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Make ventilatory support meet patient demand

Patient-ventilator asynchrony appears in many different types. The presence of each type of asynchrony is associated with specific patient and ventilator risk factors, and adverse effects. Each type of asynchrony can be categorized according to its relationship to specific phases of the delivered breath: breath initiation, flow delivery and breath cycling/termination.

Asynchrony Begets More Asynchrony

As asynchrony has a negative impact on respiratory mechanics, it may predispose patients to increased and/or different types of asynchrony.

IMAGE 1. The influence of patient-ventilator asynchrony on respiratory mechanics and subsequent asynchrony11,14,17,20

Managing Patient-Ventilator Interaction

In circumstances where there is a mismatch between patient demand and ventilatory delivery, the result is frequently patient-ventilator asynchrony (e.g. fighting the ventilator), which may negatively influence patient outcome.21, 22  Conversely, passive mechanical ventilation in which patient demand is eliminated, via sedative or neuromuscular blockade, may also produce diaphragmatic injury or ventilator-induced diaphragmatic dysfunction.21

IMAGE 2. Scenarios of patient ventilator interaction during mechanical ventilation21

VENTILATOR AND PATIENT FACTORS INFLUENCING THE OCCURRENCE OF ASYNCHRONY6
PATIENT FACTORS: VENTILATOR FACTORS:
Intrinsic Respiratory Rate Mode
Minute Ventilation Minute Ventilation
Respiratory Drive Triggering criteria
Airway Resistance Cycling criteria
Lung Volume Rise Time
Compliance Tidal Volume
Respiratory Muscle Function Expiratory Time
VENTILATOR AND PATIENT FACTORS INFLUENCING THE OCCURRENCE OF ASYNCHRONY6
PATIENT FACTORS: VENTILATOR FACTORS:
Intrinsic Respiratory Rate Mode
Minute Ventilation Minute Ventilation
Respiratory Drive Triggering criteria
Airway Resistance Cycling criteria
Lung Volume Rise Time
Compliance Tidal Volume
Respiratory Muscle Function Expiratory Time

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Influence of underlying patient condition

Respiratory mechanics significantly impact patient-ventilator interaction. Therefore, specific patient conditions that influence respiratory mechanics may predispose patients to specific types of asynchrony.

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
PATIENT CHARACTERISTICS Increased lung compliance
Higher airway resistance
Longer time constant
RELATIONSHIP TO ASYNCHRONY Increased presence of intrinsic PEEP (PEEPi) is a common cause of ineffective efforts with flow triggering, as the patient effort required to trigger the ventilator must first overcome any alveolar pressure present at the end of exhalation11
Additional airway resistance may extend ventilator inspiratory time. Patients with a lower cycling-off threshold of peak inspiratory flow are prone to delayed cycling, shortened expiratory time (already compromised by increased expiratory resistance) and additional air-trapping.20

Influence of underlying patient condition

Respiratory mechanics significantly impact patient-ventilator interaction. Therefore, specific patient conditions that influence respiratory mechanics may predispose patients to specific types of asynchrony.

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
PATIENT CHARACTERISTICS Increased lung compliance
Higher airway resistance
Longer time constant
RELATIONSHIP TO ASYNCHRONY Increased presence of intrinsic PEEP (PEEPi) is a common cause of ineffective efforts with flow triggering, as the patient effort required to trigger the ventilator must first overcome any alveolar pressure present at the end of exhalation11
Additional airway resistance may extend ventilator inspiratory time. Patients with a lower cycling-off threshold of peak inspiratory flow are prone to delayed cycling, shortened expiratory time (already compromised by increased expiratory resistance) and additional air-trapping.20
ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)
PATIENT CHARACTERISTICS Decreased lung compliance
Higher airway resistance
Shorter time constant
RELATIONSHIP TO ASYNCHRONY In contrast to COPD patients, stiff-lung ARDS patients with a higher cycling-off threshold of peak inspiratory flow are prone to premature cycling, which may or may not be accompanied by double-triggering. This premature cycling leads to decreased tidal volume delivery and consequent increases in work of breathing.19
ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)
PATIENT CHARACTERISTICS Decreased lung compliance
Higher airway resistance
Shorter time constant
RELATIONSHIP TO ASYNCHRONY In contrast to COPD patients, stiff-lung ARDS patients with a higher cycling-off threshold of peak inspiratory flow are prone to premature cycling, which may or may not be accompanied by double-triggering. This premature cycling leads to decreased tidal volume delivery and consequent increases in work of breathing.19

