[1]

Patient-ventilator asynchrony

The patient-ventilator asynchrony is the mismatch between the patient effort and the ventilator delivery — it occurs in roughly a quarter of the ventilated patients and is associated with the longer ventilation, the longer ICU stay and the worse outcomes. The major types are the ineffective triggering (the patient effort that fails to trigger the breath — the most common, due to the auto-PEEP, the over-sedation, the weak effort), the double triggering (the breath stacking — the second breath before the exhalation, due to the inspiratory time shorter than the neural time), the auto-triggering (the false breaths from the leak or the circuit motion), the flow starvation (the patient pulling harder than the ventilator delivers — the scalloped flow curve), and the delayed cycling (the ventilator cycles off after the patient has stopped inspiring). The discipline is to read the waveforms regularly and fix the cause — the trigger sensitivity, the cycling-off threshold, the rise time, the inspiratory time, the PEEP (for the auto-PEEP), or the mode switch (the PAV+, the NAVA).[7]

Reading the ventilator waveforms — five patterns and what they mean

1

Scalloped inspiratory flow curve (flow starvation)

In the pressure support or the PC, the inspiratory flow curve should be a smooth descending ramp. If it is CONCAVE (scalloped), the patient is pulling harder than the ventilator delivers — FLOW STARVATION (the patient is "fighting the ventilator"). Fix by increasing the rise time or the pressure support, lengthening the inspiratory time, or switching to a more responsive mode.

2

Expiratory flow not returning to baseline (auto-PEEP/air-trapping)

The expiratory flow curve should reach zero before the next breath. If it is still above zero at the end-expiration, there is the INCOMPLETE EXHALATION = the AIR TRAPPING (the intrinsic/auto-PEEP). Seen in the COPD, the asthma, the high RR, or the too-short expiratory time. Manage by reducing the RR, shortening the inspiratory time, applying the external PEEP about 80% of the auto-PEEP.

3

Double triggering (breath stacking)

Two breaths delivered with little or no exhalation between them — the patient triggers a second breath before the first has cycled off. Causes: the inspiratory time too short for the neural time (the delayed cycling), the high drive, the low support. Consequence: the stacked Vt, the high transpulmonary pressure, the VILI risk. Fix by lengthening the inspiratory time or raising the support or the cycling threshold.

4

Ineffective triggering (missed breaths)

The patient effort visible on the flow/pressure trace (a brief deflection) that does NOT trigger a ventilator breath. Causes: the auto-PEEP (the patient must first climb the intrinsic PEEP), the over-sedation, the weak respiratory muscle, the insensitive trigger. Manage by treating the auto-PEEP (bronchodilators, lower RR, external PEEP), reducing the sedation, setting a more sensitive trigger, or the NAVA.

5

Auto-triggering (false breaths)

The ventilator delivers breaths the patient did not initiate — the rapid cycling from the leak, the circuit motion, the water in the circuit, or the too-sensitive trigger. Manage by checking the circuit for the leaks/water, reducing the trigger sensitivity, or switching to the NAVA (the neural trigger is leak-proof).

Non-invasive ventilation: the interfaces and the contraindications

The NIV is delivered through an interface — the mask or the helmet that connects the circuit to the patient. The choice of the interface determines the tolerance and the leak. The oronasal mask (covering the nose and the mouth) is the standard first choice — the most effective for the acute respiratory failure, but the highest risk of the skin breakdown and the claustrophobia. The full-face mask (covering the nose, the mouth and the eyes) provides the best seal for the high pressure but is poorly tolerated. The nasal mask is comfortable but the mouth leak limits its use in the acute setting (better for the chronic NIV). The total face mask (covering the whole face) is an alternative for the claustrophobia and the skin-bridge breakdown. The helmet (the hood that covers the head and the neck) is the most comfortable and the lowest skin-breakdown, with the growing evidence (the HELMET trial) of the comparable or the superior outcomes in the ARDS — though it requires the higher pressures to overcome the larger internal volume.[1][1]

