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“One of the symptoms of an approaching nervous breakdown is the belief that one's work is terribly important.”
I read with great interest a recent letter penned by Taylor and Camporota in response to an investigation on airway pressure release ventilation [APRV] by Zhou and colleagues. Their brief communication proposed an equation for estimating the amount of intrinsic PEEP [PEEPi] generated during APRV and, consequently, argued that the driving pressure in APRV is likely less than that reported in the study by Zhou et al.
In this post I will briefly explain and critique their mathematical approach, propose a simpler equation for estimating PEEPi in APRV [based on far fewer physiological assumptions] and finally reaffirm why, in my opinion, driving pressure is a troublesome variable, particularly in APRV.
Intrinsic PEEP in APRV
Ultimately, the mathematical approach proposed by Taylor and Camporota seeks to estimate the amount of trapped volume in the lung at the end of the expiratory time [T-Low] and then multiply this residual volume by the elastance [or stiffness] of the lung; this, then, gives the residual pressure or PEEPi.
In other words:
How can we calculate the remaining ['residual'] volume at the end of the expiratory time during APRV? One can understand by inspecting the expiratory flow waveform on a ventilator [see figure 1A]. If we assume the time it takes for the lung to fully empty to be 4 time constants and we multiple this time by the peak expiratory flow rate [PEFR] then we get the total expired volume if the lung were left to empty completely. Geometrically, this can be seen as one-half the rectangular area [i.e. the blue highlighted triangle] defined by the PEFR and the duration of 4 time constants.But in APRV, the lung isn’t allowed to fully empty, so the ‘residual volume’ described above is the total triangular volume in figure 1A less the actual released volume [in red]. This remaining area of the triangle - in purple - defines the amount of volume left in the lung at the end of T-Low [figure 1B]. If this value is then multiplied by the elastance [i.e. stiffness, the inverse of compliance], then the recoil pressure remaining in the airway – that is, the PEEPi – is revealed.
There are both practical and theoretical problems with this formulation. The practical problems are that airway resistance and compliance [and therefore elastance] are burdensome to calculate correctly at the bedside. In a patient on APRV, determining these respiratory variables, essentially, mandates switching the patient to volume control. Further, accurate calculation typically requires heavy sedation and, potentially, paralysis to maintain synchrony during end-expiratory and inspiratory holds. Finally, patients with the same respiratory mechanics and identical APRV settings can have different PEEPi levels based solely on the ventilator given inherent differences in device manufacture.
Theoretically, as described in part 1 of the ‘APRV Trilogy,’ time-constants are problematic because both calculated resistance and compliance are physiologically-coupled. Only when all lung units are homogenous does compliance totally uncouple from resistance and this is simply impossible in ARDS. Additionally, both calculated airway resistance [and compliance] are volume-dependent – for example resistance tends to fall as lung volume rises, presumably due to the tethering open of airways. Similarly, compliance [and elastance] are also volume dependent; should these calculations be made on a standardized level of PEEP? If, during the elastance [or resistance] calculation, the clinician uses an extrinsic PEEP [PEEPe] of 10 cm H2O, can the stiffness [and resistance] of the lung at this clinician-selected PEEPe be used interchangeably with the stiffness [and resistance] of the lung at the PEEPi generated during APRV? No, methinks.
A Simpler Method
As described in part 2 of the ‘APRV Trilogy,’ a simpler assumption [with much less physiological and mathematical coupling] is to presume that flow, volume and pressure all decay mono-exponentially. Using this approach, if flow falls by 25% then pressure [from P-High] also falls by 25%. As an example, if PEFR is 60 L/min and at the end of T-low, the expiratory flow is 45 L/min then flow has fallen by 25%. If P-High were set to 30 cm H2O and we assume that it too fell by 25%, then PEEPi becomes 22.5 cm H2O. If P-Low were set to zero, then the driving pressure is 30 cm H2O – 22.5 cm H2O or 7.5 cm H2O. The astute reader may recognize by the aforementioned assumptions that the estimated PEEPi – and driving pressure – simply become the following:
A Fool’s Errand?
Yet the problem with both of the aforementioned calculations is that driving pressure still only speaks to the change in pressure within the ‘airway compartment’ and cannot definitively provide the true stress across the lung, over time. It is entirely possible that a patient with severe ARDS secondary to trauma-induced pancreatitis and a patient with equally severe ARDS from bilateral aspiration pneumonia have the same respiratory mechanics; however, their trans-pulmonary pressures – and therefore stress across the lung – may be markedly different. With disparate stress across the lung, the mechanical power felt by the lung skeleton may be intensely dissimilar despite equal driving pressures. Importantly, PEEP will lower mechanical power upon the lung only to the extent that PEEP homogenizes pulmonary stress raisers. If the application of PEEP does not homogenize the lung, then it will simply increase the power felt by the lung during both the mechanical and spontaneous breaths of APRV.
In part 3 of the ‘APRV Trilogy,’ I proposed a theoretical model for visualizing mechanical power in APRV using pulmonary and extra-pulmonary ARDS as clinical points-of-departure. Please see that post [and especially its first figure] on how, theoretically, the risk of ergotrauma may become quite high in a patient with severe pulmonary ARDS, despite a driving pressure of less than 8 cm H2O.
Dr. Kenny is the cofounder and Chief Medical Officer of Flosonics Medical; he is also the creator and author of a free hemodynamic curriculum at heart-lung.org