Ventilatory Management of Obstructive Airway Disease

Published on 07/03/2015 by admin

Filed under Critical Care Medicine

Last modified 07/03/2015

Print this page

This article have been viewed 1965 times

Ventilatory Management of Obstructive Airway Disease

John Marini

Chapter Outline

Positive-pressure ventilators have been in widespread clinical use for more than 4 decades. Our understanding of respiratory muscle function and ventilatory failure has undergone major revision over that period, helping to gear equipment and treatment strategies more effectively to patient requirements. Some of the more important advances in this area concern the interactions of patients having obstructive pulmonary disease (airflow obstruction [AO]) with the mechanical ventilator. Others concern physiologic principles important in withdrawing machine support from ventilator-dependent patients, many of whom have chronic obstructive pulmonary disease (COPD) or asthma. With these advances in mind, the purpose of this chapter is to provide an updated physiologic background for understanding mechanical ventilation in patients with AO, as well as to review selected aspects of this problem that are frequently overlooked and, though noteworthy, may be unfamiliar to many practitioners. Noninvasive ventilation, a modality of immense value in the treatment of alert patients with moderately severe obstructive illnesses, will not be extensively addressed here, as it is covered in other chapters of this text.

Special Challenges of Patients with Severe Airflow Obstruction

By assuming a major portion of the ventilatory workload, mechanical ventilation affords the opportunity to rest the respiratory muscles while maintaining pH homeostasis and oxygenation, thereby averting progressive ventilatory failure, respiratory arrest, or both. Unfortunately, these benefits are not cost-free—mechanical ventilation is expensive, uncomfortable, and inherently hazardous; few would dispute the desirability of avoiding the need for its implementation or of accelerating the process of its withdrawal. Although deceptively simple in concept, the management of patients with AO who require mechanical support often proves to be a rather complex clinical undertaking. To manage respiratory failure effectively in patients with severe AO, it is important to understand their distinctive problems. Patients with severe AO may be characterized by a number of salient clinical features. Paramount among these are increased work of breathing and mechanical compromise of the ventilatory pump that must contend with it. Such patients are also distinguished by their susceptibility to the hazards of machine support.

Increased Work of Breathing

The mechanical breathing workload during passive ventilation can be quantified as the product of mean inflation pressure and minute ventilation. The mean inflation pressure (Pm) is approximated in a modification of the equation of motion of the respiratory system:

In this equation R = resistance; VT is tidal volume; C is respiratory system compliance (the inverse of elastance); and PEEPi is auto-PEEP, the positive end-expiratory alveolar pressure in excess of set PEEP because of dynamic hyperinflation (Fig. 10.1).

Figure 10.1 Depiction of the elements of the inspiratory equation of motion and their associated work of breathing. Stippled area is resistive work, and striped areas represent the elastic work associated with tidal volume and auto–positive end-expiratory pressure, respectively.

Increased resistance to airflow is responsible (directly or indirectly) for many of the physiologic disturbances that typify this disease. Flow resistance, an important determinant of Pm, is increased by structural and functional narrowing of the airway. Structural changes include a reduced number of airway channels, as well as narrowed cross-sectional airway caliber. In this already narrowed tapering network of tubes, the additional reduction of airway caliber caused by mucosal edema, functional compression, increased bronchomotor tone, or secretion accumulation noticeably increases the work of breathing because resistance relates linearly to the airway length but inversely to the fourth power of airway radius. For similar reasons, resistance within these critically narrowed airways is highly volume dependent, so that loss of lung volume is accompanied by loss of elastic recoil tension, reduction of cross-sectional area, tendency for expiratory airway collapse, and major increases in the frictional workload.1,2

Although each factor just enumerated contributes to AO, functional compression of the airway during exhalation is of overriding importance in many patients with components of emphysema or vigorous expiratory effort. Loss of elastic recoil encourages collapse of these narrowed bronchi as their transluminal distending pressure gradients decline (or reverse) during the course of exhalation. In most patients who require mechanical ventilatory support, dynamic airway collapse occurs even during tidal breathing, so the average airway resistance is often several times higher during exhalation than during the inspiratory phase of ventilation. This compressive mechanism underlies the phenomenon of air trapping and such hyperinflation-related consequences as loss of inspiratory power and reduced compliance of the respiratory system.

