The pressure–time curve reports the elastic and resistive loads; the flow–time curve reports the division of the cycle into inspiratory and expiratory time and is the earliest sign of gas trapping; the volume–time curve confirms what entered and left the lung.

Driving pressure is $\Delta P = P_{plat} - PEEP_{tot} = 19\ \text{cmH}_2\text{O}$, up from $10$. With tidal volume and PEEP fixed, the only explanation is falling compliance, $C_{rs} = V_T/(P_{plat} - PEEP_{tot})$, now about half its earlier value. A rising driving pressure at a fixed tidal volume is the strongest mechanical signal of progressive lung injury. Confirm the hold, exclude a new pneumothorax, atelectasis and abdominal distension, reduce tidal volume toward $4$–$5\ \text{mL}/\text{kg}$, and reassess PEEP decrementally. If $\Delta P$ stays high with a $P_aO_2/F_iO_2$ below about $80$, refer for extracorporeal support. (Parent chapters 01 and 03.)

Attributing a rising peak pressure to secretions while ignoring a rising plateau. Secretions raise the peak alone; a rising plateau means elastic injury.

Dynamic hyperinflation with intrinsic PEEP, here $PEEP_i = 13 - 5 = 8\ \text{cmH}_2\text{O}$. The trapped volume raises intrathoracic pressure, impedes venous return and lowers cardiac output. The immediate manoeuvre is mechanical: disconnect the endotracheal tube, allow passive deflation and compress the chest bilaterally, then reassess blood pressure. Rebuild the settings around expiratory time — rate 8–10/min, shorter inspiratory time, I:E of at least 1:3, low extrinsic PEEP — and deepen sedation, adding neuromuscular blockade if spontaneous effort defeats the strategy. (Parent chapter 05.)

Reaching for fluids or vasopressors first, or raising the rate. Both increase trapping and deepen the collapse.

A concave, upward-bowing pressure–time curve gives a stress index above $1.1$: tidal overdistension, because each increment of volume requires more pressure as compliance falls during inflation. Reduce PEEP in steps of $2$–$3\ \text{cmH}_2\text{O}$ and re-measure; a curve that straightens toward $1.0$ confirms overdistension. The converse applies: a convex curve with a stress index below $0.9$ implies tidal recruitment and may tolerate more PEEP. (Parent chapter 03.)

Chasing hypoxaemia with more PEEP without checking the stress index, or measuring it during active inspiratory effort. The index is valid only in a passive patient on constant flow.

$\text{RSBI} = f / V_T = 38 / 0.21 \approx 181\ \text{breaths}/\text{min}/\text{L}$, far above the threshold of $105$. The rapid, shallow pattern reflects an unfavourable balance between respiratory load and capacity — resistance, reduced compliance, dynamic hyperinflation or cardiac dysfunction. Do not extubate; treat reversible factors (fluid overload, secretions, pain, delirium, ischaemia) and re-test later. (Parent chapter 13.)

Treating a single number as decisive. The index is a supportive predictor; a "pass" still requires an adequate cough, manageable secretions and a protected airway.

Double triggering, or breath stacking: most often reverse triggering, in which a diaphragmatic contraction is entrained to the mandatory breath in a sedated patient, or a short inspiratory time that leaves the patient to trigger again. The stacked volume causes regional overdistension and volutrauma and threatens barotrauma and haemodynamic compromise. Assess for reverse triggering, deepen sedation, lengthen inspiratory time or increase flow so the demand is met, and consider raising the set rate toward the intrinsic rhythm; refractory cases may need neuromuscular blockade. (Parent chapters 01 and 13, with adaptive modes in chapter 17.)

Lowering the set tidal volume to make the average look acceptable while continuing to accept stacked breaths. The injurious breath is the second one.

These are ineffective triggering efforts. Intrinsic PEEP is a threshold load: before flow can begin, the diaphragm must lower alveolar pressure below the airway opening pressure and then overcome the trigger sensitivity. Extrinsic PEEP at roughly $60$–$80\%$ of the measured auto-PEEP — here about $6$–$8\ \text{cmH}_2\text{O}$ — raises end-expiratory airway pressure toward alveolar pressure, reducing the threshold load without raising total PEEP while it stays below the intrinsic level. Titrate to comfort and recheck total PEEP. (Parent chapter 05.)

