Intrinsic (or auto-) positive end-expiratory

Laurent Brochard
Introduction
The mechanisms generating intrinsic or auto-positive end-expiratory pressure (PEEP) during controlled mechanical ventilation in a relaxed patient also occur during spontaneous breathing or when the patient triggers the ventilator during an assisted mode [1, 2]. These include an increased time constant for passive exhalation of the respiratory system, a short expiratory time resulting from a relatively high respiratory rate and/or the presence of expiratory flow limitation. Whereas dynamic hyperinflation and intrinsic or auto-PEEP may have haemodynamic consequences, this is not frequently a major concern in spontaneously breathing patients or during assisted ventilation because the spontaneous inspiratory efforts result in a less positive or more negative mean intrathoracic pressure than during controlled mechanical ventilation. The mainconsequence of dynamic hyperinflation during spontaneous and assisted ventilation is the patient's increased effort to breathe and work of breathing [1, 2]. To what extent does intrinsic (or auto-) positive end-expiratory pressure influence work of breathing? For air to enter the lungs, the pressure inside the chest has to be lower than the pressure at the mouth (spontaneous breathing) or at the airway opening (assisted ventilation). In the case of intrinsic (or auto-) PEEP, by definition, the end-expiratory alveolar pressure is higher than the pressure at the airway opening. When the patient initiates the breath, there is an inevitable need to reduce airway pressure to zero (spontaneous breathing) or to the value of end-expiratory pressure set on the ventilator (assisted ventilation) before any gas can flow into the lungs. For this reason, intrinsic or (auto-) PEEP has been described as an inspiratory threshold load. In patients with chronic obstructive pulmonary disease (COPD) this load has sometimes been measured to be the major cause of increased work of breathing [3]. During assisted ventilation, is the trigger sensitivity important to reduce intrinsic (or auto-) positive end-expiratory pressure? Because the problem of intrinsic or (auto-) PEEP has to do with the onset of inspiration, one may reason that increasing the inspiratory trigger sensitivity to initiate a breath with a lower pressure or flow deflection should reduce the work of breathing induced by hyperinflation. These systems are based on the detection of a small pressure drop relative to baseline (pressure-triggering system) or on the presence of a small inspiratory flow (flow-triggering systems). Unfortunately, increasing the trigger sensitivity induces only a small reduction in the total work of breathing. The reason for this lack of effect relates to the need for the inspiratory trigger to sense changes in airway pressure or in inspiratory flow. Thus, intrinsic PEEP needs to be counterbalanced first by the effort of the inspiratory muscles, in order for this effort to generate a small pressure drop (in the presence of a closed circuit) or to initiate the inspiratory flow (in an open circuit) [4]. The consequence of intrinsic or (auto-) PEEP is that the inspiratory effort starts during expiration. This is easily identified by inspection of the expiratory flow-time curve [1]. Asaconsequence, it cannot be detected by any of the commercially available trigger systems. Can the set external positive end-expiratory pressure reduce dynamic hyperinflation and work of breathing? Responses to these two questions are the same as during controlled mechanical ventilation in a relaxed patient [1]. Their consequences are, however, very different. External PEEP reduces the difference between the alveolar and the ventilator proximal airway pressure, i.e., intrinsic (or auto-) PEEP. The inspiratory threshold load resulting from intrinsic (or auto-) PEEP is thus reduced by addition of external PEEP. Thus, the total work of breathing is reduced, especially in patients withhigh levels of intrinsic (or auto-) PEEP, such as those subjects with COPD [5, 6]. Although external PEEP reduces work of breathing, it does not minimise hyperinflation. The level of dynamic hyperinflation is not modified by external PEEP, unless this PEEP is set higher than the minimal level of regional intrinsic PEEP, and then hyperinflation increases. Increasing hyperinflation can aggravate the working conditions of the respiratory muscles by placing them at a mechanical disadvantage and can result in significant haemodynamic compromise by decreasing venous return and increasing right ventricular outflow resistance. Hyperinflation in excess of intrinsic (or auto-) PEEP occurs usually when the set PEEP is positioned at values above 80% of the mean “static”intrinsic PEEP [7]. For this reason, titration of external PEEP based on measuring intrinsic (or auto-) PEEP would be desirable. Unfortunately, a reliable measurement of intrinsic (or auto-) PEEP in the spontaneously breathing subject is