂, work of breathing, and comfort. Remove the valve immediately for rising work of breathing, desaturation, or distress -taking it off instantly restores the open exhalation path.
In-line on the ventilator: use the in-line valve (PMV 007, aqua), then adjust the vent for the cuff-deflation leak: reduce or remove set PEEP (the restored upper airway supplies physiologic PEEP, and added PEEP just escapes the open airway), increase set tidal volume to compensate for the leak, and silence/adjust the low-volume and low-pressure alarms (returned volume reads low by design, not from a circuit fault).
Pimp Questions
Why must the tracheostomy cuff be fully deflated before placing a Passy-Muir valve?
The PMV is a one-way valve: air enters through the trach on inhalation but can only exit up around the tube and out the upper airway on exhalation. An inflated cuff blocks that exit, so air stacks with every breath, intrathoracic pressure climbs, and the patient can suffer barotrauma or fatal respiratory arrest. The cuff must be 100% deflated and a leak confirmed before the valve goes on.
A patient is in distress and desaturating minutes after a PMV was placed. First move?
Remove the valve immediately. Distress after PMV placement means air cannot escape, usually an incompletely deflated cuff, upper-airway obstruction, or a trach tube too large for the airway. Taking the valve off instantly reopens the exhalation path through the trach. Then suction, re-check that the cuff is fully down, and evaluate for obstruction before any re-trial.
📋 On Rounds
On Rounds
Pimp Questions
What is driving pressure and why does it matter?
Driving pressure = Pplat − PEEP. It reflects the stress on functional lung units. A driving pressure > 15 cmH₂O is independently associated with increased ARDS mortality even when TV and Pplat are within targets. It may be the most important vent parameter to minimize.
What is auto-PEEP and when does it occur?
Air trapping due to incomplete exhalation before the next breath -common in COPD/asthma. Causes hemodynamic compromise (reduced venous return) and barotrauma. Detected by expiratory hold maneuver. Treated by reducing RR, increasing I:E ratio (longer expiratory time), and bronchodilators.
The vent is alarming with high peak pressures. How do you troubleshoot?
Peak pressure = airway resistance + compliance + PEEP. High peak + normal plateau (< 30) = airway resistance problem: bronchospasm (give albuterol), mucus plug (suction), kinked ETT, biting tube (bite block/sedation), small ETT. High peak + high plateau (> 30)
What is driving pressure and why is it more important than tidal volume alone?
Driving pressure = Plateau pressure − PEEP. It represents the actual distending pressure applied to the lung parenchyma. Goal: < 15 cmH₂O. A landmark meta-analysis by Amato (2015) showed driving pressure was the ventilator variable most strongly associated with survival in ARDS -more predictive than tidal volume or plateau pressure alone.
📋 Daily Vent Check Presentation
"Mr. Patel is intubated day 3 for hypoxemic respiratory failure from aspiration pneumonia. Current vent settings: AC/VC, TV 420 mL (6 mL/kg PBW), RR 18, PEEP 8, FiO₂ 0.55. This morning's ABG: pH 7.38, pCO₂ 42, pO₂ 74 -P/F ratio 135, consistent with moderate ARDS. Pplat is 24, driving pressure 16. He had a SAT trial this morning -he was following commands but became tachypneic. We are holding the SBT today and will reassess tomorrow. He is on propofol and fentanyl, RASS −1. Fluid balance is negative 200 mL over the past 24 hours."
Clinical Examples
Case 1: ARDS, Severe Pneumonia
Presentation: 45M admitted with severe bilateral pneumonia and hypoxemic respiratory failure. SpO₂ 82% on 15L NRB, intubated emergently. ABG post-intubation: pH 7.34, PaO₂ 70 on FiO₂ 0.8 → P/F ratio 88 (severe ARDS, <100).
Vent Strategy (ARDSNet): Mode AC/VC. PBW ~63 kg → TV 6 mL/kg PBW = 378 mL (set 380 mL). RR 18, PEEP 12, FiO₂ 0.8. Confirm Pplat after first breath: target <30 cmH₂O. Driving pressure (Pplat − PEEP) target <15 cmH₂O. ARMA, 2000
Escalation: P/F ratio persists <150 after 12–16h on optimized settings → initiate prone positioning for 16h/day. Consider neuromuscular blockade (Cisatracurium (Nimbex)) if severe patient-ventilator dyssynchrony. Repeat ABG 30 min after every vent change.
Teaching point: Always use PBW (predicted body weight, from height and sex), not actual body weight, for TV calculation. Over-ventilating causes ventilator-induced lung injury (VILI) and increases mortality, even a few extra mL/kg matters.
Case 2: COPD Exacerbation, Auto-PEEP Risk
Presentation: 68F with severe AECOPD, on BiPAP for 4h with worsening hypercapnia (pH 7.18, pCO₂ 92). BiPAP failure → intubated with RSI using Ketamine (Ketalar) + Succinylcholine (Anectine).
