Chest wall effect on the monitoring of respiratory mechanics in acute respiratory distress syndrome

Abstract

The respiratory system mechanics depend on the characteristics of the lung and chest wall and their interaction. In patients with acute respiratory distress syndrome under mechanical ventilation, the monitoring of airway plateau pressure is fundamental given its prognostic value and its capacity to assess pulmonary stress. However, its validity can be affected by changes in mechanical characteristics of the chest wall, and it provides no data to correctly titrate positive end-expiratory pressure by restoring lung volume. The chest wall effect on respiratory mechanics in acute respiratory distress syndrome has not been completely described, and it has likely been overestimated, which may lead to erroneous decision making. The load imposed by the chest wall is negligible when the respiratory system is insufflated with positive end-expiratory pressure. Under dynamic conditions, moving this structure demands a pressure change whose magnitude is related to its mechanical characteristics, and this load remains constant regardless of the volume from which it is insufflated. Thus, changes in airway pressure reflect changes in the lung mechanical conditions. Advanced monitoring could be reserved for patients with increased intra-abdominal pressure in whom a protective mechanical ventilation strategy cannot be implemented. The estimates of alveolar recruitment based on respiratory system mechanics could reflect differences in chest wall response to insufflation and not actual alveolar recruitment.

Figure 1

Graphical representation of the traditional "elastic" lung and chest wall model. The vertical lines anchored to the base represent the resting volumes of each structure and the arrows the elastic recoil pressure according to the volume of the respiratory system. RV - residual volume; FRC - functional residual capacity; TLC - total lung capacity.

Figure 2

Respiratory system (in black), transpulmonary (in light gray) and chest wall (in dark gray) pressure volume curves constructed using end-inspiratory pauses (diagram A) and positive end-expiratory pressure steps and end-expiratory pauses (diagram B). The effect of chest wall mechanics is non-significant, as shown by overlapping transpulmonary and end-expiratory airway curves (diagram B).

Figure 3

Diaphragm net effect: during insufflation, the increase in transversal and coronal axes in the caudal area of the rib cage passively tensions the diaphragm, preventing the intra-abdominal pressure from affecting the thoracic cavity. IAP - intra-abdominal pressure.

Figure 4

Exemplification of different chest wall responses to deformation as the load a subject must overcome to push a car up an inclined plane. A) Viscoelastic response to rapid deformation: The force [in the respiratory system, pressure change ∆P] required to push the car up (in the respiratory system, volume gain, ∆V) is related to the weight of the vehicle and to the slope of the inclined plane (in the respiratory system, chest wall elastance). Once the force is removed, the vehicle will return to its initial position with a magnitude of force identical to that necessary to push the car up. B) Viscoelastic response to slow deformation. If, after the ascent, the load (pressure) is sustained over time (PEEP insufflation), the car continues moving through a plateau (ΔV), where the required force is negligible. C) If the car is pushed up a new slope with the same characteristics (no change in chest wall elastance), the necessary force will be of equal magnitude to that of phase A.

Figure 5

Graphical representation of the end-expiratory lung volume (EELV), airway pressure and esophageal pressure as a function of the PEEP-IAP gradient. Note the marked decrease in end-expiratory lung volume (EELV) when the IAP level exceeds the programmed PEEP. The increase in airway pressure when the IAP exceeds the absolute value of PEEP may be explained by the increase in end-inspiratory esophageal pressure; however, the end-expiratory Pes remains non-responsive to the increase in IAP. EELV - end-expiratory lung volume; PEEP - positive end-expiratory pressure; IAP - intra-abdominal pressure.

Figure 6

Action algorithm proposed for patients with respiratory distress syndrome. ARDS - acute respiratory distress syndrome; MV - mechanical ventilation; PBW - predicted body weight; PEEP - positive end-expiratory pressure; Pes - esophageal pressure; P_L - transpulmonary pressure; ∆P_L - inspiratory transpulmonary pressure change.

Figure 7

Relationship between the mechanical behavior of the respiratory system (bottom images) and end-expiratory lung volume (EELV) changes (top image) after a PEEP step. The increase in airway pressure (Paw, bottom left) coincides with the increases in both pleural (Ppl, bottom right) and transpulmonary (P_L, bottom middle) pressures, resulting from the initial volume gain (MPV, minimum predicted volume), reflecting the combined mechanical response of the lung and chest wall. After the first ventilatory cycle at the new PEEP level, the pleural pressure begins to decrease, and consequently, the transpulmonary pressure increases, which generates volume gain (TDV, time-dependent volume, above), which, in this case, depends on the lung mechanical characteristics. PEEP - positive end-expiratory pressure.