Peak Airway Pressure: Why the Fuss?

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Aman Thind
Aman Thind
Critical care medicine fellow at the Cleveland Clinic. Interests: Cardiopulmonary physiology, shock, POCUS, mechanical ventilation, and ARDS. Music genres: Blues, Rock, and Heavy metal

The Pre-brief

You are taking signout from your colleague in the morning:

A patient with severe ARDS, paralyzed. Initial vent settings: VCV, TV = 350, RR = 28, Flow = 60 lpm with square waveform. Overnight, switched to decelerating ramp waveform (all other settings same) as they were able to achieve lower peak inspiratory pressure by doing so.

You ask yourself: was this change actually lung-protective?


I would love to take credit for the title of this article but this is stolen from this excellent narrative review.[1] Nonetheless, it is reflective of how some of us feel about peak inspiratory pressure (PIP). It is natural to have some inherent dread about high PIP. It is inherently true that extremely high pressures delivered by the ventilator may lead to lung injury. It is perhaps not widely appreciated that the peak pressure alarm in ventilators is not simply an alarm. The ventilator also cycles the inspiration off when the upper limit of PIP (set by the user) is reached. This engineering feature is a testament to the potential dangers of high ventilatory pressures.

By definition, peak inspiratory pressure (PIP) is the highest pressure delivered by the ventilator at any instant during a single ventilatory cycle. For simplicity, the following discussion is limited to passive ventilation in a paralyzed patient. So, is PIP directly related to lung injury? To answer this question, it is important to carefully study how the PIP is ‘spent’. At this point, it would be helpful to brush over the previous articles on the equation of motion (Part 1 & Part 2). In summary, ventilatory pressure has two distinct components (Figure 1):

The equation of motion in a passive mechanically ventilated patient with square waveform would be as follows:

Peak inspiratory pressure = (Resistance x Flow) + (Elastance of respiratory system x Tidal volume) + PEEP

(a) Resistive (dynamic) component:
The product of respiratory system resistance and flow. This can be higher due to an increase in resistance (e.g. asthma) and/or flow (e.g. higher set flow or shorter I-time for a given tidal volume).

(b) Elastic (static) component:
The product of respiratory system elastance and volume. This is increased in cases of increased lung and/or chest wall elastance (e.g. ARDS, IPF) and with high set tidal volume. Note that clinically, elastic pressure (elastance x volume) is nothing but driving pressure (plateau pressure – PEEP). For simplicity, let’s assume a PEEP of zero so that elastic pressure = driving pressure = plateau pressure.

Components of peak inspiratory pressure: further analysis

Straight off the bat, it should become obvious that the resistive component of PIP should have no bearing on lung injury. Resistive pressure is dissipated entirely in parts of the respiratory system that contribute to resistance (mainly small airways). On the other hand, elastic pressure is “spent” on the elastic structures: lung and chest wall. For simplicity, we will ignore the effect of chest wall for now. Hence, to get any information about the potential for ventilator-induced lung injury, we have to filter the resistive component and tease out the elastic component of PIP. This can be achieved by measuring airway pressure after applying a post-inspiratory pause in airflow. (Remember, resistive component = resistance x flow; if flow is zero, resistive component is zero.) This is nothing but plateau pressure (Figure 1).

It’s about the plateau, not the peak

If the peak pressure is reported to be high, the next question should be – what is the plateau pressure (Pplat)? A high plateau pressure should raise concerns about lung injury. More precisely, it’s the ‘transpulmonary Pplat’ that’s the most direct marker of lung stress, but that’s a discussion for another day. For determining lung stress, knowing the Pplat still brings you much closer to the truth than simply knowing PIP. From this discussion, it becomes clear that the higher the ratio of resistive and elastic loads, the greater would be the difference between PIP and Pplat. This can occur when resistance is high (e.g. asthma), and/or when inspiratory flow is set high on the vent.

Vent settings do not alter respiratory mechanics

Here’s a fundamental truth – what we dial on the ventilator does not affect the underlying respiratory mechanics (elastance and resistance). Hence, as long as the tidal volume remains the same, the ‘elastic pressure’ (elastance x tidal volume) will remain the same, and choosing one ventilator setting over another to “lower PIP” is a fundamentally flawed concept. Instead, one should ponder – what could have caused the lowering of PIP with changing the ventilator setting? Since the elastic pressure is constant the change in PIP would have occurred due to a change in resistive pressure, which, again, is inconsequential as far as lung stress is concerned.

