The Daily Ventilator Check: A Bedside Ready Reckoner for the Modern Internist

A Masterclass in Mechanical Ventilation Assessment

 

Dr Neeraj Manikath

 

 

 

1. The Silent Descent: A Clinical Introduction

It was 7:15 AM on a Tuesday. The night team had signed out the 58-year-old woman in Bed 12 as "stable on the vent." She had been admitted three days prior for severe community-acquired pneumonia evolving into ARDS. Her settings were volume-control, TV 6 mL/kg (360 mL), RR 16, PEEP 10, FiO₂ 60%. Her morning SpO₂ was 93%, and her blood pressure was 110/60. By all conventional metrics, she was "fine."

 

When I walked into the room for the morning round, the ventilator screen was glowing with a serene, repetitive waveform. But the patient was not serene. Her eyes were wide, her forehead beaded with sweat, and her accessory muscles were taut, pulling desperately against the catheter mount. The respiratory rate on the screen was 16, but her actual breathing rate was 32. The night team had noted a "mild tachycardia" of 115 bpm, attributing it to fever.

 

I reached for the ventilator, performed a 2-second expiratory hold, and the screen revealed an auto-PEEP of 12 cm H₂O. Her actual end-expiratory pressure was 22 cm H₂O. She was dynamically hyperinflating, trapped in a breath stacking cycle that was silently crushing her right ventricle and turning her alveoli into overstretched balloons. We were torturing her under the guise of "stable settings."

 

This case is not an anomaly; it is a daily reality in our ICUs. The ventilator is the most powerful organ-support device in modern medicine, yet it is often treated like a complicated microwave—set by a recipe, monitored by a single number (SpO₂), and adjusted only when the alarm screams. A "daily ventilator check" is not a checkbox on a morning rounds template. It is a physiological dialogue. It requires the clinician to translate pixels on a screen into the mechanics of a living, breathing lung.

 

This review is born from 25 years of standing at the bedside, tuning ventilators by hand and mind. It is a ready reckoner for the postgraduate trainee and the practicing consultant—a distillation of how master clinicians think, inspect, and intervene at the ventilator interface. Every paragraph herein is designed to be actionable. Let us decode the machine.

 

 

 

2. The Pathophysiology We Actually Use: The Equation of Motion

Most textbooks drown you in the physics of respiratory mechanics. At the bedside, you only need one equation—the Equation of Motion of the Respiratory System. Everything you see on the ventilator screen is a derivative of this single truth:

 

Pvent + Pmus = (Elastance × Volume) + (Resistance × Flow)

 

Let’s translate this into clinical English:

● Pvent is the pressure the machine generates.

● Pmus is the pressure the patient generates (which can be positive if they fight, or negative if they pull).

● Elastance × Volume is the Static Pressure—the pressure required to hold the lung open at that volume (Elastance is the inverse of Compliance).

● Resistance × Flow is the Dynamic Pressure—the pressure required to push the gas through the tubes and airways at that speed.

 

🪙 Clinical Pearl: The ventilator only measures Pvent at the machine end of the circuit. If Pmus is negative (patient actively inhaling), Pvent will drop (triggering the machine). If Pmus is positive (patient actively exhaling or fighting), Pvent will rise. You cannot interpret ventilator pressures without simultaneously asking: "What is the patient's muscle doing?"

 

When you understand this equation, the daily check becomes a mathematical detective game. If the peak pressure (Ppeak) rises, but the plateau pressure (Pplat) stays the same, the (Resistance × Flow) term has increased. The patient has bronchospasm, a mucus plug, or a kinked tube. If Ppeak and Pplat both rise together, the (Elastance × Volume) term has increased. The lung is stiffer (worsening edema, fibrosis, pneumothorax) or the volume is too high (overdistension).

 

 

 

3. The M-A-C-H-I-N-E Mnemonic: A Systematic Daily Check

A master clinician never approaches the ventilator randomly. We use a systematic, stepwise assessment to ensure nothing is missed. I teach the M-A-C-H-I-N-E mnemonic to all my registrars:

 

● M - Mechanics & Modes

● A - Auto-PEEP & Airway Resistance

● C - Circuit & Cuff

● H - Hemodynamics & Heart

● I - Interactions (Patient-Ventilator Synchrony)

● N - Numbers (FiO₂, SpO₂, PaO₂, PaCO₂)

● E - Escalation & Extubation Readiness

 

Let us dissect each letter with the granularity required at the bedside.

