Show Summary Details
Page of

Failure to ventilate in critical illness 

Failure to ventilate in critical illness
Chapter:
Failure to ventilate in critical illness
Author(s):

Vito Fanelli

and V. Marco Ranieri

DOI:
10.1093/med/9780199600830.003.0100
Page of

PRINTED FROM OXFORD MEDICINE ONLINE (www.oxfordmedicine.com). © Oxford University Press, 2020. All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use (for details see Privacy Policy and Legal Notice).

date: 30 November 2020

Key points

  • During assisted ventilation, patient and ventilator pumps share the work of breathing, avoiding both respiratory muscle atrophy and fatigue.

  • Deterioration of patient/ventilator interplay causes asynchrony, which is associated with prolonged mechanical ventilation, and longer intensive care unit and hospital length of stay.

  • Depending on the phase of the respiratory cycle, there are three types of asynchrony—asynchrony during the triggering phase; asynchrony during delivery of inspiratory flow; asynchrony during the cycling phase from inspiration to expiration.

  • Bedside analysis of flow and airways pressure traces allows recognizing patient–ventilator asynchrony. Altered mental status, discomfort, activation of accessory inspiratory and expiratory muscles, tachycardia, and hypertension are all signs associated with patient ventilator asynchrony.

  • Continuous adjustment of sedation, ventilator trigger, flow rate, and criteria of cycling from inspiration to expiration allow to minimize asynchronies.

Introduction

Mechanical ventilation is a life-saving therapy that is effective in reducing the work required to breathe and improves alveolar ventilation. Since its first description in 1952 during the polio epidemic, mechanical ventilation has become common practice for many physicians, and its technology has improved to provide better care for critically-ill patients [1]‌.

In the most severe forms of acute respiratory failure, the use of deep sedation and neuromuscular blocking agents dictate the adoption of controlled mechanical ventilation. The medical practitioner sets ventilator parameters with the aim of reducing oxygen consumption, improving gas exchange and oxygen availability in the whole organism.

In less severe forms of respiratory failure or during the resolution phase of the disease that has imposed the use of mechanical ventilation, assisted controlled ventilation allows patients to contribute to work of breathing, thus avoiding deep sedation, muscle atrophy, and long-term dependency from the ventilator.

The most robust model that helps to understand the complex interaction between patient and ventilator during respiratory failure is the equation of motion that states [2]‌:

P mus +   P aw   =   V * R   =   V T * E   +   PEEP i
[eqn 1]

where Pmus is the pressure developed by inspiratory muscles, Paw is the pressure applied to respiratory system by the ventilator, Vʹ‎ is the inspiratory flow, R is the airways resistance, VT is the tidal volume, E is the elastance of the respiratory system and PEEPi is the intrinsic PEEP. Based on this equation, respiratory failure occurs when there is an imbalance between the inspiratory muscle generating force and the inspiratory load through its resistance, elastic, and PEEPi components. Therefore, mechanical ventilation restores the balance, helping respiratory muscle to overcome inspiratory load. In particular, during controlled mechanical ventilation, the contribution of inspiratory muscles (Pmus) is negligible, and the ventilator generates pressure (Paw) to overcome the elastic (E) and resistive forces (R) of the respiratory system. This generates flow (Vʹ‎) and changes in volumes (VT). On the other hand, during assisted ventilation, both the inspiratory muscles and the ventilator pump work together to share the work required to overcome resistance and elastic loads, and the threshold pressure of PEEPi. Any deterioration of this complex interplay causes patient–ventilator asynchrony, which exposes the patient to the risk of failure to ventilate, meaning no rest for their muscles and deterioration of gas exchange. The aim of this current chapter is to define the most common examples of asynchronies between patients and the ventilator, explaining physiopathological mechanisms and common solutions at the bedside. It is noteworthy that around 25% of intensive care unit (ICU) patients experiences asynchrony with the ventilator and those who are failing to ventilate because of asynchrony are exposed to many risks, including prolonged mechanical ventilation [3,4], longer ICU, and hospital length of stay [4]‌.

