Lung mechanics during mechanical ventilation

Muscle contraction uses energy. If the muscle moves, external work is performed. This can be measured as the force multiplied by the distance that the muscle has shortened. In many biological situations the length of the muscle is fixed; when this occurs the internal work (within the muscle cell) is difficult to measure. The power that the muscle produces is the product of work and its duration.

In the ventilated patient, work is performed during each breath by the ventilator and energy is dissipated. The external work causes gas to move and this can be measured. Internal work may be performed if the respiratory muscles contract, but no gas flows and this is often not measured. Clearly, considerable amounts of internal work can occur in an occult manner.

The respiratory muscles form a complex geometrical arrangement around the chest wall and the force exerted during contractions cannot be measured directly. However, as the transpleural pressure difference causes gas to move, pressure is used in place of force to calculate work. For similar reasons, the distance that the respiratory muscles move is substituted by the volume of gas which moves when calculating the external work performed during breathing. The external work of breathing is measured by integrating simultaneous measurements of transpleural pressure and the volume change at the mouth.

If the patient is fully ventilated, the machine is performing all the work of breathing. Work is performed principally in expanding the lung against the elastic recoil of the lung and chest wall and, when gas is flowing, in overcoming resistance. Further work is dissipated due to gas compression and rarefaction within the breathing circuit. Under these circumstances, ventilator work can easily be calculated. If pressure is measured at the mouth and inspiratory flow is constant, the work is represented by the area under the pressure-time graph. If this technique is to be used to assess inspiratory work sequentially, the measurement must be made under standardized flow and volume conditions. Additionally, the method assumes that the ventilator is performing all inspiratory work and that the patient is making no effort. Inspiratory effort will reduce the pressure measured at the mouth and the airway pressure-time diagrams will be irregular and convex inwards ( Fig 1 and Fig..2).

Fig. 1 Airway pressure is measured during constant flow lung inflation. Note the straight upstroke suggestive of a linear relationship between volume and pressure. Compliance can be measured during gas flow (dynamic) or after an inspiratory pause (static).

Fig. 2 The upstroke of the pressure-time curves should be linear. If the patient is hyperinflated, pressure rise per unit volume change will accelerate. If pressure changes decelerate, recruitment must be occurring.

The shape of the pressure curve depends on the mechanics of the lung and chest wall. From the relaxed end-expiratory point, the volume-pressure relationship is linear and the slope of the line is related to lung compliance. Dynamic compliance can be calculated by dividing delivered volume by peak end-expiratory pressure.

Hyperinflation of the lung and recruitment of alveoli alter the shape of the pressure-time curves. As lung volume increases, more pressure is required to inflate the chest and the pressure-time curve is non-linear. If lung volume is reduced, recruitment of alveoli may occur during inflation and less pressure is required at the end of inflation.

Hyperinflation of the lung and recruitment of alveoli alter the shape of the pressure-time curves. As lung volume increases, more pressure is required to inflate the chest and the pressure-time curve is non-linear. If lung volume is reduced, recruitment of alveoli may occur during inflation and less pressure is required at the end of inflation.

/Q exceeds 1.0.

The effect of mechanical ventilation on this important physiological concept is seen when the effect of posture and loss of muscle tone are considered. When supine, dependent areas of the lung show a decrease in compliance; therefore these lung units are further down the pressure-volume relationship. For a given change in pressure, lung expansion is reduced and ventilation declines. Therefore such dependent areas of the mechanically ventilated lung have a negative effect on the ■

overall VlQ state of the lung, and both a higher inspired oxygen tension and increased ventilation are required.

The effect of common disease states can be seen clearly in terms of VlQ. Intrapulmonary shunt predominates in acute respiratory distress syndrome, although two

types of gas exchange have been demonstrated. There are areas of low VlQ, suggesting very poorly ventilated areas of lung, and also other lung units with ■ ■

essentially normal VlQ levels. In contrast, in airflow limitation shunt is typically low and dead-space increased. When VlQ relationships are measured, four different

patterns of distribution occur and the net effect is one of bimodal changes in VlQ. Clearly, ventilatory strategies to optimize mechanical ventilation will be fundamentally different in patients with small-volume lungs compared with patients whose primary pathology is hyperinflation.

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