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Ventilator Alarms—Causes and Evaluation 

Ventilator Alarms—Causes and Evaluation
Chapter:
Ventilator Alarms—Causes and Evaluation
Author(s):

John W. Kreit

DOI:
10.1093/med/9780190670085.003.0006
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date: 12 July 2020

When a patient is intubated and placed on mechanical ventilation, the clinician must write a series of ventilator orders, and this will be covered in Chapter 8. It’s important to recognize, though, that several other parameters are typically set by the respiratory therapist without direct physician input. The most important are the critical values that will trigger a ventilator alarm.

ICU ventilators constantly monitor many machine and patient-related variables, including airway pressure, flow rate, volume, and respiratory rate, and it seems like there’s an alarm for almost everything. Unfortunately, since these alarms are so common, many nurses and physicians either ignore them or reflexively “silence” them through the user interface. While it’s true that some alarms are of little or no significance, others may indicate an important and potentially life-threatening problem. That’s why it’s essential that all physicians caring for mechanically ventilated patients be able to identify the reason for every ventilator alarm and understand its causes and implications. Ventilator alarms are listed in Box 6.1.

PEEP = positive end-expiratory pressure; FIO2 = fractional inspired O2 concentration

Once an alarm sounds, you can determine its meaning and significance only by going to the bedside and looking at the user interface. There, most ventilators display the reason for the current alarm(s)—yes, there can be more than one at a time—and even show which alarms have been active in the recent past. Once you identify the specific alarm, you need to determine its potential causes and know how to quickly and accurately diagnose and correct the problem.

In this chapter, I will discuss only the most common and clinically important ventilator alarms. These are:

  • High airway pressure

  • Low airway pressure

  • High respiratory rate

  • Low respiratory rate

  • Low exhaled tidal volume

High Airway Pressure

Recall that the pressure generated by the ventilator (airway pressure; PAW) is constantly measured proximal to the expiratory valve. On most machines, it is displayed both graphically in real-time as a pressure–time curve and digitally as the maximum or peak (PPEAK) airway pressure during the preceding breath. After mechanical ventilation is initiated, the respiratory therapist will set a high airway pressure limit, which is typically 15–20 cmH2O above PPEAK.

It’s important to understand that when PAW exceeds the set pressure limit, the ventilator immediately cycles from inspiration to expiration, and the patient receives no gas flow. So, until the underlying problem has been identified and corrected, the patient will get very little if any ventilation!

The most common cause of a high airway pressure alarm is the spike in PAW produced when a patient coughs. This is almost always self-limited and requires no intervention. Patient–ventilator asynchrony that causes the patient to attempt to exhale before inspiratory flow stops can also cause an abrupt increase in PAW. In the absence of these two problems, high airway pressure alarms occur almost exclusively when patients are receiving volume control (VC) breaths.

Volume Control Breaths

Figure 6.1 is a plot of PAW and alveolar pressure (PALV) during a passive VC breath with constant inspiratory flow and PEEP of 5 cmH2O. A brief, end-inspiratory pause is also shown. As discussed in Chapters 1 and 5, at all times during a mechanical breath, PAW is equal to the sum of the pressures needed to overcome viscous forces (PV), the elastic recoil generated by the delivered volume (PER), and total end-expiratory pressure (PEEPT). This is expressed mathematically as:

PAW= PV+ PER+ PEEPT
(6.1)

Figure 6.1 Simultaneous plots of airway (PAW) and alveolar (PALV) pressure versus time during a passive mechanical breath with constant inspiratory flow and 5 cmH2O PEEP. An end-inspiratory pause briefly delays expiration. PAW reaches a peak (PPEAK) at end-inspiration and falls to a plateau pressure (PPLAT) during the end-inspiratory pause. PPLAT is the sum of the elastic recoil pressure generated by the tidal volume (PER) and total PEEP (PEEPT). The difference between PPEAK and PPLAT is the pressure needed to overcome viscous forces at end-inspiration (PV).

