Elastic Equilibrium Volume Research Articles

Mechanical interaction between patient and ventilator in biphasic positive airway pressure (BIPAP)--digital and mechanical simulations

Biphasic Positive Airway Pressure (BIPAP) and the closely related Airway Pressure Release Ventilation (APRV) are characterised by asynchronous actions of ventilator and patient. Clinical observation and physiological reasoning suggest, that in BIPAP patient and ventilator can interact in various ways. This study was to elucidate the mechanical interaction. Ventilation and interaction between patient and ventilator were analysed in digital and mechanical simulations of BIPAP with a variety of patient effort magnitudes and durations, machine pressures and phase durations, and passive respiratory system (RS) mechanics. Patient efforts were most likely to effect a breath if they were strong relative to the machine pressure swing, and if they occurred late in a ventilator phase. Conversely, efforts occurring with or shortly after a machine pressure swing or relatively weak efforts were more or less ineffective. The postulated permanently unrestricted spontaneous breathing in BlPAP mode, although indeed assured in the technical sense, has to be qualified: Every change in machine pressure defines a new balance of the forces driving the RS, and the lung volume will approach a new elastic equilibrium volume ( = relaxation volume); the speed of this approach is determined by the time constant (tau = R x C) of the RS. Patient efforts are most effective when the RS is at or close to an equilibrium. An increase in the assisting machine pressure swing can unload the patient and assure a minimum ventilation, but it reduces the patient"s influence on ventilation and thus potentially patient comfort. In contrast, Automatic Tube Compensation (ATC), an assist component accelerating the RS by reducing resistances, combines unloading with more patient influence; this has to be weighed against the potential disadvantage of higher peak flows.

LUNG VOLUMES AND ELASTICITY

The respiratory system is an elastic structure changing volume when pressures are generated by inspiratory or expiratory muscles. If the muscles are relaxed the respiratory system returns to its relaxation volume (Vr) (referred to in the pediatric literature as the elastic equilibrium volume [EEV]), which in normal subjects is the end-expired volume or functional residual capacity, FRC, where alveolar pressure is equal to atmospheric pressure.

Pressure-volume curves and compliance in acute lung injury: evidence of recruitment above the lower inflection point.

Measuring elastic pressure-volume (Pel-V) curves of the respiratory system and the volume recruited by a positive end-expiratory pressure (PEEP) allows one to study the pressure range over which recruitment occurs in acute lung injury (ALI), and to explain how recruitment affects the compliance. Pel-V curves were measured with the low flow inflation technique in 11 patients mechanically ventilated for ALI. Curve I was recorded during inflation from the volume attained after a prolonged expiration (6 s) at PEEP (9.0 +/- 2.2 cm H2O), and Curve II after expiration to the elastic equilibrium volume at zero end-expiratory pressure (ZEEP). By using the end-expiratory volume of the breaths, the curves were aligned on a common volume axis to determine the effect of a single complete expiration. In each patient, Curve II (from ZEEP) was shifted toward lower volumes than Curve I. The volume shift, probably due to derecruitment, was 205 +/- 100 ml at 15 cm H2O (p < 0.01) and 78 +/- 93 ml at 30 cm H2O (p < 0.01); thus, during inflation from ZEEP, the volume deficit was successively regained over a pressure range up to at least 30 cm H2O. At any pressure, compliance was higher on the curve from ZEEP than from PEEP, by 10.0 +/- 8.7 ml/cm H2O at 15 cm H2O (p < 0.01), and by 5.4 +/- 5.5 at 30 cm H2O (p < 0.01). It is concluded that in ALI, a single expiration to ZEEP leads to lung collapse. High compliance during insufflation from ZEEP indicates that lung recruitment happens far above the lower inflection point of the Pel-V curve.