The contraindications to the NIV are the situations where the NIV cannot work or will harm: the cardiac or respiratory arrest, the inability to protect the airway (the reduced GCS, the copious secretions), the facial trauma or the surgery (the poor mask seal), the haemodynamic instability (the severe shock, the uncontrolled arrhythmia), the undrained pneumothorax (relative — the tension risk), the agitation or the non-cooperation that prevents the mask tolerance, and the recent upper GI surgery (the insufflation risk). The principle is that the NIV is for the patient who can protect the airway, can tolerate the mask, and whose failure of the NIV is not catastrophic — the prompt intubation for the worsening.[1]

The NIV interfaces — the practical trade-offs
InterfaceSealToleranceLeakBest forLimitation
InterfaceSealToleranceLeakBest forLimitation
Oronasal maskGoodModerateModerateThe standard first choice for the acute respiratory failure (COPD, CPO)Skin bridge breakdown; claustrophobia
Full-face maskBestLowLowThe high-pressure requirement (the BiPAP IPAP > 20)Poorly tolerated; eye irritation
Total face maskGoodModerate-HighModerateThe claustrophobia; the skin breakdown over the nose bridgeLarger dead space; CO2 rebreathing risk
Nasal maskModerateHighHigh (mouth leak)The chronic NIV (the OSA, the neuromuscular)Mouth leak limits the acute use
Helmet (hood)Good (neck seal)HighestLowThe prolonged NIV; the ARDS (the HELMET trial); the difficult mask fitHigher pressures needed; the CO2 clearance; the cost
Mouthpiece (lip seal)PoorVariableHighThe chronic NIV (the neuromuscular, the daytime ventilation)Not for the acute; needs the intact bulbar function
[1]

Starting and titrating BiPAP in the COPD exacerbation

1

Fit the oronasal mask and explain to the patient

Choose the oronasal mask (the standard for the acute). Hold the mask to the face for the first few breaths before strapping (lets the patient acclimatise, reduces the claustrophobia). Explain that the pressure will rise but the breathing will get easier. The initial acclimatisation is the key to the tolerance.

2

Set the initial EPAP at 4-5 cmH2O and the IPAP at 10-12 cmH2O

Start low and titrate up. The EPAP (the expiratory positive airway pressure) splints the airway and counteracts the intrinsic PEEP; the IPAP (the inspiratory positive airway pressure) augments the Vt and unloads the respiratory muscles. The difference (the IPAP minus the EPAP) is the pressure support that drives the ventilation.

3

Set the FiO2 for the SpO2 88-92% (the COPD target)

In the COPD, target the 88-92% (the CO2-retainer). In the pure type-1 respiratory failure, target the 92-96%. Avoid the hyperoxia (the Haldane effect, the absorption atelectasis, the oxygen toxicity).

4

Titrate the IPAP up by 2-3 cmH2O every 5-10 min to the target

Raise the IPAP (in 2-3 cmH2O steps) until the Vt is adequate (the 6-8 mL/kg), the respiratory rate falls (below 25), and the patient is comfortable. Most COPD patients need the IPAP of 15-20. Watch the leak, the skin, and the haemodynamics (the high intrathoracic pressure drops the venous return).

5

Check the ABG at 30-60 min — the pH and the PaCO2 trend

The NIV success is judged by the ABG at 1 hour: the pH rising (toward the 7.35), the PaCO2 falling, the respiratory rate falling, the patient more comfortable. The failure (the persistent acidosis, the rising RR, the distress) is the prompt intubation — do NOT persist with the failing NIV (the failure of the NIV has a higher mortality than the primary intubation).

6

Plan the discontinuation — the weaning as the cause resolves

As the bronchodilation, the steroids and the antibiotics work, titrate the IPAP down and increase the off periods. The COPD NIV is usually discontinued within 24-72 hours of the cause resolution. Do not abandon abruptly — the graded reduction prevents the rebound.

[1]

High-flow nasal cannula (HFNC)

The high-flow nasal cannula (the HFNC, the HFNO) delivers the heated, the humidified oxygen at the high flow (the 30 to 60 L/min) through the wide-bore nasal prongs. It sits between the standard oxygen (the low flow, the cold, the dry) and the NIV — it is NOT a ventilator (it does not guarantee the pressure or the Vt), but it delivers the physiological benefits beyond the FiO2: the low-level PEEP (the 3 to 5 cmH2O at the 30 to 50 L/min, proportional to the flow), the washout of the dead space (the anatomical dead space of the nose, the pharynx and the trachea is flushed, reducing the CO2 rebreathing and the Vt needed for the same alveolar ventilation), the reduced work of breathing (the lower inspiratory resistance, the matched flow to the patient demand), the heated humidification (the mucociliary clearance, the secretion mobilisation), and the reduced inspiratory resistance.[5][10]

