Welcome to the world of ventilab

This blog is born from the desire to make ventilab's contents available worldwide.

It contains my translations of posts from the original ventilab blog. As you might now, the posts in Italian are over 200: I will keep on adding content (both new posts as they are published and old ones) as time goes on, hopefully managing to make all posts available in time.

If you have interest in a specific post, please let me know via email (ventilabinternational@gmail.com).

Comments to posts are deeply welcome: I hope interesting discussions on mechanical ventilation can be born here also, as is the case for the Italian blog.

Translations have not been reviewed by the authors of the original posts, and any mistakes are solely my responsibility.

Happy reading :)

Federica

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Cardiogenic oscillations and respiratory activity

Original post written on 21st January 2022 by Giuseppe Natalini

Let’s continue the analysis of the case presented and discussed in previous posts (here and here). 

Many readers have lingered on the oscillations which can be seen on the pressure trace (and, to a smaller extent, on the flow trace). Two interpretations were given: 1) they are a sign of the patient’s respiratory activity, not in sync with the ventilator; 2) they are cardiac artefacts.

In order to understand which interpretation is correct (or if both are) let’s analyze the traces (see Figure 1) systematically using the RESPIRE method (see this and this post in Italian -to be translated in English soon).

The steps R (Recognizing important curves) and E (Exhalation - ventilator) have already been proposed in Figure 1 and 2 on this post.

 

Figure 1

Now lets process with the S (Suppose the patient is passive). With pressometric ventilation,  we expect to see a constant inspiratory pressure and decreasing flow. Expiration, in any ventilation modality, should have a constant pressure (at PEEP level) and a decreasing flow. The white dashed line in Figure 2 shows how the curves could be if the patient did not have any respiratory activity. 

Figure 2

 

Now let's see where to place the patient (P): in the middle between the pressure trace (above) and the flow trace (below) (Figure 3),

Figure 3

 

and let's start to think about how the patient's possibile inspiratory activity (I) might modify the curves (Figure 4).

Figure 4

 

With the RESPIRE method (which has a physiological basis which we are not going to discuss here for the sake of simplicity), the patient’s inspiratory activity “attracts” the curves towards his position: it “raises” the flow trace and “lowers” the pressure trace compared to what we would expect.

In case of patient’s activity, the variations in flow and pressure must both agree with each other, meaning that both traces have to “move towards” or “move away” from the patient. Patient’s activity could be evident on one of the two curves only: only on the flow trace during ventilator’s expiratory time, on flow or pressure (depending on the mechanical ventilator in use) during ventilator’s inspiratory time. If the variations of flow and pressure are not in agreement, meaning that one curve “moves towards” while the other “moves away” from the patient, this can never be attributed to the patient's activity.

Looking at inspiratory flow in the area shown in Figure 4 (“insp”), we can see a little flow increment compared to what we would expect (the curve moves towards the patient). If this was due to patient activity, the airway pressure should decrease (move towards the patient) or stay unchanged. In this case we can see that, in the highlighted area, airway pressure is slightly higher than what we can see in other parts of inspiration (it moves away from the patient) and, using RESPIRE, we attribute this condition to expiratory activity. When flow and pressure suggest antithetical respiratory activities (inspiration on the flow trace, expiration on the pressure trace) we can exclude that this can be attributed to patient's activity: we can therefore conclude that, on these images, there is no patient’s inspiratory activity.

The next step is to search for the moments when pressure remains constant and flow is absent (R: release/relaxation): this is the only condition during which the pressure measured by the ventilator becomes the same as the pressure in the lungs.

Figure 5

The phase without flow at a constant (although there are small oscillations) pressure can be seen at the end of inspiratory flow. The pressure value in the mechanical ventilator is 23 cmH2O (Figure 5), which is the pressure in the patient’s lungs at the end of inspiration if it is obtained in the absence of any patient’s expiratory activity (we have already excluded the presence of any inspiratory activity in the previous step).

We are going to end this analysis by trying to find the patient’s expiratory activity (E).

In Figure 6 and 7 we can see two short, minimal but obvious drops in flow, one during inspiration and one during expiration.