 

 

 

M - Mechanics & Modes: Decoding the Settings

First, acknowledge the mode. Do not just read the label; understand the philosophy. Is the machine controlling volume (Volume Control/AC) or pressure (Pressure Control/PC)? Is it controlling time (mandatory breaths) or letting the patient dictate time (Spontaneous/Support modes)?

 

⚡ Clinical Hack: In Volume Control, the machine guarantees the volume but sacrifices the pressure. The pressure will fluctuate based on lung stiffness and airway resistance. In Pressure Control, the machine guarantees the pressure but sacrifices the volume. The volume will fluctuate based on lung stiffness. Never chase a "normal" pressure in Volume Control without checking Pplat, and never chase a "normal" volume in Pressure Control without checking the delivered TV.

 

The Driving Pressure Paradigm (ΔP):
The most actionable mechanical metric of the last decade is Driving Pressure (ΔP = Pplat - PEEP). It represents the actual strain applied to the lung parenchyma with each breath.

 

Why is it superior to Pplat alone? Because Pplat includes PEEP. If you increase PEEP from 10 to 15, Pplat might rise from 25 to 30. A novice might panic ("Pplat is >30!"). But the master clinician calculates ΔP: 30 - 15 = 15. The strain on the lung hasn't changed; you've just shifted the baseline.

 

● Target: ΔP < 15 cm H₂O. If ΔP > 15, you are overdistending the functional lung, regardless of what the "ideal body weight" TV calculation told you.

 

🦪 Oyster: If you are in Pressure Control and cannot easily measure Pplat, calculate Driving Pressure dynamically: ΔP = Delivered Tidal Volume / Respiratory System Compliance. (Compliance = TV / [Pplat - PEEP]). If your compliance is 30 mL/cm H₂O and your TV is 360 mL, your ΔP is 12. Keep it under 15.

 

 

 

A - Auto-PEEP & Airway Resistance: The Hidden Killers

Auto-PEEP (or intrinsic PEEP) is the pressure that remains in the alveoli at the end of expiration when the patient hasn had enough time to empty their lungs. It is the silent assassin of the ICU.

 

How to detect it:

1. Look at the flow scalar: If the expiratory flow does not reach the zero baseline before the next inspiration begins, auto-PEEP is present. This is the most reliable visual cue.

2. The Expiratory Hold: Press the expiratory hold button on the ventilator for 2-3 seconds at the very end of expiration. The pressure will equilibrate and reveal the total PEEP (Total PEEP = Set PEEP + Auto-PEEP).

 

🪙 Clinical Pearl: Auto-PEEP is not just a COPD phenomenon. It happens in ARDS when the respiratory rate is too high (e.g., >20 bpm), even with low tidal volumes. A 6 mL/kg breath at 25 bpm still produces a high minute ventilation, leaving insufficient expiratory time if the airways are obstructed or compliance is low.

 

Airway Resistance (Raw):
Calculate it daily: Raw = (Ppeak - Pplat) / Flow.
If Flow is 60 L/min (1 L/sec), and Ppeak is 30, Pplat is 20, Raw is 10 cm H₂O/L/sec. Normal is <10.
If Raw suddenly spikes from 8 to 20, do not order a bronchodilator. First, check the ETT for a kink, check the bite block, and suction for a mucus plug. The tube itself can be the resistance.

 

 

 

C - Circuit & Cuff: The Hardware Check

The most sophisticated physiological reasoning is useless if the physical circuit is flawed.

 

1. The Leak Check: If the returned tidal volume is significantly less than the delivered volume, you have a leak. 🦪 **Oyster:** Where is the leak? If the measured Ppeak is disproportionately low alongside the volume loss, the leak is *above* the pressure sensor (i.e., in the circuit, the humidifier, or the exhalation valve). If Ppeak is normal but the returned volume is low, the leak is *below* the pressure sensor—almost always a **deflated ETT cuff** or a bronchopleural fistula. Inflate the cuff to 25-30 cm H₂O using a manometer. Stop guessing with the "pilot balloon" squeeze.