Dynamic Hyperinflation (Air Trapping)

Expiration is normally a passive process that uses elastic energy stored during inflation to drive expiratory airflow. If the energy potential stored during inflation is insufficient to return the system to a relaxed equilibrium before the next inspiration begins, flow continues throughout expiration and alveolar pressure remains positive at end expiration, exceeding the clinician-selected PEEP value (Fig. 10.2).^3–9 This positive distending pressure within the alveoli increases the driving pressure for expiratory airflow and increases lung volume, thereby helping to overcome airflow resistance. Unfortunately, such hyperinflation also places the expiratory musculature at a mechanical disadvantage. Furthermore, because the hyperinflating end-expiratory alveolar pressure encourages deflation, it must first be counterbalanced by positive pressure applied to the central airway or by negative pleural pressure before inspiration can begin.^10,11 Thus PEEPi adds to the other components of the equation of motion to elevate the mean inflation pressure and inspiratory work of breathing. The process of air trapping contributes to an increase in the respiratory work of breathing in at least two other ways. Hyperinflation drives the respiratory system upward toward the least compliant portion of the pressure-volume relationship, incurring increased elastic work per liter of ventilation (see Fig. 10.1). At these higher volumes the lung approaches its elastic limit as the recoil tension of the distended rib cage becomes expiratory rather than inspiratory in nature. Finally, hyperinflation tends to convert more of the well-perfused (“zone 3”) lung into less-well-perfused tissue, thereby increasing ventilatory deadspace and the minute ventilation requirement.

Figure 10.2 The auto–positive end-expiratory pressure (PEEP) effect. Auto-PEEP is the positive flow driving the difference between alveolar and airway opening pressures at end expiration. As depicted here, it can vary widely from site to site within the lung.

Generally, the resistance increase in patients with chronic AO and many of those with severe asthma concentrates within small airways.¹ Yet for certain asthmatic patients, the central airways and larynx contribute impressively to total resistance, accounting for the helpfulness of helium-oxygen (heliox) mixtures in some (but not all) patients during exacerbated asthma.¹² According to some reports, heliox helps to reduce air trapping in patients with COPD as well. Although there is some concern regarding the generalizability and accuracy of such observations, several mechanisms can be invoked, even if the primary site of expiratory obstruction is too peripheral for helium to reduce resistance there. These mechanisms include reduced inspiratory turbulence, faster expiratory flow in non–flow-limited channels with increased wave speed, modestly decreased CO₂ production, and perhaps reduced associated gas trapping.

Of note, dynamically positive end-expiratory alveolar pressure can also exist without hyperinflation, provided that airway collapse does not occur. In these instances expiratory muscle contraction increases pleural pressure, alveolar pressure, and the speed of expiratory airflow, obviating the need for hyperinflation to complete exhalation in the allotted time. Such mechanisms are employed by normal subjects during heavy exercise or when faced with major respiratory workloads. Indeed, many untrained normal subjects expire to positions below the equilibrium point of the respiratory system when exposed to PEEP. In this way the respiratory muscles can begin contraction from a mechanically advantageous position, and the expiratory muscles can share in the ventilatory work. Using this strategy, PEEP actually provides a boost to inspiration, experienced early in the cycle when the expiratory muscles relax. This “work-sharing” strategy, although effective for a normal individual, cannot be implemented by patients who experience dynamic airway collapse during tidal breathing. Because forceful expiratory efforts succeed not only in raising alveolar pressure but also in intensifying dynamic airway collapse, flow rate is determined strictly by lung volume and is not accelerated by expiratory muscle activity after the first third of expiration has been completed.

When dynamic collapse occurs during tidal respiration and breathing requirements are high, there is little alternative to hyperinflation, CO₂ retention, or both. At the chosen level of minute ventilation, maintaining the lower lung volume may be either too energy costly or physically impossible. For this reason, many patients with severe obstruction do not or cannot decrease their lung volumes when recumbent. Such considerations may help to explain the dyspnea experienced by most patients with severe AO on assuming horizontal positions. For the same recumbent angle, the lateral position allows slightly more decompression than does the supine position because lung volume influences airway caliber, airway resistance, and tendency for collapse as the lung deflates.¹³ Patients with obesity have a lower resting lung volume and therefore exhibit higher airway resistance and tendency for dependent atelectasis and symptoms when airways are narrowed by bronchoconstriction or disease. Likewise, patients with acute respiratory distress syndrome have higher than normal airway resistance in dependent zones.

