By Tom Pietrantonio, BSRT, RRT-ACCS, NREMT

MedCenter Air

It wasn’t until 1967, in a landmark article published in Lancet, that Ashbaugh, Bigelow, Petty, and Levine first described the clinical entity that they called “acute respiratory distress in adults” (Bernard, 2005). Twenty-five years later, in 1992, the American-European Consensus Conference (AECC) was tasked with developing a standardized definition of acute respiratory distress syndrome (ARDS). The AECC definition was eventually replaced by the Berlin definition in 2013. However, despite our best efforts in research and treatment over the last half-century, the mortality rate of ARDS remains excessively high at 40%.

The use of airway pressure release ventilation (APRV) has some clinicians skeptical about its ability to effectively treat ARDS in the patient care environment. However, after years of research, we are now being introduced to a new concept of APRV called, Time-Controlled Adaptive Ventilation (TCAV).

This article is part one in a two-part series, where the first part is a discussion on the pathophysiology of ARDS and the current evidence on APRV. The second part will focus on how we can effectively use APRV in the patient care environment.

NORMAL ALVEOLI

There are approximately 480 million alveoli in the human lung. Alveoli are unique in that they are not individual units within the lung. Rather, they are all interdependent and interconnected, and each alveolus shares walls with adjacent alveoli. Each alveolar unit is homogeneous in appearance, and mechanically they exhibit a viscoelastic property during inspiration and expiration. All living tissues display viscoelastic behavior, which is characterized by time and frequency-dependent behavior of the material responses. Unlike elastic materials, which attain equilibrium instantaneously following the application of external loading, in viscoelastic materials, this process is delayed and impeded by internal viscous stresses (Suki, Stamenovic, & Hubmayr, 2011). The interconnected structure of alveoli, which consists of complex variations in connective tissue, give alveoli a great deal of stability during normal tidal volume ventilation. When the lung is damaged, alveolar heterogeneity occurs which results in ineffective gas exchange and alveolar function.

PATHOPHYSIOLOGY OF LUNG INJURY

The lungs are susceptible to developing ARDS either by a direct or indirect lung insult. At the micro-alveolar level, lung injury is the result of both primary and secondary mechanisms. The primary mechanisms of lung injury are the loss of surfactant function and increased alveolar stress caused by repeated recruitment and derecruitment of the alveoli. The secondary mechanisms of lung injury are characteristic of alveolar overdistention and the release of inflammatory mediators (Nieman, et al., 2017). Secondary mechanisms of lung injury can only occur when the primary mechanisms are present (Table 1).

It is well known that one of the primary insults of direct lung injury, is mechanical ventilation. Both the initiation of mechanical ventilation after intubation and clinician experience can greatly affect patient outcomes. Gajic, et al studied ventilator-induced lung injury in patients without acute lung injury (ALI) at the onset of mechanical ventilation, and they concluded that approximately 25% of patients who did not have acute lung injury from the outset and who were ventilated for 48 hrs. developed ALI, a majority during the first 3 days of mechanical ventilation. The ARDSnet trial back in 2000 was stopped early after ventilating with lower tidal volumes (6cc/kg/IBW) were found to be efficacious with a reduced mortality (P = 0.005) when compared to ventilating with higher tidal volumes (12cc/kg/IBW). Protti, et al studied the effects of static and dynamic lung stress and strain during mechanical ventilation, and they found that all animals ventilated with large dynamic stress and strain developed severe pulmonary edema, whereas those ventilated with the smallest dynamic and largest static stress and strain never did. Subsequently, when stress and strain were mainly dynamic, transpulmonary (and airway) pressure increased and hypoxemia and hypercarbia developed, despite no change in ventilatory settings; these alterations never occurred when stress and strain were mainly static.

According to Villar and Slutsky, “maybe ALI / ARDS is a consequence of our efforts to ventilate patients, rather than the progression of the underlying disease”? If what Villar and Slutsky claim is to be true, then, “acute lung injury and acute respiratory distress syndrome is no longer a syndrome that must be treated but is a syndrome that should be prevented”.  Perhaps, based on what we currently know, we need to re-think about the way we mechanically ventilate our patients. Instead of protocolizing strategies that conform the patient to the ventilator, we should be conforming the ventilator to the patient.

