Patient-Ventilator Interaction

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49 Patient-Ventilator Interaction

V. Marco Ranieri, Cesare Gregoretti, Vincenzo Squadrone

The clinical management of patients with acute respiratory failure is based on the assumption that significant abnormalities in respiratory mechanics, respiratory muscle performance, and control of breathing are the underlying mechanisms responsible for acute respiratory failure.1 The effects of mechanical ventilation on gas exchange, respiratory muscle load, and dyspnea depend on the matching between the ventilator settings and the patient’s respiratory physiology. However, mechanical ventilation is rarely optimized, which would require that ventilator settings be based on accurate and reproducible measurements of lung and chest wall mechanics, respiratory muscle function, and respiratory drive.2–5

image Respiratory Physiology

The goal of the intrinsic ventilatory control system is to integrate the timing and intensity of the phrenic nerve signal, inputs from chemoreceptors and pulmonary stretch receptors, and variations in metabolic demands. Contraction of the respiratory muscles leads to the generation of flow and volume to provide adequate alveolar ventilation with minimal work of breathing.6 During spontaneous breathing,7 the respiratory muscles generate pressure (Pmus) to generate flow against the resistive properties (RRS) and volume against the elastic properties (ERS) of the respiratory system to eventually overcome intrinsic positive end-expiratory pressure (PEEPi). Under these circumstances, the act of spontaneous breathing can be described at any instant as follows:

(Equation 1) image

where Pres represents the resistive pressure and is a function of flow (Pres = Flow × RRS), and Pel represents the elastic recoil pressure and is a function of volume (Pel = Volume × ERS). Assuming that RRS and ERS are linear, the equation becomes:

(Equation 2) image

In patients with acute respiratory failure requiring ventilatory support, pressure generated by the ventilator (Pappl) is added to the pressure generated by the contraction of the respiratory muscles according to the following equation:

(Equation 3) image

The complex interaction among all the variables in equation 3 can be summarized by the concept of neuroventilatory coupling (Figure 49-1).8 Under normal conditions, as well as at the onset of acute respiratory failure, the spontaneous contraction of the respiratory muscles suddenly generates flow and volume; the slope of the relationship between effort and ventilatory output is conditioned by the contractile properties of the respiratory muscles and the impedance of the respiratory system. When positive pressure is applied to assist the action of breathing in most common modes of mechanical ventilation (pressure-support or pressure-assist mandatory ventilation), the coupling between effort and output is compromised. During assist-control ventilation, flow and volume remain constant despite changes in muscle contraction; during pressure-support ventilation, despite coupling between inspiratory effort and ventilatory output, any increase in respiratory impedance decreases the amount of delivered flow and volume.8 During noninvasive ventilation (NIV), air leaks may further compromise the coupling between patient effort and ventilatory output.9

image

Figure 49-1 Neuroventilatory coupling. Under normal conditions, as well as at onset of acute respiratory failure, spontaneous contraction of respiratory muscles suddenly generates flow and volume. The slope of the relationship between effort and ventilatory output is conditioned by the contractile properties of the respiratory muscles and impedance of the respiratory system. When positive pressure is applied to assist the action of breathing in most common modes of mechanical ventilation, the coupling between effort and output is compromised. During assisted mandatory ventilation (AMV), flow and volume remain constant despite changes in muscle contraction. During pressure-support ventilation (PSV), despite a sort of coupling between inspiratory effort and ventilatory output, any increase in respiratory impedance decreases the amount of delivered flow and volume. VT, tidal volume.

image Patient and Ventilator Variables

Patient Variables

The patient interacts with the ventilator based on three physiologic variables2,10,11:

1 Ventilatory drive, or when inspiration starts12
2 Ventilatory requirements, or how much flow and volume are necessary to satisfy metabolic demands5
3 Timing of the integrated circuits generating the respiratory rhythm, as measured by the duration and ratio of inspiratory time to total breath cycle duration10

Ventilator Variables

Three phase variables define inspiration13,14:

• The trigger that begins inspiration (pressure, volume, flow, and time dependent)
• The limit that cannot be exceeded during inspiration (pressure, volume, and flow)
• The cycling-off criteria

In other words the ventilator interfaces with the patient’s physiology based on three technologic variables:

1 The inspiratory trigger, or when the ventilator starts to deliver flow, volume, and pressure15,16
2 The delivery mechanisms—that is, the algorithm used by the ventilator to assist ventilation through the delivery of flow, volume, or pressure17–22
3 The cycling-off criteria, or when the ventilator stops assisting inspiratory effort and lets the patient exhale spontaneously20,21

Features of ventilators such as blowers and inspiratory, expiratory, and positive end-expiratory pressure (PEEP) valves are also important in determining the interaction between patient and ventilator.23–26

To unload the respiratory muscles, restore sufficient gas exchange, and relieve the patient from dyspnea, the healthcare team must establish an interface between patient and ventilator. To do so, there are two options: total ventilator-controlled mechanical support or partial patient-controlled support.

