Effective mechanical ventilation requires the synchronized function of two pumps. One pump, the mechanical ventilator, is governed by the settings chosen by the clinician. The other, the patient’s respiratory system, is controlled by groups of neurons in the brain stem that set the respiratory rate, inspiratory flow rate, and tidal volume based on input from peripheral and central chemoreceptors, intrapulmonary receptors, and the cerebral cortex. Ideally, these two pumps should work together so that the ventilator simply augments and amplifies the activity of the respiratory system. This is important because asynchrony between the ventilator and the patient reduces patient comfort, increases the work of breathing, predisposes the patient to respiratory muscle fatigue, and may even impair oxygenation and ventilation.
Patient–ventilator asynchrony most commonly occurs either during ventilator triggering or during the inspiratory phase of the respiratory cycle. This chapter explains how to detect asynchrony and describes how to reduce or eliminate it.
Asynchrony During Triggering
A mechanical breath is triggered when patient inspiratory effort causes the demand valve to open, which allows gas to flow into the lungs. As described in Chapter 4, the ventilator senses patient effort by detecting changes in either pressure or flow within the ventilator circuit. Three signs of patient–ventilator asynchrony may be evident during the triggering phase of a mechanical breath:
• Ineffective triggering
• Multiple triggering
As the name indicates, ineffective triggering occurs when patient inspiratory effort is insufficient to trigger a mechanical breath. This can be detected in two ways. First, examine the patient while listening to the ventilator and look for any uncoupling of respiratory effort and mechanical breaths. Inspiratory efforts can be subtle and may be visible only as retractions just above the suprasternal notch. If the patient makes an inspiratory effort but does not receive a mechanical breath, triggering is ineffective. Second, look at the pressure–time curve on the ventilator user interface. As shown in Figure 11.1, patient inspiratory effort may be (but is not always) reflected by a drop in PAW during the expiratory phase. The absence of an accompanying mechanical breath is diagnostic of ineffective triggering.
Ineffective triggering has three causes:
• Poor inspiratory effort (usually due to over-sedation)
• An inappropriately low (i.e., insensitive) trigger sensitivity
• Inability to overcome the “threshold load” produced by intrinsic PEEP (PEEPI)
The last cause is by far the most common. Recall from Chapter 10 that 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 PAW or the base flow sufficiently to trigger a mechanical breath.
When ineffective triggering is present, its cause must be identified and, if possible, corrected. The recognition and management of dynamic hyperinflation and PEEPI was discussed in Chapters 9 and 10, and I’ll only emphasize a few points here.
• You can screen for dynamic hyperinflation by examining the flow–time curve on the user interface. As shown in Chapter 9, Figure 9.17, PEEPI must be present if expiratory flow does not return to zero prior to the next mechanical breath. PEEPI can then be quantified by measuring PAW during a brief end-expiratory pause (Figure 9.16).
• Remember that PEEPI usually occurs in the setting of significant obstructive lung disease when the interval between mechanical breaths is insufficient to allow the respiratory system to return to its equilibrium volume. Intrinsic PEEP can most effectively be reduced by decreasing tidal volume, respiratory rate, or both.
Auto-triggering occurs when the ventilator initiates mechanical breaths in response to a drop in pressure or flow that is not produced by patient effort. Occasionally, this is caused by the back and forth movement of water in the ventilator circuit or by the heartbeat of a patient with a wide pulse pressure. More often, the drop in PAW or base flow is caused by a leak in the ventilator circuit. This may occur at a tubing connection or result from gas escaping around the cuff of the endotracheal or tracheostomy tube.
How does a leak cause auto-triggering? Remember that flow-triggering occurs whenever flow passing through the expiratory limb of the ventilator circuit falls below the base flow by a set amount (the flow-sensitivity). This, of course, usually means that the patient has started to inhale. But you can see that triggering will be independent of patient effort if there is a big enough leak in the ventilator circuit. Similarly, during pressure-triggering, a breath will be initiated if a leak causes a sufficient drop in PAW. Unlike flow-triggering though, this will happen only if expiratory PAW is positive; that is, if extrinsic PEEP (PEEPE) is present. That’s because a leak can decrease PAW only if it’s above atmospheric pressure. For example, if PEEPE is 5 cmH2O and pressure sensitivity is set at –2 cmH2O, a leak will trigger a mechanical breath when PAW drops below 3 cmH2O. If PEEPE is zero, there’s no way that PAW can fall below atmospheric pressure to –2 cmH2O without patient inspiratory effort.