The HFNC is the first-line for the acute hypoxaemic respiratory failure without the hypercapnia (the pneumonia, the ARDS, the pulmonary embolism, the post-operative) — the FLORALI trial (the Frat 2015, the NEJM) showed the HFNC reduced the intubation and the 90-day mortality compared with the standard oxygen and the NIV in the moderate-severe hypoxaemic respiratory failure (the PaO2/FiO2 below 300), particularly in the more severe subgroup (the PaO2/FiO2 below 200). The HFNC is NOT for the hypercapnic respiratory failure (the COPD with the CO2 retention — the BiPAP is the first-line) and it is not a substitute for the intubation in the failure of the airway protection or the severe distress.[5]

The ROX index (the SpO2/FiO2 divided by the respiratory rate, all as the fractions or the integers per the source) is the validated predictor of the HFNC success — a ROX of at least the 3.85 at the 2, 6 or 12 hours predicts the success; a ROX below the 3.59 (the 2 hours), the 3.45 (the 6 hours) or the 3.16 (the 12 hours) predicts the failure and the need for the intubation. The discipline is to set a time-bound HFNC trial (the 1 to 2 hours) and to intubate early if the ROX falls or the patient distress worsens — the delayed intubation after the prolonged HFNC failure is associated with the higher mortality.[6]

Starting and assessing the HFNC — the practical protocol

1

Set the initial flow at 30-40 L/min and titrate up to the patient tolerance

Start at 30-40 L/min and increase by 5-10 L/min every few minutes to the target (commonly 50-60 L/min). The flow is the PEEP and the dead-space-washout variable. Higher flow = more support, but the nasal dryness and the claustrophobia limit the tolerance in some.

2

Set the FiO2 to the target SpO2 (92-96% for the type-1 failure)

Start at the FiO2 of 0.5-1.0 and wean as the oxygenation improves. Target the 92-96% for the type-1, the 88-92% for the COPD-retainer. The closed-loop oxygenation (the FreeO2, the O2 closed-loop) is an emerging automation that reduces the mean FiO2.

3

Set the temperature at 34-37°C (the humidification)

The heated humidification is part of the mechanism (the mucociliary clearance). Lower temperature = more condensation in the tubing; higher = the patient discomfort. 34-37°C is the standard.

4

Reassess at 1-2 hours — the ROX index and the clinical picture

Calculate the ROX (SpO2/FiO2 ÷ RR) at 1-2 hours. A ROX above the 3.85 supports the continued HFNC. A falling ROX, the rising RR, the persistent distress, the worsening work of breathing, or the rising lactate is the intubation. Do not persist with the failing HFNC.

5

Decide the trajectory — the improvement, the stability, or the failure

The improvement → the wean of the FiO2 and the flow. The stability → the continued HFNC with the monitoring. The failure → the prompt intubation (the delayed intubation after the HFNC failure is the harm).

The ventilator liberation: the structured strategy

The liberation from the mechanical ventilation is the daily, the protocolised process — the earlier the safe liberation, the better. The structured strategy is the SAT + SBT (the spontaneous awakening trial and the spontaneous breathing trial) — the daily interruption of the sedation (the SAT), and if passed, the SBT. The SAT-SBT pairing (the ABC trial, the Girard 2008) reduced the ventilation days and the mortality compared with the usual care plus the SBT. The principle is that the sedation is the enemy of the liberation — the lighter the sedation, the earlier the patient can breathe.[1][1]

The weaning categories are the simple (the patient passes the first SBT and is extubated — about 70 per cent), the difficult (the patient passes the SBT after up to three attempts or within 7 days — about 20 per cent), and the prolonged (the patient fails the three attempts or the 7-day mark — about 10 per cent). The prolonged weaning carries the higher mortality — the cause is sought and treated (the cardiac, the respiratory-muscle weakness, the electrolyte, the sedation, the secretions, the delirium, the malnutrition, the over-ventilation from the high mandatory rate).[1][1]

