The response of the ventilator to a patient’s effort is influenced by ventilator variables including the trigger variable that initiates the breath, pressure delivery, and the cycle variable that terminates the breath.

The trigger variable is controlled by either a flow or pressure signal derived from the airway. Figure 15.2 illustrates a comparison of two trigger variables. For pressure triggering, the patient must decrease the pressure in the ventilator circuit, by an isometric contraction of the respiratory muscles, to a preset value to completely open the inspiratory valve and initiate a mechanical breath. In flow triggering, the patient must generate a change in flow, sensed between the ventilator’s inspiratory and expiratory pneumotachographs, by an isotonic contraction of the respiratory muscles. It has been generally believed that there are distinct advantages of flow triggering (Carmack et al. 1995; Branson et al. 1994; Giuliani et al. 1995; Sasson et al. 1994; Heulitt et al. 2000, 2003; Sanders et al. 2001). However, current ventilators are microprocessor controlled, replacing mechanical responses to patient triggering seen in older generation ventilators. The result of the microprocessor controller is a faster response time with decreased trigger delay. This improvement may negate the advantages in adult patients with larger endotracheal tubes and mature respiratory muscles. This does not appear to be true in neonatal and pediatric patients. As can be seen in Fig. 15.2 (Sanders et al. 2001), flow triggering results in a faster response time and decreased effort necessary to trigger in a pediatric-sized animal model during pressure support ventilation. These differences are important because during triggering, the initial phase of patient effort reflects essentially patient work until the inspiratory valve opens completely and delivers gas to the proximal airway. This is illustrated in Fig. 15.3, where a tracing of pressure, flow, and volume is recorded at an animal’s airway during pressure support. In this example, there is a waveform illustrating the opening and closing of the inspiratory valve with a tracing of the animal’s muscular response, illustrated by an EMG tracing of the diaphragm. In a study of pediatric-sized lambs, WOB during flow triggering was reduced by 47 % during pressure support and 19 % in CPAP (Carmack et al. 1995). However, there have been no controlled studies in pediatric and neonatal patients to determine if these differences affect outcome measures such as length of ventilation.

It is important to note that despite the differences illustrated in the type of triggering, there are also differences related to the design characteristics of the ventilator. These differences relate to ventilator control algorithms that can affect trigger delay. Trigger delay is the time from the beginning of inspiratory muscle activity and the beginning of mechanical inflation (increase in pressure at the proximal airway). Increased trigger delay has been associated with the design characteristics of the pneumatics and electronics of ventilator system and correlated with respiratory drive (Leung et al. 1997) more time to trigger with less drive. This is especially important in small preterm infants, who have intrinsically short inspiratory times. For instance, if the inspiratory time is 0.2 s and the trigger delay is 100 ms, the patient will be halfway through the inspiratory phase before mechanical assistance is appreciated.

In a study between two microprocessor-controlled neonatal ventilators, it was found that there was a significant difference in trigger delay and work of breathing between these two ventilators (Heulitt et al. 2000) illustrating the role of ventilator design on both work of breathing and triggering. Once triggering occurs, there is pressurization of ventilator circuit and subsequently the patient.

Control variables include pressure, flow, and volume. Once the trigger variable is met and the inspiratory valve opens fully, there is pressurization of the ventilator circuit by the delivery of fresh gas flow. This pressurization of the system is illustrated in Fig. 15.4. The phase of this pressurization can be subdivided into the inspiratory positive pressure area or area 2 on Fig. 15.4 (Chatmongkolchart et al. 2001), which follows area 1, and is the amount of effort expended to activate the mechanical breath. Area 2 is defined by the start of the inspiratory pressure curve with the return of pressure to baseline and ending at the onset of expiration. Area 2 represents the ability of the ventilator to pressurize the system or the actual area of pressure versus time applied during inspiration. The variables that control the delivered pressure depend upon the mode of ventilation and the controller utilized in that mode. For example, in a mode with a preset tidal volume (e.g., volume assist-control), upon triggering the ventilator operates under a preset flow-time profile for the delivery of the tidal volume, and the ventilator determines the mechanical inflation time. In contrast, in a mode where there is a preset pressure (e.g., pressure support ventilation), the inflation time is influenced by both the patient and the ventilator. MacIntyre et al. (1990) demonstrated that if a rise in flow is not commensurate with the patient’s demand during pressure support ventilation, there may be a too rapid rise in flow, or flow may be inadequate to meet the patient’s effort. In either case patient-ventilator asynchrony can result. Current ventilators also have dual control capability. Some modes (e.g., PAV, PRVC, VS) offer a theoretical compensation for these limitations. Breaths are regulated by one variable to meet a target variable. For example, in PRVC, the clinician sets a target volume and then regulates the delivered pressure between each breath to reach that volume target. In contrast, in PAV the ventilator delivers pressure that is proportional and set by the clinician to instantaneous flow and volume and thus the patient’s own P _mus. Thus, depending upon the mode, it may or may not reflect corresponding changes in patient’s effort.

The cycle off variable is the variable that controls the end of inspiration. This can be a clinician-controlled variable. As can be seen in Fig. 15.5, the timing of this trigger signal may not correspond to the end of neural inspiration and the peak of diaphragmatic activity or contraction of inspiratory muscles after the close of the inspiratory valve. Thus, if flow stops either before or after the patient’s own inspiratory flow, expiratory flow occurs before the end of inspiratory effort. In this situation, P _mus continues to increase even though inspiratory flow is zero (inspiratory valve closed) or is revered, and the muscle tension is applied to the elastic recoil of the respiratory system rather than obtaining further inspiratory flow. Thus, at the end of mechanical inspiration, P _mus continues to increase the muscle tension applied to overcome elastic recoil of the respiratory system causes a short mechanical inflation and low elastic recoil at end-inspiration and can promote re-triggering or ineffective triggering. The effects of asynchrony depend on the type of asynchrony present (Georgopoulos and Roussos 1996) and will be discussed further below. In the newborn, use of flow cycling is important in achieving expiratory synchrony because of the rapidity with which the respiratory time constant can change.