Figure 6.1 Simultaneous plots of airway (PAW) and alveolar (PALV) pressure versus time during a passive mechanical breath with constant inspiratory flow and 5 cmH2O PEEP. An end-inspiratory pause briefly delays expiration. PAW reaches a peak (PPEAK) at end-inspiration and falls to a plateau pressure (PPLAT) during the end-inspiratory pause. PPLAT is the sum of the elastic recoil pressure generated by the tidal volume (PER) and total PEEP (PEEPT). The difference between PPEAK and PPLAT is the pressure needed to overcome viscous forces at end-inspiration (PV).

and as:

PAW= (R ×V˙) + (ΔV/C)+ PEEPT
(6.2)

If we look only at what determines PPEAK during a VC breath, Equation 6.2 becomes:

PPEAK= (R ×V˙EI)+ (VT/C) + PEEPT
(6.3)

Here, V˙EI is the flow rate at end-inspiration, and VT is the delivered tidal volume.

If we have excluded coughing and patient–ventilator asynchrony, the remaining causes of an acute rise in PPEAK are shown by Equation 6.3. If we assume that there hasn’t been a recent, unrecognized increase in V˙EI, VT, or extrinsic PEEP, we are left with the causes listed in Box 6.2.

ET = endotracheal; PEEP = positive end-expiratory pressure

That list requires some clarification. First, “increased lung volume” doesn’t mean that VT has increased, but instead that a portion of the lungs receives more volume. For example, occlusion of the left main bronchus by mucous or right main bronchus intubation causes the entire tidal volume to enter the right lung. This may or may not reduce lung compliance. If compliance is unchanged, doubling the volume must double the pressure needed to balance the elastic recoil of the right lung. If over-distension leads to a fall in compliance, then PER will increase even more. Second, the effect of airway secretions depends on the extent of bronchial obstruction. Narrowing of the airway lumen increases resistance and PV. Complete obstruction, as just mentioned, increases PER.

So how do you determine which of these problems is responsible for an increase in PPEAK? The first step is to measure PAW during an end-inspiratory pause. As discussed in Chapter 1, when flow stops, viscous forces disappear, and PPEAK rapidly falls to a “plateau” pressure (PPLAT) that equals the total elastic recoil pressure of the respiratory system (PER + PEEPT). The difference between PPEAK and PPLAT is the pressure needed to overcome viscous forces (PV) at end-inspiration. You can now determine whether the rise in PPEAK is due to an increase in total elastic recoil or viscous forces.

Figure 6.2 shows the effect of reduced compliance and increased resistance, lung volume, and intrinsic PEEP (PEEPI) on PPEAK, PPLAT, PV, and PER. An acute rise in PPEAK that is accompanied by a small PPEAK – PPLAT gradient must be due to a fall in compliance or an increase in lung volume or PEEPI. You can screen for the presence of PEEPI by examining the flow–time curve on the user interface (Chapters 9 and 10). If each mechanical breath begins before expiratory flow reaches zero, PEEPI must be present. If PPLAT is much less than PPEAK, there has been an increase in airway resistance.

Figure 6.2 The effect of increased volume, resistance, and PEEPI and reduced compliance on PPEAK, PPLAT, PV, and PER.

Figure 6.2 The effect of increased volume, resistance, and PEEPI and reduced compliance on PPEAK, PPLAT, PV, and PER.

Appropriate tests must now be performed to diagnose or exclude the causes of increased PV, PER, or PEEPI listed in Box 6.2. As shown in Box 6.3, this evaluation consists of a focused physical examination, a chest radiograph, airway suctioning, and sometimes fiber-optic bronchoscopy. Treatment, of course, depends on the identified cause(s).

ET = endotracheal; PAW = airway pressure; CXR = chest X-ray; PEEP = positive end-expiratory pressure

Other Types of Mechanical Breaths

Unlike VC breaths, PAW is constant during pressure control (PC), adaptive pressure control (aPC), pressure support (PS), and adaptive pressure support (aPS) breaths, so high airway pressure alarms are almost always due to coughing or patient–ventilator asynchrony. Since PAW increases during aPC and aPS breaths to maintain a clinician-set tidal volume, a high-pressure alarm will occasionally occur if a large increase in PAW is needed to counteract a rise in airway resistance or a fall in compliance or patient inspiratory effort.