2. The Condensation Check: Water pooling in the circuit acts as a pendelluft reservoir, causing chaotic flow triggers and false auto-PEEP readings. Drain it.

3. The Tube Position Check: Lip marks shift. A tube taped at 22 cm at the lip can migrate to 18 cm with patient movement, resulting in right mainstem intubation and left lung collapse. Check the depth every shift.

 

 

 

H - Hemodynamics & Heart: The Cardio-Pulmonary Axis

The lung and the heart share a thoracic cavity. Changing the ventilator is an intervention on the cardiovascular system.

 

🪙 Clinical Pearl: PEEP does not decrease preload; it decreases venous return. In a volume-responsive patient (sepsis), decreasing venous return drops cardiac output and blood pressure. But in a heart failure patient with a dilated, overfilled RV, decreasing venous return is therapeutic—it decompresses the right heart. Master clinicians use PEEP as a pharmacological agent for the heart.

 

The RV Disaster:
ARDS causes pulmonary vascular constriction (hypoxia, hypercapnia, high alveolar pressure). The RV fails silently.
Signs of RV failure on the vent:

● Sudden rise in Pplat with a simultaneous drop in blood pressure.

● A widened pulse pressure variation (>15%) on the arterial line.

● Refractory hypoxemia (because a failing RV shunts blood away from the lungs via intracardiac pathways).

 

⚡ Clinical Hack: The PEEP Challenge. If you increase PEEP and the blood pressure drops >10%, you have reduced venous return to an empty heart—give fluids. If you increase PEEP and the blood pressure stays the same or rises, you have decompressed a failing RV—keep the PEEP, consider diuresis.

 

 

 

I - Interactions (Patient-Ventilator Synchrony): The Visual Assessment

Step away from the numbers. Stand at the bedside and watch the patient's chest and the ventilator screen simultaneously. Are they dancing together, or fighting?

 

1. Trigger Asynchrony: The patient starts to inhale, but the ventilator delays its breath. Look for a negative pressure deflection on the pressure waveform before the machine ramps up.

○ Fix: Increase trigger sensitivity (e.g., flow trigger to 2 L/min), or treat auto-PEEP (auto-PEEP creates a threshold load the patient must overcome before triggering).

2. Flow Asynchrony: The patient wants a deep, fast breath, but the machine delivers a slow ramp. The patient will pull vigorously against the set flow. The pressure waveform will show a "concave" shape during inspiration.

○ Fix: Increase the flow rate (e.g., to 60-80 L/min) or switch to Pressure Control (which delivers decelerating flow, matching initial high demand).

3. Cycling Asynchrony (Double-triggering): The machine cuts off the breath, but the patient is still inhaling. The patient immediately triggers a second breath, stacking volume.

○ Fix: Increase the inspiratory time (Ti) or increase the flow rate to shorten the breath, depending on the patient's neural rhythm. Ensure sedation is adequate.

 

🦪 Oyster: Refractory tachypnea on AC mode is almost always double-triggering. The ventilator screen shows a rate of 16, but if you watch the patient, they are taking 32 mini-breaths. Increase the flow rate or adjust Ti. Do not just increase sedation to blunt the drive; fix the machine's timing.

 

 

 

N - Numbers (FiO₂, SpO₂, PaO₂, PaCO₂): The Gas Exchange

Oxygenation Targets:
Chasing an SpO₂ of 100% in ARDS is a mistake. It requires toxic levels of FiO₂ or PEEP.

● Target SpO₂: 88-92% in moderate-severe ARDS. 94-98% in mild lung disease.

● The P/F Ratio: (PaO₂ / FiO₂). A quick bedside hack without an ABG: SpO₂ / FiO₂ (S/F ratio) closely correlates with P/F. If SpO₂ is 90% and FiO₂ is 60%, S/F is 150. You are in severe ARDS territory.

 

Carbon Dioxide Targets:

● Permissive Hypercapnia: We allow PaCO₂ to rise to 50-60 mmHg (sometimes up to 80 in extreme cases) to keep tidal volumes low and protect the lungs. 🪙 **Clinical Pearl:** **Permissive hypercapnia is only permissible if the pH is tolerable.** A pH of 7.20 is acceptable; a pH of 7.10 causes pulmonary vasoconstriction (worsening RV load) and myocardial depression. If pH < 7.15, buffer with sodium bicarbonate or initiate rescue therapies (prone, ECCO₂R).