Vent Strategy: Mode AC/VC. TV 6–8 mL/kg PBW. RR 12–14/min (low rate = more time to exhale). High inspiratory flow rate (60–80 L/min) to shorten inspiratory time. Target I:E ratio 1:4 (vs. normal 1:2) to maximize expiratory time and prevent breath stacking. Start PEEP 5.
Auto-PEEP check: Perform end-expiratory hold maneuver, press hold, read auto-PEEP off the ventilator display. Auto-PEEP >5 cmH₂O = air trapping. Treatment: decrease RR, increase expiratory time, aggressive bronchodilators (Albuterol + Ipratropium); if critical, briefly disconnect ETT and allow full passive exhalation.
Permissive hypercapnia: Target pH 7.25–7.35, not a normal pCO₂. Do not raise RR to normalize CO₂, this worsens air trapping. Hemodynamic stability is the goal, not a normal ABG.
Case 3: Ventilator Weaning, SAT + SBT Protocol
Presentation: 55M intubated day 5 for Category E PE with hemodynamic instability, now improving. On AC/VC, RR 14, TV 450 mL, PEEP 5, FiO₂ 0.35. SpO₂ 96%, hemodynamically stable, off vasopressors. RASS −1, follows commands, intact cough.
Step 1, SAT (Sedation Vacation): Hold Propofol and Fentanyl infusions every morning. Assess within 30 min: opens eyes to voice, follows commands, breathing comfortably? Fail criteria: agitation, RR >35, SpO₂ <88%, hemodynamic instability → restart sedation at half dose. Girard, 2008
Step 2, SBT (Spontaneous Breathing Trial): SAT passes → switch to PS 5 / PEEP 5 for 30–120 min. Readiness: FiO₂ ≤40%, PEEP ≤8, hemodynamically stable. Pass criteria: RR <35, SpO₂ >90%, no significant accessory muscle use, RSBI (f/VT in L) <105. Example: RR 18, TV 0.45L → RSBI = 40 → pass.
Decision: Passes both SAT + SBT → proceed to extubation. Fails repeatedly (≥3 attempts over multiple days) → discuss tracheostomy to facilitate long-term weaning, reduce dead space, and improve patient comfort.
Monitoring -Mechanical Ventilation
| Parameter | Frequency | Target / Action |
|---|---|---|
| ABG | 30 min after any vent change, then q4–6h | pH, PaCO2, PaO2, P/F ratio. Guides FiO2/PEEP (oxygenation) and RR/TV (ventilation) adjustments. |
| Daily SBT assessment | Every morning | Assess readiness: FiO2 ≤ 40%, PEEP ≤ 8, hemodynamically stable, no high-dose vasopressors, adequate mental status. RSBI < 105 (RR/TV in liters) predicts successful extubation. Girard, 2008: paired SAT + SBT improves outcomes. |
| Plateau pressure | q4–6h or with vent changes | Pplat < 30 cmH2O (lung protective). If exceeding → reduce TV, check for pneumothorax, bronchospasm, or mucus plugging. |
| Driving pressure | q4–6h | Driving pressure < 15 cmH2O (Pplat - PEEP). Strongest predictor of ARDS mortality Amato, 2015. Optimize by adjusting TV and PEEP. |
| SpO2 / FiO2 trending | Continuous SpO2, track P/F ratio | SpO2 target 88–95% in ARDS, 94–98% otherwise. Worsening P/F may indicate disease progression, fluid overload, or new complication. |
| Auto-PEEP check | q shift and with clinical concern | Expiratory hold maneuver. Auto-PEEP > 5 = air trapping → increase expiratory time (decrease RR, decrease I:E ratio). Common in COPD/asthma. |
| Sedation level (RASS) | q4h | Target RASS -2 to 0 (light sedation). Deeper sedation only if specific indication (prone, paralysis, severe agitation). Daily sedation awakening trial (SAT). |
| Daily SAT + SBT | Every morning | Girard, 2008: paired protocol -SAT first (hold sedation, assess arousal) → if passes → SBT (PS 5–8/PEEP 5 for 30–120 min). Reduces vent days and mortality. |
| VAE surveillance | Daily | Ventilator-associated events: new/worsening infiltrate, rising FiO2/PEEP after period of stability, fever, purulent secretions. Prevent with: HOB 30-45°, oral care, DVT/PUD prophylaxis, daily SBT. |
Every vent day is a bad day. The single best thing you can do for a ventilated patient is liberate them from the ventilator. Daily SAT + SBT is the most evidence-based strategy to shorten ventilator duration.
