general philosophy
Let's admit it, nobody knows exactly how to set APRV. Numerous protocols and articles recommend different approaches. There has never been a human trial comparing two different APRV protocols, so it's impossible to dogmatically say whether any protocol is better than any other protocol. The most successful clinical trial of APRV to date is Zhou 2017, which has influenced the guidelines below.
These guidelines are intended as a basic scaffold for how to approach APRV. Each patient is different, so ventilator settings will need to be titrated to the individual patient. When in doubt, different settings may need to be trialed to determine which works the best.
A review of small APRV trials dating back to 1988 found that none of them caused harm, although many used protocols that are horrific by modern standards (Jain 2016). This is evidence that APRV is a relatively forgiving ventilator mode. Slightly suboptimal settings are unlikely to cause harm.
The guideline below is designed for patients with predominantly hypoxemic respiratory failure (e.g. ARDS, atelectasis). Patients with severe obstructive lung disease aren't ideal candidates for APRV (e.g., they were excluded by Zhou 2017).
intro: discussion of parameters
P-High
- Ideally keep at 30 cm or below. However, for patients with severe obesity, may need to increase higher.
- Problems with excessive P-High:
- Lung over-distension
- Excess driving pressure and large release breaths may cause lung injury.
- May impair hemodynamics by causing cor pulmonale.
- Problems with inadequate P-High:
- Derecruitment & hypoxemia.
- Low minute ventilation and hypercapnia.
- P-high is what provides the driving pressure for the release breath, which is the mechanism whereby APRV provides mechanical support to the work of breathing. Inadequate P-high may cause inadequate ventilator support, causing increased work of breathing.
P-Low
- Most APRV protocols in use set P-low to zero, but some do use positive P-low of ~5 cm (Zhou 2017).
- Benefit of setting P-Low above zero.
- Should make APRV more lung-protective, by avoiding atelectasis and wide fluctuations in airway pressure which drive large tidal volumes (Mireles-Cabodevila 2016; Chatburn 2016).
- May allow for management of severe hypoxemia without increasing the P-High to dangerous levels.
- Drawbacks of setting P-low above zero:
- Will reduce tidal volume and thereby promote hypercapnia.
- Reduction in driving pressure and expiratory flow velocity may reduce secretion clearance.
T-High
- T-high is the main driver of the release frequency.
- Release frequency = 60/(T-High + T-Low)
- Initially a frequency of 10-14 releases/minute is reasonable.
- As patients wean off ventilator support, T-High will be increased and the release frequency will decrease.
- Ideally the T-High should be greater than nine times the T-Low, so that >90% of the overall time is spent at T-High.
- If you're increasing T-Low above 0.7 seconds, consider increasing T-high as well.
- Problems with inadequate T-high:
- Too many releases may lead to de-recruitment (by lowering the mean airway pressure).
- APRV stops being lung-protective, starts resembling generic pressure-control ventilation.
- Insufficient time for CO2 in blood to diffuse into gas within the airways (“diffusive” CO2 clearance).
- Problems with excessive T-high:
- Too few releases may cause hypercapnia.
- Release breaths are what provides mechanical support to assist the patient's work of breathing. So if the T-High is too long, the vent isn't doing much to support the patient's work of breathing (this starts to resemble CPAP).
T-Low
- Trickiest setting, requires ongoing attention if the lung physiology changes.
- Among a patient who is exhaling passively, T-Low may be gauged by comparing the end-expiratory flow rate to the peak expiratory flow rate. The usual target is an end-expiratory flow rate of 75% the peak expiratory flow rate.
- Problems with inadequate T-low (will tend to increase the end-expiratory flow rate >75%)
- Release breath is too small, leading to ineffective ventilation. Ventilator does little to support the work of breathing.
- Problems with excessive T-low (will decrease the end-expiratory flow rate <50-75%)
- Release breath is too large, causing derecruitment (leading to hypoxemia and also hypercapnia).
- Repetitive closing/opening of alveoli during release breath causes trauma to lungs (atelectotrauma).
- End-expiratory flow rate <50% the peak flow rate suggests that APRV isn't functioning in a lung-protective manner.
#1: initial settings
- P-High
- Transitioning from volume-cycled ventilation: set equal to plateau pressure.
- Transitioning from pressure-cycled ventilation: set equal to peak pressure.
- Often start ~25 cm.
- P-Low
- Set to zero.
- T-High
- Set to 5 seconds.
- T-Low
- Set to 0.5 seconds initially.
- Adjust to achieve an end-expiratory flow equal to 75% of the peak expiratory flow rate (Jain 2016).
- FiO2
- Start high, titrate down rapidly based on oxygen saturation.