 

 

 

E - Escalation & Extubation Readiness

When to Escalate (The Rescue Pathway):
If ΔP > 15, P/F < 150, and the patient is fighting the vent despite optimal sedation, you are losing the mechanical battle.

1. Prone Positioning: The definitive rescue. P/F improves by 20-40 mmHg in 1 hour by homogenizing V/Q match and reducing ΔP. Do it early (within 12-24 hrs of severe ARDS).

2. Recruitment Maneuvers: Highly controversial. The ART trial showed stepwise incremental PEEP recruitment increased mortality. Master clinicians use sustained inflation (PC 20, PEEP 20 for 2 mins) only if a quick derecruitment event occurred (e.g., disconnection), and only if hemodynamics are pristine.

3. ECCO₂R / ECMO: When ΔP cannot be kept < 15 without lethal acidosis, it's time to call the center.

 

When to Watch (Preparing for Extubation):
Do not delay the liberation process. The longer the vent, the higher the mortality.

● The Rapid Shallow Breathing Index (RSBI): f/Vt. < 105 predicts success. But do it during a spontaneous breathing trial (SBT), not on full support.

● The Cuff Leak Test: If the patient has been intubated > 7 days with a traumatic intubation or active upper airway infection, deflate the cuff. If the leaked volume is > 15% of the delivered TV, the airway is safe. If < 15%, treat with IV dexamethasone 8 mg q8h for 48 hours before extubating.

 

⚡ Clinical Hack: The "T-piece vs. PS" debate is dead. The latest evidence shows Pressure Support of 5-8 cm H₂O + PEEP 5 for the SBT is superior to a pure T-piece. It reduces the work of breathing through the ETT while still testing the patient's endurance.

 

 

 

4. Diagnostic Nuances: Subtle Signs That Separate Good from Great

A good clinician reacts to alarms. A great clinician reads the waveforms before the alarm ever sounds.

 

● The Sudden Spike in Ppeak: The good clinician orders a CXR and ABG. The great clinician auscultates for unilateral absent breath sounds (mucus plug), checks the ETT depth (right mainstem), and checks the circuit temperature (condensation/obstruction).

● The "Scuba Diver" Expiratory Pattern: If the patient actively purses their lips or uses their abdominal muscles to push air out on expiration, they are fighting to overcome auto-PEEP or high airway resistance. This is a visual diagnosis of expiratory flow limitation.

● The Over-distension Sign: On the pressure waveform in Volume Control, if the peak pressure curve flattens out at the top (a "beaked" waveform), the lung is reaching its elastic limit. You are overdistending. Drop the TV immediately.

 

🦪 Oyster: The EtCO₂ to PaCO₂ Gap. Normally, EtCO₂ is 2-5 mmHg lower than PaCO₂ due to alveolar dead space. If the gap widens (e.g., EtCO₂ 30, PaCO₂ 60), dead space has massively increased. This is the earliest physiological marker of a pulmonary embolism, severe ARDS progression, or a massive mucus plug. If EtCO₂ suddenly drops without a change in ventilation, suspect a catastrophic drop in cardiac output (PEEP crushing the RV, or a massive PE) or a circuit leak.

 

 

 

5. Management Intricacies: Drug Choices, Doses, and Sequencing

Managing the ventilated patient requires a meticulous choreography of drugs and settings.

 

Sedation Sequencing:

1. First line: Propofol (10-50 mcg/kg/min). Fast onset, fast off. Allows daily neuro checks. Pitfall: Hypotension, propofol infusion syndrome (watch triglycerides and lactate if > 48 hrs at high doses).

2. Second line: Midazolam (2-5 mg/hr). For prolonged runs (>3-4 days). Pitfall: Active metabolites accumulate in renal/hepatic failure, causing delirium.

3. The Adjunct: Fentanyl (25-100 mcg/hr). Analgesia-first sedation. Opioids blunt the respiratory drive, which is highly desirable if the patient is tachypneic and double-triggering.