Ideally, at the same moment when inspiratory muscles are contracting, patients should receive enough assistance from the ventilator to satisfy their ventilation needs and rest their muscles. This is until the switch from inspiration to expiration takes place. For this to happen, it is necessary that the ventilator promptly recognizes the inspiratory effort without delay, through an efficient trigger. Moreover, the machine should provide enough flow for the needs of the patient by matching the patient’s neural inspiratory time with that of the ventilator. Toward this end, it is easily understood that the perfect synchrony between patient and ventilator is a goal to achieve by the physician assessing the patient’s ventilator demands [3]‌. Necessary interventions to improve patient–ventilator interaction can be made by a bedside analysis of flow and airway pressure traces that are displayed on the ventilator’s screen [5].

There are three types of asynchrony:

  • Asynchrony during the triggering phase.

  • Asynchrony during delivery of inspiratory flow.

  • Asynchrony during the cycling phase from inspiration to expiration.

This classification takes into account the phase of the respiratory cycle in which the asynchrony occurs [5]‌.

Asynchrony between the patient’s ventilatory drive and ventilator’s trigger

Asynchrony during the triggering phase occurs when there is a discrepancy between the patient’s ventilatory drive and the ventilator’s trigger activation (Table 100.1). Inspiratory effort required to activate the trigger is an important part of the inspiratory effort [6]‌. Newer ventilators are equipped with pressure triggers that are as efficient as the flow triggers in terms of the time that elapses between effort and opening of the inspiratory valve. To date, due to the sensitivity of the trigger systems on newer ventilators, there is a greater risk of AutoTrigger than in their low-sensitivity counterparts. In fact, simple cardiac oscillations, movement of the condensate within the systems of the tubes or air leaks within the system, can activate the trigger [7]. The risk is that breaths, which are delivered by the ventilator without inspiratory effort, may lead to dynamic hyperinflation of the respiratory system, especially in heavily-sedated patients. Consequently, this removes every positive effect of assisted ventilation in terms of respiratory muscle activity. AutoTrigger may be recognized as a breath delivered by the ventilator that is not preceded by a drop in airway pressure as a consequence of inspiratory effort. In this case, it is important to verify the sensitivity of the trigger itself and adjust the level of sedation, such that the patient is not too deep [8].

Table 100.1 Different types of patient–ventilator asynchrony, in relation to the phase of the respiratory cycle in which are realized possible causes and remedies to implement

Type of asynchrony

Phase of respiratory cycle

Aetiology

Diagnosis

Solution

  • Asynchrony during triggering phase:

    • Autotrigger.

    • Trigger delay.

    • Ineffective triggering.

Inspiration

  • Autotrigger:

    • High trigger sensitivity; cardiac oscillations; movement of condense into tubing system; air leaks.

  • Trigger delay:

    • Depressed respiratory drive; over-assistance by the ventilator; increased elastic load (PEEPi).

  • Ineffective triggering:

    • Depressed respiratory drive; over-assistance by the ventilator; Increased elastic load (PEEPi).

  • Autotrigger:

    • Lack of decrease in the airway pressure tracing at the beginning of inspiration.

  • Trigger delay:

    • Time delay between the abrupt decrease of expiratory flow (with distortion of morphology) until it reaches zero line and the beginning of airway pressure increase

  • Ineffective triggering:

    • Time delay between the abrupt decrease of expiratory flow (with distortion of morphology) until it reaches zero line and the beginning of airway pressure increase.

  • Autotrigger:

    • Check trigger sensitivity; reduce the level of sedation; correct underlying respiratory alkalosis.

  • Trigger delay:

    • Reduce the level of sedation; reduce the level of assistance by the ventilator; minimize PEEPi, essentially increasing expiratory time.