- Automatic Tube Compensation (ATC) must be turned on.
#2: adjustment based on oxygenation & ventilation
hypoxemia
- Hypoxemia generally indicates under-recruitment, although other possibilities exist (e.g. right-to-left shunt due to cor pulmonale, cardiogenic shock).
- Interventions to improve recruitment:
- Reduce T-Low by 0.05-0.1 second if end-expiratory flow rate is <75% of peak expiratory flow rate or if release breath is >8 cc/kg.
- Increase P-high by 1-2 cm if <30 cm (or <35cm in morbid obesity).
- Increase T-High by 0.5-1 second.
- Last resort: Increase P-Low by 1-2 cm.
hypercapnia
- Tolerate permissive hypercapnia down to pH of ~7.15 (or even lower if hemodynamically tolerated). Before trying to reduce the PaCO2, think very carefully about whether you truly need to do this.
- If the patient is tolerating a high PaCO2 and doing well clinically, the best thing is often to leave this alone. The interventions listed below will tend to reduce the PaCO2, but may do this at the cost of being less lung-protective.
- The best way to improve pH may be to manipulate the metabolic acid/base status (e.g. IV bicarbonate for non-anion-gap metabolic acidosis).
- Interventions
- If patient isn't breathing spontaneously, wean sedation to encourage this (see “patient effort” below).
- Increase P-High by 1-2 cm (up to ~30 cm or ~35cm in obesity).
- T-High manipulation here is a double-edged sword:
- Increasing T-high may improve recruitment and thereby improve CO2 clearance… if patient is de-recruited.
- Reducing the T-high will increase the frequency of releases, thereby increasing the minute ventilation.
- Judgement (regarding how well recruited the patient is) & trial-and-error may be needed.
- Decrease P-low by 1-2 cm (if positive).
- Last resort: May increase T-Low by 0.05-0.1 second if end-expiratory flow rate is >>50% of the peak expiratory flow rate. However this is generally undesirable because it may cause derecruitment.
hypocapnia
- Hypocapnia may be an indication that the patient is ready for weaning – more detail on this below.
- Interventions
- Decrease P-High if able from an oxygenation standpoint.
- Increase T-High.
- Decrease T-low.
#3: additional parameters to monitor
expiratory tidal volumes during pressure release
- Optimal volumes might be ~6-8 cc/kg (1).
- Undesirable to have volumes >>8 cc/kg IBW.
- May be caused by lung overdistension –> decrease P-high.
- May be caused by alveolar de-recruitment during release –> reduce T-low.
patient effort
- Ideally patient should breathe spontaneously over APRV, without dyspnea.
- Severe ARDS: ideally patient performs ~10-30% of total minute ventilation
- Mild-moderate ARDS: ideally patient performs ~30-60% of total minute ventilation
- If patient isn't performing enough effort:
- Consider weaning sedation if over-sedated.
- Consider weaning support level (e.g. reduce P-high and increasing T-high).
- If patient is performing too much effort:
- Consider adding sedation if patient is anxious/agitated.
- Consider increasing support level (e.g. increasing P-high and reducing T-high) if concern that patient may fatigue.
expiratory flow deceleration angle
- Perfect angle in a normal lung is ~45 degrees.
- Low angle (“steep” flow curve) may reflect de-recruitment or restriction (e.g. ARDS, abdominal compartment syndrome – example above on the right).
- High angle (“flat” flow curve) may reflect over-distension or obstruction (e.g. bronchospasm or secretions in large airways).
- Changes in angle may be more useful than the absolute value. For example, sudden increase in angle could signal acute airway obstruction.
weaning off APRV
readiness for weaning
- Patient should be spontaneously breathing at a reasonable rate (e.g. 10-25 breaths/minute). Goal is a patient who is calm but conscious. This may be facilitated by:
- Anxiolysis: consider adding dexmedetomidine while weaning down propofol (OK to use combination of low doses of both simultaneously).
- Pain control: consider adding ketamine infusion to allow weaning down opioids.
- T-High is fairly long (e.g. ~8-10 seconds).
- FiO2 50% or lower.
- P-Low of zero.
- Not significantly hypercapneic.
- Ready to assume more of the work of breathing (e.g. not in severe shock).
weaning: “drop and stretch”
- Decrease P-high in increments of 2 cm and prolong the T-high by increments of 0.5-2 seconds.
- May be done every 4-8 hours as tolerated.
- Monitor for desaturation, increased work of breathing, or tachypnea.
liberation from the ventilator
- Once you reach P-high of 20 cm and stretch the T-high to ~20-30 seconds, the patient is doing nearly all the work of breathing (you're very close to being on CPAP).