Assuming that added PEEP always worsens hyperinflation. In the spontaneously breathing, flow-limited patient it is usually therapeutic; in the passive patient it can raise end-expiratory lung volume, and the rate must instead be reduced.

The sawtooth reflects a mobile or unstable airway — mucus strands dropping across the lumen, or oscillation of the airway wall — and is closely associated with retained secretions. It is not bronchospasm, although the two coexist. Suction, review humidification and position, and re-examine the loop; resolution confirms the cause. (Parent chapter 14, with airway mechanics in chapter 05.)

Escalating bronchodilators for a pattern caused by secretions, or misreading the sawtooth as auto-PEEP. The notches sit on the flow tracing, not the end-expiratory baseline.

A circuit disconnection or large leak — including endotracheal tube dislodgement or cuff failure. Trace the circuit from the Y-piece to the tube and check the cuff. Reconnect and manually ventilate with a self-inflating bag on 100% oxygen while completing the diagnosis; a displaced tracheostomy tube is a lost airway. (Parent chapters 10 and 14.)

Assuming the ventilator has failed and cycling the power. In a patient losing saturation, the airway, not the machine, is the priority.

Deliberate controlled hypoventilation. Reduce the rate to $6$–$10$/min, shorten inspiratory time with high flow to an I:E of at least 1:4, keep tidal volume at 6–8 mL/kg, and accept hypercapnia to a pH floor of about 7.20–7.25. Deepen sedation and add neuromuscular blockade if spontaneous effort shortens expiratory time, and if the blood pressure falls, disconnect and decompress first. Recheck total PEEP after every adjustment. (Parent chapter 06.)

Pursuing normocapnia by raising the rate, which shortens expiratory time, worsens trapping and can precipitate pulseless electrical activity.

Reduce the ventilator to lung-rest parameters: tidal volume $1$–$3\ \text{mL}/\text{kg}$ predicted body weight, plateau pressure at or below $20$–$25\ \text{cmH}_2\text{O}$, driving pressure at or below $10\ \text{cmH}_2\text{O}$ (many centres target $\leq 8$), rate $4$–$10$/min with apnoea accepted, PEEP $10$–$15\ \text{cmH}_2\text{O}$, inspiratory time $1.5$–$2.0$ s, and $F_iO_2$ $0.21$–$0.40$. Mechanical power is collapsed while the membrane manages gas exchange. Watch for atelectasis at very low volumes and adjust sweep and blood flow, not the ventilator, for carbon dioxide. (Parent chapter 15.)

Continuing conventional protective ventilation because the numbers "look acceptable". The point of extracorporeal support is to unload the native lung, not to leave it at injurious stress.

Acute-on-chronic hypercapnic respiratory failure: the raised bicarbonate indicates chronic compensation, so the fall in pH is smaller than the carbon dioxide rise alone would produce. Start controlled oxygen and non-invasive ventilation, and target the patient's chronic baseline rather than a normal $P_aCO_2$. (Parent chapters 05 and 07.)

Sudden loss of exhaled carbon dioxide means loss of delivery to the lung: circuit disconnection, tube dislodgement, massive pulmonary embolism, or cardiac arrest. Cross-check the pressure waveform; a flat channel with a flat capnogram points to disconnection, and the airway is addressed first. (Parent chapters 10 and 14.)

Beaking toward the upper inflection point indicates overdistension of aerated units. Reduce PEEP and, if necessary, tidal volume, and confirm the change with the stress index; loops are supportive rather than standalone evidence. (Parent chapter 03.)

Interpret a stress index below $0.9$ (convex) as tidal recruitment, $0.9$–$1.1$ (straight) as adequate, and above $1.1$ (concave) as overdistension. Change PEEP in the direction the curve indicates and re-measure. (Parent chapter 03.)

A "curare cleft" is a spontaneous inspiratory effort during expiration, historically seen in partially paralysed patients. It signals intact diaphragmatic activity and may herald reverse triggering, so reassess sedation and synchrony. (Parent chapters 01 and 13.)