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Severe Obstructive Lung Disease 

Severe Obstructive Lung Disease
Chapter:
Severe Obstructive Lung Disease
Author(s):

John W. Kreit

DOI:
10.1093/med/9780190670085.003.0013
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date: 03 July 2020

Although COPD, asthma, bronchiectasis, and bronchiolitis have very different causes, clinical features, and therapies, they share the same underlying pathophysiology. They are referred to as obstructive lung diseases because airway narrowing causes increased resistance and slowing of expiratory gas flow. Mechanical ventilation of patients with severe obstructive lung disease often produces two problems that must be recognized and effectively managed: over-ventilation and dynamic hyperinflation.

Over-Ventilation

Here, I’m referring to excessive minute ventilation in patients with chronic, compensated hypercapnia that reduces the PaCO2 below the patient’s baseline (but not necessarily below normal). This causes alkalemia due to an apparent metabolic alkalosis. Over a period of several days, reduced renal bicarbonate reclamation and regeneration will decrease the serum bicarbonate concentration and return the blood pH toward normal. The problem is that this eliminates the metabolic compensation required for the patient to maintain their usual PaCO2.

Let’s look at an example. A patient with severe COPD has a baseline PaCO2 of 80 mmHg, a serum bicarbonate concentration of 40 meq/L, and an arterial pH of 7.30. He is admitted to the ICU with a COPD exacerbation that has caused his PaCO2 to increase to 100 mmHg and his pH to fall to 7.14. He is intubated and ventilated using CMV-VC with a set, mandatory rate of 18, and he does not trigger any spontaneous breaths. About a half-hour after intubation, blood gas measurements show a PaCO2 of 60 mmHg, a calculated bicarbonate concentration of 40 meq/L, and a pH of 7.46. Several days later, his PaCO2 is still 60 mmHg, but the bicarbonate concentration has fallen to 32 meq/L, and the pH has dropped to 7.38.

So what’s the problem? The problem is that when you decide that the patient’s respiratory status has returned to baseline and perform a spontaneous breathing trial, his PaCO2 will acutely increase back to its baseline level of 80 mmHg, his pH will fall to 7.22, and he will be placed back on CMV. You can see that the patient will never get off the ventilator because he no longer has the metabolic compensation needed for his baseline minute ventilation and PaCO2.

Fortunately, the vast majority of patients with chronic hypercapnia will maintain their baseline PaCO2 during mechanical ventilation, if you let them. Unfortunately, as in the case I just described, an inappropriately high set respiratory rate and failure to recognize its consequences are common. Consequently, this is also a common cause of chronic ventilator-dependence in patients with severe obstructive lung disease.

So how do you avoid this problem? First, determine your patient’s baseline PaCO2. Look at their blood gas measurements for the past few years. If there aren’t any, look at their serum bicarbonate (or total CO2) concentrations. If they’re chronically elevated, you can be pretty sure that the patient has chronic hypercapnia. You can estimate the baseline PaCO2 by assuming that chronic respiratory acidosis causes the serum bicarbonate concentration to increase by about 4 meq/L (from 24 meq/L) for every 10 mmHg elevation (from 40 mmHg) in the PaCO2. For example, a patient with a chronic serum bicarbonate concentration of 36 meq/L would be expected to have a PaCO2 of about 70 mmHg. Second, make sure that you set a low mandatory rate. Many patients with chronic hypercapnia only need 6–10 breaths per minute. The best way to avoid over-ventilation is to make sure that the patient always triggers spontaneous breaths. This can easily be confirmed by noting that the total respiratory rate exceeds the set rate on the ventilator–user interface.

