- Initial settings
- Troubleshooting hypoxemia & acidemia
- Questions & discussion
APRV can be a bit scary for folks who aren't used to it. Everyone has slightly different ways of setting the parameters. However, over time I've come to believe that APRV is a more forgiving mode than most realize. Perfect is the enemy of good. As long as the settings are reasonable, the clinical effects are likely to be the same.
So far, we have had considerable success with APRV in our COVID patients. This has allowed us to support and extubate several patients successfully, while avoiding paralysis, proning, deep sedation, inhaled pulmonary vasodilators, or ECMO. Patients typically can be weaned from 100% FiO2 to 50% FiO2 on APRV within 6-12 hours as they slowly recruit. As such, APRV may be an economical mode which may reduce drug expenditures (e.g., cisatracurium) and limit the expenditure of PPE (e.g., proning a patient exposes many people repeatedly and consumes lots of PPE).
There is considerable debate regarding the pathophysiology of COVID respiratory failure. This is a complex disease, which may defy any simple mechanism. However, I continue to believe that a primary pathophysiological problem is de-recruitment. This may explain the benefits of CPAP and awake proning. It also explains why APRV works well for these patients (video on this concept below).
One group of patients who might not benefit from APRV are patients with substantial obstructive lung disease (e.g., COPD or asthma). Such patients tend to accumulate excessive intra-thoracic pressures (“autoPEEP”) with any ventilator mode. APRV could potentially exacerbate this. APRV may be used cautiously in patients with mild or moderate obstructive lung disease (with the understanding that patients may require unusually long T-low and that careful monitoring is required to ensure adequate ventilation).
- Typical range from 15-35 cm (higher than 35 might rarely be required in profound obesity).
- Initially, this is targeted at a high level (~30 cm), then inched down over time as oxygenation improves.
- Problems with excessive P-High:
- Lung over-distension.
- May impair hemodynamics by causing cor pulmonale.
- Problems with inadequate P-High:
- De-recruitment leads to hypoxemia.
- Repeated opening and closing of alveoli causes atelectotrauma.
- 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.
- Always set this to zero.
- T-high is the driver of the release frequency (i.e., the frequency of “mechanical breaths” or “dumping breaths”).
- Release frequency = 60/(T-High + T-Low). Since T-low is small, this approximates to simply 60/T-High.
- Initially the T-hi is generally set ~5 seconds, to achieve ~12 releases per minute.
- As patients wean off ventilator support, T-High will be increased (“stretched”) and the release frequency will decrease.
- Problems if T-high is too short:
- Too many releases may lead to de-recruitment (by lowering the mean airway pressure).
- APRV stops being lung-protective, and starts resembling generic pressure-control ventilation.
- Problems if T-high is too long:
- 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 (and this starts to resemble CPAP).
- Generally, 0.5 seconds is a reasonable place to start and won't be too far off for COVID patients.
- For patients with underlying COPD, longer T-low may be needed (e.g. 0.8-1.5 seconds).
- There are two potential ways to set T-low
- Traditional method: (This is complicated and requires considerable training in APRV.) Among patients who are 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. However, if the dumping breath is consistently >8 cc/kg, it may be advisable to reduce the T-low further.
- Shortcut method: (This is easier to do and requires less training.) Adjust the T-low to target a dumping breath volume of ~6-8 cc/kg. For patients who are actively breathing on the ventilator, this may be the only possible method to use (because the flow curves may vary between different breaths due to patient effort, hampering the traditional method).
- Problems if the T-low is too short:
- The release breath is too small, leading to ineffective ventilation. The ventilator does little to support the work of breathing.
- This isn't generally a major problem, so when in doubt it's generally better to err on the side of setting the T-low too short.
- Problems if the T-low is too long:
- The release breath is too large, causing de-recruitment (leading to hypoxemia and also hypercapnia).
- Repetitive closing/opening of alveoli during the release breath causes trauma to lungs (atelectotrauma).
- This is potentially a huge problem – and frankly it's the Achilles heel of APRV. Fortunately, this is avoidable with adequate monitoring and keeping T-low on the shorter side.
- Aggressively wean the FiO2 down to target a saturation of ~88-94%.
- Consistently and aggressively titrating the FiO2 to its lowest possible value allows the FiO2 to be a “de-recruitment meter.”