  • Ineffective triggering:

    • Reduce the level of sedation; reduce the level of assistance by the ventilator; minimize PEEPi, essentially increasing expiratory time.

  • Asynchrony during the delivery of inspiratory flow:

    • Rate of increase in airway pressure.

    • Inspiratory flow.

Inspiration

  • Higher or lower rate of increase in airway pressure.

  • Higher or lower inspiratory flow.

  • Rate of increase in airway pressure:

    • Lower rate of increase in airway pressure is associated with increased work of breathing and patient’s discomfort.

  • Inspiratory flow:

    • Higher inspiratory flow is associated with a decrease of inspiratory time and an increase of respiratory rate.

  • Rate of increase in airway pressure:

    • Optimize the rate of increase in airway pressure to reduce dyspnoea and to avoid short inspiratory time, especially in patients with long time constant of respiratory system.

  • Inspiratory flow:

    • Titrate the inspiratory flow to patient’s ventilation needs avoiding the miss concept that higher inspiratory flow reduces tachypnoea.

Asynchrony during the cycling phase from inspiration to expiration.

Expiration

  • Patient’s neural inspiration lasts longer than ventilator inspiratory time.

  • Patient’s neural inspiration lasts less than ventilator inspiratory time.

  • Longer neural inspiration

  • ‘Double triggering’, two breaths delivered by the ventilator for each inspiratory effort: the asynchronous breath lasts less the breath before.

  • Shorter neural inspiration.

  • Activation of expiratory muscle during ventilator inspiratory time. Consequently, it’s possible to observe a sudden increase in the airway pressure at the end of inspiration.

  • Longer neural inspiration.

  • Change the expiratory trigger in order to increase the duration of inspiration. This means the expiration begins after higher percentage of flow decay.

  • Shorter neural inspiration.

  • Change the expiratory trigger in order to decrease the duration of inspiration. This means the expiration begins after lower percentage of flow decay.

Ideally, the patient’s inspiratory effort should coincide with the ‘breath’ delivered by the ventilator. The algorithms of the most recent ventilators are based on indirect measurements of the patient’s inspiratory time, such as flow or airway pressure signals. In fact, assuming the electrical activity of the diaphragm as the most useful measure to determine the beginning of the patient’s neural inspiratory time, several studies have shown that the inspiratory time identified by the activity of the diaphragm differs significantly from that identified by the analysis of flow, oesophageal pressure and trans-diaphragmatic pressure [9]‌. The direct consequence of this discrepancy is that patient–ventilator asynchronies may be generated and they are essentially of two types–trigger delay and ineffective triggering (Table 100.1). Trigger delay is defined as a delay between the patient’s inspiratory time (or the so-called neural trigger) and the breath delivered by the ventilator. The trigger delay can be caused mainly by a depressed respiratory drive [10,11] or by an increase in the elastic load caused by high levels of intrinsic PEEP (PEEPi) [9,12]. In five ICU patients, Parthasarathy showed a significant delay between the beginning of inspiratory effort of the patient, measured by the electrical activity of the crural diaphragm, and the beginning of inspiratory flow [9]. Moreover, in this small cohort of patients, a correlation between the trigger delay and the level of PEEPi was noted. As a consequence, PEEPi represents a threshold that must be overcome before inspiratory flow could be delivered. It is important to note that in COPD patients with high levels of PEEPi, the increase of the inspiratory effort required to match the value of PEEPi may have negative haemodynamic consequences. For example, an important inspiratory effort equal to an oesophageal pressure of –15 cmH2O, in the presence of a value of PEEPi equal to 20 cmH2O, leads to a significant increase in cardiac venous return and displacement of the interventricular septum with an altered diastolic filling of left ventricle [13]. The application of an external PEEP value, equal to about 80% of the value of PEEPi, reduces inspiratory effort and improves haemodynamics [13].