In fact, the distribution of gas trapping varies regionally throughout any diseased lung, depending on the local mechanical properties of the airways. Therefore, at the end of the expiratory cycle some zones remain patent, and some have sealed much earlier in the deflation cycle (see Fig. 10.2). Consequently, the end-expiratory value of auto-PEEP detected at the airway opening may not reflect the magnitude of gas trapping.¹⁴ Clues to the presence of regional closure are often seen when the airway is occluded at end expiration; the auto-PEEP value shows an atypically slow rise to its final value as quasi-occluded small airways decompress into the common airway. In such cases, PEEP often eliminates this characteristic. During volume-controlled ventilation, plateau pressure tracks hyperinflation more reliably than direct measurements of PEEPi.

In some patients, especially those who passively receive ventilatory support, the problems presented by air trapping and dynamic hyperinflation are as much cardiovascular as pulmonary in nature. A relatively high fraction of the resulting positive alveolar pressure is transmitted to the pleural space, where it impedes venous return and confuses interpretation of hemodynamic pressure measurements made with pulmonary artery catheters (Fig. 10.3). Lung distention also adds to pulmonary vascular resistance, exacerbating the tendencies of patients with cor pulmonale toward low cardiac output and hypotension. Marked respiratory variation of systolic and pulse pressures during passive inflation indicates phasically adverse cardiac loading and strongly implies the possibility of dynamic hyperinflation (Fig. 10.4).

Figure 10.3 The hemodynamic impact of auto-PEEP (positive end-expiratory pressure) in a passively ventilated patient with severe airflow obstruction. A 40-second disconnection of the ventilator was associated with rising blood pressure and cardiac output despite a falling pulmonary artery wedge pressure.

Figure 10.4 Marked respiratory variation of systemic arterial blood pressure, indicative of the relative variation in cardiac loading conditions associated with dynamic hyperinflation. PP, pulse pressure. (From Michard F, Teboul J-L: Using heart-lung interactions to assess fluid responsiveness during mechanical ventilation. Crit Care 2000;4:282-289.)

Increased Minute Ventilation Requirement

Ventilation-perfusion () mismatching is widespread in patients with severe AO, reducing the efficiency of carbon dioxide elimination.¹ It is not uncommon for the resting minute ventilation requirement to exceed 12 L per minute (twice the normal value) in patients with exacerbated asthma or extensive emphysema and strong chemical drives to breathe. Not only do such increases in ventilation requirement act as a linear cofactor in the work of the breathing equation already discussed, but the high minute ventilation requirement itself increases most components of inspiratory pressure: flow, elastance (the reciprocal of compliance), tidal volume, and auto-PEEP. It is not surprising, therefore, that enormous increases in the oxygen consumption rate of the ventilatory muscles have been observed in patients with obstructive lung disease. During exacerbations, the oxygen consumed by ventilation and the metabolic demands associated with heightened vigilance, agitation, or anxiety may double the total body oxygen consumption observed during fully supported breathing. The prevalent combination of impaired matching, hypoventilation, and diffusion impairment result in arterial oxygen desaturation that generally responds well to modest supplementation of inspired oxygen.

Reduced Mechanical Efficiency

In patients with exacerbated COPD or decompensated asthma, the oxygen consumed in the ventilatory task is disproportionate to the amount of mechanical work actually performed. The muscles of the hyperinflated ventilatory system are inefficiently aligned, force-length relationships of the shortened end-inspiratory fibers are suboptimal, and normally efficient coordination among the various muscles of the ventilatory group is often disrupted.14–16 The energy cost of breathing, therefore, is greatly increased for the pressure and mechanical work actually generated by the breathing effort.

Problems and Hazards of Ventilation with Positive Pressure

Patients with AO who require mechanical ventilation present special challenges to the clinician for yet another reason: an unusual predisposition to its adverse consequences that are only loosely related to the airflow resistance. For reasons that are not entirely clear, patients with COPD have been reported to have an increased incidence of gastrointestinal ulceration and bleeding, especially during stress periods. This tendency is accentuated to an important degree by poor nutrition, stress, and the therapeutic use of high-dose corticosteroids. In modern intensive care unit practice, the incidence of ulceration has been greatly attenuated by the use of proton pump inhibitors and other means of acid suppression.