Dynamic Hyperinflation

Since a lot of time is needed for complete exhalation, patients with severe air flow obstruction are likely to receive or trigger another mechanical breath before the respiratory system has returned to its resting or equilibrium volume. This is referred to as dynamic hyperinflation, and this topic was covered in Chapter 10. The more end-expiratory lung volume exceeds the equilibrium volume, the greater the remaining elastic recoil and the higher the alveolar (elastic recoil) pressure. This end-expiratory alveolar pressure is called total PEEP (PEEPT), and the difference between total and set (extrinsic) PEEP (PEEPE) is called intrinsic PEEP (PEEPI).

Both the presence and severity of air flow obstruction and dynamic hyperinflation can be determined by examining the flow–time curve on the ventilator user interface. As shown in Figure 13.1, as obstruction worsens, it takes more and more time for complete exhalation to occur. Dynamic hyperinflation and PEEPI must be present if a mechanical breath occurs before expiratory flow reaches zero.

Figure 13.1 Inspiratory (Insp) and expiratory (Exp) flow curves in patients with mild, moderate, and severe obstructive lung disease. Dynamic hyperinflation and PEEPI are present when the next mechanical breath occurs before expiratory flow reaches zero (arrow).

Figure 13.1 Inspiratory (Insp) and expiratory (Exp) flow curves in patients with mild, moderate, and severe obstructive lung disease. Dynamic hyperinflation and PEEPI are present when the next mechanical breath occurs before expiratory flow reaches zero (arrow).

As discussed in Chapter 3, both PEEPI and PEEPE increase pleural pressure (PPL) and intramural right atrial pressure (PraIM) throughout the respiratory cycle. This reduces venous return, which can decrease cardiac output and blood pressure. It’s long been recognized that hypotension is much more likely to occur with intrinsic than extrinsic PEEP, but it’s important to understand that the type of PEEP is irrelevant. What matters is the clinical setting in which it occurs (Figure 13.2). Extrinsic PEEP is used to improve oxygenation in patients with ARDS. Since compliance is low, the increase in lung volume and PPL produced by a given PEEP level is small, PPL remains negative (sub-atmospheric) throughout inspiration, and hemodynamic effects are typically small or absent. On the other hand, since PEEPI occurs in patients with normal or high (emphysema) lung compliance, the same level of PEEP causes a larger increase in lung volume and PPL, and adverse hemodynamic effects are common.

Figure 13.2 The relationship between lung volume and alveolar (PALV), pleural (PPL), and lung transmural (PlTM) pressure in a patient with low lung compliance and extrinsic PEEP (PEEPE) (A), and a patient with obstructive lung disease, normal lung compliance, and intrinsic PEEP (PEEPI) (B). PEEP causes a larger increase (∆V) in end-expiratory volume (VEE) and pleural pressure (∆PPL-1) when lung compliance is normal. During tidal inflation (VT), PPL is much more likely to be positive (∆PPL-2) when lung compliance is normal.

Figure 13.2 The relationship between lung volume and alveolar (PALV), pleural (PPL), and lung transmural (PlTM) pressure in a patient with low lung compliance and extrinsic PEEP (PEEPE) (A), and a patient with obstructive lung disease, normal lung compliance, and intrinsic PEEP (PEEPI) (B). PEEP causes a larger increase (∆V) in end-expiratory volume (VEE) and pleural pressure (∆PPL-1) when lung compliance is normal. During tidal inflation (VT), PPL is much more likely to be positive (∆PPL-2) when lung compliance is normal.

As dynamic hyperinflation worsens and PEEPI increases, patients with obstructive lung disease are more and more likely to develop hypotension. Although this may happen at any time, it’s most common immediately after intubation, and there are several reasons for this. First, patients are often volume-depleted because empiric diuresis is commonly used in an attempt to treat possible congestive heart failure and stave off intubation. Second, sedative-hypnotics, narcotics, and anesthetics directly dilate systemic arterioles while eliminating respiratory distress–induced adrenergic activation. Finally, over-zealous manual bag-mask ventilation or an excessively high set respiratory rate may cause or worsen dynamic hyperinflation. By generating high levels of PEEPI and PPL, this may markedly reduce venous return and even cause pulseless electrical activity (PEA).