Total Ventilator-Controlled Mechanical Support

In this mode, the patient’s breathing pattern is totally controlled by the ventilator. The pressure generated by the respiratory muscles is abolished by paralysis or sedation. Flow, volume, and pressure are imposed by the ventilator, and the patient’s breathing pattern is totally replaced by that of the ventilator. The risk of patient-ventilator asynchrony is therefore abolished, but there are potential risks associated with sedation and paralysis,27 respiratory muscle atrophy,28 lung damage due to overdistention,29 patient discomfort,30 and difficulty weaning after prolonged controlled mechanical ventilation.1

Partial Patient-Controlled Mechanical Support

With this mode, spontaneous breathing activity is partially preserved.31 The need for sedation and paralysis may be reduced, disuse atrophy of the respiratory muscles may be minimized, and the weaning process may be accelerated, provided the patient’s ventilatory demand and ventilator settings are synchronized.32 The ability to restore gas exchange, unload respiratory muscles, and relieve patient dyspnea with partial patient-controlled mechanical support therefore depends on the absence of patient-ventilator asynchrony.33

Although there are no well-accepted definitions, patient-ventilator asynchrony is common; it is often unrecognized, underestimated, and inappropriately treated.3–5,22,33–35 The cause of patient-ventilator asynchrony can be described as occurring because of a mismatch between the three physiologic variables characterizing spontaneous breathing (ventilatory drive, ventilatory requirements, and duration and ratio of inspiratory time to total breath cycle duration) and the three technologic variables characterizing ventilator function (trigger function, gas delivery algorithm, and cycling criteria).

image Respiratory Drive–Ventilator Trigger Asynchrony

During partial ventilatory assistance (assisted breath), the inspiratory synchronization system (inspiratory trigger) detects any patient inspiratory effort and activates a mechanical act. Therefore, inspiratory effort is tracked in order to couple the patient’s effort with the delivery of pressure, flow, or volume. The goal of a good inspiratory trigger is to reduce as much as possible the duration and intensity of the muscular effort that comes before mechanical support, while avoiding autotrigger effects.36 Auto-triggering can be defined as a mandatory breath not following a patient’s inspiratory effort.

It has been suggested that a trigger (independently of its algorithm) must have a response time less than 100 ms. However, the inspiratory effort necessary to trigger a breath may be a significant part of the total inspiratory effort, representing 17% and 12% of the total inspiratory effort during pressure and flow triggering, respectively.15–23,34,35 Aslanian and coworkers found that even though the time required for triggering was 43% shorter, and effort during the time of triggering was 62% less with flow triggering than with pressure triggering, effort during the post-triggering phase was equivalent for both pressure and flow triggering.37 The clinical benefit of flow triggering therefore appears to be much less relevant than commonly stated.3

Inspiratory phase asynchrony may be due to problems with inspiratory triggering, and this can be correlated with respiratory drive. Phase lag quantifies the delay between the commencement of inspiratory muscle activity and the beginning of mechanical inflation (Figure 49-2).3,10,11 The presence of a threshold load, such as dynamic intrinsic PEEP, may further complicate patient-ventilator interaction during the triggering phase.15 Giuliani et al. suggested that effort during triggering determines patient effort during the remaining portion of inspiration.38 Leung and coworkers demonstrated that the higher the level of ventilator-applied pressure, the lower the respiratory drive, but the longer the time required to trigger the ventilator. As a result, respiratory muscles generate smaller inspiratory swings in intrathoracic pressure but over a longer inspiratory time.2 Another problem is related to the fact that pressure is mostly detected inside the ventilator; therefore, any resistive load (e.g., endotracheal tube or upper airways during noninvasive ventilation) reduces the responsiveness of the gas delivered by the ventilator in response to patient effort.22

image

Figure 49-2 Representative tracings show interaction between patient effort and triggering of ventilator. Delay between beginning of inspiratory muscle activity (dotted line) and beginning of mechanical inflation (solid line) can cause an inspiratory phase asynchrony. Flow, flow generated at airway opening; Paw, pressure applied at airway opening; Pes, esophageal pressure.

