Airway pressure release ventilationThis is an introduction to the invasive ventilation mode Airway Pressure Release Ventilation (APRV).  My understanding is evolving and I’m trying to incorporate the more recent concept of driving pressure into my knowledge. I hope to receive some feedback on these musings as I struggle to integrate new thinking and understanding in the management of ARDS.


So what is APRV?

At the simplest level, APRV is a form of continuous positive airway pressure (CPAP) which utilises releases of CPAP to a pressure of zero intermittently. The pattern of these CPAP releases to zero are such that they represent a severe, inverse ratio ventilation. The second aspect of APRV is that the releases to 0 (exhalation) are very brief, typically 0.25 to 1 second. The brevity of the pressure release or expiratory phase is as equally important to the technique of APRV as the long inspiratory time or inhalation-exhalation ratio (I:E ratio).


What is inverse ratio ventilation?

Under normal resting circumstances we take longer to exhale than inhale, for instance one second to breath in, two seconds to breath out. This is caused by changes in the diameter of small airway which varies with the intrathoracic pressure. Breathing in generates a relative negative intrathoracic pressure which pulls the small airways open, increasing their diameter and causing an increase in flow compared to exhalation. During exhalation, intrathoacic pressure is relatively increased, removing the splinting influence on the small airways and reducing their diameter and therefore airflow. The I:E ratio is dynamic and is influenced by the patients individual pathology. As a traditional rule of thumb, we set our ventilators on 1:2 ratios for this reason.

So why would we want to do the reverse of this? Imagine a group of alveoli, half the group are atelectic (collapsed) due to oedema or exudate, the other half are open. Now imagine that these alveoli are receiving gas flow at a traditional 1:2 ratio. The healthy alveoli increase and decrease their volume with the tidal volume. However, the atelectic alveoli only start to open towards the end of the tidal breath and then collapse again, the volume and pressure is not applied long enough to keep them open through the breath cycle. The time that it takes for the alveoli to open is described as a time constant, but, in hypoxic patients where large section of lung tissue are atelectic, the time constants differ between the collapsed and the healthy lung. The idea of inverse ratio ventilation is to increase the inspiratory time to allow areas of lung with slower time constants (the collapsed/atelectic areas) enough time to open.


So the next question you ask is why is the expiration so short?

Using an inverse ratio we have overcome the problem of different parts of the lung having different time constants and not being able to keep alveoli open long enough to contribute to gas exchange. The next problem is keeping the alveoli that we have now recruited, open, this is usually achieved with positive end expiratory pressure (PEEP). When using APRV, the recruited alveoli are kept opened because they don’t have time to collapse when the pressure lease or exhalation occurs. The airway pressure although set to zero, never reaches zero at the alveoli level; there simply isn’t time. This is why PEEP is not necessary in APRV. Given that the alveolar pressure does not approach zero in the expiratory phase, adding PEEP would likely increase intrinsic PEEP and negatively effect carbon dioxide removal and possibly impair haemodynamics. The ideal expiratory time should not allow the expiratory flow to drop less than 75% of its peak flow rate. To see this, you need to look at the flow-time wave form on the ventilator. In conventional ventilation you want to see the expiratory flow reach zero before the next breath starts, this prevents breath stacking and intrinsic PEEP; remember you have already set a PEEP level in conventional ventilation.


So APRV is a way of optimising an “open lung” approach in the ventilation of patients with ARDS. In theory, the prolonged inhalation maximises recruitment of alveoli with different time constants and keeps them open by not allowing sufficient time on exhalation to collapse. Some of the lung injury that occurs as a result of how we ventilate lungs is caused by the cyclical collapse and opening of alveoli, an “open lung” approach aims to minimise this and APRV is one approach to achieve it.


Which patients might benefit from APRV?

Some centres may use APRV as their primary mode of ventilation and simply alter settings according to individual pathology. Most critical care units, my own service included, use APRV as a rescue therapy in the more severe acute respiratory distress syndrome (ARDS) patients.