 

🪙 Clinical Pearl: If the patient is tachypneic and fighting the vent, increasing propofol will drop their blood pressure before it stops their breathing. Opioids (fentanyl boluses) specifically target the respiratory drive. Give 50-100 mcg fentanyl, watch the rate drop to 18, then maintain with a drip.

 

Neuromuscular Blockade (NMB):

● Indication: Severe ARDS (P/F < 150) with refractory patient-ventilator dysynchrony or dangerous transpulmonary pressures.

● Drug: Rocuronium (bolus 50 mg, then infusion 10-40 mcg/kg/min).

● Pitfall: Myopathy. Never use NMB without deep sedation (RASS -5) and continuous EEG monitoring (to ensure they are not "awake" under the paralysis). Limit to 48 hours maximum.

 

Diuresis in ARDS:
The lung is a wet sponge. Improving oxygenation requires drying the sponge, but without crashing the systemic circulation.

● Drug: Furosemide drip (0.1-0.5 mg/kg/hr) rather than boluses. Boluses cause abrupt preload drops and hemodynamic chaos; drips provide gentle, sustained negative fluid balance. Target a negative balance of 1-2 L/day once the patient is out of the shock phase.

 

 

 

6. State-of-the-Art Updates: The Paradigm Shifts

The landscape of mechanical ventilation has undergone tectonic shifts in the last 5 years. If you are practicing based on textbooks from 2010, you are harming patients.

 

1. Driving Pressure is the North Star: The Amato meta-analysis (2015) and subsequent RCTs proved that Tidal Volume relative to ideal body weight is a poor surrogate for lung strain. A 6 mL/kg TV in a patient with a tiny functional lung (low compliance) still overdistends the alveoli. ΔP < 15 cm H₂O is the independent predictor of survival. Adjust TV to achieve ΔP < 15, even if that means dropping TV to 4 mL/kg.

2. The ROSE Trial (2019): Early continuous neuromuscular blockade (cisatracurium) for 48 hours in severe ARDS did not improve mortality compared to light sedation with rescue paralysis. The days of "paralyze all early ARDS" are over. Use NMB only for dysynchrony that cannot be fixed by sedation or vent adjustments.

3. The ART Trial (2017): The massive ALVEOLI and ART trials debunked aggressive stepwise recruitment maneuvers (incrementing PEEP to 30-40 cm H₂O). They increase barotrauma and mortality. Individualized PEEP titration based on best compliance/lowest ΔP is the modern standard.

4. High-Flow Nasal Cannula (HFNC) Post-Extubation: The HIGH-WEAN trial and subsequent data show HFNC post-extubation reduces reintubation in high-risk patients compared to conventional oxygen. It provides PEEP (3-5 cm H₂O), washes out dead space, and reduces work of breathing. Use it immediately after pulling the tube.

 

 

 

7. When to Escalate vs. When to Watch: Decision Thresholds

The internist's greatest virtue at the bedside is knowing when to act and when to sit on their hands. Panic kills; complacency kills. Here are the rational thresholds.

 

When to WATCH (Accept Permissive Sub-optimal States):

● SpO₂ 88-92%: In severe ARDS, this is a victory. Do not increase PEEP or FiO₂ to chase 95% if ΔP is already 14. You will overdistend or toxify the lung.

● PaCO₂ 55-60 mmHg (pH 7.25-7.35): Permissive hypercapnia is protective. It reduces tidal stretch. Do not increase TV to normalize CO₂.

● Blood Pressure 90/50: If the patient is on PEEP 16 for ARDS and has a MAP of 90 on norepinephrine, do not add more fluids. The PEEP is compressing the RV. Treat with diuresis or prone positioning to offload the right heart.

 

When to ESCALATE (Red Alert Thresholds):

● ΔP > 15 cm H₂O: Drop the TV. If TV is already at 4 mL/kg and ΔP is still > 15, you have exhausted lung-protective ventilation. Time for prone positioning.

● P/F < 150 for > 12 hours: Despite optimized PEEP/FiO₂, prone early. Do not wait for day 3. Prone positioning reduces 28-day mortality by 16% when done early and for >16 hrs/day.

