Airway pressure release ventilation: An alternative mode of mechanical ventilation in acute respiratory distress syndrome

APRV: A PRESSURE-CONTROLLED MODE THAT ALLOWS SPONTANEOUS BREATHS

Reprinted from Frawley PM, Habashi NM. Airway pressure release ventilation: theory and practice. AACN Clinical Issues 2001; 12:234–246, with permission from Wolters Kluwer Health/Lippincott, Williams & Wilkins.

Airway pressure release ventilation (APRV), first described by Stock et al in 1987,¹¹ is essentially a pressure-control mode—ie, the clinician sets a high and a low pressure. However, it also allows spontaneous breathing through the entire breathing cycle (Figure 2).^12,13

A baseline high pressure (P high) is set first. Mandatory breaths are achieved by releasing the high baseline pressure in the circuit very briefly, usually to 0 cm H₂O (P low), which allows the lungs to partially deflate, and then quickly resuming the high pressure before the unstable alveoli can collapse.

In theory, the optimal release time (the very short time in low pressure, or T low) in APRV should be determined by the time constant of the expiratory flow. The time constant (t) is the time it takes to empty 63% of the lung volume. It is calculated as:

t = C × R

where C is the combined compliance of the lung and chest wall, and R is the combined resistance of the endotracheal tube and the natural airways. In diseases that lead to lower lung compliance (such as ARDS), the time constant is shorter. A practical equilibrium time—or the time it takes for the lung volume in expiration to reach steady state (no expiratory flow)—is about 4 time constants.¹⁴

Since the release time in APRV is much shorter than the equilibrium time, a residual volume of air remains in the lung, creating intentional auto-PEEP. Ideally, this intentional auto-PEEP should be high enough to avoid derecruitment (optimally above the lower inflection point). In APRV the auto-PEEP is controlled by the settings, and this intentional restriction of the expiratory flow is critical to avoid derecruitment of unstable alveolar units.

The amount of time spent at the higher pressure (T high) is generally 80% to 95% of the cycle (ie, the lungs are “inflated” 80% to 95% of the time), and the amount of time at the lower pressure (T low) is 0.6 to 0.8 seconds.

Thus, APRV settings provide a relatively high mean airway pressure, which prevents collapse of unstable alveoli and over time recruits additional alveolar units in the injured lung. The major difference between this mode and more conventional modes is that in APRV the mean inspiratory pressure is maximized and end-expiratory pressure is due to intentional auto-PEEP. In addition, spontaneous breathing is allowed throughout the entire cycle (Figure 2).¹³

Although APRV does not approximate the physiology of spontaneous breathing with healthy lungs, it is nonetheless relatively comfortable and well tolerated. Its theoretical advantage in patients with lung injury is its ability to maximize alveoli recruitment by maintaining a higher mean inspiratory pressure, while the peak alveolar pressure remains lower than with conventional ventilation (Figure 1).

Other modes that are similar to APRV

Other modes of mechanical ventilation very similar to APRV are biphasic positive airway pressure (BiPAP) and bilevel ventilation.

BiPAP differs from APRV only in the timing of the upper and lower pressure levels. In BiPAP, T high is usually shorter than T low. Therefore, in order to avoid derecruitment, P low has to be set above zero with both a high and a low PEEP level.¹³

No studies have demonstrated one mode to be more beneficial than the other, although BiPAP might be more predictable, as both pressures are known.

Bilevel ventilation works like APRV but incorporates pressure support to spontaneous breathing. The use of pressure support may affect the positive physiologic effects (see section below) of unsupported spontaneous breathing. Nevertheless, this strategy might be useful to address severe hypercapnia in the context of APRV.

INITIAL VENTILATOR SETTINGS IN APRV

As we described in the previous section, P high and T high are set to increase end-inspiratory lung volume, recruitment, and oxygenation. P low and T low regulate end-expiratory lung volume, and their settings should prevent derecruitment but ensure adequate alveolar ventilation (Table 1).

P high. In selecting an initial P high, we measure the plateau pressure in a conventional mode using an accepted protective strategy, such as volume-control mode. If the plateau pressure is lower than 30 cm H₂O, we use this pressure as our initial P high. If the plateau pressure is higher than 30 cm H₂O, we select 30 cm H₂O as an initial P high to minimize peak alveolar pressure and reduce the risk of lung overdistention.

P low is set at 0 cm H₂O.

T high is set at 4 seconds and is then adjusted if necessary.

T low is probably the most difficult variable to set because it needs to be short enough to avoid derecruitment but still long enough to allow alveolar ventilation. We usually start with a T low of 0.6 to 0.8 seconds.

ADJUSTING THE VENTILATOR SETTINGS

For hypoxemia. Physician-controlled variables that affect oxygenation in APRV are:

• Mean airway pressure (dependent primarily on P high and T high)
• Fraction of inspired oxygen (Fio₂).

Inadequate oxygenation usually requires increasing one or both of these settings.

Physician-controlled variables that affect alveolar ventilation in the APRV mode are:

• Pressure gradient (P high minus P low)
• Airway pressure release time (T low)
• Airway pressure release frequency.¹⁴ Frequency is related to total cycle time of mandatory breaths by the following equation³:

frequency = 60/cycle time = 60/(T high + T low).

Note that if T low remains constant, adjusting T high will adjust frequency (the more time the lung remains inflated, the lower the respiratory frequency). Conversely, some ventilators allow adjustment of frequency, making T high the dependent variable. The goal of this mode is to recruit alveoli and improve oxygenation, so we usually do not modify the pressure gradient to improve ventilation.

Reprinted from Frawley PM, Habashi NM. Airway pressure release ventilation: theory and practice. AACN Clinical Issues 2001; 12:234–246, with permission from Wolters Kluwer Health/Lippincott, Williams & Wilkins.

In practice, physicians rarely calculate the time constant for each patient to set T low. Hence, T low is usually adjusted according to the flow-time curve on the ventilator, so that the pressure release ends when expiratory flow reaches approximately 40% of the peak expiratory flow, ie, approximately 1 time constant (Figure 3).¹³

For hypercapnia. A frequent and expected consequence of lung-protective ventilation strategies is hypercapnia, termed “permissive” hypercapnia because it is allowed to some extent. In APRV, some degree of CO₂ retention is not unusual. When the measured Paco₂ becomes extreme, we usually increase the frequency of releases by shortening T high, recognizing that this adjustment may affect recruitment by lowering the mean airway pressure.

Spontaneous breaths. A positive aspect of APRV that contributes to its tolerability for patients is that it allows for spontaneous respiration. In some studies of patients with ARDS ventilated with APRV, spontaneous breathing accounted for 10% to 30% of the total minute ventilation and was responsible for an improvement in ventilation-perfusion matching and oxygenation.^15,16 We titrate our patients’ sedation to a goal of spontaneous breathing of at least 10% of total minute ventilation.