Supplemental oxygen should be administered to maintain Spo2 greater than 88% in both asthma and COPD. Asthma rarely leads to severe hypoxemia unless it is associated with another pulmonary condition such as lobar pneumonia or there is significant hypoventilation and hypercarbia. For patients with COPD, the administration of supplemental oxygen can lead to excessive hypercarbia, a condition termed hyperoxic hypercarbia. In addition to the well-known decrease in minute ventilation that can occur because of the relief of the patient’s hypoxic drive (or inducing sleep), it is thought that supplemental oxygen can cause hypercarbia by releasing CO2 from hemoglobin (Haldane effect), increasing dead-space fraction by releasing hypoxic pulmonary vasoconstriction in poorly ventilated areas (thus worsening V/Q mismatch) and causing bronchodilation from a direct effect of CO2 on the airway. When supplemental oxygen is given by face mask, these effects can be magnified because patients decrease their minute ventilation and entrain less air.
Helium is less dense than is nitrogen and has nearly the same viscosity; so, theoretically, a mixture of helium and oxygen should reduce turbulence in airways, thus allowing more gas for the same pressure gradient. In both asthma and COPD, helium-oxygen mixtures have been used with varying success. Studies have been inconclusive when using helium-oxygen delivered by face mask or by ventilator, and no definite conclusions can be made regarding its efficacy in either condition. Overall, the evidence appears weaker in COPD than in asthma, either for improving ventilation or when used to drive impact nebulizers. It should be noted that because of the differences in density of helium-oxygen mixtures versus nitrogen-oxygen mixtures, mechanical ventilator flow sensors need to be calibrated for helium-oxygen for proper functioning. A recent meta-analysis of 11 trials in adults and children of driving nebulizers with helium-oxygen mixtures appeared to show benefits in improvement of airflow limitation and hospital admission (number needed to treat to prevent one admission = 9) when given in the emergency room for acute asthma.
For asthma, where increased mucus production is part of the pathophysiology of airway obstruction, it might seem that bronchoscopy would be a valuable tool, especially in patients on mechanical ventilation. In fact, there was initial enthusiasm for the use of bronchoscopy in asthma, but this was tempered by reports of bronchoscopy-induced bronchospasm in patients with asthma receiving bronchoscopy for reasons not necessarily related to their asthma. It was postulated that the severe bronchospasm was caused by mechanical stimulation of vagal afferents in the airway by the bronchoscope. A subsequent study found bronchospasm in only 1 of 10 patients with mild asthma undergoing bronchoscopy and no change in FEV1 after the procedure in any of the subjects. These subjects were pretreated with aminophylline before the procedure, and all had a history of only mild asthma. Subsequently, there have been multiple case reports of successful bronchoscopic lavage, sometimes with acetylcysteine or deoxyribonuclease (DNAse), to improve lung function among patients with asthma who are intubated. Overall, it appears from a limited number of cases that bronchoscopy with lavage in patients with asthma on mechanical ventilation is well tolerated and can result in improvements in lung mechanics. However, data are too limited to make any definitive conclusions about the role of bronchoscopy in the routine care of patients in the ICU with an asthma exacerbation. For respiratory failure caused by COPD, there has not been any study showing benefit with the use of bronchoscopy as a therapeutic tool.
Mechanical ventilation aims to decrease the patient’s work of breathing and support gas exchange. Work of breathing is increased during acute exacerbation of asthma or COPD due to both increased resistive and elastic load. Airway narrowing increases resistive work, whereas air trapping and increased lung volumes increase elastic work. The latter occurs because expiratory flow obstruction and dynamic hyperinflation place the respiratory system on a less compliant part of its pressure-volume curve, thereby increasing the elastic component of the work of breathing. Ventilator management must balance the goal to achieve adequate oxygenation (Spo2 = 88%-92%) and ventilation with avoidance of further hyperinflation and barotrauma.
Because of the increase in airway resistance and, in COPD, also compliance, the time constant of the respiratory system (equal to the product of resistance and compliance) is increased in patients with obstructive lung disease, especially during acute exacerbations. Consequently, the expiratory time may not be sufficient to allow complete lung emptying, resulting in an increase in end-expiratory lung volume above functional residual capacity (or equilibrium volume if positive end-expiratory pressure [PEEP] is applied). This is known as dynamic hyperinflation. Accordingly, alveolar pressure is higher than is the pressure at the airway opening at the end of expiration and this increase is termed “auto” (or “intrinsic”) PEEP. Note that although dynamic hyperinflation is always accompanied by auto-PEEP, auto-PEEP can also occur without hyperinflation or even at an end-expiratory volume lower than functional residual capacity in a subject who is actively exhaling. For example, patients with very low respiratory compliance and impending respiratory failure (eg, acute respiratory distress syndrome [ARDS]) may use the expiratory muscles to “push” the respiratory system below functional residual capacity at end exhalation, such that the first phase of the ensuing inspiration is passive because it is driven by the outer recoil of the respiratory system. This “work sharing” is a protective mechanism to partly unload the fatigued inspiratory muscles at the expense of the expiratory muscles.
