Normally, expiratory flow stops and expiration ends only when the respiratory system has returned to its equilibrium volume and alveolar pressure (PALV) is zero (Figure 10.1A). This is the point at which the elastic recoil of the lungs and the chest wall are equal and opposite (see Chapter 1). Clinician-added or “extrinsic” positive end-expiratory pressure (PEEPE) creates a new, higher equilibrium volume, and end-expiratory alveolar pressure (PALVee) equals PEEPE (Figure 10.1B).
When the time available for expiration (expiratory time; TE) is insufficient to allow the respiratory system to return to its equilibrium volume with or without PEEPE (Figure 10.2), flow persists at end-expiration, and PALVee exceeds PEEPE by an amount referred to as intrinsic PEEP (PEEPI). PALVee is then the sum of extrinsic and intrinsic PEEP, which is called total PEEP (PEEPT).(10.1)
Intrinsic PEEP (or auto-PEEP) results from dynamic hyperinflation, which is illustrated in Figure 10.3. When TE is too short to allow the entire tidal volume (VT) to be exhaled, there is a progressive increase in lung volume. The accompanying rise in elastic recoil increases expiratory flow, which eventually allows a relatively constant end-inspiratory and end-expiratory lung volume (and PEEPI) to be established.
Dynamic hyperinflation and PEEPI almost always occur in patients with severe obstructive lung disease, in whom slowing of expiratory flow prevents complete exhalation even when TE is normal or prolonged. Occasionally, patients without airflow obstruction develop dynamic hyperinflation when TE is excessively shortened by a rapid respiratory rate, a long set inspiratory time (TI), or both.
Diagnosis of Dynamic Hyperinflation and Intrinsic PEEP
Dynamic hyperinflation should always be suspected in mechanically ventilated patients with obstructive lung disease. The presence of breath sounds or wheezing that continues throughout the entire expiratory phase is the most suggestive sign, although its absence certainly does not exclude the diagnosis. Dynamic hyperinflation must also be strongly suspected when patients develop one or more characteristic complications, specifically hypotension and ineffective ventilator triggering (discussed later in this chapter).
As discussed in Chapter 9, you can screen for PEEPI by examining the flow–time curve on the user interface (Figure 10.2). If expiratory flow doesn’t reach zero before the next mechanical breath, dynamic hyperinflation must be present. The higher the end-expiratory flow, the more severe the dynamic hyperinflation, and the greater the PEEPI.
PEEPT and PEEPI can be measured during a brief end-expiratory pause (Chapter 9). Remember that the ventilator measures airway pressure (PAW) proximal to the expiratory valve. Throughout expiration, when the expiratory valve is open, PAW equals zero (atmospheric pressure) or the set level of PEEPE, not PALV. When the valve is closed during an end-expiratory pause, flow stops, pressure equilibrates between the alveoli and the pressure sensor, and PAW equals PALVee (PEEPT) (Figure 10.4). PEEPI can then be calculated as the difference between PEEPT and PEEPE.
Also recall that the measurements performed during an end-expiratory pause will be accurate only if the patient is not attempting to breathe. Often, sedation will sufficiently minimize patient effort. Alternatively, accurate pressure measurements can usually be obtained once respiratory drive has been decreased by a brief period of hyperventilation.
As shown in Figure 10.5, dynamic hyperinflation can be directly quantified by stopping ventilation in a pharmacologically paralyzed patient and measuring expired volume until flow reaches zero. The volume of the expired gas is the difference between end-inspiratory volume (VEI) and the equilibrium volume (EV) of the respiratory system. The difference between end-expiratory volume (VEE) and EV can then be determined by subtracting the tidal volume. Since it provides little clinically useful information and requires neuromuscular blockade, this measurement is typically restricted to research studies.
Consequences of Dynamic Hyperinflation
Dynamic hyperinflation can cause three important adverse effects in mechanically ventilated patients.
• Reduced cardiac output and hypotension
• Ineffective ventilator triggering
As discussed in Chapter 3 and shown in Figure 10.1A, mechanical ventilation causes a cyclical increase in pleural (PPL) and lung transmural (PlTM) pressure. By increasing end-expiratory lung volume, both PEEPE and PEEPI cause an additional, continuous rise in PPL and PlTM (Figures 10.1B and 10.2), which leads to further reduction in venous return and further increase in RV afterload, respectively. If sufficiently large, the decrease in preload and increase in afterload will cause cardiac output and blood pressure to fall.
By increasing lung volume throughout the respiratory cycle (Figures 10.2B and 10.3), dynamic hyperinflation predisposes to alveolar over-distension, and this may lead to alveolar rupture, which is usually referred to as “barotrauma.” Air tracks along the bronchovascular bundles and enters the mediastinum (pneumomediastinum). From there, air may enter the pleural space (pneumothorax), the subcutaneous tissues (subcutaneous emphysema), and even the pericardial space (pneumopericardium) or the abdominal compartment (pneumoperitoneum). Pneumothorax interferes with gas exchange and may cause hypotension by further increasing PPL and reducing venous return. Pneumopericardium may impair cardiac filling and cause cardiac tamponade.
