ICU Physiology in 1000 Words: Driving Pressure & Stress

Index
Review Articles, ARDS and ALI, Critical Care, Mechanical Ventilation 1 Comment

Feb 132016

By Jon-Emile S. Kenny [@heart_lung]

The problem with the lung in the acute respiratory distress syndrome [ARDS] is not that it is
stif f , but rather, that it is small [1]. In the 1980s, CT scans of the lungs of patients with
ARDS revealed that the f unctional lung was attenuated in size and that dependent densities
f ormed [2]. These images led to the notion of the ‘baby lung’ as the size of aerated lung in
ARDS patients approximated the size of a child’s lung. Appropriately, the degree of
dependent consolidation correlates with shunt f raction, degree of hypoxemia and pulmonary
hypertension [3]. However, in any given patient, it is dif f icult to predict the exact size of
the ‘baby lung.’ Regardless, the af orementioned physiology provides strong rationale f or
the notion of smaller tidal volume or ‘lung protective’ ventilation. The larger the mismatch
between the size of the ventilator-delivered volume and the size of the ‘baby lung,’ the
larger the dif f erence in airway pressure. As somewhat of an analogy, consider two balloons
comprised of the same elastic material [i.e. their specif ic elastances are equivalent], but one
has a capacity of 100 mL and the other a capacity of 500 mL. Delivery of a 500 mL breath
to each of these balloons will result in a dif f erent stress across the balloon [i.e. the
distending pressure] and dif f erent strain [i.e. the increase in balloon volume relative to its
resting size]. In the intubated patient [free of respiratory effort], this physiology is
represented by a calculated dif f erence in respiratory system compliance [Crs]; that is, f or a
given change in thoracic [lung and chest wall] volume, there is a dif f erence in measured
airway pressure.

Given the above, a complex statistical analysis of previously published randomized

controlled trials on tidal volume [Vt] limitation and positive end-expiratory pressure [PEEP]
in ARDS patients was undertaken [4]. The authors hypothesized that the change in airway
pressure in response to a volume-limited ventilator-delivered breath would be the best
physiological surrogate f or assessing the stress and strain of the ‘baby lung.’ The driving

pressure [ΔP] is equal to [equation 1]:

The driving pressure is equal to the end-inspiratory plateau pressure [Pplat] minus the
positive end expiratory pressure [PEEP], such that [equation 2]:

Contemplating this equation can certainly cause some mathematical consternation because
it is conf using as to what the independent [clinician-controlled] and dependent [system
output] variables are. For this, an illustration may prove f ruitf ul [diagram 1].
Diagram 1: ΔP = driving pressure, Paw = airway pressure, Pplat = plateau pressure, Crs =
respiratory system compliance, Vt = tidal volume

From diagram 1, it can be seen that there are two independent variables, the Vt [or ΔV] and
the PEEP as these are both selected by the clinician in a volume-limited mode of ventilation.
Consequently, the true dependent variable is the Pplat while the Crs is a derived variable
that f orms the slope of the ΔV/ΔP relationship.

The f irst complicating matter here is that changes in both Vt and PEEP by the clinician can
change the Crs [the slope of the line] – if a change in ventilator setting [e.g. an increase in
PEEP] results in over-distension, the slope of the Crs will bend down and rightwards
[diagram 2, curve A], while if there is recruitment, the slope of the Crs will bend up and
lef twards [diagram 2, curve B]. As Crs can co-vary, it may conf ound what a change in Pplat
[and theref ore ΔP] represents. This, in my opinion, may make it dif f icult to design a trial
that provides the clinician with a universal target value f or ΔP. Nevertheless, it can be
inf erred that if ΔP remains the same, or f alls, it likely represents a ‘baby lung’ that is not
overly stressed by a change in ventilator setting.