Finally, an excessive elastic load may generate the second type of asynchrony—ineffective triggering. Ineffective triggering is defined as a reduction in oesophageal pressure of more than 1 cmH2O that is not able to open the inspiratory valve, or has not achieved an increase of inspiratory flow >100 mL/sec [10]. At the bedside, ineffective triggering has been shown to represent nearly 90% of patient–ventilator asynchrony events [4]‌ and it can be identified through the analysis of flow traces displayed on the mechanical ventilator. The start of this trigger is indicated by the point at which the expiratory flow decreases suddenly during expiration, altering its normal morphology and reaching the zero line. The time elapsed between this point and the point at which the airway pressure begins to rise is the ‘triggering delay’. If a breath delivered by the mechanical ventilator does not follow this abrupt reduction in expiratory flow, ineffective triggering occurs (Table 100.1). Ineffective triggering is caused by high levels of ventilator assistance in either pressure-support or assisted-controlled ventilation [10]. It has been demonstrated that the amount of ineffective triggering is proportional to the level of assistance by the ventilator [10]; in fact, increasing the level of assistance reduces the work of breathing and the degree of dyspnoea, but also increases the number of ineffective triggering. It is important to note how breaths before ineffective triggering are characterized by larger tidal volumes, shorter expiratory time, and higher values of PEEPi [10,14]. Consequently, the increase in the elastic load due to the PEEPi threshold may be an important risk factor for ineffective triggering [10,12,14]. Of note, ineffective triggering has been associated with poor outcome, highlighting the need to recognize asynchrony and promptly correct it. In a cohort of 60 ICU patients under mechanical ventilation within 24 hours, those who showed ineffective triggering breaths were more that 10% of total breaths in 10 minutes of observation had poorer outcomes as demonstrated by longer duration of mechanical ventilation, fewer ventilator-free days and a lower likelihood of home discharge [4].

Many attempts have been made to reduce the time delay between a patient’s inspiratory time and flow delivered by the ventilator. In this respect, synchrony during the triggering phase has been improved significantly with the neutrally-adjusted ventilatory assist (NAVA) ventilation mode [15]. In fact, with this method of assisted ventilation, the signal recognized by the ventilator to deliver the inspiratory flow is very close to the patient neural time and it uses neural electromyography activity of the diaphragm [15]. In this case, therefore, the trigger will not consist of changes in pressure or flow signals that are greatly influenced by the extent of respiratory elastic load. During NAVA, the level of assistance is proportional to every millivolt of electrical activity of the diaphragm, and the inspiration ends when the peak value of electrical activity of the diaphragm decreases to a fixed percentage. In this way, the level of assistance is proportional to the electrical activity of the diaphragm, leaving part of the work of breathing to the patient; it terminates when the diaphragm is relaxed and the electrical activity is decreased [16].

Asynchrony between the patient’s ventilatory requirements and flow delivered by the ventilator

Good patient–ventilator synchrony is achieved even when the mean inspiratory flow is adjusted to the patient’s ventilator requirements. In fact, flow asynchrony has been related to the increase in the speed of airway pressurization, the patient’s ventilator drive, and the ventilator’s performance [17]. Both airway pressurization rates that are too slow or too fast may produce discomfort for the patient [18] (Table 100.1). A slow rate of airway pressurization may not reduce the patient’s dyspnoea and, indeed, increases the work of breathing, especially in the presence of impaired respiratory mechanics as in COPD or in patients with restrictive diseases [17]. In 11 COPD patients under assisted ventilation, the same inspiratory pressure was applied with a different rate of airway pressure increasing, ranging from 0.1 to 1.5 seconds. In this cohort of patients, Bonmarchand showed that progressively slower rates of airway pressure increasing were associated with an increased work of breathing, while respiratory rate, tidal volume, and PEEPi remained unchanged [17].