Figure 6

Figure 7

In both cases, we can see at the same time a rise in pressure. They appear therefore to be signs of the patient’s expiratory activity. 

The oscillations in airway pressure are frequent and regular: we can see 13 of them in the 7 seconds of recording (Figure 8), corresponding to about 110 oscillations per minute.  

Figure 8

 

This was very similar to the patient’s heart rate. We have to conclude that the airway pressure variations (and minimal flow variations) are cardiogenic oscillations, meaning that they are induced by the patient’s heart beat. 

 

This gives rise to two interesting considerations: 

1. Cardiogenic oscillations are expression, to all effects, of the patient’s respiratory activity, which originates from the patient’s heart beat instead of originating from the activity of the patient’s respiratory muscles. 

Cardiogenic oscillations induce the variations of pressure in the lung, which are behind pressure and flow variations. This is just like the respiratory muscles, which generate alveolar pressure variations (although of much greater entity) in order to originate airway flow. For this reason, RESPIRE identifies cardiogenic oscillations as patient’s respiratory activity, and don’t make a distinction between the heart or respiratory origin since they have, from the mechanical point of view,  the same impact.

2) The mechanism behind cardiogenic oscillations is far from trivial. If we observe them in Figure 8, the positive peaks generated by cardiogenic oscillations on the airway pressure trace (where you can see the dashed white lines) remind us of vascular pressure peaks during systole.

Beyond their morphology, their duration is more in agreement with the lesser duration of systole compared to diastole.

If we think carefully, matching the peaks due to cardiogenic oscillations with systole is in contradiction with the variation in heart volume: in fact, during systole the heart volume decreases, therefore its imprint on the lungs should decrease, generating a small pulmonary expansion and a subsequent reduction in intrapulmonary pressure: just the opposite of what we have observed in our case.

Nonetheless, during systole the intrathoracic vascular volume increases and the pulsatile wave of the pulmonary artery is transmitted to gas contained in the airways. Both these mechanisms increase the vascular imprint on aerated spaces and therefore increase the intrapulmonary pressure during systole.

Cardiac contractions and pulmonary artery pulse induce volume and pressure variations of opposite sign on the alveoli.

The direct effect of the heartbeat manifests itself clearly on the iuxta-cardiac lung areas (especially on the lower left lobe), while in other areas of the lung the variations have an opposite direction compared to the inferior left lobe (1, 2).  

This data can be consistently interpreted as follows: in the lower left lobe, the prevailing mechanism is that of the direct compression-decompression of the heart on the lungs, i.e. the heart volume reduces in systole and the lung parenchyma expands in systole while the opposite happens in diastole. In the other areas of the lung the direct transmission of the heartbeat is not relevant, but the systolic increase in intrapulmonary blood volume and the direct transmission of the arterial pulmonary blood vessels’ pulsatile wave becomes significant, with an increase of compression of lung aerated spaces in systole and their decompression in diastole. The total net effect sees the prevalence of the impact of pulmonary artery pulse on heart contraction, as we can perceive from our case-study by observing a systolic peak on airway pressure.

This interpretation is confirmed by the observation that the cardiogenic oscillations persist with an open chest cavity, when the heart is not in direct contact with the lungs and that they are eliminated by clamping the pulmonary artery while the heart is still beating (3).

Let’s finish our analysis of expiratory activity by focusing our attention on the last very evident difference between the hypothetical curves obtained with a passive patient and the ones effectively recorded. During the expiratory phase, we can see that the pressure stays well above the applied PEEP level for a long time, and that PEEP level is reached only at the end of expiration (Figure 9). 

Figure 9

 

This behaviour is definitely abnormal, and it could be due to the expiratory activity of the patient only if it were associated with an increase in expiratory flow, which we do not see. The flow decreased exponentially during the entire expiration, as usually happens for passive patients. Moreover, we can see that the absolute value of the expiratory flow’s peak is significantly lower than the inspiratory flow’s peak. This confirms the fact that it is unlikely that this could be due to the patient’s expiratory activity, since it would eventually increase the expiratory flow’s peak.