Ineffective triggering is due to the ventilator’s inability to detect the patient’s “request” for an assisted breath despite substantial inspiratory effort (Figure 49-3). This phenomenon usually occurs with high levels of ventilator assistance and short expiratory times. Mechanical characteristics that may induce ineffective triggering include low elastance, high resistance, and intrinsic PEEP; ineffective triggering is not correlated to an increase in the patient’s inspiratory effort.2 The application of external PEEP below the intrinsic PEEP level can reduce the inspiratory effort required to trigger the ventilator.39 Parthasarathy and coworkers demonstrated that prolonging mechanical inflation into neural expiration reduces the time available for unopposed exhalation, resulting in the need for a greater inspiratory effort to trigger the ventilator.40 Younes and colleagues found that ineffective triggering in ventilator-dependent patients exacerbates dynamic hyperinflation.41

image

Figure 49-3 Representative tracings show ineffective triggering due to ventilator’s inability to detect patient’s “request” for an assisted breath. A substantial inspiratory effort (arrows) generates only a bump in the flow and pressure tracings instead of a mandatory assisted breath. Flow, flow generated at airway opening; Paw, pressure applied at airway opening; Pes, esophageal pressure.

New trigger algorithms aim at improving patient-ventilator interaction during sudden changes in flow or respiratory rate or in the presence of air leaks during NIV. This can be achieved with volume triggers, triggers linked to flow waveform algorithms, combining pressure and flow signals in the same trigger algorithm, or using both pressure and flow triggers. However, all inspiratory trigger drawbacks may be overcome by using a neural trigger obtained by means of a dedicated nasogastric tube with a multiple array of electrodes placed in the distal esophageal portion.8,42,43

image Ventilatory Requirement–Gas Delivery Asynchrony

Gas delivery asynchrony occurs when ventilator-delivered flow, volume, and pressure are insufficient to meet the patient’s ventilatory demand. Ward and coworkers demonstrated that increasing the flow rate could be used as a means of reducing the patient’s respiratory drive and active respiratory muscle work,17 although doing so may exert an excitatory effect on respiratory rate and on the rate of rise of inspiratory muscle activity.3,20,21,44–50 Laghi and colleagues demonstrated that the imposed inspiratory time during mechanical ventilation determines respiratory frequency independent of inspiratory flow and tidal volume.20 Pressure-targeted breaths may better match the patient’s ventilatory requirements, because flow is the dependent variable during constant pressure delivery. In addition, rapid pressurization of the airways is coupled with high inspiratory flow only at the beginning of inspiration, thus reproducing the physiologic flow profile.51 However, during a pressure-targeted breath, the pressure-rise time setting—the time taken to reach the pressure set on the ventilator—may influence patient-ventilator interaction because its modification determines the dependent flow output.13,14

image Inspiratory Time–Ventilator Cycling Asynchrony

A breath can be pressure-, time-, volume-, or flow-cycled.14 Ventilator-patient asynchrony occurs when the patient is trying to exhale, but the ventilator is still delivering gas.37,40,52 In patients ventilated with a time-cycled breath, expiratory phase asynchrony takes place when the patient’s neural inspiratory time is shorter or longer than the ventilator inflation time. For proper cycling off the ventilator and optimal patient-ventilator synchrony, the patient’s inspiratory flow and ratio of inspiratory time–to–total breath cycle duration must be tracked.

During flow-cycled breaths, inspiratory time is determined exclusively by the time taken for the exponentially declining flow to reach the flow threshold value (when cycling between inspiration and expiration occurs).34,53 As a consequence, a flow-cycled ventilation mode (e.g., pressure-support ventilation [PSV]) is cycled when inspiratory flow decay reaches a given threshold value. The inspiratory flow threshold value, also called expiratory trigger, thus controls the inspiration-to-expiration switch in these modalities.13,54 The aim is to detect the very end of patient inspiration through inspiratory flow measurement. The goal of these ventilatory modes is to optimize synchronization between spontaneous patient inspiratory time and ventilator inspiratory time. However, for proper cycling off and optimal patient-ventilator synchrony, the ventilator always has to track the patient’s inspiratory flow.40,55,56

image Patient-Ventilator Asynchrony During Pressure-Support Ventilation

Three phases may influence patient-ventilator interaction during PSV: the threshold value of inspiratory flow decay (expiratory trigger), the pressure ramp (pressure slope), and the level of PSV.

