Dynamic PEEP? | Ventilation Strategies for Metabolic Acidosis w/ Melody Bishop, RRT

foamfrat
Aug 21
7 min read

A little over a year ago, I made a short reel discussing ventilating a patient in a severe metabolic acidosis. In the video, I mentioned that minimal to no PEEP might be appropriate. Not because the patient doesn’t need PEEP, but because the shortened cycle time at higher respiratory rates can unintentionally generate dynamic PEEP on its own. But what if it was intentional? What if the presence of a wider pressure when the ventilator switches into exhalation would cause the air to exit more rapidly?

In this podcast, I discuss my thought process with respiratory therapist extraordinare, Melody Bishop @melodybishop_rt. She helps surface some definitions and distinctions to terms like air-trapping, Set PEEP, & auto-PEEP while we discuss ventilation strategies in metabolic acidosis. The blog below was what I had sent her before the podcast to get all my thoughts & illustrations down in writing. As always, follow your local guidelines, and I hope you enjoy listening in on the conversation.

To pitch this thought experiment appropriately, we need to all be thinking of the same patient presentation. Imagine a young patient with DKA who has no underlying obstructive physiology. The patient is tiring out and is no longer adequately compensating for their metabolic acidosis (indicated by a rising PaCO2). If they were compensating but perhaps just unresponsive, we would not intubate unless the airway was in imminent danger (e.g., aspiration).

The general metabolic acidosis strategy is not to just increase minute volume but to increase alveolar minute volume. This means you want the majority of your minute volume to come from actual volume, rather than just increasing the rate but with smaller volumes (dead space breathing).

Common vent strategies begin by optimizing tidal volume (7-8 cc/kg) and then using the flow waveform to adjust the respiratory rate. If you spin the respiratory rate up too high, you will start cutting into either your inspiratory or expiratory time.

Let’s break down why this matters in the context of acidosis:

Terminating the inspiratory phase too early reduces alveolar minute ventilation, favoring ineffective dead space ventilation. That’s a significant issue when the patient relies on full tidal ventilation to compensate for their acid-base imbalance.

Excessively shortening the expiratory phase raises concerns about air trapping and dynamic hyperinflation.

In the illustration below, you can see the flow waveform returns to baseline at the end of inspiration and expiration.

After a brief look at the illustration above, you can visualize a lot of time spent riding the baseline. This is the time when you are neither inhaling nor exhaling - you are either holding your breath waiting to exhale, or you have finished exhaling and waiting for the next breath. Neither of these is ideal when trying to achieve compensatory alveolar minute volumes in a metabolic acidosis. My buddy Bryan Winchell calls these no-flow areas "time on the table."

So let's say we start increasing the rate.

In the following example, the I:E is set to favor the expiratory phase. This is pretty normal when you start in a 1:2 ratio. Your vent will eventually begin to rob time from the inspiratory phase before the expiratory phase.

The clinician looks at the waveform and realizes that while they are fully exhaling, they are not getting the full breath in. You are left to either decrease the rate, or increase the inspiratory time. This is done by either adjusting the I:E ratio directly and it indirectly adjusting the inspiratory time, or adjusting the inspiratory time directly and it indirectly adjusting the I:E.

So let's say you decide to increase the inspiratory time without decreasing the rate, but you also drop your PEEP to zero. Now we get the full breath in, but we are not allowing the exhalation to reach baseline.

Instead of setting the PEEP, could you create it by shortening the exhalation phase? This concept is not new and has been applied in modes like APRV for a long time. In APRV, the goal is an increase in mean airway pressure, so you have very short periods where you allow them to exhale. The goal is to release as much CO2 as possible in as short a time as possible. What other patient population do we want them to release as much CO2 in as short of a time as possible? This seems like it would apply to a severe metabolic acidosis as well.

In the illustration below, you will see the T-CAV APRV mode, where the P-Low (PEEP) is set to zero, but the time at that pressure (T-Low) is set short enough that it never actually reaches zero.

So, let's say this actually works (we can call it the dynamic PEEP concept) and we do see that it releases more CO2 over a shorter amount of time, allowing us to increase the rate without sacrificing volume. How in the world do we know what our actual alveolar pressures are? In the video I made, I paused the screen and dropped a line on the pressure/flow graph to show that when the vent switched to exhalation, the patient was exhaling at a rate of 21.6 L/min, which correlated to an airway pressure of 1.8 cmH2O.