Signs of auto-PEEP include the following: (i) Inspiratory efforts by the patient that do not trigger the ventilator (patient-ventilator dyssynchrony) because auto-PEEP essentially acts as an additional pressure trigger; (ii) expiratory flow does not reach zero before the next inspiration. However, in the presence of flow limitation, end-expiratory flow can be minuscule despite significant auto-PEEP; or (iii) a biphasic expiratory flow pattern (sharp spike followed by almost a plateau at a very low flow rate) caused by rapid emptying of a small volume of gas from the large airways followed by a very slow emptying of distal alveoli.
Given that expiration is either passive or flow is not increased by activation of expiratory muscles in the presence of flow limitation, the only strategies to decrease dynamic hyperinflation at a given minute ventilation are (i) relief of bronchoconstriction (eg, β2-agonists); (ii) reduction of the inspiratory-to-expiratory time ratio, with ensuing prolongation of expiratory time; and (iii) possibly, use of a helium-oxygen gas mixture.
There is no general agreement as to whether PEEP should be used in airflow obstruction. Part of this lack of consensus stems from the fact that whether PEEP has a beneficial or detrimental effect on respiratory mechanics in this setting depends on the underlying mechanism of auto-PEEP.
When the underlying pathophysiologic mechanism for auto-PEEP is expiratory flow limitation, PEEP will not impair expiratory flow until the critical pressure at the “choke point” is reached. This pressure has been reported to range from 70% to 85% of auto-PEEP. Consequently, setting PEEP up to 70% of auto-PEEP measured at zero end-expiratory pressure will not cause substantial further hyperinflation and will instead decrease the work of breathing in a patient who is spontaneously breathing and decrease the pressure that the inspiratory muscles must generate to trigger the ventilator. In a patient on controlled, rather than assisted, ventilation, applying PEEP up to 70% of auto-PEEP may still be beneficial because it favors a more uniform distribution of tidal volume. In fact, the value of auto-PEEP measured with an end-expiratory pause is the average of many different values of individual respiratory units. When inspiration starts from zero end-expiratory pressure, units with the lowest auto-PEEP receive proportionally more tidal volume than those with the highest auto-PEEP, which start to inflate only later during inhalation. In this setting, PEEP acts as an “equalizer” of auto-PEEP within individual lung units, promoting more uniform distribution of ventilation and improved (V/Q) matching.
If, instead, auto-PEEP is due to airflow obstruction without flow limitation (ie, there is no “flutter”/“waterfall” mechanism), then extrinsic PEEP will be transmitted all the way up to the alveoli and will result in further hyperinflation, increased (elastic) work of breathing, and hypotension.
From the earlier discussion, it follows that the clinician must determine whether the patient is flow limited to decide whether and how much PEEP to apply. The classical method of obtaining isovolume pressure-flow curves by changing pressure at the airway opening while measuring flow at a given absolute lung volume has been applied in patients with COPD on mechanical ventilation. Signs indicative of expiratory flow limitation include the following: (i) a biphasic expiratory flow-volume curve showing a sharp peak expiratory flow that falls abruptly to a much lower flow (Figure 21.2), which then decreases linearly with exhaled volume at a very slow rate; (ii) the value of end-expiratory flow does not decrease substantially when expiratory time is prolonged, that is, even with very long expiratory times it is hard to reach zero flow; (iii) if PEEP is applied stepwise, inspiratory plateau pressure will not increase until the critical pressure threshold is achieved. This test can also be used to set PEEP at the highest value that will not cause a significant increase in plateau pressure when an end-expiratory hold button is not available; (iv) if an end-expiratory hold can be performed with the ventilator, stepwise application of PEEP will result in a decrease of auto-PEEP of similar magnitude to the increase in PEEP until flow limitation is reversed (usually 70%-85% of auto-PEEP at zero end-expiratory pressure).
Permissive hypercapnia was originally conceived as a strategy for the ventilation of patients with acute severe asthma, in whom the goal was no longer to restore adequate alveolar ventilation and Paco2 but to limit airway pressures to avoid barotrauma (eg, pneumothorax) and cardiocirculatory failure. It is implemented by reduction of tidal volume to 4 to 6 mL/kg and reduction of respiratory rate with prolongation of expiratory time. Paco2 of 60 to 80 mm Hg and pH as low as 7.15 are considered acceptable in the absence of contraindications such as intracranial hypertension. The main side effects of this strategy are as follows:
For patients with acute severe asthma and hypoxemia or hypercapnia that is refractory to other therapies, extracorporeal membrane oxygenation (ECMO) or extracorporeal CO2 removal (ECCO2R) has been used successfully to maintain gas exchange. More recently, extracorporeal techniques have been used to allow early extubation, ambulation, and weaning and to prevent intubation in patients failing NPPV or awaiting lung transplantation.