(1) The expiratory trigger sensitivity can be fixed (default at 25% of peak flow ) or can vary from 5% to 90% or from 5 to 25 L/min (Figure 49-4).57 It can also be linked to algorithms where there is a ranking logic of expiratory cycling criteria that links cycling to expiration. Setting the expiratory trigger at a higher percentage of peak inspiratory flow (i.e., 50% to 70% of decay of peak inspiratory flow) in patients with obstructive pulmonary disease improves patient-ventilator synchrony and reduces inspiratory muscle effort.58

image

Figure 49-4 Representative tracings show different settings for expiratory trigger sensitivity on a flow-time plot. Top to bottom, Expiratory trigger set at 25%, 50%, and 75% of peak flow. Ventilator inspiratory time is influenced by preset flow expiratory trigger sensitivity, at which point the ventilator switches to expiration.

In addition, the modification of cycling-off criteria may have a beneficial effect on reducing the dynamic hyperinflation and inspiratory effort in chronic obstructive pulmonary disease patients, especially at low levels of pressure support.59

The proper adjustment of expiratory trigger threshold may be also important in improving patient-ventilator synchrony and in decreasing the work of breathing during acute lung injury. Unlike in obstructive pulmonary disease, setting the lower threshold at 5% of the peak inspiratory flow might be the optimal value for patients with acute respiratory distress syndrome or acute lung injury.60

Chiumello et al. found in patients recovering from acute lung injury during PSV at 15 cm H2O, the lowest cycling-off criteria reduced the respiratory rate and increased the tidal volume without modifying the work of breathing.61

The expiratory sensitivity setting is crucial when ventilators are used to deliver NIV, because air leaks may cause an abnormal prolongation of the inspiratory time; during this time, the patient may make efforts to exhale against the machine or to inhale, without receiving any ventilatory support (inspiratory hang-up) (Figure 49-5).62–66 In addition, leak-compensating capabilities differ markedly between ventilators.56,67

image

Figure 49-5 Representative record of air leaks during noninvasive face mask pressure-support ventilation. Presence of air leaks causes prolonged ventilator inspiratory time (arrows). Flow, flow generated at airway opening; Paw, pressure applied at airway opening; Pes, esophageal pressure.

(2) The setting of the pressure-rise time (pressure slope) can also affect the expiratory threshold by modifying the dependent inspiratory flow.61,68–71 Although there is some evidence that rapid pressure-rise times might reduce a patient’s work of breathing,69 a fast pressure increase may lead to particularly high peak inspiratory flow, which may cause premature termination of inspiration when the fixed percentage criterion for expiratory cycling is reached (Figure 49-6).22,59,71

image

Figure 49-6 Representative tracings show different pressure-rise time sensitivities on a flow-time plot. Left to right, Pressure-rise time set at 90%, 60%, and 30% of maximal pressurization time. Ventilator inspiratory time (shaded area) is influenced by preset pressure-slope sensitivity that generates a different peak inspiratory flow. Paw, pressure applied at airway opening; Flow, flow generated at airway opening.

Prinianakis et al. assessed the effects of varying the rate of pressure change during noninvasive PSV on the breathing pattern of patients with COPD, as well as inspiratory effort, arterial blood gases, tolerance to ventilation, and amount of air leakage. No significant changes were observed in breathing pattern and arterial blood gases between the differing amounts of pressure change. The pressure-time product of the diaphragm, an estimate of its metabolic consumption, was significantly lower with all rates of pressure change than with spontaneous breathing, but it was significantly lower with the fastest rate. Interestingly, air leak—assessed by the ratio between expired and inspired tidal volumes—increased, and the patients’ tolerance of ventilation, measured using a standardized scale, was significantly poorer with the fastest rate of pressure change.72 In invasively ventilated patients recovering from acute lung injury, Chiumello et al. found that the shortest inspiratory rise time reduced the work of breathing.61