Not uncommonly, none of these causes is evident, and auto-triggering is due simply to an inappropriately high sensitivity (i.e., very sensitive) setting. This is particularly likely during flow-triggering when the sensitivity is set at or below 1 L/min.
Auto-triggering should be suspected in any patient who has a persistent and unexplained respiratory alkalosis. Like ineffective triggering, the diagnosis can usually be made by simultaneously looking at the patient and listening to the ventilator. In most cases, it’s fairly obvious that mechanical breaths are not preceded by patient inspiratory effort.
Once auto-triggering has been confirmed, attention must be directed to identifying and correcting the cause. Make sure that flow-sensitivity has been set above 1 L/min. Carefully examine the ventilator circuit for leaks and drain any water that’s present. Auscultate over the neck to detect air escaping around the cuff of the endotracheal or tracheostomy tube.
If the cause of auto-triggering remains unclear, it’s probably due to an unrecognized leak, so here’s what you do to confirm it. First, if the ventilator is set for flow-triggering, change it to pressure-triggering. Sometimes this, by itself, will eliminate the problem. If auto-triggering persists, reduce PEEPE to zero (if this is safe to do). For the reasons discussed previously, if auto-triggering stops, it must have been due to a leak, and additional efforts must be made to identify the source.
This type of patient–ventilator asynchrony occurs when a single inspiratory effort triggers several (usually two) mechanical breaths in rapid succession (Figure 11.2). When you see multiple triggering, it almost always means that the patient wants a much larger tidal volume. This causes the patient to continue to inhale after the ventilator cycles, which immediately triggers another mechanical breath. Multiple triggering can usually be minimized or eliminated by increasing the delivered tidal volume. When low tidal volume ventilation is needed for a patient with ARDS, increased sedation is often the only way to improve patient comfort and reduce patient–ventilator asynchrony.
Asynchrony During Inspiration
Two signs of patient–ventilator asynchrony during inspiration are:
• Abnormally low airway pressure
• A spike in airway pressure at end-inspiration
Abnormally Low Airway Pressure
This occurs primarily with VC breaths and is a sign of inadequate inspiratory flow. Recall from Chapter 5 that inspiratory flow during VC breaths cannot be increased by patient effort. Patients who are dyspneic and tachypneic pull vigorously in an unsuccessful attempt to inflate their lungs more rapidly. Since the ventilator circuit is a closed system, when a patient inhales faster than gas enters the lungs, PAW must fall, and this causes the PAW–time curve to have a characteristic “scooped out” appearance. As shown in Figure 11.3, the degree and duration of the PAW drop correlate with the magnitude of the imbalance between the set inspiratory flow and the demands of the patient. Notice that peak airway pressure (PPEAK) often falls as this imbalance worsens.
The solution to this problem, of course, is to increase the inspiratory flow rate. At the same time, an effort should be made to identify and, if possible, correct the problem(s) leading to tachypnea and high flow requirements. Common causes include pain, anxiety, sepsis, and metabolic acidosis. Alternatively, you can switch from volume control to adaptive pressure control (aPC) breaths. But be careful. Even though aPC breaths are better able to match inspiratory flow demands, the ventilator provides less and less support as patient effort increases. This is reflected by a relatively small increase in airway pressure during inspiration and indicates that the patient is doing much or even most of the work of breathing (Figure 11.4).
End-Inspiratory Pressure Spike
When inspiratory time (TI) is too long, the patient tries to exhale before mechanical inflation ends. Simultaneous, oppositely-directed flow from the ventilator and the patient causes an abrupt rise in PAW, which can be detected by looking at the PAW–time curve on the user interface (Figure 11.5). This is also a common cause of a high airway pressure alarm (see Chapter 6). When this problem is identified, TI can be reduced either directly or by increasing the set flow rate, depending on the breath type and the ventilator being used (see Chapter 5).
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