EMCrit Lecture – Dominating the Vent: Part II

When I was a resident, every vent lecture either put me to sleep or left me dazed and bewildered. I gave a lecture of that ilk when I started working after fellowship. I had become part of the problem. I decided there must be a way to make vent management more understandable and if not interesting, at least bearable.

This lecture was up on the soon to be defunct EMCrit Lecture site. It offers a path to managing any patient on the ventilator in the ED. I have tried to simplify as much as possible while still maintaining an evidence-based approach.

This is Part II, it deals with the obstructive strategy. Last week, we spoke about the strategy for patients with  lung injury.

Your goal with these patients is to let them have adequate time to breathe out.

There are only 4 things you need to remember for an obstructive patient

Vt (Tidal Volume) = 8 ml/kg, don’t mess with it

Flow Rate = 60-80 lpm, shortens insp times (this really doesn’t do much good, and super-high IFRs should not be used. Increasing IFR will also increase peak pressure)

Resp Rate = Lung protection, start at 10 work your way down if necessary

FiO2/PEEP = Oxygenation, should need much O2 (40%)m I recommend PEEP of 0, but certainly keep it less than 5

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  1. Richard Chang says

    Hey Scott,

    Great lecture, I liked the format.

    One question- do you paralyze all your intubated asthmatics? Theoretically this should decrease metabolic demand and lower CO2 production, but I haven’t found any data on this.

    Rich Chang
    Hennepin C0unty Medical Center

    • emcrit says


      I don’t ever paralyze, but I sedate and analgeze the heck out of the asthmatic patient to the point where there is no spontaneous breathing and they are essentially rock-like. This has all the advantages of paralysis and none of the problems.


  2. Thomas Ton says

    Thanks Scott for the great lecture. I just have a question regarding deadspace. Like you stated, Va for a normal CO2 when not intubated is 60cc/kg/min and double that for intubated patients. What if the patient is not intubated but trached instead? Does it matter if I use 120cc/kg/min to include the ventilator tubing/circuit deadspace? Please advise. Also, I would love to hear your explanation for not using PEEP in COPD patients? Besides decreased venous return and increased in intrathoracic pressure, are there any other reasons?

    Keep up the great work.


  3. Terry Ross says

    One concept that I am struggling with is in treating acute copd exacerbations . They have “obstructed” lungs and are hypercapneic. So do you set the rate at 10, 18, 36 or somewhere in between and adjust based on Plateau pressures and blood gasses?

    Also would you use Zeep or a Peep of 5?


    • says

      Titrate RR to normalize pH, not PaCO2 as most of these pts are chronic retainers. If Plat is high, accept low pH. ZEEP is fine, 5 is essentially not doing anything negative; would not go beyond that.

  4. Mike says

    Hi Scott.

    I understand the concept of not having to use PEEP for someone with obstructive respiratory distress. However, I also have read that using PEEP at approximately 80% of the estimated auto-PEEP decreases the work of breathing needed to initiate a spontaneous breath and increases patient comfort.

    I was wondering what your opinion of this rationale was and whether you often adjust the PEEP above 5. Additionally, if you’re using NIV with a COPD patient, do you use the same approach?


  5. Josh Farkas says

    Hi Scott,

    Great lecture, thanks for all the education. I want to share a trick I learned recently when I got a call from a community hospital that was transferring us an intubated asthmatic that they couldn’t ventilate, asking for help with the ventilator. This forced me to realize that there is one ventilator prescription that will provide safe, idiot-proof ventilation for most COPD/asthma patients… a universal vent prescription. It is Pressure Control mode with 5 cm PEEP, 30 cm Pressure Support, 60% FiO2, respiratory rate of 14/min (to generate a peak pressure of 35cm). For this to work the patient should be deeply narcotized or paralyzed and not over-breath the vent much.

    The beauty of pressure control mode is that if the patient gets more obstructed or tachypneic, they will never develop PEA or pneumothorax because the peak pressure is absolutely limited to 35 cm (their ventilation may deteriorate — but hypercapnia is very well tolerated in most intubated patients). This is useful in any situation where the pressures can’t be monitored closely (i.e., back of an ambulance, busy overcrowded ED, ventilator without graphics, etc).

    Yeah, I know you don’t like using PEEP in obstruction. I like PEEP to balance out autoPEEP and reduce work of triggering the vent, but in the crashing asthmatic they should be deeply sedated and not triggering so it doesn’t really matter. I doubt we take our coffee the same way either. For folks who don’t like PEEP, you could use Pressure Control, 0 cm PEEP, 35 cm Pressure Support, 60% FiO2, rate 12/min.


    • says

      ummm, not so much. Pressure control in no way protects from the problems of hyperinflation. Hyperinflation problems come from your resp rate, not the mode of ventilation. PC leaves you with a situation in which the patient may have variable and insufficient tidal volumes. So instead of decreased venous return (pneumothorax doesn’t happen anymore with low tidal volume/low rr ventilation) you get a patient who gets no oxygen to their alveoli. If you like PEEP, knock yourself out. As I mentioned in the podcast, there has never been a documented benefit.

      • Josh Farkas says

        I was hoping to avoid the pressure-cycled vs. volume-cycled ventilation debate. I’ve gone between institutions which preferred one or the other, and the only constant is that everyone is convinced that their way is best. Vent mode is religion in the ICU.