⚡ Summary
Summary
Escalate in Order
Nasal cannula (up to 6 L) → venturi mask → non-rebreather → high-flow nasal cannula → NIV → intubation. High-flow nasal cannula is not just more oxygen: it washes out nasopharyngeal dead space and delivers a few cmH₂O of PEEP, which is why it works in hypoxemic failure where a non-rebreather has stopped working.
CPAP or BiPAP
CPAP is one continuous pressure and fixes oxygenation, so it is the choice in cardiogenic pulmonary edema, where it also cuts preload and afterload. BiPAP adds an inspiratory boost above the expiratory pressure, and that difference is the tidal volume, so it is what fixes ventilation in a hypercapnic COPD exacerbation. NIV in COPD and cardiogenic edema reduces intubation and mortality; it is far weaker evidence in pneumonia and ARDS.
Four Reasons to Intubate
Failure to protect the airway, failure to oxygenate, failure to ventilate, and anticipated clinical course. The fourth is the one that gets under-called: a patient who is predictably deteriorating is safer intubated now, in daylight with a full team, than at 3 am as a crash airway.
The Two Knobs
Oxygenation is FiO₂ and PEEP. Ventilation is respiratory rate and tidal volume. A low saturation means turn up PEEP or FiO₂; a high CO₂ means increase minute ventilation. Confusing the two is the commonest ventilator error, and raising the rate for a hypoxemic patient just causes breath stacking.
Starting Settings
Volume control, tidal volume 6 to 8 mL/kg of predicted (not actual) body weight, rate 12 to 16, PEEP 5, FiO₂ 100% then wean down quickly. Predicted body weight is calculated from height, because lung size tracks height, not weight: dosing a 6-foot obese patient on actual weight delivers a frankly injurious volume.
Watch Plateau Pressure, Not Peak
Keep plateau pressure below 30 cmH₂O and driving pressure below 15. A high peak with a normal plateau is an airway problem (secretions, bronchospasm, a kinked or biting tube); a high peak with a high plateau is a lung or chest wall compliance problem (pulmonary edema, ARDS, pneumothorax, abdominal distension). The measurement takes an inspiratory hold and it tells you which of those two you are dealing with.
Sudden Deterioration: Think DOPE
Displaced tube, Obstruction, Pneumothorax, Equipment failure. Disconnect from the ventilator and bag by hand: easy bagging points to the machine, difficult bagging points to the patient, and this single maneuver also relieves the breath stacking that causes hypotension in obstructive disease.
Wean With a Daily SBT
Screen daily and pair a spontaneous awakening trial with a spontaneous breathing trial, which reduces ventilator days and mortality. Rapid shallow breathing index below 105 predicts success. Passing an SBT is not enough on its own: the patient still needs to protect the airway and manage their secretions, and a cuff leak test is worth doing where laryngeal edema is a risk.
📄 One Pager
Text version
ICU · Ventilator · One Pager
Mechanical Ventilation
Know your numbers every morning. When in doubt -disconnect and bag. DOPE for acute deterioration. SAT + SBT daily to get them off the vent.
Initial Settings
ModeAC/VC (most common)
Tidal volume6–8 mL/kg PBW
Rate14–16 /min
FiO₂1.0 → wean to SpO₂ 94–98%
PEEP5 cmH₂O (start)
Acute Deterioration -DOPE
- D -Displacement (ETT too deep/dislodged)
- O -Obstruction (mucus plug, biting)
- P -Pneumothorax → needle decompress
- E -Equipment failure → bag the patient
Pressure Interpretation
- High Peak, Normal Plat: Airway resistance → suction, bronchodilator
- High Peak + High Plat: Compliance problem → PTX, ARDS, edema
- Driving pressure = Pplat − PEEP. Target ≤ 15.
Weaning -Daily SAT + SBT Girard 2008
- Stop sedation daily (SAT)
- SBT on CPAP 5 / PS 5–8 for 30–120 min
- RSBI < 105 = ready to extubate
- Pass both → extubate
📣 Sample Presentation
One-Liner
"Mr. Brown is a 64-year-old intubated for COPD exacerbation with hypercapnic respiratory failure. Currently on AC/VC: TV 450, RR 16, PEEP 5, FiO₂ 30%. Morning ABG: pH 7.38, pCO₂ 52, pO₂ 88."
Key Points to Cover on Rounds
Intubation indication: hypercapnic respiratory failure (pH 7.22, pCO₂ 78 on presentation, failed BiPAP). Current ABG improved: pH 7.38, pCO₂ 52 (his baseline is ~48). Vent: AC/VC, TV 450 mL (6 mL/kg), RR 16, PEEP 5, FiO₂ 30%. Plateau 22, no auto-PEEP. Sedation: propofol off, RASS 0, following commands. SAT passed, SBT with PSV 5/5 × 30 min -RR 18, TV 380, no distress. Plan: extubate today. BiPAP standby. Nebs q4h.
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