Achieving Balance

Often the optimization of patient-ventilator interaction causes the clinician to adjust the ventilator in order find a balance between two harmful extremes. For example, determining the appropriate trigger sensitivity involves striking a balance of between ineffective efforts (i.e. overlyinsensitive trigger) and auto-trigger (i.e. overly sensitive trigger). A review of the asynchrony evidence reveals many of these scenarios. Like many circumstances related to asynchrony, the success of a given ventilator adjustment may be confounded by several related patient and ventilator factors.

IMAGE 3. Clinical consequences of asynchrony due to suboptimal breath triggering threshold, cycling threshold, pressurization rate/rise time, and level of assistance:1,2,5,11, 23 , 24

Adverse Consequences of Patient-Ventilator Asynchrony

Though it is unclear whether asynchrony is a marker of disease severity or the cause of negative outcome, there is significant evidence associating asynchrony with mortality, delayed weaning and increased hospital length of stay. However, it is clear that asynchrony has a negative influence on gas exchange, respiratory muscle function, patient comfort, and lung protection. It is possible that these are the mechanisms of injury by which asynchrony influences patient outcome. 

MECHANISM INJURY
RESPIRATORY MUSCLE FUNCTION Asynchrony may work synergistically with multiple other factors related to critical illness to impose excessive muscle loading on the respiratory muscles. Ventilatory muscle failure occurs when respiratory muscle demand overwhelms respiratory muscle capability. Therefore, additional work of breathing associated with asynchrony may have a negative impact on respiratory muscle function, potentially leading to dyspnea, discomfort and increased time on ventilator.2,23,25 Likewise, sustained exposure to excessive muscle loading predisposes patients to structural damage of the respiratory muscles.24
ALTERED GAS EXCHANGE Patient-ventilator asynchrony may have a negative effect on gas exchange.1
Both double-triggering and delayed cycling may result in incomplete lung emptying and consequent dynamic hyperinflation, which may lead to ventilation-perfusion mismatch, causing hypoxemia and hypercapnia.26
Auto-triggering may result in hyperventilation, causing hypocapnia and alkalemia.1
DEFEATING LUNG PROTECTIVE VENTILATION In the wake of the ARDSnet trial, lung protective ventilation (lower tidal volumes, ~6-8 mL/kg/min) has become the standard of care for the prevention of additional lung injury in patients with acute respiratory distress syndrome.27
However, lung protective ventilation in the presence of increased respiratory drive may lead to an increase incidence of double triggering.5 Double-triggering leads to significantly increased tidal volume5, resulting in the delivery of potential harmful volumes.26
DYSPENEA AND DISCOMFORT Asynchrony is associated with increased dyspnea and discomfort, which may result in sleep disruption and/or increased need for sedation. Both sleep disruption and additional sedation are associated with negative outcomes in mechanically ventilated ICU patients.
DYSPNEA Dyspnea results from the increased demand on respiratory muscles required to overcome imposed load. As several types of asynchrony are associated with increased work of breathing,2,19 asynchrony may play a role in the etiology of dyspnea.
Ineffective efforts,5 and flow asynchrony,2 are associated with increased dyspnea
Schmidt et al. determined that in 35% of patients with dyspnea, ventilator asynchronies were involved in the pathogenesis of dyspnea28
DISCOMFORT Multiple studies have demonstrated a relationship between discomfort and asynchrony
Vitacca et al demonstrated that increasing pressure support level was associated with an increase in both the incidence of ineffective efforts and patient discomfort.5
Vignaux et al determined that an asynchrony index of > 10% was associated with a significant increase in discomfort.29
SLEEP Asynchrony has been implicated in sleep disruption.30
Interventions to decrease asynchrony have been demonstrated to increase rapid eye movement (REM) sleep by two-fold and slow wave sleep by three-fold.30
In patients with preexisting pulmonary comorbidity, sleep loss may be associated with decreased pulmonary function, which may delay weaning.31
SEDATION In a study by Pohlman et al, asynchrony was responsible for 42% of all increases in sedation.17
Multiple studies have demonstrated that sedation in ICU patients is associated with increased duration of mechanical ventilation, hospital and ICU length of stay, and mortality.32

