Chapter 18: Obstructive Lung Disease

Obstructive pulmonary diseases include chronic obstructive pulmonary disease (COPD), asthma, bronchiectasis, and cystic fibrosis. Patients with this underlying pathology are a significant fraction of those requiring respiratory support. Although this chapter deals primarily with COPD and asthma, the principles related to mechanical ventilation are similar for other obstructive lung diseases.

With COPD, flow limitation leads to air trapping with increased work-of-breathing and respiratory muscle dysfunction. Asthma is episodic and associated with airways inflammation and bronchospasm. COPD and asthma are chronic diseases that are often managed well in the community. But exacerbations of either can result in respiratory failure necessitating mechanical ventilation.

Respiratory Muscle Dysfunction

Because of the hyperinflation with COPD, the normal dome shape of the diaphragm is flattened and the zone of apposition is decreased. The result is less efficient diaphragmatic function. If the diaphragm is sufficiently flattened, during contraction the lateral rib cage moves inward instead of outward, leading to paradoxical breathing (Table 18-1). Accessory muscles of inspiration (intercostals, scalenes, sternomastoid, pectoralis, and parasternal) become the primary muscle groups for breathing. In patients with COPD where chronic respiratory muscle dysfunction has developed, reserve is limited and fatigue can occur with increases in respiratory muscle load.

Auto-Positive End-Expiratory Pressure

Auto-positive end-expiratory pressure (auto-PEEP) is end-expiratory alveolar pressure due to air trapping. Due to the heterogeneity that exists in the lungs, air trapping and auto-PEEP may differ between lung units. As a result, the auto-PEEP level measured is an average value. Long-time constants (Table 18-2) resulting from increased resistance and compliance in COPD necessitate more expiratory time to prevent air trapping and auto-PEEP. Auto-PEEP requires a greater inspiratory pressure to initiate flow into the lungs (difficulty triggering the ventilator) and the hyperinflation resulting from air trapping causes an increased work-of-breathing. The airways resistance with COPD is characterized by flow limitation.

Patients with severe acute asthma also develop air trapping and auto-PEEP. The air trapping occurs due to increased airways resistance with bronchospasm, inflammation, and secretions. Some lung units may be hyperinflated to the point that they compress adjacent lung units. The auto-PEEP and increased resistive load results in large intrathoracic pressure changes during the breathing cycle, resulting in pulsus paradoxus. Hyperinflation causes tidal breathing on a less compliant part of the pressure-volume curve, which decreases compliance and increases the work-of-breathing. The measured auto-PEEP during mechanical ventilation in some patients with asthma may not reflect the magnitude of air trapping because of complete airway obstruction (Figure 18-1). These patients should receive a respiratory pattern to minimize air trapping and breathing effort. Anxiety and a high respiratory drive make this difficult.

Nutrition

It is common that patients presenting with COPD exacerbation are nutritionally depleted, with caloric and protein deficiencies and electrolyte imbalances. This compromises respiratory muscle function and contributes to respiratory failure. Nutritional support is important, but care must be taken to avoid overfeeding, which results in increased carbon dioxide production and, thus, a greater load on the respiratory muscles.

Although often lifesaving, invasive mechanical ventilation should be avoided if possible in patients with COPD. Morbidity (aspiration, barotrauma, nosocomial infection, cardiovascular dysfunction) in chronic pulmonary disease patients is high during invasive mechanical ventilation and some of these patients become ventilator-dependent once intubated. As a result, noninvasive ventilation (NIV) has become standard practice for patients with COPD during an exacerbation. For many of these patients, intubation is avoided with the use of NIV. Moreover, there is a survival benefit afforded to the patient with the use of NIV. With severe acute asthma, NIV can be attempted but success is less likely than with COPD. Use of NIV in severe asthma is an area of controversy, but there is accumulating evidence supporting its use in selected patients with asthma and cystic fibrosis.

Indications

Patients presenting with a COPD exacerbation are hypercapnic, hypoxemic, exhausted, and with respiratory muscle dysfunction (Table 18-3). Mechanical ventilation is indicated to unload the work-of-breathing, rest respiratory muscles, decrease Paco₂ to the patient's baseline, and treat hypoxemia.

A clinical dilemma with asthma is determining when conventional therapy has failed and respiratory support is required. Many patients presenting with acute asthma are young and otherwise healthy, and they can maintain ventilation despite the marked increase in breathing effort. These patients may maintain Paco₂ less than or equal to 40 mm Hg until they are completely exhausted. When CO₂ retention occurs, severe hypercapnia and acidosis can rapidly develop. Thus, mechanical ventilation should be provided when Paco₂ exceeds 40 mm Hg and sooner if the patient is showing signs of exhaustion (Table 18-4). At this point, the patient is fatiguing and waiting longer before initiating ventilation results in further hypoventilation.