Should patients be allowed to breathe spontaneously?

Patients can breathe spontaneously or be paralysed. I believe this mode is optimised when the patient is spontaneously breathing. I’ve paralysed patients on APRV who remained hypoxic with spontaneous breathing and have several times seen hypoxia and hypercapnia worsen, this was usually in the most severe of ARDS patients. Some hypothesise that spontaneous breathing improves ventilation to dependent lung regions (basal and posterior zones). My practice is to allow patients to breathe spontaneously, often requiring a reduction in sedation. I’ve also seen patients spontaneously breathing and nursed in the prone position, no neuromuscular blockade. In my opinion, your patient is more likely to experience hypercapnea if you don’t allow spontaneous breathing when using APRV.


How can a patient breath spontaneously with a very long I:E ratio and be comfortable and not stack breaths?

APRV is essentially a variant of bi-phasic inspiratory positive airway pressure (BIPAP). This area of terminology can get confusing due to copy right issues between manufacturers. In terms of invasive ventilators, BIPAP, BI-level and DuoPap are the same thing. What’s important to understand in these modes is that the patient can breathe spontaneously in the inspiratory portion of the mandatory breath and not just between mandatory breaths. If you don’t have a specific APRV mode on your ventilator, but have a version of BIPAP, you could set the mode to provide APRV with some adjustments of alarms and settings, but it’s a pain and will likely trigger lots of unnecessary alarms. Most modern ventilators will have a bespoke APRV mode built into their software. Breathing spontaneously with APRV is analogous to breathing on a CPAP circuit with very high CPAP and with the occasional complete release of the CPAP. The expiratory valve is always open so although resistance to exhalation will be felt, it is not obstructed. Patients can be weaned and extubated from APRV without changing to conventional modes. Pressure support for spontaneous breaths should not be applied in APRV. Firstly, in severe ARDS cases, this would likely increase peak pressures above 30cmH2O if a high pressure high setting is needed. Secondly, pressure support will interfere with the expiratory time if a spontaneous breath is triggered in that phase, increasing the expiratory phase and causing alveolar collapse between CPAP pressure cycles.


APRV settings.

This can seem very confusing compared to conventional ventilation, but it’s actually quite simple.

There are two groups to consider, pressure and time settings.

You set a pressure high (PH) and a pressure low (PL).

Then you need to set a time high (TH) and a time low (TL).

That’s it.

Pressure low is always set at 0, so there are only three settings to adjust, if you exclude oxygen. Once you have inputted the initial settings, it’s the titration of these settings to your partial pressure of oxygen and carbon dioxide which can be a little counter intuitive, but a simple memory card can help you out here (see references).

When it comes to fine tuning APRV settings there are a few key things to keep in mind. Broadly speaking, increasing PH, TH and decreasing TL augment recruitment and therefore oxygenation, this may increase carbon dioxide. If hypercapnea is the problem, increasing PH and TL will increase carbon dioxide clearance, however, increasing TL may be off-set by causing de-recruitment and reduced oxygenation. In the setting of hypocapnea, reducing PH, reducing TL and increasing TH will increase carbon dioxide.

Never forget sedation, especially in the context of hypercapnea. Allowing increased spontaneous breathing by reducing sedation is often my first strategy when dealing with hypercapnea. All this needs to be taken in context of the patients haemodynamic state and your overall goals, always take permissive hypercapnea into consideration. If the cause of hypoxia is a primary COPD are asthma exacerbation, this is absolutely not the mode to use.


Weaning during APRV can also be a little counter intuitive. In my own ITU, we tend to convert back to conventional ventilation modes, usually pressure regulate synchronised intermittent ventilation (PSIMV) or a form of BIPAP. Alternatively you can wean using APRV. Firstly, the PH needs to be weaned, to at least 15cmH2O. Then TH can be gradually extended to ten seconds and TL reduced to 0.3 seconds. At this point the patient is essentially breathing on conventional CPAP and you either convert to another spontaneous support mode or extubate.