"Intrinsic" PEEP (PEEPi): role of expiratory muscles

In normal subjects breathing at rest, lung volume at end-expiration corresponds with the elastic equilibrium volume, or relaxation volume (Vr), of the respiratory system. If expiratory duration is not long enough, then inspiration may begin before the system has returned to Vr, such that end-expiratory lung volume is higher than Vr. This condition is named dynamic pulmonary hyperinflation and intrinsic positive end-expiratory pressure (PEEPi), also called auto PEEP, corresponds to the elastic recoil of the lung at end-expiration [1, 2]. In the spontaneously breathing subject, this dynamic hyperinflation occurs mainly when the rate of lung emptying is decreased owing to high respiratory resistance or flow limitation. The highest degrees of dynamic hyperinflation are, thus, encountered in patients with airway diseases, particularly chronic obstructive pulmonary disease (COPD) patients. In the ventilated patient, external determinants may also induce dynamic pulmonary hyperinflation, or increase the magnitude of dynamic hyperinflation that was already present before the onset of mechanical ventilation. These additional external determinants include a preceding inflation volume that is too large, a time available for expiration that is reduced or a decreased rate of lung emptying owing to high resistance associated with the tube, the ventilator tubing or devices [3]. Dynamic pulmonary hyperinflation has important pathophysiological and therapeutic implications mainly in critical care medicine [3]. In particular, it implies that as the inspiratory muscles start to contract they must first offset the elastic recoil pressure of the system before inspiratory flow can begin and lung volume can increase. PEEPi associated with dynamic pulmonary hyperinflation thus corresponds to an inspiratory threshold load and is associated with an increased inspiratory work of breathing. This has led several investigators to give external PEEP or continuous positive airway pressure (CPAP) in the belief that this would unload the inspiratory muscles and, therefore, reduce the inspiratory work of breathing [4–6]. It must be stressed, however, that PEEPi and dynamic pulmonary hyperinflation are not always linked. In fact, alveolar pressure can also remain positive throughout expiration when the expiratory muscles contract [1, 5]. With respect to this, recent studies have shown that in many patients with stable but severe COPD [7] as well as in many mechanically ventilated patients [8, 9], expiration is a mechanically active process. These observations, thus, provide strong evidence that the active nature of expiration is an important determinant of PEEPi in such patients and, therefore, that the importance of dynamic pulmonary hyperinflation has been overestimated. Since a positive end-expiratory alveolar pressure resulting from an expiratory muscle contraction does not represent an inspiratory threshold load, the level of external PEEP that is needed in such patients must be significantly less than conventionally thought. The contribution of expiratory muscle contraction to the increase in end-expiratory alveolar pressure has to be taken into account when applying external PEEP or CPAP to offset PEEPi or these procedures might, in fact, result in enhanced pulmonary dynamic hyperinflation with further deleterious consequences [4, 10]. In this issue of the European Respiratory Journal, ZAKYNTHINOS and co-workers [11] report on a method for detecting expiratory muscle use and quantifying its contribution to PEEPi. The two points at issue in this and other studies [7–9] are:

Intrinsic PEEP and cardiopulmonary interaction in patients with COPD and acute ventilatory failure.

Deviation of end-expiratory lung volume from the elastic equilibrium volume of the respiratory system is recognized as a cardinal feature in mechanically-ventilated patients with severe chronic obstructive pulmonary disease (COPD) and acute ventilatory failure (AVF). The presence of dynamic hyperinflation implies that alveolar pressure remains positive throughout expiration. At the end of the expiration, this positive pressure is named intrinsic positive end-expiratory pressure (PEEPi). Recent studies have suggested that, in COPD patients with expiratory flow limitation, the application of external PEEP during assisted mechanical ventilation, or the use of continuous positive airway pressure (CPAP) in spontaneously breathing patients, can counterbalance and reduce the inspiratory threshold load imposed by PEEPi, without causing further increase in lung volume and alveolar and intrathoracic pressures until a critical value of PEEP (Pcrit) is reached. Above this critical limit further hyperinflation is observed. A specific and characteristic role of PEEPi in compromising the heart function in COPD patients during AVF may be identified based on: 1) an increase in right ventricular impedance due to lung hyperinflation; 2) an increase in the venous return to the right ventricle and, consequently, a leftward shift of the septum caused by the large negative deflections in intrathoracic pressure due to the inspiratory threshold load; 3) a further increase in venous return to the right ventricle, with the eventual collapse of the vena cava caused by the expiratory recruitment of abdominal muscles; and 4) hypoxia and hypercapnia consequent to acute ventilatory failure, which may further increase right ventricular impedance and venous return to the right ventricle. All these phenomenon are directly correlated to the large negative intrathoracic pressure developed by the respiratory muscles to overcome the inspiratory threshold caused by intrinsic positive end-expiratory pressure (preload effect), and to the increase in lung volume (afterload effect). Application of positive end-expiratory pressure/continuous positive airway pressure in chronic obstructive pulmonary disease patients during acute ventilatory failure may, hence, unload the respiratory muscles as well as the heart.

