Patient-Ventilator Dyssynchrony

Abstract

In mechanically ventilated patients, assisted mechanical ventilation (MV) is employed early, following the acute phase of critical illness, in order to eliminate the detrimental effects of controlled MV, most notably the development of ventilator-induced diaphragmatic dysfunction. Nevertheless, the benefits of assisted MV are often counteracted by the development of patient-ventilator dyssynchrony. Patient-ventilator dyssynchrony occurs when either the initiation and/or termination of mechanical breath is not in time agreement with the initiation and termination of neural inspiration, respectively, or if the magnitude of mechanical assist does not respond to the patient's respiratory demand. As patient-ventilator dyssynchrony has been associated with several adverse effects and can adversely influence patient outcome, every effort should be made to recognize and correct this occurrence at bedside. To detect patient-ventilator dyssynchronies, the physician should assess patient comfort and carefully inspect the pressure- and flow-time waveforms, available on the ventilator screen of all modern ventilators. Modern ventilators offer several modifiable settings to improve patient-ventilator interaction. New proportional modes of ventilation are also very helpful in improving patient-ventilator interaction.

Keywords: assisted mechanical ventilation; critical illness; dyssynchrony; mechanical ventilation.

Figure 1.

Schematic illustration of the respiratory system and the applied pressures. The respiratory system is presented as a balloon at passive functional residual capacity (FRC) (continuous line). Two dashed lines indicate volumes above (ΔV₁) and below (ΔV₂) FRC. In mechanically ventilated patients during inspiration ventilator pressure (Paw) and pressure developed by inspiratory muscles (Pmus_I) generate flow and the volume increases above passive FRC. The sum of these two pressures is dissipated to overcome elastic pressure (Pel), and resistive pressure (Pres). All these pressures have positive values in the equation of motion. Pressure developed by contraction of expiratory muscles (Pmus_E), elastic recoil pressure due to volume below passive FRC and resistive pressure due to V’_E have negative values in the equation. V’_I : inspiratory flow; Rrs: resistance of the respiratory system; V’_E: expiratory flow; Ers: elastance of the respiratory system. Modified from Kondili et al. Br J Anaesth 2003;91:106-19, with permission of Oxford University Press [43].

Figure 2.

Airway pressure (Paw), flow and esophageal pressure (Pes) time curves in a patient ventilated with pressure support ventilation. Observe that the second decrease in Pes, which represents inspiratory effort of the patient, is not followed by a mechanical breath. This is ineffective effort (IE) during expiration and is manifested by a slight decrease in Paw associated with a simultaneous decrease in expiratory flow (red arrows). Notice that the signal of flow distortion is much clearer than the corresponding Paw change. In every mechanical breath, there is a time lag between the start of neural inspiration (first dotted line) and the start of mechanical inspiration (second dotted line). This time lag is the triggering delay. Observe the spike early in expiratory flow (black arrows) after each breath that suggests high airway resistance and long-time constant causing incomplete exhalation (flow is not zero before the next breath). Dynamic hyperinflation causes triggering delay and, combined with a relatively weaker patient effort (second Pes deflection smaller than the others) leads to ineffective triggering.

Figure 3.

Flow and esophageal pressure (Pes) time curves in a patient ventilated with pressure support ventilation. The start of neural inspiration (dotted line) is indicated by a rapid decrease in Pes associated with a rapid decrease in expiratory flow (expiratory flow returns rapidly to zero line). The two subsequent patient efforts are not accompanied by a mechanical breath and represent ineffective efforts (IE, red arrows). Both can be identified by the associated flow distortion. The first IE takes place during mechanical inspiration and causes an increase in inspiratory flow waveform. The second IE happens during expiration and is manifested by a decrease in expiratory flow. The spike early in expiratory flow (black arrow) due to high airway resistance and the incomplete exhalation (flow is not zero before the next breath) are signs of dynamic hyperinflation.

Figure 4.

Airway pressure (Paw), flow and transdiaphragmatic pressure (Pdi) time curves of a patient ventilated on pressure support ventilation are illustrated. As indicated by the absence of Pdi increase, there is no inspiratory effort before the second mechanical breath (autotriggered breath, see blue shaded area). We can observe that, in comparison to patient-triggered breaths, where a decrease in Paw is observed before the start of mechanical inflation (grey shaded areas), there is no distortion in the Paw- (no decrease in Paw) and flow-time curve in the autotriggered breath. Moreover, the shape of the inspiratory flow-time curve is different compared to that of patient-triggered breaths. Notice the absence of dynamic hyperinflation in this patient (expiratory flow returns to zero after each breath).

Figure 5.

Delayed opening of the expiratory valve. Flow, airway pressure (Paw), gastric pressure (Pgas) and esophageal pressure (Pes) time waveforms in a patient ventilated with pressure support ventilation. There is a significant time delay (blue shaded area) between the end of neural inspiration, recognized by a rapid increase in Pes, and the end of mechanical inspiration, signified by the termination of inspiratory flow (inspiratory flow equals zero). Observe the rapid increase of Paw towards the end of mechanical inspiration, indicating inspiratory muscle relaxation.

Figure 6.

Reverse triggering in a patient ventilated with assist pressure control ventilation. There is an inspiratory effort of the patient (dotted lines), as evidenced by the rapid increase in electromyographic activity of the diaphragm (EAdi) after every mechanical inflation (1:1 relationship). The time interval between the initiation of mechanical and neural inspiration is fixed. Indirect evidence of patient inspiratory activity during mechanical inflation is the notch in Paw (grey shaded area). Paw: airway pressure; V_T: tidal volume.

Figure 7.

Reverse triggering in a patient ventilated with assist volume control ventilation. Esophageal pressure (Pes) decrease reveals patient inspiratory efforts (blue line) after every mechanical inflation in 1:1 relationship. Indirect evidence of patient inspiratory activity during mechanical inflation is the flow distortion (grey shaded area) and the disappearance (blue arrows) of plateau airway pressure (Paw) in the flow-time and Paw-time waveform, respectively. In this patient, a reverse triggered breath was strong enough to trigger the ventilator at the end of the mechanical inspiration, causing breath stacking (red shaded area). Inflated tidal volume (V_T) during breath stacking increased from 444 ml to 800 ml (double arrow).

Figure 8.

Flow, airway pressure (Paw), esophageal pressure (Pes) and transdiaphragmatic pressure (Pdi) time waveforms in a patient ventilated with pressure support ventilation. Observe the vigorous contraction of inspiratory muscles (Pdi increase) during the mechanical inspiration. The magnitude of this contraction causes a rounded inspiratory flow and a large decrease of Paw (gray shaded area) from the expected square-shaped form during inspiration. Rounded flow and Paw decrease are signs of low ventilator assist with respect to patients ventilator demands.

Figure 9.

High assist in a patient ventilated with pressure support ventilation. Observe the square shaped airway pressure (Paw) and the abrupt decrease in inspiratory flow to flow threshold for cycling off towards the end of inspiration (arrows). There is also a significant cycling off delay (blue shaded area), seen often at high assist levels. Esophageal pressure (Pes) and electromyographic activity of the diaphragm (EAdi) decrease rapidly but mechanical inflation continues. Importantly, expiratory muscles contract during the whole expiration.