(3) The pressure-support level also determines the dependent flow output. During NIV, patient-ventilator asynchrony is a common occurrence, mainly owing to air leaks.9,63 Because air leaks may determine modification in flow output, reducing PSV level even by 1 or 2 cm H2O may reduce air leaks, thus improving patient-ventilator asynchrony.9

In conclusion, modifications of inspiratory rise time and cycling-off criteria must be carefully adjusted during PSV, as well as the level of PSV. Dyssynchrony at the termination of a PSV breath can be corrected by varying the cycling-off criteria (e.g., the expiratory trigger threshold) or modulating inspiratory flow (e.g., modifying the pressure slope or varying the set pressure level).9 Automated modes designed to achieve an optimal expiratory cycling during PSV may deserve further investigation.73–74

image Total Patient-Controlled Mechanical Support

Optimization of patient-ventilator interactions can be obtained only by continuous matching between the triggering, flow delivery, and cycling functions of the ventilator and the patient’s ventilatory drive, spontaneous inspiratory flow demand, and ratio of inspiratory time to total breath cycle. This implies continuous measurement of physiologic variables and continuous adaptation of the ventilator to the spontaneous variations in these variables. Future development in ventilator technology should be oriented toward systems with the capability to automatically interface between physiologic parameters and ventilator output. Such technology will be based on closed-loop algorithms able to achieve total patient-controlled mechanical support.4

The design features of an automatic control system in a mechanical ventilator include (1) what activates the system (the input), (2) what the system produces (the output), and (3) the protocol used to link input and output (the controlling algorithm). In a closed-loop system, the output will activate and condition the input. When changes in output are opposite to changes in input, the closed loop is said to be negative. The closed loop is positive when variations in output mirror variations in input. The most common example of a negative closed-loop control system in the clinical setting is the ventilator humidifier. In this case, the input is the temperature inside the chamber, and the output is the temperature of the gas being delivered to the patient. The controlling algorithm is designed to keep the latter constantly above a value set by the operator. If the output (i.e., the temperature of gas delivered to the patient) is lower than the preset level, the algorithm will increase the input (i.e., the temperature in the chamber); if the output is higher than the preset level, the algorithm will decrease the input. Closed-loop systems are hence able to stabilize and limit the performance of a mechanical system.

In the case of acute respiratory failure, the patient is unable to provide sufficient output (i.e., minute ventilation). The ventilator should therefore be able to detect the input from the patient and continuously adapt the output. If the input is increasing (i.e., ventilatory requirements are increasing), the ventilator will increase the output (i.e., apply more positive pressure); if the input is decreasing (i.e., ventilatory requirements are decreasing), the ventilator will decrease the output (i.e., apply less positive pressure). The controlling closed loop eventually applied by the ventilator must therefore be positive. Positive closed-loop control systems are inherently unstable in the sense that they tend to (1) “run away” with ventilatory assistance—if the pressure generated by the ventilator is higher than the pressure required to offset the passive properties of the respiratory system, the ventilator will continue to deliver flow and volume while the patient stops his or her inspiratory effort and tries to initiate expiration; and (2) “extinguish” ventilatory assistance—if the patient does not produce any inspiratory effort, the ventilator will not produce any ventilatory support.

Based on closed-loop algorithms, new modes of mechanical ventilation have been proposed. Such approaches represent modifications of PSV and are characterized by the patient’s ability to control the amount of assistance provided by the ventilator. They are differentiated by the patient-related variable used to close the loop.

image Proportional Assisted Ventilation (PAV), Proportional Pressure Support (PPS), and Proportional Assisted Ventilation Plus (PAV+)

During proportional assisted ventilation (PAV) and proportional pressure support (PPS), the ventilator generates pressure in proportion to patient-generated flow and volume75,76; the ventilator amplifies patient effort without imposing any ventilatory or pressure targets. Ventilator-generated pressure rises as long as inspiratory muscle effort is produced by the patient. During PAV or PPS, the preset parameter is therefore not a pressure target. During these modes of mechanical support, the clinician adjusts the percentage of flow-assisted or volume-assisted ventilation after determining the patient’s resistance and elastance. In other words, the physician must determine how much to reduce the load imposed by the patient’s elastance77 and resistance.78,79