Ineffective Ventilator Triggering
Consider what must occur before a patient with dynamic hyperinflation can trigger a mechanical breath (Figure 10.6). During expiration, the respiratory system is above its equilibrium volume, inward elastic recoil raises PALV above the pressure at the expiratory valve (PAW), and gas flows from the lungs (Figure 10.6A). PAW is equal to PEEPE. If the patient attempts to trigger a breath before PALV has reached PEEPE, they must first stop expiratory flow. This can be done only by generating enough inspiratory pressure to eliminate the pressure gradient that is driving flow. That is, they must lower PALV until it reaches PEEPE (Figure 10.6B). Since PALV equals PEEPT, this requires a pressure equal to PEEPI. Once expiratory flow stops, additional muscular effort is needed to trigger the ventilator (Figure 10.6C). As discussed in Chapter 4, if pressure triggering is used, PALV must be reduced enough to lower PAW by the set sensitivity. If the ventilator is set for flow triggering, PALV must be decreased until the base flow falls by the set flow sensitivity.
Let’s look at some examples to help clarify these concepts. If PEEPI is 10 cmH2O, PEEPE is 0 cmH2O (PEEPT = 10 cmH2O), and the set pressure sensitivity is –2 cmH2O, a patient must first lower PALV from 10 cmH2O to zero and then generate an additional 2 cmH2O to trigger the ventilator (total of 12 cmH2O). If PEEPE and PEEPI are both 5 cmH2O (PEEPT = 10 cmH2O), PALV must be reduced from 10 cmH2O to 5 cmH2O to stop expiratory flow, and an additional 2 cmH2O is needed to trigger the ventilator (total of 7 cmH2O).
By forcing patients to stop expiratory flow before they can take another breath, dynamic hyperinflation produces a threshold load on the inspiratory muscles. Dynamic hyperinflation also forces patients to breathe at a higher, less compliant portion of the pressure–volume curve (see Chapter 1, Figure 1.3). Take a deep breath and then perform tidal breathing near total lung capacity. You’ll discover that it’s very difficult and very uncomfortable, and you’ll be able to better appreciate the effort required to sustain ventilation.
Ineffective triggering occurs when a patient is unable to generate the inspiratory pressure needed to trigger the ventilator. This can usually be detected at the bedside by noting chest wall expansion and accessory muscle activity that do not trigger a mechanical breath. As shown in Figure 10.7, airway pressure and flow tracings may also reveal ineffective inspiratory efforts. Ineffective triggering will be discussed again in Chapter 11.
Management of Dynamic Hyperinflation
There are two ways to reduce the adverse effects of dynamic hyperinflation. The first is to decrease dynamic hyperinflation itself by allowing the respiratory system to get closer to its equilibrium volume. The second is to treat the adverse hemodynamic effects of PEEPI.
Reducing Dynamic Hyperinflation
Since patients almost always have significant obstructive lung disease, bronchodilators and steroids may increase expiratory flow and reduce end-expiratory volume. At the same time, three ventilator adjustments can be made to allow more complete exhalation.
• Decrease the set respiratory rate (RR). If the patient is making no spontaneous efforts, this will reduce the total rate and increase the time between breaths, which will allow more complete emptying.
• Decrease the tidal volume (VT). Since less volume is delivered, less must be exhaled, and the respiratory system will get closer to its equilibrium volume. With VC and aPC breaths, this is done by changing the set VT. With PC breaths, VT is reduced by lowering the driving pressure.
• Reduce inspiratory time (TI). If respiratory cycle duration (TI + TE) is unchanged, a decrease in TI must lengthen TE, and this will reduce end-expiratory volume. Depending on the ventilator and the type of mechanical breath, inspiratory time can be decreased either by changing the set TI or by increasing the set inspiratory flow rate.
It’s important to recognize several important limitations of these ventilator adjustments.
First, inspiratory time is almost always very short to begin with, so decreasing it further does little to reduce dynamic hyperinflation. Let’s say that a patient has a respiratory rate of 12. This means that every respiratory cycle lasts for 60/12 = 5 seconds. If TI is initially 1 second, TE will be 4 seconds. If you reduce TI to 0.5 second, TE increases only to 4.5 seconds, and this is likely to have no clinically significant effect on PEEPI.
Second, when attempting to reduce RR, VT, or both, you will often encounter two problems. First, decreasing the set rate will have no effect if the patient is triggering additional mechanical breaths. Second, reducing VT will not be beneficial if the patient increases their respiratory rate to compensate for the drop in minute ventilation.
Because of these limitations, patients with dynamic hyperinflation-induced hypotension who are unresponsive to volume expansion (see next section) may require sedation and neuromuscular blockade to allow sufficient reduction in RR or VT to reduce PEEPI. This usually leads to significant hypercapnia and respiratory acidosis, which can be treated, if necessary, with intravenous (IV) sodium bicarbonate.
Since PEEPI-induced hypotension is caused largely by a decrease in venous return, it can be treated by rapidly expanding intravascular volume. As discussed in detail in Chapter 3, this raises systemic venous pressure, increases the gradient driving blood into the RA, and improves RV and LV preload. Typically, 500 ml boluses of normal saline or Lactated Ringers are given until hypotension resolves or no further effect is seen.
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