Ventilator Settings for COPD

Mechanical ventilation of the patient with COPD can be challenging. At best, these patients are returned to their baseline characterized by dyspnea, increased work-of-breathing, and abnormal gas exchange. Of primary concern during respiratory assistance of these patients is patient-ventilator synchrony to avoid unnecessary effort and anxiety. Heavy sedation or paralysis is not used beyond the initiation of mechanical ventilation. Ventilator settings that assure patient comfort in addition to adequate gas exchange is important (Table 18-5 and Figure 18-2).

Either pressure-controlled ventilation (PCV) or volume-controlled ventilation (VCV) can be used. An advantage of PCV is that flow varies with the patient's demand. However, in the setting of increased auto-PEEP, tidal volume is reduced with PCV. With VCV, tidal volume does not decrease with increased auto-PEEP, but there is a risk of an increased plateau pressure and overdistention.

Pressure support ventilation (PSV) can be problematic with COPD. Termination of inspiration with PSV is flow-cycled (eg, a fixed fraction of peak flow). Termination of inspiration may be either prolonged or premature, increasing respiratory demand and activating accessory muscles of exhalation to terminate flow if patient and ventilator termination of inspiration is not synchronous. PCV may be preferred over PSV because it allows rate and inspiratory time to be set. In the early phase of respiratory support, a fixed inspiratory time may be better tolerated and is set per patient comfort (0.6-1.0 second).

If VCV is used, flow is set high enough to satisfy inspiratory demand and promote patient comfort. Peak flow should be set to produce an inspiratory time of 0.6 to 1.0 second. When the flow demand of the patient is greatest at the beginning of inspiration, a ramp flow pattern is useful. The lower end-inspiratory flow with the ramp flow pattern may improve gas distribution to long-time constant regions. However, there are some patients who are more comfortable with a constant inspiratory flow pattern. When a shorter inspiratory time (longer expiratory time) is necessary to manage auto-PEEP, a constant inspiratory flow may be necessary. Rate should be set at 8 to 15/min, depending on the degree of hypercapnia and the development of auto-PEEP.

High plateau pressures are usually not a problem in COPD unless auto-PEEP is present. As a result, V_T in the 6 to 8 mL/kg range should be used. Plateau pressure should be kept as low as possible (< 30 cm H₂O) to minimize overdistention.

Auto-PEEP is always a concern when ventilating patients with COPD. Efforts to minimize auto-PEEP and its effects on triggering should be maximized. Therapy to reverse airways resistance (eg, bronchodilators, steroids) and mobilize secretions (eg, bronchoscopy, suctioning) should be used. In addition, minute ventilation should be as low as possible. Auto-PEEP produces a threshold load at the beginning of inspiration, which increases the effort required to trigger the ventilator. A common clinical sign of auto-PEEP is missed triggers. Provided the trigger sensitivity is set properly, the only reason that the patient's rate exceeds the ventilator rate is auto-PEEP. Ensuring that minute ventilation (rate and tidal volume) is not excessive reduces auto-PEEP. However, even if tidal volume is minimized, some patients with COPD are unable to generate sufficient effort to overcome auto-PEEP and trigger the ventilator. In this setting, applied PEEP counterbalances auto-PEEP and improves triggering. PEEP is increased by 1 or 2 cm H₂O increments until patient rate and ventilator rate are equal. The use of 5 cm H₂O PEEP is usually beneficial in patients with COPD, and more than 10 cm H₂O is seldom necessary to counterbalance auto-PEEP. Applying PEEP counterbalances auto-PEEP in the setting of flow limitation with COPD.

The Fio₂ requirement in patients with COPD is rarely more than 0.50. Unloading the work-of-breathing and improving V̇/Q̇ matching results in an acceptable Pao₂ with only modest Fio₂ requirement. A Pao₂ of 55 to 80 mm Hg is adequate for these patients.

It is important to avoid overventilation in patients with COPD. Paco₂ should only be decreased to the patient's baseline level. In many patients, this is a Paco₂ of 50 to 60 mm Hg or that required for a near-normal pH (> 7.30). If initial ventilator settings satisfy respiratory drive, these patients usually require minimal sedation. Full respiratory support to rest the respiratory muscles is recommended for the first 24 to 48 hours of ventilation, after which evaluation for liberation should be considered.

Ventilator Settings for Asthma

The major concern when ventilating a patient with severe acute asthma is auto-PEEP. The approach to ventilation should be focused on minimizing auto-PEEP (Table 18-6 and Figure 18-3). This often means that permissive hypercapnia must be allowed, particularly in the early phases of mechanical ventilation. Inhaled bronchodilators and systemic steroids are an important aspect of the management of these patients.

Although either VCV or PCV can be used, VCV is often necessary at the onset of respiratory support. In very severe acute asthma, a high driving pressure is needed to deliver the tidal volume due to the high airways resistance. Although a peak airway pressure of 60 to 70 cm H₂O may be necessary, a plateau pressure less than 30 cm H₂O can still be maintained. The difference between the peak pressure and the plateau pressure is an indication of the degree of airways resistance.