Diagram 2: Note, tidal volume [Vt] remains the same for both curve A and curve B

The second complicating matter here is that Crs ref lects the pressure dif f erence between
the alveolus and the atmosphere, that is, the distending pressure across the thorax. But
this does not represent the true stress on the lung which is the trans -pulmonary pressure
[Ptp] or the alveolar pressure minus the pleural pressure [2, 5]. Accordingly, a patient with
normal pulmonary compliance, but a very low chest wall compliance [e.g. obesity, extra -
pulmonary ARDS, ascites] will have a large ΔP [curve A above], but without a large stress
across the lung [6, 7]. This is important, because it is the stress and strain on the lung
which places the patient at risk f or lung injury and is also an important determinant of right
ventricular hemodynamics [2, 8]. This criticism was astutely raised in response to the
original paper with the suggestion of measuring esophageal pressure as a surrogate f or
pleural pressure [9]. The authors responded, somewhat anemically, with the f ollowing
“…the measurement of esophageal pressures would just reveal a f ixed elastic component
(chest wall), in series with lung elastance,” which lacks substance, because this is true f or
all patients who are passive with a mechanical ventilator. The question posed to the
authors is distinguishing how much of the chest wall elastance contributes to the calculated
airway pressure. The ef f ect of the chest wall on airway pressure can be clinically very
signif icant [10, 11].

One method f or qualitatively evaluating respiratory mechanics – which f lows f rom the
physiology above – is the stress index [12]. If examination of the terminal portion of the
pressure-time curve on the ventilator [again, in a volume-cycled mode of ventilation]
demonstrates curvature away from the pressure axis [which approximates curve B above]
there is said to be a stress index < 1 or tidal recruitment. By contrast, if the terminal
portion of the pressure-time curve bends towards the pressure axis on the ventilator, curve
A above is approximated, and represents tidal over -distension [stress index > 1]. Note that
on the ventilator, pressure is on the y-axis, not on the x-axis as above. Also on the
ventilator, time in on the x-axis rather than volume. The absolutely crucial point here is
that when measuring the stress index, flow must be constant [square wave delivery] as
when f low is constant, volume and time become linear analogs [13]. In other words, f low
must be constant so that def ormations of the pressure curve ref lects alteration in the elastic
properties of the lung rather than demonstrating changes in f low.
Diagram 3: cartoon of ventilator pressure-time waveform

For more inf ormation please watch the f ollowing lectures [1D, 1E, and 4D]

Ref erences:

1. Gattinoni, L., et al., The "baby lung" became an adult. Intensive Care Med, 2016.
2. Gattinoni, L. and A. Pesenti, The concept of "baby lung". Intensive Care Med, 2005.
31(6): p. 776-84.
3. Gattinoni, L., et al., Inflammatory pulmonary edema and positive end-expiratory
pressure: correlations between imaging and physiologic studies. J Thorac Imaging,
1988. 3(3): p. 59-64.
4. Amato, M.B., et al., Driving pressure and survival in the acute respiratory distress
syndrome. N Engl J Med, 2015. 372(8): p. 747-55.
5. Akoumianaki, E., et al., The application of esophageal pressure measurement in
patients with respiratory failure. Am J Respir Crit Care Med, 2014. 189(5): p. 520-
31.
6. Gattinoni, L., et al., Acute respiratory distress syndrome caused by pulmonary and
extrapulmonary disease. Different syndromes? Am J Respir Crit Care Med, 1998.
158(1): p. 3-11.
7. Gattinoni, L., et al., Bench-to-bedside review: chest wall elastance in acute lung
injury/acute respiratory distress syndrome patients. Crit Care, 2004. 8(5): p. 350-5.
8. Jardin, F. and A. Vieillard-Baron, Right ventricular function and positive pressure
ventilation in clinical practice: from hemodynamic subsets to respirator settings.
Intensive Care Med, 2003. 29(9): p. 1426-34.
9. Costa, E.L., A.S. Slutsky, and M.B. Amato, Driving pressure as a key ventilation
variable. N Engl J Med, 2015. 372(21): p. 2072.
10. Talmor, D., et al., Mechanical ventilation guided by esophageal pressure in acute
lung injury. N Engl J Med, 2008. 359(20): p. 2095-104.
11. Brochard, L., Measurement of esophageal pressure at bedside: pros and cons. Curr
Opin Crit Care, 2014. 20(1): p. 39-46.
12. Grasso, S., et al., Airway pressure-time curve profile (stress index) detects tidal
recruitment/hyperinflation in experimental acute lung injury. Crit Care Med, 2004.
32(4): p. 1018-27.
13. Bekos, V. and J.J. Marini, Monitoring the mechanically ventilated patient. Crit Care
Clin, 2007. 23(3): p. 575-611.