Patient-ventilator asynchrony

Abstract

Patient-v entilator asynchrony (PVA) is a mismatch between the patient, regarding time, flow, volume, or pressure demands of the patient respiratory system, and the ventilator, which supplies such demands, during mechanical ventilation (MV). It is a common phenomenon, with incidence rates ranging from 10% to 85%. PVA might be due to factors related to the patient, to the ventilator, or both. The most common PVA types are those related to triggering, such as ineffective effort, auto-triggering, and double triggering; those related to premature or delayed cycling; and those related to insufficient or excessive flow. Each of these types can be detected by visual inspection of volume, flow, and pressure waveforms on the mechanical ventilator display. Specific ventilatory strategies can be used in combination with clinical management, such as controlling patient pain, anxiety, fever, etc. Deep sedation should be avoided whenever possible. PVA has been associated with unwanted outcomes, such as discomfort, dyspnea, worsening of pulmonary gas exchange, increased work of breathing, diaphragmatic injury, sleep impairment, and increased use of sedation or neuromuscular blockade, as well as increases in the duration of MV, weaning time, and mortality. Proportional assist ventilation and neurally adjusted ventilatory assist are modalities of partial ventilatory support that reduce PVA and have shown promise. This article reviews the literature on the types and causes of PVA, as well as the methods used in its evaluation, its potential implications in the recovery process of critically ill patients, and strategies for its resolution.

Figure 1. Flow and pressure waveforms, respectively, illustrating two simulated types of ineffective triggering. The first two waveforms represent a patient without problems in respiratory mechanics, with a weak spontaneous effort (Pmus) because of respiratory muscle weakness or decreased neural drive. The bottom two waveforms represent a patient with airflow obstruction and difficulty in triggering some breaths because of the presence of auto-positive endexpiratory pressure, even with a muscle effort that is “physiological” but unable to trigger ventilator breaths. In both cases, pressure-controlled ventilation (pressure sensitivity of −2 cmH₂O) was used. The dots on the waveforms indicate ineffective efforts. Paw: airway pressure; and Pmus: muscle pressure. Source: Xlung^®.

Figure 2. Volume, flow and pressure waveforms, respectively, illustrating two simulated types of auto-triggering. The first three waveforms represent a patient on pressure-support ventilation with flow sensitivity. The system with a leak causes the onset of flow-triggered breaths, without patient effort (Pmus = 0). The bottom three waveforms represent a patient on pressure-controlled ventilation,* without respiratory muscle effort, but showing regular flow and pressure oscillations, with a respiratory rate of approximately 80 breaths/min, corresponding to his/her heart rate. Pressure sensitivity was changed to flow sensitivity. The increase in the total respiratory rate was due to triggers induced by transmission of flow oscillations because of cardiac activity. Vol.: volume; and Paw: airway pressure. Source: Xlung^®.

Figure 3. Volume, flow, and pressure waveforms, respectively, illustrating two simulations of asynchrony. The first three waveforms represent a case in which, because of patient neural inspiratory time, which is longer than the ventilator inspiratory time, the first breath is always triggered by the patient, during volume-controlled ventilation. The dots indicate stacked tidal volume caused by double triggering. The bottom three waveforms represent a case of reverse triggering due to respiratory muscle effort triggered by reflex mechanisms resulting from a ventilator-delivered breath, during pressure-controlled ventilation. Note, in both cases, stacked tidal volume and increased airway pressure during asynchrony. The dots indicate reverse triggering. Paw: airway pressure; and Pmus: muscle pressure. Source: Xlung^®.

Figure 4. Flow and pressure waveforms, respectively, illustrating two types of cycling asynchrony simulated during pressure support ventilation. The first two waveforms represent a patient with COPD. Asynchrony is corrected by increasing the threshold percentage of peak inspiratory flow for termination of inspiration. The bottom two waveforms represent a patient with restrictive lung disease experiencing premature cycling. Asynchrony is attenuated by decreasing the cycling threshold percentage of peak flow. The dots indicate cycling during pressure support ventilation. Paw: airway pressure; and Pmus: muscle pressure. Source: Xlung^®.

Figure 5. Volume, flow, and pressure waveforms, respectively, illustrating simulation of correction of flow asynchrony and volume asynchrony (air hunger), evident in the second breath, during VCV. The application of PCV from the third breath onward enabled delivery of flow and tidal volume. The patient responded with decreased muscle contraction (Pmus) from the fourth breath onward. Note a slight airway pressure overshoot at the end of breath during PCV (arrow), attenuated by better adaptation of the patient. The dots indicate free-flow delivery during PCV. VCV: volume-controlled ventilation; PCV: pressure-controlled ventilation; Paw: airway pressure;; and Pmus: muscle pressure. Source: Xlung^®.