This is a modality of ventilation that seems to utilised more and more frequently in our ARDS patients with refractory hypoxaemia.
To be honest, it can be a daunting mode if you don’t understand the underlying principles behind it, so here is a guide to attempt to clear this up and make it more palatable, particularly when you need to set it up without support from those who are more familiar with it.
A BIT ON LUNG PROTECTION
Telling you to suck eggs here, but we all know it is:
- Bilateral Infiltrates on CXR
- PaO2/FIO2 ratio < 300 and falling (See ARDS / ALI calculator here)
- Plateau pressures greater than 30 cm H2O
- No evidence of left heart failure (e.g. PAOP of 18 mm Hg or greater)
As per ARDSnet, Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) require low volume, low pressure ventilatory strategies.
- Keep plateau pressures < 30 cm H2O
- Use low tidal volume ventilation (4-6 mL/kg IBW)
- PEEP to restore the functional residual capacity (FRC)
What do you normally do if plateau pressures >30 and high PaCO2?
- Increase the ventilator rate
- Permissive Hypercapnia
- High Frequency Ventilation (OSCAR trial – although no 30-day mortality benefit)
- Extracorporeal Life Support!!
WHAT IS APRV then?
- Two levels of PEEP: high (P-high) and low (P-low)
- The patient breaths spontaneously during P-high and P-low
- The time in P-high (T-high) is longer than P-low (T-low) to maintain recruitment
- Results in a degree of autoPEEP due to the short release time (T-low)
- It promotes lung recruitment of collapsed and poorly ventilated alveoli.
- The CPAP level primarily facilitates oxygenation.
- The timed releases facilitate carbon dioxide clearance.
- P-High – the upper CPAP level.
- Affects oxygenation
- P-Low or PEEP – the lower pressure setting
- Also affects oxygenation maintaining recruitment
- T-High– is the inspiratory time spent at the P-High, upper CPAP level
- T-Low or TPEEP – is the release time allowing CO2 elimination
- (P-high – P-low) determines flow out of the lungs and volume exchange (VT and PaCO2).T-High plus T-Low is the total time of one cycle
- Uses lower PIP to maintain oxygenation
- Improved alveolar recruitment
- Potential lung protective effect
- Shown to improve V/Q matching
- Better ventilation of dependent areas whilst spontaneously breathing
- Preservation of spontaneous breathing (should be 20-30% of MV)
- Less sedation required
- Reduced muscle atrophy and shorter weaning times as a result
- May improve renal perfusion
- Maintains the normal cyclic decrease in pleural pressure, which augments venous return and improves cardiac output.
- Reduction of left ventricular transmural pressure and therefore reduction of left ventricular afterload
- Less haemodynamic compromise
- Risks of volutrauma from increased transpulmonary pressure
- Increased work of breathing due to spontaneous breathing
- Increased energy expenditure due to spontaneous breathing
- Worsening of air leaks (bronchopleural fistula)
- Increased right ventricular afterload, worsening of pulmonary hypertension
- Reduction of right ventricular venous return:
- may worsen intracranial hypertension
- may worsen cardiac output in hypovolemia
- Risk of dynamic hyperinflation
GET IT GOING
- SET P-High at the Plateau
- Start at 20-25cmH2O (30 if plateau pressures already 30)
- Set to previous mean airway pressure if switching from different mode
- Try to keep below 35cmH2O
- Set T-High
- Start at minimum of about 4.0 seconds
- Progressively increase until you achieve Target PaO2.
- RR should be 8-12bpm, no more
- Set P-Low
- Start at 0 cmH2O to optimize expiratory flow.
- The large pressure ramp allows for tidal ventilation in very short expiratory times.
- Set T-Low
- Start at 0.5-0.8 seconds.
- Short enough to prevent derecruitment and long enough to obtain a suitable tidal volume.
- A tidal volume target is between 4 and 6ml/kg.
- If the tidal volume is too low, the expiratory time is lengthened
- If it is too high (>6ml/kg), the expiratory time is shortened.
- Automatic tube compensation (ATC) should be on.
- The expiratory flow from patient should end at about 50 to 75% of peak expiratory flow
- This can be determined by saving a screen and calculating peak expiratory flow.
WHAT TO DO WITH IT ONCE GOING – ABG’s are the key!
To decrease PaCO2
- Decrease T-High.
- Means more release/min
- No shorter than 3 seconds
- Check T low. If possible increase T low to allow more time for “exhalation.”
To increase PaO2
- Increase FIO2
- Increase MPaw by increasing P-High in 2 cm H2O increments
- Increase T-high slowly (0.5 sec/change)
- Recruitment Maneuvers
- Maybe shorten T PEEP (T low) to increase PEEPi in 0.1 sec. increments (This may reduce VT and affect PaCO2)
- FiO2 SHOULD BE WEANED FIRST (Target < 50% with SpO2)
- Reducing P High, by 2 cmH20 increments until the P High is below 20 cmH2O.
- Increasing T High to change vent set rate by 5 releases/minute
- The patient essentially transitions to CPAP with very few releases
- Patients should be increasing their spontaneous rate to compensate.
WHERE’S THE EVIDENCE?
There is no evidence that APRV improves clinically significant outcomes such as mortality. It does improve physiological variables in animals and humans.
My thoughts are varied. It certainly has physiologic advantages, particularly in the hands of an experienced team. But uncertainty remains and the vast majority may stick to tried and tested modalities of ventilation, backed by more evidence. The weaning alone is mildly anecdotal and worked for the team who broadcast it’s benefits. The subsets of patients we tend to put onto this mode are amongst the sickest too, so outcomes may be biased towards the bad end of the spectrum!
As we always say these days….we need more validation and more RCT’s. Thus statement, when used more than twice on a shift surely means you will only choose this mode when all else seems to have failed and not as a routine part of your ICU practise?