So, is that 1.8 cmH2O the alveolar pressure?

No. The only time you can say the pressure on both sides of a conduit are equal is in the absence of flow. Therefore, if expiratory flow is still occurring when the next breath starts, the actual alveolar pressure is higher than what is displayed on the ventilator. This changes which pressure will be higher based on the phase of the respiratory cycle. I used random pressure below to show the discrepancy.

In the inspiratory phase, the pressure on the ventilator side will be higher because it is where the flow originates.

During the expiratory phase, the alveolar pressure will be higher because the flow has reversed and now the pressure is being generated on the patient side.

Flow is the evidence of a pressure gradient. If there is no gradient, there is no flow. So, if we stop right there, we can agree that the higher pressure is always on the sending side of flow.

The higher the expiratory flow when you switch from exhalation to inhalation, the higher the PEEP.

The lower the expiratory flow when switching from exhalation to inhalation, the closer your end-airway pressure (as measured by the vent) is to your end-alveolar pressure (the actual pressure in the alveoli).

If you are effectively optimizing minute volume to compensate for a severe metabolic acidosis, your ventilator flow waveform will resemble a spontaneous breathing pattern. This means you will spend as little time as possible in the “no flow” zone. Does this mean you can’t tell how much PEEP you are providing?

Let's first see if we agree on the following:

The higher the expiratory flow when you switch from exhalation to inhalation, the more air that is trapped, and the higher the alveolar pressure.

In the example I demonstrated in the video, the exhalation flow was 26.1 L/min, and the airway pressure was 1.8 cmH2O when we switched to inspiration.

If you know the pressure decay rate or resistance, you can solve for the end-alveolar pressure.

We know that as the pressure gradient between two gases nears equilibrium, the flow and therefore the resistance decrease. Knowing that the airway pressure is 1.8 when we exhale at a rate of 26.1 L/min. If we observe the resistance, we can also determine exactly what the alveolar pressure is.

Let’s say:

Flow = 26.1 L/min → that’s 0.435 L/s
Resistance = 8 cmH₂O/L/s (estimated from vent Rinsp)
Airway pressure at end of exhalation = 1.8 cmH₂O

So, at the moment the vent switched to inhalation, the actual alveolar pressure was ~5.3 cmH₂O, which we know is higher than the 1.8 cmH₂O the vent displayed. Which is why I stated that we wouldn't think twice about setting the PEEP to 5 cmH2O in the video.

Does this make it harder for the patient to trigger a breath?

In this scenario, the patient is sedated and paralyzed, so triggering a breath is not part of their interaction with the ventilator. If I wanted a DKA patient to participate in their own breathing, I’d seriously question whether intubation was the right move in the first place. The point of intubating a DKA patient is often to take over when their compensatory efforts fail or become unsustainable.

This came up in response to Melody’s concern about whether controlled air trapping (or dynamic PEEP) could make it harder for the patient to trigger a breath. While I understand the problem in a spontaneously breathing patient, I think my brain imagines a very different kind of patient.

But I still think it is worth investigating

Even in cases where a patient isn’t paralyzed, we should ask: Does dynamic PEEP make it harder to trigger a breath?

Let's start with how the vent even knows the patient is trying to pull a breath.

Pressure Trigger: The patient must drop the pressure below the set PEEP level to initiate a breath. In this mode, PEEP (especially auto-PEEP) can increase the work of triggering.

Flow Trigger: The patient initiates a breath by generating a specific drop in flow from the ventilator’s baseline (bias) flow. The ventilator senses a drop in flow and delivers a breath.

The Hamilton T1 uses a flow trigger, not a pressure trigger. This means the patient doesn’t have to drop airway pressure below PEEP; instead, they need to draw in enough flow (e.g., 2 L/min) to trip the trigger. Flow triggering is generally more sensitive and easier for patients.

Regardless of the trigger, the patient usually has to do some work to convince the ventilator that they want a breath. The amount of work they have to do depends on how sensitive the trigger is set in comparison to the amount of work required to meet that trigger. If, for some reason, I decided to keep this patient breathing spontaneously after intubation (which I wouldn't, for the reasons stated above), they would need to generate flow against the alveolar pressure we calculated earlier, which is ~ 5 cmH2O of PEEP.

I could have worded this video better, specifically that the PEEP measured on the screen is not the same pressure as the pressure in the alveoli.

Huge thanks to Melody Bishop for coming on the show & sharing her expertise.