- If the FiO2 requirement is increasing, this suggests de-recruitment or other pulmonary deterioration (e.g., pneumothorax).
- Start at 25-35 cm, most often ~28-30 cm.
- Higher pressures are useful for patients with more profound hypoxemia and patients with morbid obesity. For example:
- Normal weight and crashing off 100% FiO2 onto APRV: set P-high to 30 cm.
- Morbid obesity and crashing off 100% FiO2 onto APRV: set P-high to 35 cm.
- Always set to zero.
- Set to 5 seconds.
- Set to 0.5 seconds initially (or 0.8 seconds in patients with COPD).
- Start at 100%, aggressively wean this down as fast as possible.
- Spontaneous breathing must be supported
- Drager or Puritan Bennett ventilators: make sure Automatic Tube Compensation (ATC) is turned on. This should provide a tailored amount of pressure designed to overcome the resistance of the endotracheal tube.
- Ventilators without automatic tube compensation: add pressure support of 5 cm.
- Some patients may experience hypotension due to increased airway pressure and reduced venous return.
- Monitor hemodynamics very carefully (e.g., cycle the blood pressure every minute).
- There should be a low threshold to initiate vasopressors pre-emptively.
- Some patients who are truly hypovolemic (e.g., due to poor oral intake and diarrhea) may require judicious fluid administration.
- This is pretty straightforward.
- Oxygen saturation reveals more about oxygen delivery than PaO2. For this reason, oxygen saturation is generally fully adequate to monitor oxygenation (there is no need for an ABG).
volume of release (“dumping”) breaths
- It's controversial how tightly this needs to be controlled.
- My preference is to keep this generally below ~8 cc/kg if possible (e.g. by reducing the T-low).
- If the dumping breaths are very small (e.g. <4 cc/kg), then consider increasing the T-low.
- The ventilator will display the percent of minute ventilation being performed by the patient's spontaneous breaths.
- The ideal amount of ventilation performed by the patient will vary based on clinical context.
- Initially, while the patient is extremely sick, ~10-30% might be a good target.
- As the patient improves, they may be able to perform more work (e.g. ~30-60% of the minute ventilation).
- If the patient isn't spontaneously breathing at all, try lightening the sedation to promote some spontaneous respiration.
- If the patient is contributing too much to the work of breathing, this could theoretically lead to fatigue over time.
- Consider adding sedation if the patient is anxious/agitated.
- Consider increasing support level (e.g., increasing P-high and reducing T-high), especially if concerned that the patient may fatigue.
- Normal minute ventilation is roughly ~6-8 liters/minute. Patients with lung disease, increased metabolism, or larger weight will need more in order to adequately clear CO2.
- Tracking minute ventilation over time is a good habit, as this may be an early indicator of a variety of problems:
- If the minute ventilation is very low (e.g. <4 liters/minute), the patient is likely hypercapneic. This may result from inadequate ventilatory support and/or over-sedation.
- If the minute ventilation is very high (e.g. >12 liters/minute), then the patient may be anxious or have increased dead-space ventilation (e.g. due to pulmonary embolism).
end tidal CO2?
- Accuracy of etCO2 in APRV may be variable, depending on the size of breaths and the breathing pattern.
- Trending this is reasonable, but it's not entirely reliable.
- Combining the minute ventilation and etCO2 trends together could provide better information than either in isolation.
- An occasional blood gas may be useful (to correlate with etCO2 and minute ventilation).
- COVID patients who are allowed to breathe spontaneously over APRV tend to defend their own CO2 – so frequent blood gas measurement doesn't seem to be necessary.
- Generally, this reflects de-recruitment (although other possibilities may include pneumothorax, left-to-right shunt due to cor pulmonale, and ventilator-associated pneumonia).
- If severe, consider lung ultrasonography to exclude pneumothorax.
- Titration of APRV settings:
- Increasing P-high is the primary way to increase mean airway pressure and promote recruitment.
- Increasing the T-high will also tend to increase mean airway pressure (but this may reduce the number of dumping breaths and thereby decrease the mechanical ventilator support).
- 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 achieve this at the cost of being less lung-protective.
- The best way to improve pH is often to manipulate the metabolic acid/base status (e.g., IV bicarbonate for non-anion-gap metabolic acidosis). Pushing the bicarbonate to ~28-32 mEq/dL will make achieving an adequate pH enormously easier if this is a problem.