 

Table 1: Causes of Direct and Indirect Lung Injury & Primary and secondary mechanisms of ARDS.

Direct Lung Injury Indirect Lung Injury Primary Mechanisms Secondary Mechanisms
Aspiration Sepsis Loss of surfactant production Alveolar over distention
Pneumonia Drug Overdose Alveolar recruitment and derecruitment Release of inflammatory mediators
Mechanical Ventilation Burns
Pulmonary Contusions Pancreatitis
Inhalation Injury Non-thoracic Trauma
Near Drowning Transfusion Reactions
Near Drowning Transfusion Reactions

 

AIRWAY PRESSURE RELEASE VENTILATION (APRV)

APRV is essentially an “open-lung” mode of mechanical ventilation that provides continuous positive airway pressure (CPAP) with quick intermittent release phases. It is a time-triggered, pressure-limited, and time-cycled mode of mechanical ventilation. To effectively ventilate a patient in APRV, the mode relies on the precise setting of four distinct parameters: pressure high (Phigh), pressure low (Plow), time high (Thigh) and time low (Tlow). If used correctly, APRV has many clinical benefits (Table 2).

 

Table 2: Benefits of APRV.

Clinical Benefits of Airway Pressure Release Ventilation (APRV)
·       Lung protective – Release volume is created by decreasing airway pressure instead of increasing airway pressure, which limits lung overdistention and barotraumas.
·       Open valve circuit – Allows the patient to spontaneous breath during the inspiration and expiration phase. Spontaneous breathing can also improve V/Q mismatching through the use of collateral channels of ventilation.
·       Limited adverse effects on cardio-circulatory function.
·       Decreased sedation use.
·       Less of a need for neuromuscular blockade (NMB) administration.

 

APRV is not a new mode of mechanical ventilation. Three decades ago, Stock and Downs first described Airway Pressure Release Ventilation (APRV) and showed benefit in a study after ten anesthetized dogs randomly received either intermittent positive-pressure ventilation (IPPV) or APRV. They concluded that APRV is an improved method of oxygenation and ventilatory support for patients with ALI that will allow unrestricted spontaneous ventilation and may decrease the incidence of barotrauma. Kollish-Singule, et al researched how dynamic alveolar heterogeneity in rat lungs is influenced by using two modes of mechanical ventilation: low tidal volume ventilation and ARPV. The low tidal volume ventilation group required higher PEEP (20-24cmH2O) levels to achieve similar alveolar characteristics of the control group, and, similarly, achieving an end-expiratory flow rate (EEFR) to peak expiratory flow rate (PEFR) of 50-75% produced similar alveolar characteristics of the control group. Although High PEEP during LTVV increased alveolar recruitment and dynamic alveolar homogeneity, alveolar size distribution was significantly different than that of the control group. In comparison, an EEFR to PEFR of 75% produced dynamic alveolar homogeneity and a closer approximation of alveolar size distribution and dynamics when compared to the control group (Kollisch-Singule, et al., 2015).

APRV: WHERE ARE WE NOW?

Despite the proven benefits, APRV is often used as a “rescue” therapy mode when other conventional ventilation strategies have failed. As with every approach to critical care medicine, early intervention is necessary, and APRV should not be an exception. Initiating APRV early would help prevent the primary and secondary mechanisms of alveolar lung injury from occurring and/or progressing.

Time-Controlled Adaptive Ventilation (TCAV) set in the APRV mode is the newest mechanical ventilation strategy for those patients with ARDS. The Time-Controlled component of TCAV involves an extended time at inspiration, which is greater than the slowest time constant, to gradually recruit and maintain a recruited “open lung” over time. The short, brief, time at exhalation is set less than the fastest time constant to prevent lung and alveolar collapse. The Adaptive component guides the clinician in setting the time duration at exhalation precisely based on improved or worsening lung mechanics by observing the expiratory flow waveform. (Nieman, et al., 2018) .