Low Airway Pressure

A low airway pressure alarm is triggered whenever PAW falls below a set low pressure limit. This is much less common than a high-pressure alarm, but it occurs in two very important situations. The first is when there’s a large leak in the ventilator circuit that prevents the set or required PAW from being reached. This most often occurs when the ventilator circuit becomes disconnected from the endotracheal or tracheostomy tube. The second is when the patient’s flow requirements exceed the inspiratory flow provided during VC breaths. The greater the difference between the required and the provided flow, the more PAW will fall (see Chapter 5, Figure 5.6).

High Respiratory Rate

This alarm is triggered when the patient’s respiratory rate exceeds a high rate limit that’s typically set 10–15 breaths per minute above the mandatory rate on the CMV and SIMV modes and between 30 and 40 breaths per minute on the spontaneous ventilation mode. The implications of a high respiratory rate alarm differ, depending on the mode of ventilation.

During CMV and SIMV, it means that the patient has a high minute ventilation (V˙E) requirement, that the set mandatory rate is far below the patient’s total respiratory rate, and that V˙E will fall (and PaCO2 will rise) if the patient’s respiratory drive decreases (e.g., with sedation). In response, the clinician should determine the cause of the high V˙E requirement, and, if it cannot be corrected, the mandatory rate should be increased.

During spontaneous ventilation, a marked increase in respiratory rate most often accompanies a drop in tidal volume. This usually results from respiratory muscle fatigue, over-sedation, or both, and indicates that the patient should be returned to the CMV mode.

Low Respiratory Rate

A low rate limit is set during spontaneous ventilation. Since there are no mandatory breaths, a low respiratory rate alarm almost always means that the patient is no longer able to maintain adequate V˙E and must be immediately switched to the CMV mode.

Low Tidal Volume

The low tidal volume limit is typically set 150–200 ml less than the set (VC, aPC, aPS) or initially delivered (PC, PS) tidal volume. A low tidal volume alarm is most often precipitated by high airway pressure. Remember that the patient gets little or no ventilation when a high-pressure alarm is active, so naturally, the exhaled tidal volume is very low. This problem is easily recognized when both alarms occur at the same time. Unless it has been caused by a brief coughing spell, the clinician must take immediate steps to diagnose and correct the problem. A low tidal volume alarm will also be triggered by a large leak in the ventilator circuit.

Other causes of a low tidal volume alarm occur only during PC and PS breaths (Box 6.4). Notice that these are the same causes of a high airway pressure alarm during VC breaths (Box 6.2). This is not just a weird coincidence. Remember that VC, aPC, and aPS breaths are volume-set and pressure-variable. If PV, PER, or PEEPI increases, PAW will increase to keep VT constant. PC and PS breaths are pressure-set and volume-variable. Since PAW cannot increase, a rise in PV, PER, or PEEPI must cause a drop in VT. Finally, since flow and volume vary with patient inspiratory effort, a low tidal volume alarm may also be triggered by a decrease in respiratory drive or effort, or by respiratory muscle fatigue. This is much more likely to occur during PS breaths, because patient effort is a more important determinant of tidal volume.

PV = pressure required to overcome viscous forces; PER = pressure required to overcome the increase in elastic recoil produced by the tidal volume; PEEPI = intrinsic PEEP

When a low tidal volume alarm occurs, the ventilator circuit should be examined for a large air leak. If there is a simultaneous high-pressure alarm, its cause must be identified, as discussed previously. If these problems are ruled out, patients receiving PC or PS breaths should be evaluated with a focused physical examination, chest radiograph, and, if necessary, fiber-optic bronchoscopy. Not surprisingly, the evaluation for a low tidal volume alarm and a high airway pressure alarm are the same (Box 6.3).