The challenge of mechanically ventilating a patient with COPD can be met by preventing autoPEEP and dynamic hyperinflation.
During the past 10 years, much of the focus in mechanical ventilation has been on preventing ventilator-induced lung injury and on optimizing care for patients with the preventing ventilator-induced lung injury and on optimizing care for patients with the adult respiratory distress syndrome (ARDS).1 Ventilatory support of the patient with chronic obstructive pulmonary disease (COPD) differs greatly from that of the ARDS patient and remains a challenge. While noninvasive positive-pressure ventilation (NPPV) is now considered the first choice for the treatment of selected patients experiencing COPD exacerbations, there are some patients for whom NPPV may not be suitable due to the severity of their conditions.2
Pathophysiology of COPD Severe airflow obstruction that imposes a significant load on the respiratory system is a major manifestation of COPD. Airflow obstruction develops when the airway diameter is narrowed by bronchospasm, mucosal or interstitial edema, and mucus, causing dynamic airway collapse during exhalation. This increases the time required for exhalation, thus elevating lung volume and alveolar pressure; end-expiratory lung volume (EELV) exceeds functional residual capacity. In contrast, EELV in individuals without COPD approximates the relaxed volume of the respiratory system. The term dynamic hyperinflation is used to describe this phenomenon of increased lung volume and is associated with the increased work of breathing (WOB) and the hypercapneic state observed in the COPD patient.3,4
The reduced expiratory airflow also causes air trapping at the end of expiration, producing alveolar pressures that are higher than atmospheric pressure before the next breath. This condition is intrinsic positive end-expiratory pressure (PEEP) or autoPEEP.
AutoPEEP increases inspiratory effort due to the greater drop in intrathoracic pressure needed to bring the alveolar pressure below that of the atmosphere. In addition, expiration becomes a struggle as more muscle work is required to expel the trapped air in the lungs.5
Aggravation of COPD worsens the situation, as muscular reserves in these individuals are limited. Hypoxemia-induced tachypnea, for example, reduces both inspiratory and expiratory times, decreasing end-inspiratory volume and further increasing EELV, dynamic hyperinflation, and the autoPEEP phenomenon. Shallow tidal volumes contribute to greater dead-space ventilation and, along with the increased WOB, elevate Paco2 levels beyond renal compensation capabilities.6 These signs are all indicative of decompensation, contributing to respiratory muscle fatigue and imminent respiratory failure.
Intubation and Mechanical Ventilation
Current medical opinion favors the use of NPPV and the avoidance of intubation and mechanical ventilation in the COPD patient due to the complications that may arise. More invasive treatment may be necessary, however, when an acute exacerbation involves worsening respiratory acidosis, despite aggressive medical therapy; inability to cough, with retained secretions; unstable hemodynamics; and deteriorating mental status.
Mechanical ventilation is also essential for postoperative COPD patients (particularly those who have undergone cardiac, lobectomy, lung-reduction, or bullectomy procedures). In providing ventilatory support for the COPD patient, the main goals are to alleviate respiratory fatigue; improve gas exchange, restoring it to the patients observed baseline level; and avoid or prevent further aggravation of dynamic hyperinflation and/or autoPEEP that might lead to cardiovascular compromise. It is precisely this combination of elements that makes ventilatory management of the COPD patient a challenge.7
Alleviating respiratory muscle fatigue may be accomplished using any mode available on the ventilator, but the choice may vary with the status of the COPD patient. For the obtunded or postoperative patient, pressure-support ventilation (PSV) is clearly unsuitable, since he or she is unlikely to make any spontaneous efforts. Therefore, either assist-control or synchronized intermittent mandatory ventilation (SIMV), with either volume or pressure targets, should be used. High inspiratory flow rates are preferred in order to reduce the inspiratory-expiratory (I:E) ratio, thus allowing more time for expiration. If the patients respiratory drive is still present after intubation, the use of PSV or of SIMV with a low rate is preferable, as this is less likely to induce or worsen any preexisting dynamic hyperinflation and autoPEEP.8 The aim is to wean the patient as soon as possible after sufficient time has elapsed to rest the respiratory muscles and to permit various medical therapies (such as bronchodilators, cortico-steroids, antibiotics, chest physiotherapy, and endotracheal suction) to take effect.
One of the hazards of assuming control of ventilation in the COPD patient is simply overventilation. In an attempt to improve acute respiratory failure, the clinician may overlook the preexisting acid-base status of the COPD patient and may ventilate the individual using normal minute volumes. Moreover, in the presence of dynamic hyperinflation and autoPEEP, acute respiratory acidosis (increased Paco2) often prevails, prompting the clinician to increase the respiratory rate and/or tidal volume.9 This action may worsen the Paco2 level, as additional air trapping is promoted by the reduced expiratory time allowed by the increases in respiratory rate or tidal volume that the clinician made. WOB becomes greater, with laborious inspiratory efforts required to drop the elevated intrathoracic pressure below that of the atmosphere. Patient-ventilator dyssynchrony may occur, since the pressure drop across the airway may not be enough to trigger the ventilator.
If the Paco2 is normalized to 40 mm Hg, acute alkalemia ensues due to the higher bicarbonate levels maintained in the COPD state. This alkalemia is a problem, as it prolongs mechanical ventilation by depressing the respiratory center and increasing respiratory-muscle weakness. Continuing mechanical ventilation in this manner for 2 to 3 days would facilitate renal excretion of bicarbonate, thereby returning the acid-base status of the COPD patient to normal. Unfortunately, when weaning is attempted, the patient is likely to develop acute respiratory acidosis or respiratory failure.