Asynchrony between inspiratory time of the patient and cycling of ventilator from inspiration to expiration

In ideal conditions, the patient’s end of inspiration should coincide with the opening of the exhalation valve of the ventilator in order to allow passive expiration. In a controlled mode, cycling of the ventilator from inspiration to expiration is determined by the amount of inspiratory flow and the respiratory rate. On the contrary, in assisted ventilation mode, the algorithm of the ventilator must recognize the end of inspiration. In the pressure-support ventilation, cycling of the ventilator from inspiration to expiration occurs as a consequence of exponential decay of the inspiratory flow; in fact, the expiratory valve opens when the flow is reduced to a threshold value, usually expressed as 30% of peak flow. However, this criterion presents some issues [12], since the patient’s inspiration may be shorter or longer than the time to deliver a given flow by the ventilator (Table 100.1). For example, if the flow delivered by the ventilator ends before the end of the patient’s neural inspiration, an asynchrony may take place—the so-called ‘double triggering’ in which two breaths are delivered by the ventilator for a single inspiratory effort. This asynchrony is easily identifiable because the asynchronous breath is shorter than the preceding breath. In fact, the asynchronous breath begins at a higher volume of elastic equilibrium. It is possible to manipulate the expiratory trigger in modern ventilators by changing the decrease percentage of flow, which determines the cycling from inspiration to expiration. Therefore, manipulation of the expiratory trigger in order to increase the duration of inspiration avoids double triggering asynchrony (see Table 100.1).

In contrast, in patients with high values of time constants of the respiratory system, as in COPD patients, the mechanical ventilator may continue to deliver flow, even after the end of a patient’s neural inspiration [19]. The time constant (τ‎) indicates the time necessary for the respiratory system to reach the volume of elastic equilibrium, and it is proportional to the value of airway resistance and compliance of the respiratory system according to the following formula:

τ   = R   cmH 2 O/L/sec   *   C   L/cmH 2 O
[eqn 2]

where R indicates the value of airway resistance and C indicates the value of respiratory system compliance.

In COPD patients, the time constant of the respiratory system may be increased due to high values of expiratory resistance and compliance because of dynamic hyperinflation and/or expiratory flow limitation. Therefore, the longer time necessary for the flow to fall at threshold value determines that the inspiratory time of the ventilator to deliver flow is longer than the neural inspiration of the patient, causing asynchrony. In COPD patients with high constants equal to 0.54 and ventilated with a pressure support of 20 cmH2O, a clear asynchrony has been shown consisting of activation of expiratory muscles during inspiratory flow delivered by the ventilator [20]. Consequently, this expiratory asynchrony is characterized by the sudden increase in airway pressure at the end of inspiration caused by activation of expiratory muscles. This asynchrony may be avoided by manipulating the expiratory trigger in order to reduce the ventilator’s inspiratory time (see Table 100.1).

Conclusion

Optimization of patient–ventilator interactions can only be achieved through a continuous adjustment of ventilator trigger, flow rate, and criteria of cycling from inspiration to expiration. These fine adjustments imply an interpretation of ventilator waveforms as flow and airway pressure. Nevertheless, it is mandatory to observe patients at the bedside, looking for signs of asynchrony, such as altered mental status, discomfort, activation of accessory inspiratory and expiratory muscles, tachycardia, and hypertension.

References

1. Sassoon C. (2011). Triggering of the ventilator in patient–ventilator interactions. Respiratory Care, 56(1), 39–51.Find this resource:

2. Purro A, Appendini L, De Gaetano A, Gudjonsdottir M, Donner CF, and Rossi A. (2000). Physiologic determinants of ventilator dependence in long-term mechanically ventilated patients. American Journal of Respiratory and Critical Care Medicine 161(4 Pt 1), 1115–23.Find this resource:

3. Thille AW, Rodriguez P, Cabello B, Lellouche F, and Brochard L. (2006). Patient–ventilator asynchrony during assisted mechanical ventilation. Intensive Care Medicine, 32(10), 1515–22.Find this resource:

4. de Wit M, Miller KB, Green DA, Ostman HE, Gennings C, and Epstein SK. Ineffective triggering predicts increased duration of mechanical ventilation. Critical Care Medicine, 37(10), 2740–5.Find this resource:

5. Georgopoulos D, Prinianakis G, and Kondili E. (2006). Bedside waveforms interpretation as a tool to identify patient-ventilator asynchronies. Intensive Care Medicine, 32(1), 34–47.Find this resource:

6. Sassoon CS, Giron AE, Ely EA, and Light RW. (1989). Inspiratory work of breathing on flow-by and demand-flow continuous positive airway pressure. Critical Care Medicine, 17(11), 1108–14.Find this resource:

7. Imanaka H, Nishimura M, Takeuchi M, Kimball WR, Yahagi N, and Kumon K. (2000). Autotriggering caused by cardiogenic oscillation during flow-triggered mechanical ventilation. Critical Care Medicine, 28(2), 402–7.Find this resource:

8. de Wit M, Pedram S, Best AM, and Epstein SK. (2009). Observational study of patient-ventilator asynchrony and relationship to sedation level. Journal of Critical Care, 24(1), 74–80.Find this resource:

9. Parthasarathy S, Jubran A, and Tobin MJ. (2000). Assessment of neural inspiratory time in ventilator-supported patients. American Journal of Respiratory and Critical Care Medicine, 162(2 Pt 1), 546–52.Find this resource:

10. Leung P, Jubran A, and Tobin MJ. (1997). Comparison of assisted ventilator modes on triggering, patient effort, and dyspnea. American Journal of Respiratory and Critical Care Medicine, 155(6), 1940–8.Find this resource:

11. Tobert DG, Simon PM, Stroetz RW, and Hubmayr RD. (1997). The determinants of respiratory rate during mechanical ventilation. American Journal of Respiratory and Critical Care Medicine, 155(2), 485–92.Find this resource:

12. Ranieri VM, Giuliani R, Mascia, et al. (1996). Patient–ventilator interaction during acute hypercapnia: pressure-support vs. proportional-assist ventilation. Journal of Applied Physiology, 81(1), 426–36.Find this resource:

13. Ranieri VM, Dambrosio M, and Brienza N. (1996). Intrinsic PEEP and cardiopulmonary interaction in patients with COPD and acute ventilatory failure. European Respiratory Journal, 9(6), 1283–92.Find this resource:

14. Ranieri VM, Grasso S, Fiore T, and Giuliani R. (1996). Auto-positive end-expiratory pressure and dynamic hyperinflation. Clinics in Chest Medicine, 17(3), 379–94.Find this resource:

15. Sinderby C, Navalesi P, Beck J, et al. (1999). Neural control of mechanical ventilation in respiratory failure. Nature Medicine, 5(12), 1433–6.Find this resource:

16. Colombo D, et al. (2008). Physiologic response to varying levels of pressure support and neurally adjusted ventilatory assist in patients with acute respiratory failure. Intensive Care Medicine, 34(11), 2010–18.Find this resource:

17. Bonmarchand G, Chevron V, Chopin C, et al. (1996). Increased initial flow rate reduces inspiratory work of breathing during pressure support ventilation in patients with exacerbation of chronic obstructive pulmonary disease. Intensive Care Medicine, 22(11), 1147–54.Find this resource:

18. Chiumello, D., et al. (2001). The effects of pressurization rate on breathing pattern, work of breathing, gas exchange and patient comfort in pressure support ventilation. European Respiratory Journal, 18(1), 107–14.Find this resource:

19. Racca F, Squadrone V, and Ranieri VM. (2005). Patient-ventilator interaction during the triggering phase. Respiratory Care Clinics of North America, 11(2), 225–45.Find this resource:

20. Jubran A, Van de Graaff WB, and Tobin MJ. (1995). Variability of patient-ventilator interaction with pressure support ventilation in patients with chronic obstructive pulmonary disease. American Journal of Respiratory and Critical Care Medicine, 152(1), 129–36.Find this resource: