Respiratory Mechanics — Detailed Review

Measurement of respiratory mechanics is still the mainstay of bedside monitoring of mechanical ventilation.
Ideally, the energy applied to the lung is optimized based on the equation of mechanical power.
Setting the ventilator considers multiple aspects of energy transfer and protection against ventilator-associated injury.
Newer technologies appear promising; particularly, electrical impedance tomography and lung ultrasound in combination with conventional monitoring are currently the direction for the future.

Mechanical ventilation can harm lung tissue through barotrauma, volutrauma, atelectrauma, oxytrauma, and biotrauma. These 5 mechanisms have their own specific pathophysiological features but share similarities in their pathways of injuring the lungs (ventilator-induced lung injury [VILI]). 1 All these mechanisms together may result in inflammation through local production and release of inflammatory mediators, which is known as biotrauma. The so-called lung-protective ventilation strategies aim to minimize the occurrence of the pathophysiological features of VILI. To prevent VILI, the amount of energy transferred from the mechanical ventilator to the patient should be limited to a bare minimum.

To do so, tidal volume (VT) and inspiratory pressures should be kept low to minimize the risk of barotrauma and volutrauma. This review provides a brief overview on the measurement of respiratory (also referred to as pulmonary) mechanics and current developments in the field to achieve this goal. WHAT ARE RESPIRATORY MECHANICS? Respiratory mechanics refer to the expression of lung function through measures of pressure and flow. From these, a variety of derived indices can be determined, such as flow, pressure, volume, compliance, resistance, and work of breathing (WOB). These factors directly affect lung volumes and therefore functional residual capacity (FRC) and gas exchange.

Waveforms are derived when one of the parameters of respiratory mechanics is plotted as a function of time or as a function of one of the other parameters. This produces scalar tracings of pressure-time, flow-time, _ and volume-time graphics, as well as flow-volume (V-V) and pressure-volume (P-V) loops. All current-generation positive-pressure ventilators—including those in the operating room—provide some monitoring of pulmonary mechanics at the bedside. Additionally, advanced respiratory mechanics monitoring modalities, such as esophageal pressure and electrical activity of the diaphragm, are available to provide sophisticated analysis of breathing efforts and diaphragmatic function.

They will only be touched upon briefly because they are beyond the scope of this article. Lung ultrasound has improved the diagnostic accuracy of these modalities and nowadays is the second mainstay of ventilator management at the bedside. WHY MEASURE RESPIRATORY MECHANICS? Artificial ventilation is a temporary measure to replace or augment the function of the inspiratory muscles, providing the necessary energy to ensure a flow of gas into the alveoli during inspiration. When this support is removed, gas is exhaled passively as the lung and chest wall recoil to their original volume. An understanding of respiratory mechanics is vital to patient assessment during mechanical ventilation in order to match the available technology to the patient’s needs.

The goals are optimizing the patient’s pulmonary physiology, providing effective gas exchange, maintaining alveolar recruitment, reducing injury potential, and ensuring hemodynamic stability. Analyzing and incorporating measurements of respiratory mechanics during your assessment will provide the information required for optimal intraoperative mechanical ventilation. Optimizing settings requires that the physician understands the intricacies of patient-ventilator interactions, particularly in terms of the measured variables as they are displayed by ventilator graphics. They represent the interaction between the ventilator and the patient’s respiratory mechanics described by the equation of motion and therefore the power applied to the lung.

The respiratory system can be simplified using a linear one-compartment model, which comprises a tube representing the airways and a balloon representing the alveoli and the chest wall. The impedance to ventilation has numerous origins, the most important of which are the following:
Elastic resistance of lung tissue and the chest wall
Resistance from surface forces at the alveolar gas-liquid interface
Frictional resistance to gas flow through the airways
Frictional resistance from deformation of thoracic tissues (viscoelastic tissue resistance)
Inertia associated with movement of gas and tissue (negligible at normal respiratory rates) The first two forms of impedance may be grouped together as elastic resistance.

These are measured when gas is not flowing within the lung and represent the total compliance of the lung and chest wall:
Compliance Crs 5 D volume/D pressure
Elastance ELrs 5 D pressure/D volume 5 1/C Respiratory Mechanics The last three forms may be grouped together as nonelastic resistance or respiratory system resistance. They occur while gas is flowing within the airways, and work performed in overcoming this frictional resistance is dissipated as heat and lost.

Impedance to flow represents resistance of the airways:
Resistance R 5 D pressure/flow Note that the linear one-compartment model does not take into account the fact that resistance and compliance are not constant in the case of lung and chest wall disease; instead, they exhibit a flow and volume dependency. Work performed in overcoming elastic resistance is stored as potential energy, and elastic deformation during inspiration is the usual source of energy for expiration during both spontaneous and artificial breathing.

In the past, adjusting the ventilator often only considered the variables positive endexpiratory pressure (PEEP), tidal volume (VT), PPlat, and DP. 2 Other components such as flow and respiratory rate were neglected. The problem is that any alterations of one component changes another and makes it even more difficult to understand the relationship of the variables, blurring the overall picture. With this in mind, Gattinoni and colleagues3 proposed the concept of mechanical power (MP) in 2016. The equation for MP is the product of ventilating frequency and the inflation energy of the tidal cycle.

The latter consists of three components: (1) the power required to overcome tissue and airways resistance during gas movement (flow-resistive work), (2) the power required to inflate the lung and chest wall from their shared initial position (VT-associated work), and (3) the (nonrecurring) power required to overcome PEEP-related recoil of the lung and respiratory system. Ultimately, in the expression for MP, every component is subsumed: PAPPL 5 PVENT 1PMUS 5 VT =C1V_  R where Pappl is the applied power to the lung and Pvent and PMus are the pressures applied by the ventilator and the muscles, respectively.

so the equation of motion Elastance (E) relates P to V, and resistance relates P to (V), can be modified to explain how the pressure at the airway opening (Paw) can be partitioned into a resistive and an elastic pressure component.   PAW ðtÞ 5 P0 1 E ðV ÞðtÞ 1R V ðtÞ Here, P0 is the starting pressure, either zero end expiratory pressure or PEEP.

Written differently, these components can be divided into the following more familiar variables, which can be measured easily at the bedside:     ð11I : E Þ Powerrs 5 RR, DV 2 , , ELrs 1 RR , , Raw 1 DV , PEEP 60, I : E where DV marks VT, ELrs is the elastance of the respiratory system (the reciprocal of compliance), RR is the respiratory rate, and I: E is the time ratio of inspiration and expiration. To begin inflation, the lung requires an energy input greater than the potential energy stored in the system by PEEP at end-exhalation. The term D V, PEEP is the energy required to equilibrate the potential energy stored in the system at the PEEP level (ie, PEEP-related MP, when related to time).

Gertler Recruitment diminishes and distention increases as airway pressure rises. Therefore, although its mechanical effects on atelectrauma may be, on balance, lung protective over its lower range, rising PEEP is unquestionably a component of MP and, as such, favors VILI by increasing lung stress and strain. MP can be calculated using the P-V curve. The power is defined as the area between the inspiratory limb of the Dtranspulmonary pressure (x)-volume curve, and the volume axis (y) and is measured in joules. 4 Following this basic idea, Collino and colleagues5 carried out a set of animal experiments in which the MP was modified by changing the PEEP. The total MP remained unchanged, with a PEEP between 0 and 7 cmH2O.

The components of energy changed, however. While the PEEP-associated energy increases, the energy decreases owing to the components of the driving pressure (DP) and the flow resistance, with a PEEP level up to 7 cmH2O. If the PEEP is raised further (up to 11–18 cmH2O), all components of MP as well as the total energy are steadily increasing. VT, driving pressure, and inspiratory flow exponentially increased MP by a factor of 2. A 1. 4 exponential increase in MP was registered with frequency, whereas a linear increase was observed with PEEP. The same MP may produce different effects in healthy or injured lungs. A power of 12 J/min may be a meaningful upper threshold of VILI and may be a predictor of survival.

MP normalized to predicted body weight was a good ventilator variable in predicting mortality in patients with adult respiratory distress syndrome (ARDS). 6

Stress is a force applied to an area, such as pressure applied to the lung parenchyma. Force applied at an angle generates shear stress. In clinical terms, lung stress refers to the distending pressure within the lung, and the counterforce (external load) is the chest wall. The best indicator of the amount of stress applied to the lungs is the transpulmonary pressure, which is difficult to measure in routine practice, but can be estimated with transpulmonary pressure measurements (eg, with an esophageal balloon, see the following information). At the bedside, plateau pressure is often used as a surrogate, although this comes with limitations.

Plateau pressure does not represent the actual force on the lung fibers but the pressure needed to expand the lungs and the chest wall consisting of the rib cage and the diaphragm. Patients with a stiff chest wall, for example, during pneumoperitoneum, will have a high plateau pressure that cannot automatically be translated into lung overdistension. 7 Maintaining a plateau pressure less than 25 cmH2O in most patients (<30 cmH2O in patients with ARDS) would limit lung strain to less than 2 cmH2O (considered detrimental) and lung stress to 22 to 24 cmH2O (considered the upper limit of stress). 8

_ The index is used to assess the shape of the pressure-time curve during constant V-V control ventilation. A linear increase in pressure (constant compliance, index 1) suggests adequate alveolar recruitment without overdistention.

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