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7. Obstructive Pulmonary Disease
Patients with obstructive pulmonary diseases, mainly including chronic obstructive pulmonary disease (COPD) and asthma, compromise a considerable proportion of mechanically ventilated patients in the intensive care unit (ICU) . Mechanically ventilated patients with comorbidity of COPD might have a longer duration of ventilation with difficult weaning. Nowadays, modern ventilators can display pressure-, flow-, and volume-time tracings, as well as pressure-volume and flow-volume curves 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 diaphragm function. This information facilitates early identification of abnormalities, detection of patient-ventilator asynchrony, and optimization of mechanical ventilation settings. In this chapter, based on the introduction of the main pathophysiologic alterations in patients with obstructive pulmonary diseases undergoing mechanical ventilation, we will discuss respiratory mechanics monitoring, specifically on the measurement of dynamic hyperinflation and air trapping. In the end, we will briefly introduce the principle for ventilation management in this population.
7.1 Dynamic Hyperinflation and Intrinsic Positive End-Expiratory Pressure
The central pathophysiologic change in patients with obstructive pulmonary disease is the airflow obstruction induced increase in airway resistance, which results in dynamic hyperinflation and intrinsic positive end-expiratory pressure (PEEP). Airflow obstruction occurs as distal airway diameter is constricted by bronchospasm, mucosal and interstitial edema, and dynamic airway collapse during expiration [2, 3]. The cause of airway obstruction during exacerbating COPD is different from that during asthma, with increased airway collapsibility resulted from lung parenchyma devastation and decreased lung elastance in the former, and with increased thickness of airway wall resulted from inflammation and decreased collapsibility in the latter [4, 5].
Normally, lung volume returns to the relaxed volume at the end of passive expiration. This relaxed lung volume is defined as a functional residual capacity (FRC) during spontaneous breathing. In patients with increased expiratory resistance due to airflow obstruction, the end-expiratory lung volume (EELV) may increase above the predicted FRC. This phenomenon is defined as lung hyperinflation, which can be further classified as static hyperinflation induced by the destruction of pulmonary parenchyma and loss of alveolar elastic recoil, and dynamic hyperinflation induced by a slowed lung emptying. Along with the increase in EELV, end-expiratory alveolar pressure increases, which is also called intrinsic PEEP .
Increased expiratory resistance resulting in longer time constant;
Reduced lung elastance resulting in decreased expiratory driving pressure;
Expiratory flow limitation defined as the inability of augmentation of expiratory flow regardless of an increased expiratory driving pressure ;
High respiratory rate with short expiratory time impairing complete exhalation to relaxed lung volume;
A high tidal volume may occur during mechanical ventilation.
The increased inspiratory load threshold
During assist mechanical ventilation, the patients with intrinsic PEEP have to generate an additional pleural pressure to counterbalance the intrinsic PEEP to trigger the ventilator. This can be considered as a wasted energy cost of breathing because inspiratory muscle contraction to counterbalance intrinsic PEEP does not generate inspiratory flow. The increased inspiratory muscle load tends to result in muscle fatigue and patient-ventilator asynchrony such as ineffective triggering [8, 9].
Increased elastic load
Because of the increase in EELV, inspiratory muscles generate tidal breathing at a higher lung volume, which represents the flattened part of the pressure-volume curve. A greater effort is needed to produce a given tidal volume.
Decreased capacity of pressure generated by inspiratory muscles
The elevated EELV and intrinsic PEEP push diaphragm downward, resulting in shortened muscular fibers and decreased diaphragm moving amplitude . The rib cage expanding action is also reduced due to the hyperinflation induced rib cage distortion. Additionally, respiratory muscle blood flow is worsened by intrinsic PEEP and dynamic hyperinflation. Consequently, the capacity of inspiratory muscles to generate inspiratory pressure decreases.
Impaired gas exchange
Several factors contribute to gas exchange impairment . Airway obstruction produces regional hypoventilation. Emphysema results in loss of the capillary bed and hyperinflated alveoli compresses the pulmonary capillaries. These factors tend to increase dead space. Besides, concomitant pneumonia and congestive heart failure also contribute to ventilation-perfusion mismatch and hypoxemia.
Positive intrathoracic pressure due to intrinsic PEEP reduces venous return and thereafter cardiac output . Dynamic hyperinflation compresses alveolar capillaries increasing pulmonary vascular resistance and right ventricular afterload, ultimately inducing right heart failure. The initiation of mechanical ventilation and the use of sedatives during endotracheal intubation produce hypotension.