Difference between functional residual capacity and elastic equilibrium volume in patients with chronic obstructive pulmonary disease.

A study was performed to determine the elastic equilibrium volume (Vr) of the respiratory system in patients with chronic obstructive pulmonary disease (COPD). Voluntary relaxed expiration from total lung capacity (TLC) was studied in three groups of subjects: seven patients with severe chronic airways obstruction (COPD), 10 normal subjects, and 15 subjects with restrictive disease. In the normal subjects and the patients with restrictive disease voluntary relaxed expiration from TLC stopped close to end tidal volume (FRC) and the volume expired in this manoeuvre was less than that expired in a slow vital capacity manoeuvre (SVC). In the patients with COPD the voluntary relaxed expiration continued beyond the end tidal volume (FRC) and the volume expired was not different from the SVC. Oesophageal (pleural) pressures and surface diaphragmatic EMG recordings in the patients with COPD supported the premise that relaxation was achieved. In patients with COPD, end tidal volume (FRC) is higher than the elastic equilibrium volume, Vr, of the respiratory system. This is in contrast to patients with restrictive disease and normal subjects in whom end tidal volume (FRC) is close to Vr. This study shows that, in patients with severe chronic obstructive pulmonary disease, Vr is at least as small as residual volume (RV).

Intrinsic positive end-expiratory pressure (PEEPi)

Positive end-expiratory pressure (PEEP) is one of the most frequently discussed topics in critical care medicine. However, alveolar pressure can remain positive throughout expiration without PEEP set by the ventilator whenever the time available to breathe out is shorter than the time required to decompress the lungs to the elastic equilibrium volume of the total respiratory system (Vr). The end-expiratory elastic recoil (Pel,rs) due to incomplete expiration has been termed auto PEEP, occult PEEP [1], inadvertent PEEP [2], endogenous PEEP, internal PEEP and intrinsic PEEP [3, 4] owing to its similarity and contrast with PEEP set by the ventilator. The purpose of this article is to provide a comprehensive review of the studies on this interesting aspect of critical care medicine, from the underlying physiological mechanism(s) to the clinical and therapeutic implications, through measurement and monitoring in the intensive care setting.

Volume-time profile during relaxed expiration in the normal dog.

Airway opening pressure, esophageal pressure, and flow were obtained during relaxed expirations in two normal anesthetized paralyzed dogs. The signal-to-noise ratio in the flow signals was greatly increased by averaging 10 different signals obtained with the same lung inflation volume. Numerical integration of an averaged flow signal then yielded the time course of the volume of the respiratory system above functional residual capacity (the elastic equilibrium volume). Comparison of volume signals obtained with different inflation volumes suggests that the resistance of the respiratory system increases with flow. The flow-volume and semilog volume curves show that expiration is induced by two apparently separate mechanisms: one causes emptying of most of the expired volume over a time interval of much less than 1 s, whereas the other contributes a relatively small amount to the expired volume over a significantly longer time (greater than or equal to 1 s). We postulate the first mechanism to be due to that of the respiratory system behaving like a single unit, with an elastance that is slightly volume dependent, emptying through a single airway which has a resistance that increases with flow. From the nature of airway opening pressure and esophageal pressure measured after occlusion in midexpiration, we conclude that the second mechanism is due to the viscoelastic properties (i.e., creep) of the respiratory system. The properties are manifest mainly in the chest wall.