        Let me flesh out my argument with a thought experiment in the style of quantum mechanics, because ultimately this comes down to physics. Imagine two identical asthmatics, Mr. AC and Mr. PC, are intubated at a small rural ED and placed on volume assist-control ventilation and pressure control ventilation, respectively. The hospital doesn’t have an ICU so they are both transferred to the tertiary hospital via 3 hour ambulance ride. Initially they are both doing fine on the ventilator but en route they develop worsening bronchospasm and the paralytics wear off so they start triggering the ventilator at 24 breaths/min.

        Mr. AC will rapidly develop progressive autoPEEP and gas trapping because his exhalation time is inadequate. With every breath, the amount of volume in this chest will increase and eventually his peak and plateau pressures will spiral to dangerously high levels. If immediate action is not taken, he is at risk of developing a pneumothorax or even PEA (as discussed in your podcast on the crashing asthmatic).

        Mr. PC also develops autoPEEP and gas trapping. However, as autoPEEP increases, the driving pressure forcing gas into his lungs (peak pressure – autoPEEP) decreases, so his tidal volume decreases. His tidal volume will progressively decrease until it reaches a volume which is low enough to be exhaled, and he will reach a new, stable equilibrium. His peak pressure will never budge from the set value, and he will not develop a pneumothorax or PEA. His oxygenation will be maintained because he is on 60% FiO2 and although the alveolar PaCO2 may double there is still plenty of oxygen in his alveoli (hundreds of mm). His ventilation will deteriorate and he will develop a respiratory acidosis. However this hypercapnia will generally be well tolerated (ie unless he is pregnant or has elevated ICP).

        Ultimately the AC vs. PC debate is tiresome, because either is fine when used by a doc and RT who know what they’re doing. Personally I’m more worried about barotrauma than ventilation, so I would favor PC in a situation with suboptimal monitoring. I’ve seen plenty of patients with scary low pH from respiratory acidosis and they do just fine; alternatively I have seen PTX/BPF due to suboptimal vent management and this causes a persistent problem. As we become increasingly aware of the safety of permissive hypercapnia in most patients, we can stop worrying so much about ventilation and focus instead on preventing ventilator-mediated iatrogenesis.

        With regards to PEEP, most patients with severe asthma/COPD will develop autoPEEP. This leads to difficulty triggering the ventilator, because in order to trigger the ventilator they have to generate more negative pressure to counteract the autoPEEP. Difficulty triggering the ventilator causes dyssynchrony and agitation (feels like being smothered). Increasing the set PEEP to a few cm below the autoPEEP will allow the patient to trigger & synchronize with the vent, they’ll feel like they can breathe again, and they will be much happier (less sedation, less delirium). There will never be a randomized controlled trial of this because it’s widely accepted in pulmonology. I believe it because I’ve treated it. With close attention to vent waveforms in lightly sedated weaning asthmatics, this will be seen. It’s irrelevant in the ED, where asthmatics should be deeply narcotized anyway.

        • Ryan says

          Great info Josh. It has been my experience that for severe asthmatics pressure control ventilation with PEEP adjusted for air-trapping works intially. However, if the condition of the patient deteriorates it generally will require a paralytic/anesthetic to prevent the patient from arrest due to severely inadequate gas exchange and/or acidosis beyond permissive > 7.10. Permissive hypercapnia is definitely a winning strategy for initial vent management.
          For those who have COPD and severe emphysema, once a patient has air-trapped enough due to tachypnea, they will become hypercarbic and drowsy/obtunded. It’s been my experience that these patients are easier to manage, since their process is usually self-limiting. It would appear that using lower PEEP values initally will allow for greater VT w/o PIP >40cmH2O. As the patients own respiratory rate slows it allows for a decreased I:E ratio promoting greater exhalation of trapped gases. In events of air trapping w/o sedative effect either from hypercarbia or medications manual ventilation by bag/mask resucitator should be seriously considered rather than using a ventilator. The difference being that a machine cannot strategically deliver breaths, whereas a human can, possibly limiting further air-trapping and breath stacking.

  6. says


    Thanks for the great overview! I have 1 question:

    Could you comment on the distinction between the flow rate and I:E ratio? If my understanding is correct (and assuming the Vt isn’t changing), the flow rate would naturally increase with decreasing I:E ratios (e.g. going to 1:4 or 1:5) because more volume would need to get into the lungs within a shorter period of time. Is that not the case?

    I love these ‘back to basics’ topics (your acid-base series is another favorite). Keep up the great work!


    • says

      Brent, There are two ways to decrease the I:E. Decrease the resp rate or increase the flow rate. If you locked the RR and the Vt then yes the flow would need to increase. This is fair less effective than decreasing RR.

  7. David Wakeland says

    In reference to “Dominating the Vent.” I have a patient in the ICU due to a scooter vs car accident. He has huge blebs from his emphysema, but now he has ARDS. I’m a third year medical student and am trying to understand what his ventilator settings should be according to the video. Currently, his PEEP is at 12, his RR is at 34, and his pH is around 7.3 with a high CO2 around 90. Also, he is not air trapping. Thanks.


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