much more difficult to obtain than in passive positive-pressure ventilation conditions. Can standard ventilatory settings influence intrinsic (or auto-) positive end-expiratory pressure? During assisted ventilation, the patient is supposed to determine the respiratory rate freely, and one may suppose that he/she will govern his/her respiratory rate to control expiratory time and minimise hyperinflation. Unfortunately, most patients will not be able to counteract fully the effects of a ventilator inspiratory time longer than their own inspiratory time [8]. Although some compensatory mechanism may exist, it will frequently be insufficient. Every setting influencing the ventilator inspiratory time may thus influence the level of dynamic hyperinflation. Is intrinsic (or auto-) positive end-expiratory pressure always synonymous with dynamic hyperinflation? In patients with spontaneous respiratory activity, recruitment of the expiratory muscles frequently participates in generating intrinsic (or auto-) PEEP independently of dynamic hyperinflation. In the case of airflow obstruction, the main consequence of an activation of the expiratory muscles is to augment intrathoracic pressure, whereas their effects on expiratory flow may be very modest, especially in the case of airflow limitation, thus promoting small airways to collapse. The activation of the expiratory muscles results from an increase in respiratory drive. Many patients with COPD already have a recruitment of their expiratory muscles at rest. This expiratory muscle recruitment results in a measurable increase in alveolar pressure. However, such expiratory muscle recruitment, although creating an intrinsic (or au- Fig. 1 Tracings of gastric (Pga), oesophageal (Poes) and airway (Paw) pressures, flow and diaphragmatic electromyographic activity (EMGdi) during an assisted breath (pressure-support ventilation). The vertical lines help to delineate the different phases of the inspiratory effort. During phase 1, the flow is still expiratory: the start of EMGdi and the abrupt decrease in both Pes and Pga all indicate that the patient performs an active inspiratory effort against intrinsic positive end-expiratory pressure (PEEP) at the same time that his/her expiratory muscles relax. Phase 2 is the triggering of the ventilator and occurs once intrinsic (or auto-) PEEP has been counterbalanced to-) PEEP, does not contribute to the inspiratory threshold load and the increased work of breathing. Indeed, at the same time that the inspiratory muscles start to decrease intrathoracic pressure, the expiratory muscles relax
and their release almost immediately abolishes this part of intrinsic (or auto-) PEEP due to the expiratory muscles [9]. This is illustrated in Fig. 1. Can intrinsic (or auto-) positive end-expiratory pressure be reliably measured? The commonly applied end-expiratory airway occlusion method that measures intrinsic (or auto-) PEEP in patients on controlled ventilation cannot be readily applied to the patient making spontaneous inspiratory efforts. For example, it is not possible to determine which amount of measured positive airway occlusion pressure, if not all, is due to expiratory muscle activity [9]. Setting the external PEEP based on this measurement could induce considerable mistakes by overestimating intrinsic (or auto-) PEEP. The only readily available and reliable method of measuring intrinsic (or auto-) PEEP in the spontaneously breathing subject is to measure the drop in oesophageal pressure occurring before flow becomes inspiratory, and subsequently subtract the part due to expiratory muscle activity determined from an abdominal pressure signal [9]. The reasoning is as follows: any rise in abdominal pressure occurring during expiration is transmitted to the intrathoracic space and increases alveolar pressure. Intrinsic PEEP is measured from the abrupt drop observed on the oesophageal pressure signal until flow becomes inspiratory (phase 1 on Fig. 1). Part of this drop in oesophageal pressure is caused by the relaxation of the expiratory muscles. This part needs to be subtracted from the oesophageal pressure drop, in order to evaluate a “corrected” intrinsic PEEP due to hyperinflation. Two main possibilities exist: to subtract the rise in gastric pressure that occurred during the preceding expiration [9] or to subtract the concomitant decrease in gastric pressure at the onset of the effort [10]. Because the correction of intrinsic (or auto-) PEEP for expiratory muscle activity has not been used in early studies, one can hypothesise that the magnitude of intrinsic (or auto-) PEEP has often been overestimated. This combined oesophageal and gastric pressure measuring technique requires the insertion of a nasogastric tube equipped with both oesophageal and gastric balloon catheters. This technique is often used for research purposes but cannot be easily used at the bedside for routine clinical monitoring.
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