Despite the exciting potential of these techniques,79–82 applied either invasively or noninvasively,73–89 no large-scale studies have demonstrated an improvement in patient outcome compared with other modes of ventilation. PAV+ provides continuous measurement of the value of elastance and resistance of the patients according to the method described by Younes and coworkers.77–79,89,90 This option requires that the physician sets only a given percentage level of gain. During invasive ventilation, PAV+ seems to considerably reduce the incidence of patient-ventilator asynchronies compared to proportional ventilation with the manual adjustment of the percentage of flow-assisted or volume-assisted ventilation according to patient’s respiratory mechanics90 (Figure 49-7). As compared to PSV, PAV+ also was able to reduce the time for ventilatory settings and changes in sedative doses.91

image

Figure 49-7 Representative tracing of flow (Flow), airway pressure (Paw), esophageal pressure (Peso), gastric pressure (Pga) and transdiaphragmatic pressure (Pdi) during PAV+ ventilation. Directional arrow (bottom) going from left to right shows the gain is reduced from 95% to 50% with subsequently increased inspiratory effort. Dotted arrows (top) indicate the measurement of respiratory mechanics automatically computed by the ventilator.

image Neural-Adjusted Ventilatory Assistance

With neural-adjusted ventilatory assistance (NAVA), electrical activity of the diaphragm is measured by means of an electrode array inserted into a nasogastric tube and placed in the lower esophagus; this information is then used to control the ventilator to generate flow, volume, and pressure.8,42,43,92 Unlike with the proportional mode described earlier, estimates of respiratory mechanics are not needed; with NAVA, the patient’s respiratory center controls the assisted positive breaths in all phases of the ventilation cycle, from triggering to cycling off of inspiration. Any change in patient ventilatory output is matched breath by breath by the ventilator, even in the presence of variations in respiratory mechanics. A NAVA level equal to 1 corresponds to a support of 1 cm H2O for 1 µV of electrical diaphragm activity (EAdi). A representative tracing of NAVA is shown in Figure 49-8.

image

Figure 49-8 Representative tracing of flow (Flow), airway pressure (Paw), esophageal pressure (Peso), and transdiaphragmatic pressure (Pdi) during NAVA ventilation. The two dotted lines define the beginning and end of patient’s inspiratory effort.

image Adaptive-Support Ventilation

Adaptive-support ventilation is an assist time–limited, pressure-targeted mode of ventilation (pressure-controlled ventilation) that relies on a negative closed-loop system of regulating ventilator settings in response to changes in both respiratory impedance (elastance and resistance) and the patient’s spontaneous efforts.93 The basic principle relies on the work of Otis and coworkers94 and Mead,6 demonstrating that for a given level of minute alveolar ventilation, there is a respiratory rate that is least costly in terms of respiratory work. With adaptive support ventilation, the operator enters the patient’s body weight and sets the desired percentage of minute ventilation. The expiratory time constant is determined by analysis of the expiratory flow-volume curve,95 adjusting inspiratory pressure, inspiratory-expiratory time ratio, and respiratory rate to obtain the prescribed minute ventilation. Adaptive support ventilation thus adjusts inspiratory pressure, inspiratory-expiratory time ratio, and mandatory respiratory rate to maintain the target minute ventilation and respiratory rate within a framework designed to avoid both rapid, shallow breathing and excessive inflation volumes. Spontaneous breathing triggers either a pressure-controlled or a spontaneous breath with inspiratory pressure support, the level of which is adjusted to meet the target respiratory rate–tidal volume combination.

Key Points

1 Patient-ventilator asynchrony is common during mechanical ventilatory support. It is often unrecognized, underestimated, and inappropriately treated in the clinical setting.
2 Patient-ventilator asynchrony takes place when the three physiologic variables of the patient’s breathing pattern—ventilatory drive, ventilatory requirements, and duration and ratio of inspiratory time to total breath cycle duration—do not match ventilator trigger, ventilator-delivered flow, and ventilator cycling criteria.
3 Clinical optimization of patient-ventilator interactions can be obtained only by continuously matching the triggering, flow delivering, and cycling functions of the ventilator with the patient’s physiologic variables.
4 Optimization of patient-ventilator interactions during invasive or noninvasive ventilation implies continuous measurement of physiologic variables and continuous adaptation of the ventilator to the spontaneous variations in these physiologic variables.
5 Future developments in ventilator technology should be oriented toward a system with the capability to automatically interface between physiologic parameters and ventilator outputs. Such technology will be based on closed-loop algorithms able to achieve total patient-controlled mechanical support.