- At this point you can rapidly wean settings to CPAP at 15 cm (e.g. over ~6hr). Make sure automatic tube compensation is on throughout this period (it should always be on during APRV).
- Patient may be extubated directly from CPAP of 10-15 cm.
- Extubate to BiPAP or HFNC to maintain ongoing support.
- Do not transition to standard nasal cannula for 24 hours.
Acknowledgments: Thanks to Emily Parent RRT for help writing this guideline.
More on APRV here.
References
- Zhou Y et al. Early application of airway pressure release ventilation may reduce the duration of mechanical ventilation in acute respiratory distress syndrome. Intensive Care Medicine 2017.
- Daoud EG et al. Airway pressure release ventilation: What do we know? Respiratory Care 2012.
- Habashi NM. Other approaches to open-lung ventilation: airway pressure release ventilation. Critical Care Medicine 2005.
Notes
- Some authors have previously suggested that very large tidal volumes might be lung-injurious even in APRV mode (Miller 2017). Zhou 2017 achieved average lung volumes of ~7.4 +/- 1 ml/kg, suggesting that the achievement of lung-protective tidal volumes using APRV is quite feasible. In fact, within this study there was no significant difference in tidal volume between the APRV and the low-tidal-volume group.
Great content as always. I do think one pitfall is worth mentioning. This all works great when using a Draeger ventilator. At my institution we use Puritan Bennett ventilators, which do not do actual APRV but instead do “bilevel”. The pitfall is that on the PB vents, spontaneous breaths overwhelm the “dumps”. By that I mean that the patient is able to prolong the Tlow with pretty much any spontaneous breath. So you’ll set Tlow at 0.55 seconds, and if you don’t pay attention to the flow/time tracing, you will miss that your patient is exhaling for 1.2 seconds, getting Vt of 1L, and derecruiting– the exact opposite of lung protective ventilation. I would also submit that it’s these complexities of setting the Tlow which have led to difficulty demonstrating what I know just has to be true–well-set APRV is the best ventilatory strategy for sick patients.
Thanks. I completely agree – these are huge pet peeves of mine: First, different vent manufacturers have different names for similar modes, which causes enormous confusion. Second, as you point out, an analogous mode may work differently on different ventilators.
If APRV continues to be supported by evidence then vent companies will be forced to get better APRV-like modes or go extinct. It’s not a very complex mode, and indeed when vent companies try to make it “better” (e.g. adding pressure support to the spontaneous breaths at T-Hi) that is often counterproductive.
I actually second that comment. I use mindray, and the APRV has a different setting (instead of Thigh and Tlow, it has T slope???). The BiLevel looks more like the APRV setting mentioned here
How can I use APRV settings on Oxylog 3000 if we’re doing intrahospital transfer so that we don’t derecruit the lung.
I don’t know how to use an Oxylog, maybe someone else can help with this.
In general most travel vents and OR vents can do pressure control. These can be set up to do pressure control – inverse ratio ventilation (PC-IRV), which isn’t as good as APRV but it can work in a pinch as a way to deliver a lot of mean airway pressure. To do this you need to extend the inspiratory time such that the inspiratory time is overall much greater than the expiratory time. PC-IRV won’t be able to do very precise dumping breaths, so you *will* need PEEP to prevent de-recruitment. For example, you might set up something along the lines of Pressure Control 30cm/15cm PEEP, resp rate 12, inspiratory time 4 seconds. That would get your 4-second breaths and 1-second exhalation for I/E ratio of 4.
I’ve been trying to conceptualize why APRV is superior to PC-IRV as you’ve described. Is it because of breath shape? or time at achieved mean airway pressure is still less? I think I need to understand how a ventilator controls dumping breaths- does it actually control the reversed flow out of the lungs, as opposed to just opening a valve and allowing outflow that is produced by the pressure of distension of the lungs and chest wall? (Using a Hamilton t1 ventilator)
I think the difference is perhaps most greatest regarding patient comfort. on APRV spontaneous breaths are supported so this is fairly comfortable. PC-IRV is probably less comfortable. in a paralyzed or passive patient, there might not be a huge difference between the two modes
There is full BiPAP mode on Oxylog 3000, which can be set in the inverse ratio described by Josh.
Hi
I am new to APRV and I am trying to get to grips with the concept and vent settings. We have Puritan Bennett ventilators so have to set up APRV through the BILEVEL route. I am ‘happy’ with the initial settings. I am a bit confused when it comes to setting up PS for any spontaneous breaths. Does this need to be on any particular setting and does it depend at all on the P high and P low values. Thank you for your help.