In absence of any expiratory activity, we must conclude that an expiratory airway pressure higher than expected is due to a problem in the ventilator. We will discuss this extensively in a future post.  

In conclusion, our analysis of patient-ventilator interaction shows that any respiratory muscles’ activity is absent for the entire duration of the respiratory cycle: the patient is completely passive.

There is a patient’s activity which can be seen on the graphical monitoring, and which is due to the heartbeat (the cardiogenic oscillations). The cardiogenic oscillations are indistinguishable, when using RESPIRE, from patient’s activity because they are respiratory movements generated by intrathoracic pressure variations: only their small impact on flow and airway pressure, which is frequent and regular, and present in all the phases of the respiratory cycle, lets us discriminate cardiogenic oscillations from respiratory muscles’ activity.

 

While waiting to discuss what really got my attention while examining this case, I send a smile to all of ventilab’s friends, as always. 

References

1. Collier GJ, Marshall H, Rao M, Stewart NJ, Capener D, Wild JM. Observation of cardiogenic flow oscillations in healthy subjects with hyperpolarized 3He MRI. J Appl Physiol 2015; 119:1007-1014

2. Dubsky S, Thurgood J, Fouras A, R Thompson B, Sheard GJ. Cardiogenic airflow in the lung revealed using synchrotron-based dynamic lung imaging. Sci Rep 2018; 8:4930

3. Suarez-Sipmann F, Santos A, Peces-Barba G, Bohm SH, Gracia JL, Calderón P, Tusman G. Pulmonary artery pulsatility is the main cause of cardiogenic oscillations. J Clin Monit Comput 2013; 27:47-53

 

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Ventilation modalities and graphical monitoring

Original post published on 8th January 2022 by Giuseppe Natalini

Last week I published a 7 second long strip showing pressure and flow curves from a mechanically ventilated patient, asking you to anonymously suggest an interpretation. This week about a thousand people have read the post, and fifty people have given their own interpretations on the traces.

I read with great attention all the answers, and I noticed one thing: almost all of ventilab’s readers have focused their attention on aspects which were different from the one I had planned to discuss. It’s amazing how many things only 7 seconds of pressure and flow curves monitoring can tell us! I am really happy to have let you express yourselves on the matter before I did. Listening before talking lets me offer different levels of interpretation for this short strip, making the discussion more exhaustive.

I have decided to publish a series of close up posts in which we will evaluate all the considerations that ventilab’s readers have written on the form from 29/12/2021’s post. 

I will leave the post explaining why this monitoring has attracted my attention and how this permitted me to find and solve the problem for last.

Today we will see what these 7 seconds can tell us on the modality of ventilation and on the ventilator's settings.

What is the ventilation modality and what are the ventilator settings? 

Recognizing the ventilation modality and ventilator settings from graphical monitoring (that is to say, from simple pressure and flow traces) means to have truly understood mechanical ventilation. It is an  exercise that I suggest to ALWAYS do: it's the only way to reach an understanding of the real way mechanical ventilation works, overcoming the blanket of smoky clouds that often is an obstacle to correct interpretation.

Figure 1 shows the original image:

Figure 1

Ventilator settings have been estimated as an inspiratory pressure approximately between 25 and 28 cmH2O and a PEEP between 5 and 7 cmH2O: reasonable answers, since from the images it was not possible to be more accurate. In reality, applied pressure was 24 cmH2O and PEEP was 6 cmH2O.

It was noted that the duration of inspiration and expiration is similar, therefore I:E ratio is 1:1 and respiratory rate is around 25 breaths/minute. Calculation of respiratory rate is simple: in about 7 seconds we see almost 3 breaths (only the last part of the expiration is missing from the last breath). Dividing 7 seconds by 3 I obtain the duration of a single breath (2.33”) rounded down, I then round it up to 2.4”. If a breath lasts about 2.4”, respiratory rate is about 25 breaths/min, with an inspiratory time of 1.2” and an expiratory time lasting the same. Having said that tidal volume was 230 ml, minute ventilation was 5.75 l/min.

The proposed ventilation modalities were: pressometric ventilation, pressure-controlled ventilation, volume-targeted pressure-controlled ventilation, assisted-controlled pressometric ventilation, APRV.