Even when able to cough with maximal force, patients with severe AO have difficulty in clearing contaminated secretions from the central and peripheral airways, predisposing to bronchial and lung infections. This tendency is accentuated when the airway is intubated or when noninvasive ventilation is provided with poorly humidified gas mixtures. These interventions accentuate the impediment to coughing efficiency, may encourage secretion thickening, and promote entry of contaminated secretions from the upper airway. In conjunction with mucus plugging, air trapping, and the tendency toward parenchymal infections, markedly inhomogeneous ventilation predisposes the ventilated patient with severe AO to the varied forms of barotrauma—pneumomediastinum, subcutaneous emphysema, and tension pneumothorax. Because the lungs cannot collapse, even a small pneumothorax in a ventilated patient with severe AO can rapidly develop a tension component, leading to ventilatory and circulatory compromise.

The hemodynamic sensitivity to positive-pressure ventilation of patients with AO arises for several reasons. The overexpanded lungs press outward on the chest wall, raising intrapleural pressure. When breathing efforts are silenced, as they are immediately after sedation and intubation, mean intrathoracic pressure abruptly changes from modestly negative to markedly positive. Increased pleural pressure raises the right atrial back-pressure to venous return. Simultaneously, increased peripheral vascular capacitance (caused in part by drug effects) and reduced peripheral vascular tone limit the rise in mean systemic pressure, the upstream driver of venous return. Blood pressure routinely falls, and cardiac output falls disproportionately to oxygen demand. Absolute values of measured central vascular pressures (central venous and wedge pressures) may therefore be misleadingly high and do not reflect intravascular filling and preload adequacy.⁷ Marked respiratory variation of systolic and pulse pressures with the ventilatory cycle (“paradox”) is a hemodynamic marker of relative hypovolemia caused by such mechanisms (see Fig. 10.4). Depending on choice of tidal volume, backup frequency, and set (and auto) PEEP, the afterload to right ventricular ejection may rise with any further lung expansion, whereas the tendency for alveolar deadspace creation is accentuated. Consequently, great care must be taken not to ventilate excessively and to provide adequate intravenous fluid support during this period. This advice pertains especially to patients with AO who require cardiac resuscitation.¹⁷

Interactions of Pressure-Targeted Modes with Auto-PEEP

Pressure-targeted modes of ventilation, exemplified by pressure control, airway pressure release ventilation (APRV), and pressure support, have become increasingly popular to employ in the care of intubated patients, as well as in those receiving noninvasive ventilation by facemask. Because the development of auto-PEEP reduces the pressure difference between airway opening and alveolus that drives inspiration, it has a powerful influence on ventilation efficacy (Fig. 10.5). As already described, auto-PEEP varies not only with airway mechanics but also with the pattern of breathing and minute ventilation. For a fixed value of applied airway pressure, inspiratory tidal volume in patients with AO will be more sensitive to the frequency and the inspiratory time fraction (an expression of the inspiratory-to-expiratory [I : E] ratio) than are normal subjects or those with restrictive disease¹⁸ (Fig. 10.6). Faster breathing frequencies, for example, allow auto-PEEP to build, and this auto-PEEP must first be counterbalanced for inspiratory airflow to begin. If the patient is passive or the amount of inspiratory muscle force remains constant, delivered tidal volume falls as the auto-PEEP builds.

Figure 10.5 Interaction of alveolar (red line) and applied airway (fine line) pressures in a patient ventilated with pressure-targeted ventilation. Auto-PEEP diminishes the driving pressure of the subsequent ventilatory cycle.

Figure 10.6 Relative sensitivity of patients with airflow obstruction to the settings of frequency and inspiratory time fraction for a fixed pressure target in pressure-controlled ventilation. This sensitivity is induced primarily by the impact of these settings on auto-PEEP (positive end-expiratory pressure).

This auto-PEEP/driving pressure interaction may result in an intriguing phenomenon resembling chaotic respiration during noninvasive ventilation with a leaky mask interface.¹⁹ The coupled PEEPi and tidal volume form a “feed-forward” system in which a building auto-PEEP of one cycle adversely influences the tidal volume of the next one. But this smaller tidal volume also reduces the auto-PEEP that follows that restricted cycle, which in turn allows the subsequent breath—the third in the cycle—to have a larger effective driving pressure and tidal volume, and the cycling variation continues. This may account for some of the wide variability in breathing rhythm often observed in these patients.²⁰ If the mask leak volume is a function of the I : E ratio, it can be shown mathematically and experimentally that fractal and chaotic tidal volume delivery may occur, even when the patient’s effort and mechanics remain unchanged (Fig. 10.7).¹⁹ The consequences for comfort and sleep efficiency are likely to be significant, but clinical data are lacking on these issues at this time.