Annotated References

Appendini L, Purro A, Gudjonsdottir M, et al. Physiologic response of ventilator-dependent patients with chronic obstructive pulmonary disease to proportional assist ventilation and continuous positive airway pressure. Am J Respir Crit Care Med. 1999;159(5):1510-1517.

This study found that in difficult-to-wean patients with chronic obstructive pulmonary disease, proportional assisted ventilation (PAV) improves ventilation and decreases inspiratory muscle effort. It also found that the combination of PAV and continuous positive airway pressure can unload the inspiratory muscles to values close to those in normal subjects.

Beck J, Sinderby C, Lindström L. Effects of lung volume on diaphragm EMG signal strength during voluntary contractions. J Appl Physiol. 1998;85(3):1123-1134.

These authors found that variations in end-expiratory lung volume between breaths can affect the transformation of respiratory muscle activation into mechanical output (neuromechanical coupling).

Calderini E, Confalonieri M, Puccio PG, et al. Patient-ventilator asynchrony during noninvasive ventilation: the role of the expiratory trigger. Intensive Care Med. 1999;25(7):662-667.

This article describes the loose patient-ventilator synchrony in the presence of air leaks and noninvasive pressure-support ventilation.

Laghi F, Karamchandani K, Tobin MJ. Influence of ventilator settings in determining respiratory frequency during mechanical ventilation. Am J Respir Crit Care Med. 1999;160(5):1766-1770.

These authors found that during assist-control mode, ventilator inspiratory time can determine respiratory frequency independently of inspiratory flow and tidal volume.

Leung P, Jubran A, Tobin MJ. Comparison of assisted ventilator modes on triggering, patients’ effort, and dyspnea. Am J Respir Crit Care Med. 1997;155(6):1940-1948.

This study found that when receiving assist-control ventilation or high levels of pressure support, one-quarter to one-third of a patient’s inspiratory efforts may fail to open the inspiratory valve triggering the machine. The number of ineffective triggering attempts increases in proportion to the level of ventilatory assistance and is not correlated to the magnitude of inspiratory effort at a given level of assistance.

Parthasarathy S, Jubran A, Tobin MJ. Cycling of inspiratory and expiratory muscle groups with the ventilator in airflow limitation. Am J Respir Crit Care Med. 1998;158(5):1471-1478.

These authors found that the continuation of a mechanical mandatory breath into neural expiration is associated with a waste of inspiratory effort, defined as failure of the subsequent inspiratory attempt to trigger the ventilator.

Parthasarathy S, Tobin JM. Effect of ventilator mode on sleep quality in critically ill patients. Am J Respir Crit Care Med. 2002;166(11):1423-1429.

These authors found that inspiratory assistance during pressure support causes hypocapnia, which combined with lack of a backup rate and wakefulness drive can lead to central apneas and sleep fragmentation, especially in patients with heart failure. A backup rate, as during assist-control volume-targeted ventilation, prevents the development of apneas and perhaps decreases arousals.

Sinderby C, Navalesi P, Beck J, et al. Neural control of mechanical ventilation in respiratory failure. Nat Med. 1999;5(12):1433-1436.

This article describes a completely new mode of detecting inspiratory effort, based on the measurement of electrical activity of the diaphragm by means of an electrode array inserted into a nasogastric tube and placed in the lower esophagus. Output generated from the electrodes, filtered out for, is used to control the ventilator that finally generates the respiratory output.

Tobert DG, Simon PM, Stroetz RW, Hubmayr RD. The determinants of respiratory rate during mechanical ventilation. Am J Respir Crit Care Med. 1997;155(2):485-492.

The authors examined the rate response of eight normal volunteers during both quiet wakefulness and non-rapid-eye-movement (non-REM) sleep in the setting of mechanical ventilation through a nasal mask in an assist-control mode with a machine backup rate of 2 breaths per minute. They found that both tidal volume and inspiratory flow settings affect the respiratory rate and can affect carbon dioxide homeostasis. During non-REM sleep, hypocapnia resulted in wasted ventilator trigger efforts. Thus, ventilator settings appropriate for wakefulness may cause ventilatory instability during sleep.

Younes M, Webster K, Kun J, et al. A method for measuring passive elastance during proportional assist ventilation. Am J Respir Crit Care Med. 2001;164(1):50-60.

A noninvasive method to continuously measure elastance of the respiratory system during proportional assisted ventilation is described.

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