● pH < 7.15 with PaCO₂ > 60: The acidosis is causing myocardial depression and pulmonary vasoconstriction. Buffer with Bicarb (if Na < 145) and call for ECCO₂R/ECMO.

● Sudden Refractory Hypoxemia: (SpO₂ drops from 90% to 70% on stable settings). This is not "worsening ARDS"—ARDS does not drop SpO₂ by 20% in 5 minutes. Think: mucus plug, pneumothorax, ETT migration, circuit disconnect. Auscultate, check circuit, grab a suction catheter, and order a stat portable CXR.

 

⚡ Clinical Hack: The Suction First Rule. When SpO₂ drops suddenly and Ppeak rises, do not reach for the FiO₂ dial. Reach for the suction catheter. A centrally located mucus plug blocking the mainstem bronchus is the most common cause of sudden refractory desaturation. Clear the airway first; oxygenate second.

 

 

 

8. The Master Mnemonic: The D-O-P-E-S Quick Troubleshoot

When the ventilator alarms, the adrenaline spikes. The novice clicks "silence." The master clicks "think." For sudden catastrophic changes (desaturation, high pressure alarms, hemodynamic collapse), use D-O-P-E-S:

 

Letter	Catastrophe	30-Second Bedside Action
D	Disconnection/Disconnect	Trace the circuit from the Y-piece to the machine. Check humidifier seals.
O	Obstruction (Mucus/Bite)	Suction immediately. Insert bite block. Check for water in circuit.
P	Pneumothorax	Auscultate for unilateral absence. Check for subcutaneous emphysema. Call for needle decompression if tension.
E	Equipment (Ventilator failure)	Disconnect from the vent. Bag the patient manually (Bag-valve-mask on 100% FiO₂). Then troubleshoot the machine.
S	Stacking (Auto-PEEP)	Disconnect from the vent for 5-10 seconds to let the trapped air escape ("manual derecruitment"). Reconnect with lower RR or higher flow.

 

 

 

9. The Daily Ventilator Checklist Summary Table

This table is your morning rounds cheat sheet. Print it, laminate it, and anchor it to every ICU bed.

 

Parameter	How to Check	Target / Normal	Red Flag (Action Required)
Mode / Settings	Read screen, confirm with order	AC/PC or SIMV/PS as indicated	Mode mismatch (e.g., AC in awake tachypneic patient)
Tidal Volume	Read Exhaled TV	6-8 mL/kg IBW (4-6 in ARDS)	TV < 4 mL/kg or > 8 mL/kg
Driving Pressure (ΔP)	Pplat - PEEP (or TV/Crs)	< 15 cm H₂O	> 15 cm H₂O (Drop TV, consider Prone)
Pplat	Inspiratory Hold (0.5-2 sec)	< 30 cm H₂O	> 30 cm H₂O (Check for overdistension)
Ppeak	Read screen	Varies (Pplat + [Raw x Flow])	Spike in Ppeak without Pplat spike (Suction/Check tube)
Auto-PEEP	Expiratory Hold; Flow scalar	0 cm H₂O	> 5 cm H₂O (Lower RR, increase exp time, treat Raw)
PEEP / FiO₂	Read screen; adjust per P/F	SpO₂ 88-92% (ARDS), 94-98% (Normal)	FiO₂ > 60% with PEEP > 12 (Consider prone if P/F <150)
Compliance (Crs)	TV / (Pplat - PEEP)	50-100 mL/cm H₂O	< 30 mL/cm H₂O (Stiff lungs, edema, fibrosis)
Resistance (Raw)	(Ppeak - Pplat) / Flow	< 10 cm H₂O/L/sec	> 15 cm H₂O/L/sec (Bronchospasm, plug, kink)
EtCO₂	Read screen	35-45 mmHg	Sudden drop (PE, shock, leak); Sudden rise (hypercapnia, fatigue)
Synchrony	Observe chest vs. screen waveform	Smooth rhythm, no fighting	Double-trigger, trigger delay, concave pressure trace
Hemodynamics	MAP, Pulse Pressure Variation	PPV < 10%, MAP > 65	PPV > 15% (Fluids if PEEP dropped MAP; RV failure if PEEP stabilized)
Circuit/Airway	Visual check, cuff manometer	ETT secure, cuff 25-30 cmH₂O, no leaks	Tube migration, leak, water in circuit

 

 

 

10. The Art of Liberation: A Final Word

The daily ventilator check is not just about keeping the patient alive; it is about preparing them for the day the machine is removed. Every morning, ask yourself: "Why is this patient still on the ventilator today?"