Other complications such as hypotension, reduced cardiac output, and barotrauma may arise (if not already present) due to the effects of dynamic hyperinflation and autoPEEP in the ventilated COPD patient. With overzealous ventilation, dynamic hyperinflation and autoPEEP effects are accentuated, thus impeding venous return and compressing the right ventricle and pulmonary veins. Left ventricular preloading is reduced, cardiac output drops, and hypotension develops.10 Barotrauma is a condition that manifests itself primarily following the overdistension of lungs with acute (ARDS) or chronic (COPD) disease. Dynamic hyperinflation and autoPEEP contribute to this problem by amplifying the already reduced airflow and increased expiratory time of COPD patients. Hyperinflated alveolar lung units may leak or rupture from the increasing volume and pressure, thus leading to pneumothoraces or bronchopleural fistulae.11
Monitoring ventilatory and physiological parameters is of particular importance in guiding the direction of ventilator changes. As the phenomenon of autoPEEP is of great concern in the ventilated COPD patient, attention should be paid to the observation required to detect autoPEEP (the difference between the ventilator-set PEEP and the total PEEP measured when all airflow has stopped). This is equivalent to the average alveolar pressure. Quantifying autoPEEP, though, is not a precise process. AutoPEEP can vary among individual lung units due to different degrees of obstruction; autoPEEP is not uniformly distributed throughout the lung, but varies in direct proportion to the airway resistance present in a particular lung unit. The amount of autoPEEP is not synonymous with airflow obstruction, since it may also be attributable to high minute ventilation.12 AutoPEEP adds to WOB, which can increase the threshold load for inspiration and increase the workload expended to trigger a breath. In this case, increasing the ventilator-set PEEP to 80% of the autoPEEP level can dramatically improve the triggering variable of a spontaneous or assisted breath. WOB is diminished as the pressure-gradient drop required to initiate inspiration is reduced.
A number of methods can be used to detect autoPEEP in the mechanically ventilated patient. On some ventilators, a 2-second pause can be invoked following the end of expiration. This technique, however, is valid only if the patient is not breathing spontaneously. This limits the procedures application to the heavily sedated, paralyzed, or physically exhausted COPD patient. An esophageal balloon avoids this problem, but may not be readily available in all hospital intensive care units. If the patient has a central venous pressure (CVP) line, autoPEEP effects can be detected due to the increased WOB reflected by greater changes in pleural pressure (which are transmitted to intrathoracic blood vessels and can be measured via CVP or pulmonary artery catheter). Thus, a large decrease in CVP during a spontaneous or assisted breath suggests that a high inspiratory threshold is needed to trigger the ventilator.
AutoPEEP can also be detected on ventilators equipped with graphic waveform monitoring. Although not readily quantifiable, autoPEEP is easily recognized on the expiratory portion of the flow waveform. If expiratory flow does not return to zero before the next inspiration, autoPEEP is present. For patients who are making spontaneous efforts to breathe, observing their respiratory efforts and the ventilators response is another useful technique, provided the ventilators sensitivity is set correctly (at -1 cm H2O or on flow triggering). Since autoPEEP increases the pressure gradient required to inhale, the patients effort may not be able to trigger the ventilator; the result is a missed breath or cycle. Clinical signs associated with autoPEEP (in patients making spontaneous efforts to breathe) include accessory muscle use, retractions, and increased ventilatory drive.
To limit dynamic hyperinflation and autoPEEP in the ventilated COPD patient, permissive hypercapnia1 is probably the most desirable approach. As the term implies, higher Paco2 levels are allowed. Low tidal volumes limit peak alveolar (plateau) pressure to less than 30 cm H2O for patients with COPD.13 With a lower tidal volume, I:E ratio is decreased, allowing longer expiration so that the hyperinflated COPD lung can empty. Consequently, this method is unlikely to induce alkalemia, cause or aggravate dynamic hyperinflation and autoPEEP, or overdistend the alveolar lung units in the ventilated COPD patient. Reducing respiratory rate and increasing inspiratory flow also increase expiratory time and facilitate emptying of the lung. Other techniques used to decrease the amount of autoPEEP include increasing the ventilator-set PEEP, giving bronchodilator therapy, and removing secretions.
Dynamic hyperinflation, autoPEEP, and their associated complications (including persistent respiratory acidosis, hypotension, and barotrauma) are more likely to occur with improper ventilatory management of the COPD patient. The cardinal problem is overventilation, which leads to several disturbances. Acute alkalemia, for example, can be avoided if the preexisting, compensated acid-base status of the COPD patient is maintained. With this goal in mind, ventilator settings should be adjusted not to normalize Paco2, but to achieve a near normal pH. This technique deters the renal excretion of bicarbonate (the level of which is elevated in response to the insufficient elimination of Paco2 by the patient with COPD). Maintenance of this elevated bicarbonate level will prevent the development of acute respiratory acidosis during weaning from mechanical ventilation.14
Marvin Mah, RRT, is an RCP in the Department of Respiratory and Critical Care, Singapore General Hospital, Singapore. Graeme ACourt RRT, is a manufacturers clinical ventilation consultant based in Singapore.
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