Since resistance remains constant over short time intervals, the only way a vent change can lead to a change in resistive pressure is by altering the flow. Let’s review a few vent changes:

(i) Peak flow setting in VC:
      Irrespective of the flow profile (square or decelerating ramp), increasing the peak flow leads to an increase in resistive pressure, and hence PIP (Figure 2). Note that increasing peak flow will also cause a reduction in I-time for the same tidal volume. In some ventilators, the user sets the I-time and the peak flow is adjusted depending on the set TV.

(ii) Changing the flow profile from decelerating ramp to square waveform in VC:
      Using basic geometrical analysis, one can appreciate that if the peak flow rate is kept constant, a given tidal volume can be delivered in half the time with a square waveform, compared to decelerating ramp (Figure 3 and 4). On the other hand, if the square waveform is delivered at half the peak flow rate of decelerating ramp, the I-time will remain the same for a given tidal volume. How does this affect resistive pressure?

(A) If the peak flow is kept the same, switching from decelerating ramp to square waveform always increases the resistive pressure (Figure 4).

(B) If the I-time is kept the same & peak flow is halved, the effect on resistive pressure is difficult to predict and depends on the underlying respiratory mechanics.

(iii)Changing mode from VC to PC to achieve the same tidal volume:
      The effect on resistive pressure will depend on several factors including flow profile in VC, shape characteristics of the flow curve in PC (which will depend on respiratory mechanics), and the relative I-time between the two modes. From personal experience, a common scenario is a switch from VC (especially square waveform) to PC with a longer I-time – with the sole purpose of a lower PIP. Overall, the point of this discussion is to emphasize that if tidal volume stays the same, Pplat would have to remain constant, and any change in PIP is due to a change in resistive pressure. The choice between ventilator modes should not be guided by PIP.

Let’s go over some clinical examples:

  • Case in the pre-brief: In this case, flow profile was changed from square to decelerating ramp with same flow rate (I-time doubled). This will result in lower PIP due to lower resistive pressure, as discussed in point (ii) above. However, since TV is constant, elastic pressure (& lung stress) will remain unchanged. Contrarily, this maneuver may have inadvertent adverse consequences. Square waveform is particularly useful in ARDS patients with high set RR. Doubling the I-time by switching to decelerating ramp would increase the chances of auto-PEEP.
  • Now consider two passively ventilated patients with status asthmaticus. Patient 1 is on VCV, TV = 600 cc, RR = 12, Flow = 60 lpm with square waveform, PIP = 85 cmH20 and Pplat = 18 cmH20. Patient 2 is on VCV, TV = 500 cc, RR = 16, Flow = 30lpm with decelerating ramp, PIP = 48 cmH20 and Pplat = 32 cmH20. Which patient is at higher risk for lung injury? The answer, clearly, is patient 2. Both patients have very high resistance. PIP is especially high in patient 1 due to higher flow rate and square waveform. On the other hand, patient 2 has lower PIP due to lower flow rate and decelerating ramp waveform. However, Pplat in patient 1 is acceptable, whereas in patient 2 is dangerously high (likely suggestive of higher auto-PEEP due to suboptimal settings). Overall, patient 1 is in a much better spot than patient 2.

The Debrief

  • Peak inspiratory pressure is determined by a combination of elastic and resistive pressures. Only the elastic pressure (Pplat) determines lung stress.
  • For a given value of resistance and tidal volume, increasing the flow rate or switching to square waveform with same flow rate increases resistive pressure without affecting elastic pressure (Pplat)
  • In general, vent changes that alter resistive pressure while keeping tidal volume (and hence elastic pressure) same are inconsequential as far as lung injury is concerned.
  • One should resist the temptation to make changes just to lower the resistive pressure as it may lead to unintended adverse consequences.


  1. Manning HL. Peak airway pressure: why the fuss? Chest. 1994 Jan;105(1):242-7. doi: 10.1378/chest.105.1.242. PMID: 8275740.


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