Utilizing CVP waveforms to assess the intensity of inspiratory efforts

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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

Real case: You are passing by the room of an awake mechanically ventilated patient with advanced IPF. Peeking in from outside the room, the following CVP waveform catches your attention (figure 1). What can you interpret about the patient’s respiratory efforts from this image?

Introduction

In a recent post, we discussed the mechanistic basis of how vigorous inspiratory efforts may worsen lung injury. In the discussion that followed, the need for closer assessment of respiratory muscle intensity was highlighted. A dedicated review on this issue will be presented in a future article. For now, we will focus on a lesser appreciated tool – the CVP waveform.

As a primer, it is helpful here to refresh the concepts of intramural, extramural, and transmural pressures across a distensible structure (e.g. alveolus, heart) (Figure 2). Take the example of the right atrial pressure or CVP. What we measure with the catheter is the intramural CVP. The actual distending pressure of the right atrium is the transmural CVP.

The gold standard for assessing the degree of inspiratory effort in a spontaneously breathing patient is to analyze the esophageal pressure (Pes) swings during inspiration. Esophageal pressure monitoring is used as a surrogate for pleural pressure (Ppl), which is the pressure that surrounds the lung. However, pleural pressure is also the extramural pressure of the heart and the thoracic vessels. Therefore, changes in pleural pressure are instantly transmitted to the pressure inside these structures. Figure 3 will help visualize this better. This is the key rationale behind why the degree of inspiratory reduction in CVP can be used as a surrogate for inspiratory Ppl swings.

It is imperative to mention here that ΔPes (and hence ΔCVP) to assess inspiratory efforts is best utilized in non-intubated patients, or those with minimal ventilatory support (e.g. pressure support of 5-10 mmHg). Significant PPV support will drive up the Pes and interfere with the reading.

Technical considerations

The ubiquity of central venous catheters in the ICU makes this an attractive tool. The only real requisite is that the site of pressure measurement has to be intrathoracic: either the right atrium or the superior vena cava. PICC lines can be used if the lumen is fully patent: check for the ease of blood draw and observe the waveform. Naturally, femoral central lines cannot be used for this purpose. Identify the breathing vigorously, this drop will be much more sudden. Remember that this reading will be in millimeters of mercury (mmHg). To convert it into cmH20, multiply it by approximately 1.35.

Theoretical pitfalls

As mentioned before, the CVP displayed on the monitor is intramural CVP. Mathematically, this is the sum of transmural CVP and the extramural pressure (which is Ppl) (see figure 2). Hence, changes in intramural pressure can be produced by changes in not only Ppl, but also transmural CVP. Since transmural CVP is the distending pressure of the right atrium, changes in transmural CVP reflect changes in RA volume. During inspiration, reduction in intramural CVP may augment venous return and hence increase the RA volume. This effect would in turn tend to increase the intramural CVP and hence blunt the inspiratory drop in intramural CVP (Figure 4).

In other words, inspiratory decline in CVP will systematically underestimate inspiratory decline in Ppl or Pes.* Interestingly, the same effect will be seen if we are following PCWP swings, but will be significantly blunted. Since the entire pulmonary circulation is within the thorax, inspiratory drop in Ppl does not directly affect pulmonary venous return. However, alveolar inflation during inspiration squeezes out blood from the alveolar vessels. This does augment the pulmonary venous return but on average, the magnitude of this effect would be lower than that seen on the right side. Magder et al directly compared Pes swings with ΔCVP and ΔPCWP. As expected, they found that both ΔCVP and ΔPCWP underestimated ΔPes. However, the overall correlation was much stronger with ΔPCWP, than with ΔCVP.

Going back to the case in pre-brief: We see that the inspiratory swing in the CVP is 35 mmHg (48 cmH2O). This is massive. The patient was noted to have clinical signs of increased work of breathing. His Pocc was around 50 cmH2O! Pocc is an index of inspiratory effort (to be discussed in the next post) and this number is astronomically high. The implications of such high vigorous inspiratory effort are numerous. First and foremost, such a degree of effort is uncomfortable for the patient. Also, remember that Pmus gets added to Pvent and the eventual transpulmonary pressure in this case would be very high. This has to be considered if VILI is a concern. Furthermore, sustained vigorous efforts may lead to load-induced diaphragm injury (underassistance myotrauma). In general, for a given ventilatory load, we should aim for a good balance between ventilatory (Pvent) and patient work (Pmus). However, if increasing ventilatory support does not relieve Pmus (and instead raises tidal volume further), more analgosedation would be a consideration.

It is important to mention that this patient did not have expiratory muscle activation. This becomes important while making an assessment of inspiratory Pmus. More on these topics in the next post.

The Debrief

  • The pressure measured with a CVC is the intramural CVP.
  • Inspiratory drop in CVP can be used as a surrogate for inspiratory drop in PPl/Pes
  • Inspiratory decline in CVP will systematically underestimate inspiratory drop in Ppl. This should be kept in mind while using it for assessing the intensity of inspiratory effort.
  • PCWP swings will more closely mirror Ppl swings. Note: a cut-off of 15 cmH20 has been used to define “significant inspiratory effort”.

References

  1. Bellemare P, Goldberg P, Magder SA. Variations in pulmonary artery occlusion pressure to estimate changes in pleural pressure. Intensive Care Med. 2007 Nov;33(11):2004-8.
  2. Verscheure S, Massion PB, Gottfried S, Goldberg P, Samy L, Damas P, Magder S. Measurement of pleural pressure swings with a fluid-filled esophageal catheter vs pulmonary artery occlusion pressure. J Crit Care. 2017 Feb;37:65-71
  3. Lassola S, Miori S, Sanna A, Cucino A, Magnoni S, Umbrello M. Central venous pressure swing outperforms diaphragm ultrasound as a measure of inspiratory effort during pressure support ventilation in COVID-19 patients [published online ahead of print, 2021 Feb 26]. J Clin Monit Comput. 2021;1-11.

*Appendix

Here’s a deeper dive into the effect of increased venous return on intramural CVP. Reduction in intramural CVP increases venous return up to a certain extent. After a certain point, further reduction in intramural CVP does not increase venous return any further (this occurs when intramural CVP falls below the abdominal pressure). If prior to initiation of inspiration, if the intramural CVP is already below the abdominal pressure, its further reduction with inspiration will not lead to any increase in venous return. In this situation, intramural CVP swing will indeed mirror PPl/Pes swings. Contrarily, when the RA is stiff and overloaded at baseline, any further increase in venous return with inspiration results in exponential increase in transmural (and hence intramural) CVP. In this scenario, ΔCVP will significantly underestimate ΔPes.

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