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Re-focusing on trans-pulmonary pressure.

In the daily care of ventilated patients with ARDS, clinicians generally concern themselves with monitoring two dependent variables that relate to tidal mechanics-airway pressure and delivered tidal volume. After several decades of steadily mounting evidence, we have become quite aware that high airway pressures coupled with high airway driving pressures (end-inspiratory minus end expiratory static airway pressure) may inflict ventilator induced lung injury (VILI). Keeping tidal volume (referenced to predicted body weight) within acceptable limits has grabbed most of the press of the last decade, following the illuminating ARDSnet trial of 6 vs. 12 ml/kg. Rightly so, provided that the delivered volume can also be referenced to the size of the "baby" lung into which it is pushed. The strain corresponding to a given tidal volume is likely to correlate best with the ratio between tidal volume and functional residual volume (FRC). Until recently, the absolute capacity of the "baby lung" could not be measured easily. Even now, only a very few newer ventilators do so.

Given those limitations, monitoring pressure has more intuitive appeal to caregivers, from both conceptual and logistical perspectives. The pressure applied across the tissue is independent of lung capacity. Importantly, the ability to measure airway pressure is universal, and its monitored display is both precise and routine. Paw is considered important enough that we dutifully inscribe plateau, PEEP, mean airway pressure and auto-PEEP on our permanent patient records, attaching meaning to their values and setting alarms by their guidelines. But just how to translate those easily measured numbers into patient risk is quite another story. The airway pressure alone does not give us nearly enough information

What's Wrong With Plateau Pressure?

To judge the stress actually applied to the airspaces of the lung, we need the trans-alveolar ("trans pulmonary") pressure; we must account for the activity of the patient's inspiratory effort and the stiffness of the chest wall. Repeated application of excessive tissue stress is thought to be an important instigator of VILI. To date, virtually every published clinical trial has relied on the airway plateau pressure as the primary indicator of maximum tidal stress applied to the parenchyma. For such purposes, the plateau pressure cer tainly is better than dynamic airway pressure, as stopping flow eliminates the component of Paw dissipated against resistance ... So far, so good. But simply measuring the plateau is not enough, as it may underestimate or overestimate stresses imposed on lung tissue. While a number of recent scientific articles have sought to provide specific thresholds above which unacceptable risk begins (e.g., >26 cmH2O), this simply cannot be done without specifying additional information that is seldom at hand or if available, properly interpreted. For example, no clinical trial that has studied tidal volume or PEEP has taken account of the inspiratory muscle tone at end-inspiration, and in my view this is an important shortcoming that clouds the interpretation of the data from those trials. When minute ventilation is high (as it usually is in the first stage of ARDS), effort does not cease once the breath is triggered. If the patient actively contributes to lung expansion--and this is encouraged in many excellent centers so as to improve the distribution of ventilation and to avoid muscular atrophy--any residual inspiratory tone at end inspiration adds to the transpulmonary pressure and to lung tissue stress. Consequently, when patient effort is silenced, it is not unusual for the recorded plateau pressure to jump substantially when using volume assist control ("volume control"), or for tidal volume to fall substantially if pressure assist control ("pressure control") is in use. A tidal volume that generates a plateau pressure of 25 cmH2O, say, may seem safe enough during triggered breathing, but after muscle relaxation delivery of the same tidal volume may require a plateau of 35 cmH2O or higher. Does that plateau still seem safe? Most would say "of course not". For me, I tend to agree that it isn't but without knowing what the patient looks like and how positioned, I'm not so sure. Let me explain.

Chest Wall Compliance

Apart from the presence or absence of effort, one must remember that the airway pressure is pushing out against the chest wall as well as against the lung. Some chest walls are much stiffer than others. Skeletal deformity of the spine and ribcage can stiffen the respiratory system, as can conditions such as anasarca (severe generalized edema), and burn eschar. A more common restrictor, however is high intra-abdominal pressure caused by ascites, "third spacing" of fluid during sepsis, post-operative abdominal surgical changes, obstipation, etc. Obesity is not a reliable indicator of the likelihood of excess intra-abdominal pressure, as the belly tends to soften over time as the muscular wall accommodates. However, a process characterized by rapidly forming edema--e.g., pancreatitis--is much more likely to generate high intra-abdominal pressures than one that has been slow to develop. The measurement of bladder pressure can give a good indication of the pressure that is pressing the diaphragm upward and restricting the lung. A substantial fraction (but only a fraction) of the abdominal pressure transmits to the pleural space.