Adverse Consequences of Patient-Ventilator Asynchrony

Though it is unclear whether asynchrony is a marker of disease severity or the cause of negative outcome, there is significant evidence associating asynchrony with mortality, delayed weaning and increased hospital length of stay. However, it is clear that asynchrony has a negative influence on gas exchange, respiratory muscle function, patient comfort, and lung protection. It is possible that these are the mechanisms of injury by which asynchrony influences patient outcome. 

MECHANISM INJURY
RESPIRATORY MUSCLE FUNCTION Asynchrony may work synergistically with multiple other factors related to critical illness to impose excessive muscle loading on the respiratory muscles. Ventilatory muscle failure occurs when respiratory muscle demand overwhelms respiratory muscle capability. Therefore, additional work of breathing associated with asynchrony may have a negative impact on respiratory muscle function, potentially leading to dyspnea, discomfort and increased time on ventilator.2,23,25 Likewise, sustained exposure to excessive muscle loading predisposes patients to structural damage of the respiratory muscles.24
ALTERED GAS EXCHANGE Patient-ventilator asynchrony may have a negative effect on gas exchange.1
Both double-triggering and delayed cycling may result in incomplete lung emptying and consequent dynamic hyperinflation, which may lead to ventilation-perfusion mismatch, causing hypoxemia and hypercapnia.26
Auto-triggering may result in hyperventilation, causing hypocapnia and alkalemia.1
DEFEATING LUNG PROTECTIVE VENTILATION In the wake of the ARDSnet trial, lung protective ventilation (lower tidal volumes, ~6-8 mL/kg/min) has become the standard of care for the prevention of additional lung injury in patients with acute respiratory distress syndrome.27
However, lung protective ventilation in the presence of increased respiratory drive may lead to an increase incidence of double triggering.5 Double-triggering leads to significantly increased tidal volume5, resulting in the delivery of potential harmful volumes.26
DYSPENEA AND DISCOMFORT Asynchrony is associated with increased dyspnea and discomfort, which may result in sleep disruption and/or increased need for sedation. Both sleep disruption and additional sedation are associated with negative outcomes in mechanically ventilated ICU patients.
DYSPNEA Dyspnea results from the increased demand on respiratory muscles required to overcome imposed load. As several types of asynchrony are associated with increased work of breathing,2,19 asynchrony may play a role in the etiology of dyspnea.
Ineffective efforts,5 and flow asynchrony,2 are associated with increased dyspnea
Schmidt et al. determined that in 35% of patients with dyspnea, ventilator asynchronies were involved in the pathogenesis of dyspnea28
DISCOMFORT Multiple studies have demonstrated a relationship between discomfort and asynchrony
Vitacca et al demonstrated that increasing pressure support level was associated with an increase in both the incidence of ineffective efforts and patient discomfort.5
Vignaux et al determined that an asynchrony index of > 10% was associated with a significant increase in discomfort.29
SLEEP Asynchrony has been implicated in sleep disruption.30
Interventions to decrease asynchrony have been demonstrated to increase rapid eye movement (REM) sleep by two-fold and slow wave sleep by three-fold.30
In patients with preexisting pulmonary comorbidity, sleep loss may be associated with decreased pulmonary function, which may delay weaning.31
SEDATION In a study by Pohlman et al, asynchrony was responsible for 42% of all increases in sedation.17
Multiple studies have demonstrated that sedation in ICU patients is associated with increased duration of mechanical ventilation, hospital and ICU length of stay, and mortality.32