The weaning categories and their prognosis
CategoryDefinitionProportionPrognosisThe focus
CategoryDefinitionProportionPrognosisThe focus
Simple weaningPasses the first SBT and the extubation~70%GoodThe protocolised daily SBT
Difficult weaningPasses the SBT after up to 3 attempts or within 7 days~20%ModerateThe cause-finding (cardiac, sedation, weakness, secretions)
Prolonged weaningFails the 3 attempts or the 7-day mark~10%Poor (higher mortality)The multidisciplinary approach; the tracheostomy; the NIV-assisted extubation
[1]

The causes of the difficult-to-wean patient — the systematic search

1

1. The respiratory load is too high (the load-capacity imbalance)

The increased load: the bronchospasm, the secretions, the pulmonary oedema, the pneumonia, the ARDS, the dynamic hyperinflation (COPD). The reduced capacity: the respiratory-muscle weakness (the ICU-acquired, the neuromuscular disease, the electrolyte — the hypophosphataemia, the hypomagnesaemia, the hypokalaemia), the malnutrition, the over-sedation.

2

2. The cardiac cause (the weaning-induced cardiac dysfunction)

The weaning raises the venous return (the preload) and the afterload (the systemic vascular resistance rises as the intrathoracic pressure falls) — the failing LV cannot cope, and the pulmonary oedema ensues. Suspect in the cardiac history, the rising filling pressures, the new crackles, the S3, the echocardiogram. Treat with the diuretics, the nitrates, the afterload reduction.

3

3. The neuropsychiatric cause

The delirium, the anxiety, the depression, the sleep deprivation. The delirium is the common, the under-recognised enemy of the weaning. Screen with the CAM-ICU; treat with the orientation, the sleep, the antipsychotic (the haloperidol, the quetiapine) only if the distress is severe.

4

4. The metabolic and the endocrine cause

The hypothyroidism (the respiratory-muscle weakness), the adrenal insufficiency (the hypotension, the fatigue), the hypophosphataemia and the hypomagnesaemia (the ATP depletion, the muscle weakness), the hypokalaemia. Check and correct.

5

5. The over-ventilation and the mode

A high mandatory rate or the too-high pressure support over-ventilates the patient and suppresses the drive — the patient "forgets" to breathe. Reduce the support to the SBT level (5 cmH2O) and let the patient take over. The SIMV is the worst weaning mode (the variable load on the diaphragm) — switch to the PSV.

6

6. The airway and the secretion cause

The copious secretions the patient cannot clear (the weak cough, the thick mucus), the laryngeal oedema (the cuff-leak), the tracheal stenosis (the prolonged intubation). The mucolytics, the physiotherapy, the suction, the cuff-leak test, and the consideration of the tracheostomy for the secretion clearance.

The tracheostomy in the ventilator liberation

The tracheostomy facilitates the liberation by reducing the dead space, lowering the work of breathing (the less resistance than the long endotracheal tube), improving the secretion clearance, and allowing the lighter sedation and the oral intake. The timing is the debated question — the early (within the 2 to 4 days) versus the late (after the 10 to 14 days) — and the TRACMAN trial (the Young 2013, the JAMA) found that the early tracheostomy did not reduce the mortality or the VAP compared with the late, though it reduced the sedation use and the ICU stay in some. The practice is individualised — the tracheostomy for the patient expected to need the ventilation beyond the 7 to 10 days, and the percutaneous dilatational technique (at the bedside, by the intensivist) is the standard. The decannulation follows the successful weaning (the progressive downsizing, the capping, the cough and the secretion clearance, the swallowing assessment).[1][9]

SAQ — Recruitment manoeuvre for refractory hypoxaemia in severe ARDS

10 minutes · 10 marks

A 48-year-old man with community-acquired pneumonia has severe ARDS. On day 3 he is ventilated in volume control at 6 mL/kg predicted body weight, PEEP 12 cmH2O, FiO2 1.0, with PaO2 56 mmHg (PaO2/FiO2 56), SpO2 88%, plateau pressure 32 cmH2O. He is deeply sedated and paralysed. The registrar asks whether a recruitment manoeuvre is appropriate.

[1]

SAQ — PEEP optimisation in moderate ARDS

10 minutes · 10 marks

A 55-year-old woman is admitted with aspiration pneumonitis evolving into moderate ARDS (PaO2/FiO2 145). She is ventilated in volume control at 6 mL/kg predicted body weight, PEEP 8 cmH2O, FiO2 0.7, with a plateau pressure of 24 cmH2O and a driving pressure of 16 cmH2O. Outline your approach to optimising her PEEP.