 

If the answer is "because their lungs are still stiff," then focus on ΔP and PEEP. If the answer is "because they are too sedated," then turn down the propofol. If the answer is "because their heart is failing," then diurese and support the RV.

 

The ventilator is an iron lung, a physiological lockbox. The master clinician holds the key: a deep understanding of elastance, resistance, and the delicate dance between alveolar pressure and venous return. Do your daily checks with your eyes, your hands, and your mind. Respect the equation of motion. Protect the driving pressure. And always, always, look at the patient before you look at the screen.

 

 

 

11. References

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2. Brower RG, Matthay MA, Morris A, et al. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342(18):1301-1308. doi:10.1056/NEJM200005043421801

3. Cavalcanti AB, Suzumura ÉA, Laranjeira LN, et al. Effect of Lung Recruitment and Titrated Positive End-Expiratory Pressure (PEEP) vs Low PEEP on Mortality in Patients With Acute Respiratory Distress Syndrome: A Randomized Clinical Trial. JAMA. 2017;318(14):1335-1345. doi:10.1001/jama.2017.14171

4. Moss M, Wellman DA, Cotsonis GA, et al. An appraisal of methodology of the recent clinical trials of the ARDS Network. Crit Care Med. 2003;31(11):S268-S272.

5. Goligher EC, Dres M, Fan E, et al. Mechanical Ventilation–Induced Diaphragm Atrophy: Impact on Ventilation Duration and Outcomes. Ann Am Thorac Soc. 2016;13(8):1284-1293. doi:10.1513/AnnalsATS.201603-175OC

6. Guérin C, Reignier J, Richard JC, et al. Prone positioning in severe acute respiratory distress syndrome. N Engl J Med. 2013;368(23):2159-2168. doi:10.1056/NEJMoa1214103

7. Slutsky AS, Ranieri VM. Ventilator-induced lung injury. N Engl J Med. 2013;369(22):2126-2136. doi:10.1056/NEJMra1208707

8. Papazian L, Forel JM, Gacouin A, et al. Neuromuscular blockers in early acute respiratory distress syndrome. N Engl J Med. 2010;363(12):1107-1116. doi:10.1056/NEJMoa1001681

9. Moss M, Huang DT, Angus DC, et al. Early Neuromuscular Blockade in the Acute Respiratory Distress Syndrome (ROSE Trial). N Engl J Med. 2019;380(21):1997-2008. doi:10.1056/NEJMoa1901686

10. Thille AW, Boissier F, Benjeloun R, et al. Patient-Ventilator Asynchrony during Mechanical Ventilation: Incidence and Risk Factors. Intensive Care Med. 2016;42(4):543-551. doi:10.1007/s00134-016-4267-8

11. Brochard L, Thille AW. What to do when a patient is fighting the ventilator? Intensive Care Med. 2018;44(4):535-538. doi:10.1007/s00134-017-4904-8

12. Frat JP, Thille AW, Mercat A, et al. High-Flow Oxygen Therapy before Intubation in Hypoxemic Patients with Acute Respiratory Failure: The HIGH-WEAN Trial. Intensive Care Med. 2018;44(10):1636-1644. doi:10.1007/s00134-018-5356-4

13. Hodgson C, Andreggen V, Murray L, et al. PEEP titration in ARDS: A systematic review and meta-analysis. Crit Care. 2016;20(1):314. doi:10.1186/s13054-016-1295-4

14. Blanch L, Bernabé F, Lucangelo U. Measurement of Airway Resistance and Auto-PEEP: The Flow Interruption Technique. Intensive Care Med. 2005;31(8):1125-1130. doi:10.1007/s00134-005-2702-7

15. Jaber S, Jung B, Corneille M, et al. Post-extubation stridor: incidence and risk factors in a large ICU population. Intensive Care Med. 2005;31(11):1536-1541. doi:10.1007/s00134-005-2802-4