Two other modifiers of the enclosure that surrounds the lungs are position and pleural effusion. Recumbency tends to accentuate the measured plateau pressure that corresponds to a given tidal volume/PEEP combination. Prone positioning may influence the measured plateau, depending on the firmness of the supporting surface, body angulation, and the pliability of the abdominal compartment. Lateral decubitus positions are associ ated with less recumbent volume loss than are those of the supine orientation. The point is that the position in which a plateau pressure is recorded may influence its value. Our decisions seldom take note of that--if ever.

Large pleural effusions are generally considered to be restrictive in nature, but their effects are conditioned by the PEEP in use and by the stiffness of the surrounding chest wall. As recent work from our laboratory demonstrates, the lower the level of PEEP and the stiffer the surrounding compartment, the greater is the tendency of an effusion of given size to compress the lung. Interestingly, the plateau pressure (and the tidal compliance calculated from it) may not accurately reflect either lung compression or lung stretch, and is insensitive to the tidal recruitment and de-recruitment cycles that occur with every breath as the building airway pressure pushes the pleural fluid aside. Again, the airway pressure alone does not provide enough information, yet we rely on it for guidance.

How About Trans-Pulmonary Pressure?

For more than forty years, physiologists have used the pressure recorded in the esophagus (Pes) by a slim balloon catheter as a minimally invasive and yet representative estimator of intrapleural pressure. Because the lung is a passive structure, knowledge of the transpulmonary pressure (calculated as the difference between airway and esophageal pressure) helps greatly in estimating the pressure applied across the alveoli. In making that inference, the common assumption is that the intrapleural and interstitial pressures that surround the vulnerable alveoli are similar. At this point it must be said that interstitial pressure cannot be directly measured, and that when the lung is diseased, the intrapleural pressure may seriously differ from that in the interstitium. Moreover, pleural pressure varies throughout the thorax, and the esophageal balloon catheter can only record those pressures in its immediate region. The absolute value of Pes is influenced by the weight of the mediastinum and therefore varies with position. Changes in pleural pressure in the zones adjacent to the catheter are rather accurately transmitted. If the nearby lung is well inflated, the Pes changes may well be representative of the behavior of the lung as a whole. Conversely, if the nearby lung is airless and cannot inflate--which it tends to be in the dependent areas proximate to the balloon--even the Pes changes may not be at all representative.

Is Trans-Pulmonary Pressure the Last Word?

Sadly, serious problems will remain despite any switch we make from plateau to trans-pulmonary pressure. Esophageal pressure measurement, were it very simple to record and entirely representative of average pleural pressure, which currently, it isn't, would not allow calculation of the actual pressure applies across the alveolus. (For that, we would need interstitial pressure, which is almost certain to vary from point to point within the heterogeneously diseased lung.) Even then, the tensions at the junctions of closed and open alveoli would be underestimated, and other damaging forces (such as tidal opening and closure) could not be tracked.

That said, pursuit of the perfect should not be the enemy of the good. However imperfect it may be, the potential contribution of Pes to clinical decision-making is considerable. Whether the patient is making an inspiratory effort or has an unusually stiff chest cage, knowledge of the Pes helps assess the true pressure that surrounds the lung. In theory, the transpulmonary pressure relates much more closely to actual tissue stress than does plateau pressure alone. Re-focusing our attention on trans-pulmonary pressure is a great conceptual leap forward, even if it has taken us way too long as a medical community to recognize the wisdom of doing so.

Come Hear Dr. John Marini (one of the world's foremost authorities on Mechanical Ventilation) present his 2-Hour Workshop on Weaning at the 10th anniversary Focus Conference May 13-15, 2010


by John Marinin MD

Dr. Marini, Professor of Medicine at the Univ. of Minnesota, is a clinician-scientist whose investigative work has concentrated in the cardiopulmonary physiology and management of acute respiratory failure.
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Author:Marinin, John
Publication:FOCUS: Journal for Respiratory Care & Sleep Medicine
Date:Mar 1, 2010
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