[1]

Red flags

Clinical pearls

Evidence and trials

ARMA trial (ARDSNet 2000, NEJM) — the low-tidal-volume ventilation

RCT: 861 patients with the ALI/ARDS. Vt 6 mL/kg PBW, plateau ≤30 cmH2O vs Vt 12 mL/kg, plateau ≤50.

FLORALI trial (Frat 2015, NEJM) — the HFNC in the hypoxaemic respiratory failure

RCT: 310 patients with the acute hypoxaemic respiratory failure (the PaO2/FiO2 below 300, without the hypercapnia). HFNC vs standard oxygen vs NIV.

ROX index validation (Roca 2016, AJRCCM) — predicting the HFNC outcome

Multicentre prospective observational: 191 patients with the pneumonia on the HFNC. Derived and validated the ROX index = (SpO2/FiO2) ÷ RR.

Esteban 1995 (NEJM) and Brochard 1994 (AJRCCM) — the weaning-method comparison

TRACMAN trial (Young 2013, JAMA) — the early vs the late tracheostomy

RCT: 909 patients expected to need the ventilation beyond 7 days. Early tracheostomy (within 4 days) vs late (after 10 days).

Esteban 2004 (NEJM) — the therapeutic NIV after the extubation failure

RCT: 221 patients who developed the respiratory failure within 48 hours of the extubation. NIV vs standard medical therapy (with the intubation as needed).

Burns 2022 systematic review (Thorax) — the NIV-assisted weaning

Systematic review and meta-analysis: 20 RCTs, the critically ill adults on the invasive ventilation. Extubation to the NIV (the NIV-assisted weaning) vs the continued invasive weaning.

ABC trial (Girard 2008, Lancet) — the SAT + SBT pairing

RCT: 336 mechanically ventilated patients. Daily SAT (sedation interruption) followed by SBT vs usual sedation + daily SBT.

References

  1. [1]Esteban A, Frutos F, Tobin MJ, et al. A comparison of four methods of weaning patients from mechanical ventilation. Spanish Lung Failure Collaborative Group N Engl J Med, 1995.PMID 7823995
  2. [2]Esteban A, Frutos-Vivar F, Ferguson ND, et al. Noninvasive positive-pressure ventilation for respiratory failure after extubation N Engl J Med, 2004.PMID 15190137
  3. [3]Burns KEA, Rizvi L, Au NHC, et al. Non-invasive ventilation versus invasive weaning in critically ill adults: a systematic review and meta-analysis Thorax, 2022.PMID 34716282
  4. [4]The Acute Respiratory Distress Syndrome Network (ARDSNet) Handling of hazardous materials Ann Emerg Med, 2000.PMID 10613956
  5. [5]Frat JP, Thille AW, Mercat A, et al. DNA double-strand breaks alter the spatial arrangement of homologous loci in plant cells Sci Rep, 2015.PMID 26046331
  6. [6]Roca O, Caralt B, Messika J, et al. Epidemiology, Patterns of Care, and Mortality for Patients With Acute Respiratory Distress Syndrome in Intensive Care Units in 50 Countries JAMA, 2016.PMID 26903337
  7. [7]Chatburn RL, El-Khatib M, Mireles-Cabodevila E A taxonomy for mechanical ventilation: 10 fundamental maxims Respir Care, 2014.PMID 25118309
  8. [8]Brochard L, Rauss A, Benito S, et al. [Foreign bodies in the appendix and videoceliosurgery] J Chir (Paris), 1994.PMID 7989419
  9. [9]Young D, Harrison DA, Cuthbertson BH, Rowan K, TracMan Collaborators Images in clinical medicine. Corneal-flap dehiscence after screwdriver trauma N Engl J Med, 2013.PMID 23282001
  10. [10]Spoletini G, Alotaibi M, Masala D, Wyncoll D, Grazioli S, Kho P, Kaltsakas G, Nava S, Hill NS, Carteaux GP An update on Ayurvedic herb Convolvulus pluricaulis Choisy Asian Pac J Trop Biomed, 2014.PMID 25182446