All these answers might be right, but only one is certainly correct: the set ventilation is generically a pressometric ventilation, and there are no elements that permit answering more precisely. Pressometric ventilation is characterized by constant inspiratory pressure and decreasing inspiratory flow, and both of these features are present, as you can see in the “insp” portion of Figure 2:

Figure 2

These characteristics are common for all the pressometric ventilations. Since all ventilation modalities except volume-controlled, NAVA and PAV are pressometric, we haven’t taken such a big step forward.

Another consideration arises from this one: if almost all ventilation modalities are pressometric, does the modality of ventilation really matter? As those of you who have followed some of our courses well know, I believe that the modality has little importance, but its correct setting is of prime importance. In other words, a patient can be managed indifferently well with different ventilation modalities if for each one of them the ventilation parameters are set well. At the same time, a patient can be inadequately ventilated using each ventilation modality if its settings are not appropriate.

To say that a patient is ventilating with pressure support ventilation (or any other modality) is an information that has little value unless we specify how much support is applied, how much tidal volume and respiratory rate are generated, what does the flow profile look like, if any asynchronies are present and eventually which ones, how is the thoraco-abdominal coordination, if accessory inspiratory muscles are being used.

Going back to our clinical case, we can say that this ventilation is pressometric. In the family of pressometric ventilations, we can exclude one with certainty: pressure support ventilation. This is because during the inspiratory time we can see a pause, which can NEVER exist during pressure support ventilation because flow cycling makes sure that inspiration ALWAYS stops when there is still inspiratory flow (see 27/12/2017 post).

From the images we cannot tell if it is a pressure-controlled or a volume-targeted pressure-controlled ventilation (called PCV-VG, PRVC, IPPV with autoflow, APV, PC-target vent, volume adaptive BiLevel, et cetera in different ventilators): in case of a passive patient, the two ventilations are indistinguishable using graphical monitoring since they are both pressure-controlled ventilations. The difference can be seen only by looking at the settings panel: in pressure-controlled ventilation you set the applied pressure (and the tidal volume is variable), while in volume-targeted pressure-controlled ventilation you set desired tidal volume and the ventilator does a variable pressure-controlled ventilation, changing constantly the applied pressure in order to obtain the desired volume. In our example, it was a volume-targeted pressure-controlled ventilation, that is the desired tidal volume was 230 ml.

Assisted-controlled pressometric ventilation is a controlled pressometric ventilation in which the trigger is activated by the patient. Can you see trigger activation in Figure 1? If so, it is an assisted-controlled ventilation, if not it is a controlled ventilation. Patient-ventilator interaction will be discussed in the next post. 

Finally APRV (Airway Pressure Release Ventilation) was suggested as a possible set ventilation modality (for more information see the 11/02/2015 post). APRV is a BIPAP, meaning that it alternates between two pressure levels that let the patient spontaneously breathe in any phase. In other words, it is the alternation of two CPAPs. Differently from BIPAP (which is defined as a partially asynchronous ventilation), APRV should be completely asynchronous, not taking into account the patient’s spontaneous breathing activity in the rythmic alternance between a higher pressure (Phigh) and a lower pressure (Plow). The rationale behind this approach is interesting (synchronicity is not always good), and we can discuss it in comments if you find it interesting.

Typically, APRV should be set with a significantly longer time at Phigh than at Plow. If the ventilation shown in Figure 1 was an APRV, Phigh (which would coincide with “insp” in Figure 2) would be 25-28 cmH2O and Plow (which would coincide with “esp” in Figure 2) would be 5-7 cmH2O, and both would last 1.2”: a possible choice, even if not typical for APRV. The ripples seen on the pressure curve at Phigh would have to be interpreted as signs of the patient's spontaneous respiratory activity. As we have said before, the set ventilation was a volume-targeted pressure-controlled ventilation, but from the shown image it was reasonable to think it was an APRV.

Here we end our exercise involving reading mechanical ventilation from flow and pressure curves. We will go on next week by discussing the many comments you made on patient-ventilator interaction.

As always, a smile for all of ventilab’s friends.

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