Once the asthma severity improves, the patient can be transitioned to PCV per clinician's bias. With PCV, changes in delivered tidal volume at a fixed pressure are a reflection of changes in resistance and air trapping. As the severity of the asthma improves, delivered V_T with PCV increases. Sedation to minimize asynchrony should be used. Neuromuscular blocking agents may be necessary in some patients, although they should be avoided if possible. Prolonged weakness may occur in some patients following neuromuscular blockade. If adequate sedation is used, full respiratory support can usually be achieved.

To minimize the development of auto-PEEP, a small V_T (4-6 mL/kg) should be used. Delivered tidal volume should be chosen to ensure a plateau pressure less than 30 cm H₂O. Respiratory rate should be set based on the level of air trapping and auto-PEEP. Theoretically, a lower rate minimizes air trapping. However, in some patients with asthma, the rate can be increased to 15 to 20 breaths/min without a marked increase in auto-PEEP. A low tidal volume with a slow rate results in CO₂ retention. Maintaining pH more than or equal to 7.20 is usually sufficient. In young otherwise healthy patients with asthma, an even lower pH may be acceptable. The risk of auto-PEEP, lung injury, and hypotension usually outweighs the risks of acidosis.

Inspiratory time should be short to prolong expiratory time and reduce auto-PEEP. However, better distribution of ventilation can be achieved by lengthening inspiratory time. An initial inspiratory time of 1 second is recommended, with evaluation of the effect on auto-PEEP if inspiratory time is increased to 1.5 second. Provided that the rate is low, the increase in inspiratory time from 1 to 1.5 second does not significantly increase auto-PEEP. A descending ramp flow pattern when volume ventilation is used may enhance distribution of ventilation. However, a shorter inspiratory time can be achieved using a rectangular flow waveform. Peak flow is selected to ensure inspiratory time is appropriate.

An initial Fio₂ of 1 should be set and then reduced when pulse oximetry and blood gas data indicate adequate oxygenation. A controversy with the management of asthma is whether PEEP should be applied. Unlike COPD, the auto-PEEP that occurs in asthma is not usually due to flow limitation. In the absence of flow limitation, the addition of PEEP may not counterbalance auto-PEEP, but rather it may further increase alveolar pressure. Moreover, if the patient is being fully ventilated and making no triggering efforts, the benefit of PEEP in the setting of auto-PEEP might be questioned. Distribution of ventilation may improve with applied PEEP since those lung units without auto-PEEP may be recruited and stabilized. Applied PEEP should not be used in patients with acute asthma if it results in an increase in total PEEP and plateau pressure. If PEEP is applied in this setting, monitoring of gas exchange, plateau pressure, auto-PEEP, and hemodynamics is necessary.

Monitoring

Monitoring of patient-ventilator synchrony is important in this patient population (Table 18-7). Auto-PEEP should be monitored regularly in patients with obstructive lung disease. Evaluation of the expiratory flow waveform or observation for missed triggers is useful to identify the presence of auto-PEEP, but not its magnitude. During passive ventilation, auto-PEEP can be quantified using an end-expiratory hold. Respiratory rate, use of accessory muscles, breath sounds, heart rate, and blood pressure should also be monitored.

Barotrauma and hemodynamic compromise are common in patients with asthma if auto-PEEP and plateau pressure is excessive. Physical examination and chest radiography need to be monitored (Table 18-8). With each ventilator-patient system evaluation, plateau pressure, peak airway pressure, tidal volume, and auto-PEEP levels should be documented and trends evaluated. Continuous pulse oximetry, periodic blood gas measurements, and monitoring of hemodynamics is necessary. It should be remembered that Spo₂ provides little indication of ventilation or acid-base balance. End-tidal CO₂ is not useful because these patients have high V_D/V_T.

Liberation

Most important in the process of liberation is to ensure that the acute process that necessitated mechanical ventilation is improving. Second, ensure cardiovascular function is optimized, as many patients with COPD also have cardiovascular disease. Third, optimize electrolyte balance and nutritional status, because nutritional status and some electrolyte imbalances affect respiratory muscle function. Finally, use spontaneous awaking trials and spontaneous breathing trials to identify when liberation is possible.

Most patients with COPD can be fully liberated from mechanical ventilation. Others require long-term support (a difficult subgroup). In those patients who are tracheostomized and require long-term respiratory support, a slow-paced approach may be necessary with spontaneous breathing trials interspersed with periods of respiratory support. Nocturnal ventilation is sometimes required. In some patients with COPD, NIV can be used as a bridge to ventilator independence. NIV can be provided until the patient can breathe independently or requires reintubation.

Liberation of the patient with severe acute asthma is usually more rapid than with COPD. Once the acute phase is adequately treated, ventilator discontinuation should be considered. As the patient's status improves (ie, airflow resistance returning to baseline, auto-PEEP eliminated, and airway pressures and tidal volumes returning to normal, adequate gas exchange), sedation should be decreased or stopped, allowing the patient to resume spontaneous breathing. Once alert and cooperative, a spontaneous breathing trial is performed to assess extubation readiness.