Currently, no randomized controlled trials exist that compares the APRV-TCAV approach to other ventilation strategies aimed at treating ARDS. However, much success has been observed using the APRV-TCAV approach, as it is the primary mode of ventilation at R. Adam Cowley Shock/Trauma Center in Baltimore, MD.

Key Points:

  • Alveoli are interdependent, interconnected, and share walls with adjacent alveoli.
  • Normal alveoli are homogenous; however, when the lung is damaged, alveolar heterogeneity occurs which results in ineffective gas exchange and alveolar function.
  • Alveoli display a viscoelastic behavior which is characterized by a “time lag” with each mechanical breath.
  • The development of ARDS is caused by direct and indirect lung injury.
  • Primary mechanisms of ARDS include 1) loss of surfactant and, 2) alveolar recruitment and derecruitment.
  • Secondary mechanisms of ARDS include 1) alveolar overdistention and, 2) release of inflammatory mediators.
  • APRV is a time-triggered, pressure-limited, time-cycled mode of mechanical ventilation.
  • APRV was first described by Stock and Downs in 1987.
  • TCAV is made up of two components: Time controlled and adaptive.
  • Time-controlled focuses on setting a time during inspiration and expiration. The time set at inspiration is set greater than the slowest time constant to gradually recruit and maintain an open lung. The time set at expiration is set less than the fastest time constant to maintain an open lung by preventing lung derecruitment.
  • Adaptive focuses on setting a time during expiration based on the expiratory flow waveform. Proper analysis of the expiratory flow waveform also alerts the clinician of changes in lung mechanics.
  • APRV-TCAV is the current mode of mechanical ventilation at R. Adam/Cowley Shock Trauma Center in Baltimore, MD.

 

 

References

Bernard, G. (2005). Acute Respiratory Distress Syndrome: A Historical Perspective. American Journal of Respiratory Critical Care Medicine, 798-806.

Gajic, O., Dara, S., Mendez, J., Adesanya, A., Festic, E., Caples, S., . . . Hubmayr, R. (2004). Ventilator-associated lung injury in patients without acute lung injury at the onset of mechanical ventilation. Critical Care Medicine.

Kollisch-Singule, M., Jain, S., Andrews, P., Smith, B., Hamlington-Smith, K., Roy, S., . . . Habashi, N. (2015). Effect of Airway Pressure Release Ventilaton on Dynamic Alveolar Heterogeneity. Association of VA Surgeons, 1-9.

Network, T. A. (2000). Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal Volumes for Acute Lung Injury and the Acute Respiratory Distress Syndrome. New England Journal of Medicine, 1301-1308.

Nieman, G., Andrews, P., Satalin, J., Wilcox, K., Kollisch-Singule, M., Madden, M., . . . Habashi, N. (2018). Acute Lung Injury: How to Stabilize a Broken Lung. Critical Care, 136-147.

Nieman, G., Satalin, J., Kollisch-Singule, M., Andrews, P., Aiash, H., Habashi, N., & Gatto, L. (2017). Physiology in Medicine: Understanding Dynamic Alveolar Physiology to Minimize Ventilator Induced Lung Injury (VILI). American Physiology Society.

Protti, A., Andreis, D., Monti, M., Santini, A., Sparacino, C., Langer, T., . . . Gattinoni, L. (2013). Lung Stress and Strain During Mechanical Ventilation: Any Difference Between Statics and Dynamics? Critical Care Medicine, 1046-1055.

Silva, P. L., Cruz, F. F., Samary, C. d., Moraes, L., de Magalhaes, R. F., Fernandes, M., . . . Rocco, P. (2018). Biological Response to Time-Controlled Adaptive Ventilation Depends on Acute Respiratory Distress Syndrome Etiology. Critical Care Medicine, 609-618.

Stock, M., Downs, J., & Frolicher, D. (1987). Airway Pressure Release Ventilation. Critical Care Medicine.

Suki, B., Stamenovic, D., & Hubmayr, R. (2011). Lung Parenchymal Mechanics. Compr Physiol, 1317-1351.

Villar, J., & Slutsky, A. (2013). Is Acute Respiratory Distress Syndrome an Iatrogenic Disease? Critical Care.

 

 

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