- If you decide to try to reduce the pCO2:
- If the patient isn't breathing spontaneously, wean sedation to encourage greater spontaneous breathing (see “patient effort” above).
- If the release breaths are small (e.g. <6 cc/kg), consider increasing the T-low.
- Reducing the T-high will increase the frequency of releases, thereby increasing the minute ventilation. However, this may threaten to reduce the mean airway pressure. Thus, a simultaneous increase in P-High by 1-2 cm may be considered along with a reduction in T-High, in order to maintain a stable mean airway pressure.
initiation of weaning
readiness for weaning
- Patient should be spontaneously breathing at a reasonable rate (e.g. 10-25 breaths/minute). The goal is a patient who is calm but conscious. This may be facilitated by adequate analgosedation (more on this here).
- FiO2 ~50% or lower.
- No major issues with CO2 clearance or hypoventilation.
- Patient is clinically 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.
- This may be done every 4-8 hours as tolerated.
- Continue this until the patient is weaned down to a P-high of ~18 cm and a T-high of >10 seconds.
- Monitor for desaturation, increased work of breathing, or tachypnea. (See: monitoring section above.)
spontaneous breathing trial
This is highly controversial. I'm not aware of any high-level evidence regarding how to perform SBTs in the context of APRV. This material is largely based on adapting the general concepts of an SBT in assist/control ventilation to APRV. Once a moderate level of support is reached, the concept of an SBT is to abruptly remove all support in a somewhat aggressive fashion and carefully monitor the patient. It's preferable to determine whether the patient will fail while the ETT is still in place.
readiness for spontaneous breathing trial
- FiO2 is ~50% or lower.
- P-High has been weaned to 18 cm or lower.
- T-High has been stretched to >10 seconds.
- Patient is awake, breathing spontaneously over the APRV, and providing a substantial amount of the work of breathing (e.g. >40%).
- Patient is otherwise stable (e.g., not requiring high-dose pressor support).
technique #1: patients able to extubate to BIPAP (e.g., cooperative, no secretions, no contraindication to BiPAP)
- Spontaneous breathing trial is performed as follows:
- Ideally: Set the ventilator to CPAP at 10 cm with automatic tube compensation (ATC) on.
- Alternatively: Could use pressure support mode with a PEEP of 10 cm and a pressure support (driving pressure) of 5 cm.
- Monitor the patient for ~2 hours (to ensure there is no delayed de-recruitment).
- If the patient does well, consider extubation to BiPAP (e.g. 15 cm inspiratory pressure over 10 cm expiratory pressure).
- If the patient is unable to tolerate the trial, return them to their prior APRV setting (e.g., 18 cm P-High, etc.).
technique #2: patients who cannot be extubated to BiPAP
- Spontaneous breathing trial is performed as follows:
- Perform a traditional spontaneous breathing trial using pressure support ventilation (5 cm pressure support on top of 5 cm of PEEP).
- Monitor the patient for ~2 hours (to ensure there is no delayed de-recruitment).
- If the patient does well, consider extubation to high flow nasal cannula (e.g., 60 liters flow and 50% FiO2)
- If the patient is unable to tolerate the trial, return them to their prior APRV setting (e.g., 18 cm P-High, etc.)
questions & discussion
To keep this page small and fast, questions & discussion about this post can be found on another page here.
- Delaying APRV initiation until the patient has failed conventional ventilation and accumulated substantial lung injury.
- Early paralysis prior to trialing APRV (once the patient is paralyzed, APRV is less effective and less beneficial).
- Excessive fear of de-recruitment leading to excruciatingly slow APRV weans.
- Allowing too little time for a trial of APRV (recruitment occurs over a period of several hours, so it's often not immediately obvious that the APRV is working).
- Elmhurst ED APRV guideline (3/27/2020)
- Airway Pressure Release Ventilation (APRV) – Mechanistic and physiologic view (Maryland CC project with Nader Habashi)
- APRV ventilation mode introduction (Resus Review)
- APRV: Resurrection of the open-lung strategy? (PulmCrit)
- PseudoARDS (PulmCrit)
Image citation: APRV tracing from the Resus Review blog by Charles Bruen