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  • 1. Chiumello D, Pelosi P, Croci M, Bigatello LM, Gattinoni L. The effects of pressurization rate on breathing pattern, work of breathing, gas exchange and patient comfort in pressure support ventilation. The European respiratory journal. 2001;18(1):107-114. View Abstract
  • 2. Gilstrap D, MacIntyre N. Patient-ventilator interactions. Implications for clinical management. American journal of respiratory and critical care medicine. 2013;188(9):1058-1068. View Abstract
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  • 12. Imanaka H, Nishimura M, Takeuchi M, Kimball WR, Yahagi N, Kumon K. Autotriggering caused by cardiogenic oscillation during flow-triggered mechanical ventilation. Critical care medicine. 2000;28(2):402-407. View Abstract
  • 13. Sassoon C. Triggering of the ventilator in patient-ventilator interactions. Respiratory care. 2011;56(1):39-51. View Abstract
  • 14. Bernstein G, Knodel E, Heldt GP. Airway leak size in neonates and autocycling of three flow-triggered ventilators. Critical care medicine. 1995;23(10):1739-1744. View Abstract
  • 15. Shoham AB, Patel B, Arabia FA, Murray MJ. Mechanical ventilation and the total artificial heart: optimal ventilator trigger to avoid post-operative autocycling - a case series and literature review. Journal of cardiothoracic surgery. 2010;5:39. View Abstract
  • 16. Pohlman MC, McCallister KE, Schweickert WD, et al. Excessive tidal volume from breath stacking during lung-protective ventilation for acute lung injury. Critical care medicine. 2008;36(11):3019-3023. View Abstract
  • 17. de Wit M. Monitoring of patient-ventilator interaction at the bedside. Respiratory care. 2011;56(1):61-72. View Abstract
  • 18. Tokioka H, Tanaka T, Ishizu T, et al. The effect of breath termination criterion on breathing patterns and the work of breathing during pressure support ventilation. Anesthesia and analgesia. 2001;92(1):161-165. View Abstract
  • 19. Tassaux D, Gainnier M, Battisti A, Jolliet P. Impact of expiratory trigger setting on delayed cycling and inspiratory muscle workload. American journal of respiratory and critical care medicine. 2005;172(10):1283-1289. View Abstract
  • 20. Gentile MA. Cycling of the mechanical ventilator breath. Respiratory care. 2011;56(1):52-60. View Abstract
  • 21. Pierson DJ. Patient-ventilator interaction. Respiratory care. 2011;56(2):214-228.
  • 22. Epstein SK. How often does patient-ventilator asynchrony occur and what are the consequences? Respiratory care. 2011;56(1):25-38.
  • 23. Kallet RH. Patient-ventilator interaction during acute lung injury, and the role of spontaneous breathing: part 1: respiratory muscle function during critical illness. Respiratory care. 2011;56(2):181-189.
  • 24. Chiumello D, Polli F, Tallarini F, et al. Effect of different cycling-off criteria and positive end-expiratory pressure during pressure support ventilation in patients with chronic obstructive pulmonary disease. Critical care medicine. 2007;35(11):2547-2552.
  • 25. Branson RD, Blakeman TC, Robinson BR. Asynchrony and dyspnea. Respiratory care. 2013;58(6):973-989. View Abstract
  • 26. Kent BD, Mitchell PD, McNicholas WT. Hypoxemia in patients with COPD: cause, effects, and disease progression. International journal of chronic obstructive pulmonary disease. 2011;6:199-208. View Abstract
  • 27. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. The New England journal of medicine. 2000;342(18):1301-1308. View Abstract
  • 28. Schmidt M, Demoule A, Polito A, et al. Dyspnea in mechanically ventilated critically ill patients. Critical care medicine. 2011;39(9):2059-2065. View Abstract
  • 29. Vignaux L, Vargas F, Roeseler J, et al. Patient-ventilator asynchrony during non-invasive ventilation for acute respiratory failure: a multicenter study. Intensive care medicine. 2009;35(5):840-846. View Abstract
  • 30. Bosma K, Ferreyra G, Ambrogio C, et al. Patient-ventilator interaction and sleep in mechanically ventilated patients: pressure support versus proportional assist ventilation. Critical care medicine. 2007;35(4):1048-1054. View Abstract
  • 31. Kamdar BB, Needham DM, Collop NA. Sleep deprivation in critical illness: its role in physical and psychological recovery. Journal of intensive care medicine. 2012;27(2):97-111. View Abstract
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