Haemodynamic considerations.

The effect of APRV on a patients haemodynamics will vary depending on the individual patients physiology. However, starting an ARDS patient on a PH of 30cmH2O when the systolic blood pressure is 80mmHg is not going to help your patient, just as 15cmH2O of PEEP would not be tolerated. Some resuscitation is going to be needed first in this context. Also bear in mind that many of these patients will have hypercapnea and the increase in pulmonary vascular resistance is going to effect right ventricular stroke volume and a knock-on effect on the left ventricle and systemic perfusion. That being said,these principles apply to any shocked patient receiving invasive ventilation, particularly soon after intubation.


Since the ARDSnet trial, it has been accepted that a plateau pressure of 30 or less and a tidal volume of 6ml/Kg of ideal body weight is the standard of care in patients with ARDS.


How does APRV fit into this approach?

I’m still trying to understand this, and there is little data to help answer this question, some of the podcasts and videos below try to address this. Some answers may lie with the concept of driving pressure. What is driving pressure? This is the difference in pressure between PEEP and plateau pressure, for instance in PSIMV mode, pressure control of 20cmH2O over 10cmH2O of PEEP gives a driving pressure of 10cmH2O. The tidal volume that this driving pressure generates depends on the lung compliance and that reflects the available lung volume. Conversely settings of 30/5 generates a driving pressure of 25, current literature suggests a driving pressure of greater than 14 is injurious, despite the plateau pressure under 30 and assuming a tidal volume of 6ml/Kg, a driving pressure of 25 may cause lung injury based on more recent thinking. This may explain findings of lack of survival benefit in high PEEP trials in ARDS and evidence of over distension of the lung despite 6ml/Kg ventilation.


In APRV it can be very difficult to keep tidal volume at 6ml/kg, so is this injurious, possibly not if the driving pressure is kept low. Since PEEP is not used in APRV and high PH settings are used does this mean that we are using high driving pressures? No, although airway pressure may fall to zero in the TL window, alveolar pressure does not, this is reflected in the target of no less than 75%  of peak expiration flow. If at the alveolar level, pressure stays within 75% of the PH this would mean that with PH of 40cmH2O, the alveolar pressure may only fall to 26, keeping the driving pressure within a protective range. Now, I have no evidence that this is the case, and I will certainly be looking at the intrinsic PEEP level within the additional ventilator parameters of APRV patients in future.


A short video on APRV on the EVITA ventilator


Cadaver lung being ventilated on APRV


Pig lung on APRV


Resus review summary on APRV.


Lecture on ARDS and relationships between tidal volume, PEEP and driving pressure.


Nader Habashi podcast lecture on ARDS in trauma and APRV.


The same lecture by Nader Habashi in video format


A second lecture by Nadar Habashi


This is a handy APRV cheat sheet and optimisation algorithm I keep on my phone.


Roy Bower lecture on driving pressure (also available on iTunes)


Is lung stretch harmful? The ARDS God Gattinoni.


Gavin DentonGavin Denton @dentongavin – Current role: Critical care practitioner, critical care, West Midlands. Roles include; assessment and management of the critically ill patient, insertion of invasive lines, advanced airway management (under supervision), transfer of the critically ill patient, resuscitation (from airway, to team leader to post resus care). Trenching and support of junior doctors of the above.
Graduated from the University of Birmingham with BN(hons). BSc from Birmingham City University. About to complete MSc in health sciences from the University of Warwick.
Working background: 15 years working within various aspects of critical care. 7 years in critical care, 6 years in critical care outreach, 2 years as a critical care practitioner. Adult life support instructor. Independent non-medical prescriber.
Future aims: faculty of critical care medicine affiliation. FEEL course, POCUS training.
Clinical interests: USS, airway management.

Originally posted 2016-10-09 21:14:21. Republished by Blog Post Promoter

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