Dynamic hyperinflation may also interfere with effective ventilator triggering by producing a “threshold load” on the respiratory muscles (Chapters 10 and 11). When the respiratory system is above its equilibrium volume, a patient trying to trigger a mechanical breath must first stop expiratory flow by generating pressure equal to PEEPI. Additional pressure must then be supplied to lower airway pressure or the base flow sufficiently to trigger a mechanical breath.

Mechanical Ventilation

Recommended initial settings are shown in Table 13.1. As in other critically ill patients with respiratory failure, it’s important to provide a guaranteed tidal volume and minute ventilation, so I recommend using the CMV mode with volume control (VC) or adaptive pressure control (aPC) breaths. It’s also essential to correct arterial hypoxemia. Most patients have a modest supplemental oxygen requirement (e.g., 2–6 L/min) prior to intubation, and I routinely start these patients on an FIO2 of 0.5. If the patient has a higher oxygen requirement, an initial FIO2 of 1.0 is appropriate.

Table 13.1 Initial Ventilator Settings for Patients with Severe Obstructive Lung Disease

Mode

CMV

Breath type

VC or aPC

Tidal volume

6–8 ml/kg IBW

Respiratory rate

8

FIO2

0.5 or 1.0

PEEP

0 cmH2O

CMV = continuous mandatory ventilation; VC = volume control; aPC = adaptive pressure control; IBW = ideal body weight

As previously discussed, it’s important to start with a low mandatory rate that allows the patient to set their own minute ventilation. An unnecessarily high rate not only causes relative hypocapnia and bicarbonate excretion, it also reduces expiratory time and may precipitate or worsen dynamic hyperinflation and its hemodynamic consequences. Given the likelihood of dynamic hyperinflation, I do not use PEEPE in patients with severe obstructive lung disease.

Once mechanical ventilation has begun, assess for dynamic hyperinflation using the expiratory flow–time curve, measure PEEPI if dynamic hyperinflation is present, follow blood pressure closely, and obtain arterial blood gas measurements.

Reduce FIO2 as much as possible to maintain SpO2 in the range of 91–93%. Even if dynamic hyperinflation is present, no changes in the initial set rate or tidal volume are needed as long as ventilation is sufficient to keep the arterial pH above 7.20 and blood pressure remains normal. Reduce the set rate if pH exceeds 7.35. If blood pressure is normal and the arterial pH is less than 7.20, increase the set rate as needed to maintain pH ≥ 7.20.

If the patient develops hypotension following intubation, it’s important to consider other possible causes, even if dynamic hyperinflation is present. In general, the higher the PEEPI, the more likely it is to be causing or contributing to the hypotension. Dynamic hyperinflation is unlikely to be a contributing factor if PEEPI is ≤5 cmH2O. Intrinsic PEEP-induced hypotension can be diagnosed with certainty only if blood pressure rises rapidly during a brief period of spontaneous breathing. If clinically feasible and the patient has an arterial catheter, this can usually be determined by disconnecting the patient from the ventilator circuit for 10–15 seconds.

As discussed in Chapter 10, the treatment of intrinsic PEEP-induced hypotension must focus on two goals. First, extra-thoracic venous pressure must be increased by intravenous volume loading. This increases the gradient for venous return, which improves RV and LV preload and stroke volume. Second, dynamic hyperinflation must be reduced. Recall that this can be done by increasing expiratory flow (e.g., treating bronchospasm, clearing large-airway secretions, inserting a new, larger-diameter endotracheal tube) and by lengthening the time available for expiration by reducing the total respiratory rate, tidal volume, or both. Sometimes cardiac output and blood pressure can be restored only by sedating and pharmacologically paralyzing the patient and allowing the PaCO2 to rise. If necessary, boluses of IV sodium bicarbonate can be given to keep the arterial pH ≥ 7.20.