Best wishes,
Mike
Not sure. Ideally you want to cancel out the resistance of the ETT, so any spontaneous breaths can occur without additional airway resistance. On the Drager this can be done using automatic tube compensation. On a different ventilator you might consider adding a small amount of pressure support (e.g. 5 cm) to cancel out the tube resistance. But I’m not certain, would try to find someone with more experience using APRV on that ventilator.
With PB we use a PS set 2-3 cmh2o higher than the driving pressure. For example, if the P-high is 25 and L-low is 0, we would set the PS to 27-28 to help the patient on top of the inspiratory wave.
Excellent article! Thank you for sharing your knowledge and experience.
Hola, como y cuándo agregas la presión soporte
Excellent article, I am trying to get a clear concept of APRV, and this article is fantastic. I have a question when do you recommend this ventilator mode ??? I was watching an online lecture, and they are urging to use it as prevention for ARDS. Any thoughts ???
Thanks for the great guide, it is very helpful. I have not been working in the ICU for a while, now back to doing critical care including tele ICU, so apologize if the question is of some obvious nature. Doing Tele ICU started using APRV on Maquet Servo-I vents and have been having issues with RTs, When pt is breathing spontaneously on top of P high, TV displayed combine the transitioning from High to Low pressure volumes with spontaneous breaths volumes. So added up TVs end up being above 800 -900 even with no PS for spontaneous breaths very often.This fact make RTs unconformable using this mode. Patients are mostly COVIDs, and i am talking about more of the early stage of lung injury with good compliance.
Should we be tolerating this trend if without spontaneous breath TV just from the pressure release at at goal around 8 cc/kg/ibw? Is there any TV or frequency of of larger TVs which one should tolerate?
Have been having hard time working with RTs on setting PEEP to zero – which is the name for P low on this machine, but high TV seems to be a bigger problem.
Thanks much in advance.
I have used APRV “BILEVEL” with both the Servo I and the Servo U. Increasing the P low will decrease your tidal volume. Refer back to Refer to this article “discussion of parameters”.
Keep P low at zero, otherwise you add unnecessary resistance to your patient’s exhalation. P low of zero keeps the open valve aspect of APRV releases, allowing your patient to breath more spontaneously. Set Exp. Term 75%, and/ or keep T low 0.4- 0.6 sec. Look at TCAV protocol as well. This explains how properly setting APRV is long protective by keeping an open lung approach.
Great article! Only disagree with the liberation from the ventilator section: especially in COVID this seems to be too rapid: I’ve seen a number of patients, who deteriorated significantly if they were weaned too quickly and had major setbacks.
In my observation continuing ‘drop & stretch’ until Phigh is 10, then switching over to CPAP with a PEEP of 10 and continuing the weaning on CPAP gradually provides a less rocky road for the patients.
One problem I’ve encountered with the Servo-U ventilator and wondering if anyone has any advice/solution:
In some patients with strong spontaneous respiratory efforts, the ventilator extends the Tlow over and above the set time, which is causing even higher Vt. I’ve got screenshots showing that the Tlow is effectively closer to 0.8-1s and stays the same regardless of setting it to 0.3 to 0.5. Pressure support was switched off.
Any thoughts?
Same problem with servo-U : an undesired extended Tlow, even when I lower the Tlow to 0.3 sec…
any advices?
I switched 2 Patients with Covid pneumonia that had severe ARDS into APRV mode, the oxygenation got quite a bit betterm maybe around 10-15 mmhg O2 more than before, as long as they were breathing on their own properly,.
After an hour or so i could see they started to get exhausted, the breathing frequency raised to 30 or so and the tidal volumes were maybe 200-300 may, the CO2 went up, the Ph went down, the abg looked like shit so i had to switch them back to pressure Support with a lot of supprt (15mbar or so), and the abg looked fine again after that.
Is that an inherent weakness of APRV? i didnt see any way to get the Co2 out unless they breath themselves enough. i tried everything, more releases, slighlty longer relesases, jsut wouldnt work.
I feel like APRV just wont work on patients unless their own breathing is still somewhat usefull.
guess my question is, what do you do if you cant get the CO2 out in APRV mode.
Thought…maybe Next time try simultaneously incr’ing your Phigh and dropping your Thigh. That way u increase your volumes and take the work away from the pt. The more Phigh and less Thigh, the less work on the pt. The less Phigh + longer Thigh, the more work on the pt, prepping closer to CPAP, as lungs improve (as evidenced by improving %Trap) Hope this helps
So Helpful to have this cheat sheet! Thank you so much. 2 of my attendings use APRV exclusively and past places only used PRVC so I have been adapting.
Learning about the APRV-mode, and this helped me a lot.
We use Hamilton, and I could easily use this Guideline