Severe ARDS with Elevated Driving Pressure and Patient–Ventilator Dyssynchrony
A 46-year-old man with a BMI of 38 kg/m² is admitted to the ICU with influenza A pneumonia and 3 days of worsening hypoxemia. He is intubated and ventilated in volume-control mode: tidal volume 420 mL (predicted body weight 70 kg), respiratory rate 28/min, PEEP 14 cmH₂O, FiO₂ 0.90. Arterial blood gas: pH 7.24, PaCO₂ 58 mmHg, PaO₂ 62 mmHg, HCO₃ 24 mmol/L. Plateau pressure is 33 cmH₂O. Chest radiograph shows bilateral infiltrates; echocardiography shows normal left ventricular function and no pneumothorax. Norepinephrine 0.15 µg/kg/min maintains MAP 68 mmHg. Sedation is deep (RASS −5), yet he intermittently triggers the ventilator, and the pressure–time curve shows a concave dip before each triggered breath. Urine output is 0.4 mL/kg/h.
1. Calculate the PaO₂/FiO₂ ratio and the driving pressure, and explain what each tells you. What ventilator changes would you make now, and what targets would you use?
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Gas exchange. PaO₂/FiO₂ = 62 ÷ 0.90 ≈ 69 mmHg, which meets the Berlin definition of severe ARDS (P/F < 100 with PEEP ≥ 5 cmH₂O).
Mechanics. Driving pressure = plateau pressure − total PEEP = 33 − 14 = 19 cmH₂O. The tidal volume is already 6 mL/kg predicted body weight (420/70), so the elevated driving pressure is not from excessive tidal volume; it suggests either inadequate recruitment or regional overdistension. The target is driving pressure ≤ 15 cmH₂O and plateau pressure < 30 cmH₂O, with the lowest FiO₂ that keeps SpO₂ 88–95%.
Ventilator changes. Perform a stepwise PEEP trial (14 → 16 → 18 cmH₂O), rechecking plateau pressure, driving pressure, PaO₂ and blood pressure 20–30 minutes after each step. Keep the higher PEEP only if driving pressure falls and oxygenation improves; back off if plateau pressure exceeds 30–32 cmH₂O or driving pressure rises, which indicates overdistension. Do not increase tidal volume to correct hypercapnia.
Permissive hypercapnia. pH 7.24 with PaCO₂ 58 is acceptable permissive hypercapnia provided pH stays ≥ 7.20 and there is no raised intracranial pressure, severe right ventricular failure or pregnancy. Recheck the gas in 30–60 minutes. If pH falls below 7.20 despite respiratory rate 30–32/min, or if P/F remains < 80 on FiO₂ 1.0, this becomes an ECMO referral trigger rather than a reason for more aggressive ventilation.
2. Does this patient meet criteria for prone positioning? Describe how you would implement it and what you would do if there is no oxygenation response.
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Indication. Yes. P/F < 150 on FiO₂ ≥ 0.6 and PEEP ≥ 5 cmH₂O is the PROSEVA entry criterion, and prone positioning reduced 28-day mortality in that population. Do not wait for further deterioration.
Implementation. Use a protocolised team of at least four people with a designated leader. Secure the airway and lines, preoxygenate with FiO₂ 1.0, pause enteral feed for the turn, protect the eyes and pressure areas, and place the patient prone for at least 16 hours per session, continuing daily sessions while P/F remains < 150. Keep the abdomen free and the head turned; use a pressure-redistributing mattress and check facial, thoracic and iliac pressure points regularly. Expect transient desaturation and arrhythmia during the turn; have suction and vasopressors ready.
Assessing response. Reassess P/F after about 4 hours prone. A rise of ≥ 20 mmHg defines a responder, but the mortality benefit is not confined to oxygenation responders, so do not abandon proning solely because PaO₂ is unchanged if the patient tolerates it.
If there is no improvement. Return supine, re-optimise PEEP and sedation, consider a 48-hour cisatracurium infusion, ensure the cause is being treated (antibiotics, drainage of any collection), and assess fluid balance and right ventricular function. Persistent P/F < 80 on FiO₂ 1.0 for more than 6 hours, or refractory respiratory acidosis with pH < 7.20, should prompt ECMO centre discussion. Document complications such as tube dislodgement, facial ulceration, brachial plexus injury and haemodynamic instability.
3. What is the likely cause of the concave dip on the pressure–time curve before each breath, why does it matter, and how would you manage it?
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Interpretation. A concave dip in airway pressure before a triggered breath is flow starvation: the patient's inspiratory effort is generating more flow than the ventilator is delivering, so the set flow is inadequate for the patient's demand. It is a form of patient–ventilator dyssynchrony, not simply 'fighting the ventilator'.
Why it matters. Vigorous spontaneous effort generates high transpulmonary pressure and can worsen lung injury (patient self-inflicted lung injury), particularly in a lung with reduced aerated volume. It also increases oxygen consumption and carbon dioxide production, raises intrathoracic pressure and can compromise venous return in a patient already on norepinephrine.
Management. First confirm the mechanism: examine flow and pressure waveforms, check for auto-PEEP and tube obstruction, and verify that triggering is not autotriggering. Then deepen analgesia and sedation to RASS −4 to −5, using an opioid plus propofol, because the drive is often pain, anxiety, acidosis or hypercapnia. If dyssynchrony and high drive persist despite deep sedation in severe ARDS, start cisatracurium for 48 hours with train-of-four monitoring. Modest increases in respiratory rate (to 30–32/min) can reduce CO₂ drive if pH is below 7.20, but do not increase tidal volume. Reassess driving pressure after each change, and avoid the trap of escalating sedation indefinitely without treating the underlying cause of the high respiratory drive.