What is patient/ventilator synchrony? Broadly speaking, a patient and ventilator are in synchrony when the settings on the ventilator are matched with what the patient's respiratory system is trying to achieve. The respiratory system continually integrates feedback from chemoreceptors, stretch receptors, and baroreceptors to determine intrinsic respiratory drive. Along with cortical input, this feedback is used for breath-to-breath adjustments to respiratory effort, tidal volume, and cycle time. Breath-to-breath adjustments are generally small, assuming there are no major changes to input. If any of several different ventilator settings aren't meeting the patient's respiratory demands, asynchrony can occur.
A concise clinical review published in the American Journal of Respiratory and Critical Care Medicinein 2013 provided an excellent summary of patient/ventilator interactions. Breath trigger, gas delivery (target), and cycle settings must provide what the patient needs to prevent dyssynchrony. In the world of low tidal volume ventilation, positive end-expiratory pressure, and driving and plateau pressure targets, other settings are often overlooked. Unfortunately, patient/ventilator dyssynchrony can dramatically increase work of breathing and transpulmonary pressure, negating efforts to rest the respiratory system and protect the lung through recruitment and low tidal volumes.
A recent study published online in the Annals of the American Thoracic Society attempted to quantify the effects that tidal volume and mode have on dyssynchrony (defined as lack of simultaneous timing of patient and ventilator trigger, flow, or cycling). Researchers enrolled 19 critically ill, mechanically ventilated patients. Ten of these patients (52.6%) had acute respiratory distress syndrome (ARDS), and all had a PaO2/FiO2 ratio < 300 mm Hg (13 [68.4%] had a PaO2/FiO2 ratio < 200 mm Hg).
Ventilator targets were adjusted to provide tidal volumes of 6, 7.5, or 9 mL/kg predicted body weight, and two different modes were used: volume assist-control (VC) at a set flow rate of 50 L/min, or adaptive pressure control (APC) mode (Volume Control Plus, Puritan Bennett™ 840). Trigger, flow, and cycle dyssynchronies were measured at each volume, on each mode in every patient.
The researchers calculated a dyssynchrony index (DI) to quantify and compare patient interactions with each volume and mode. "Severe dyssynchronies" were those considered to be "clearly detrimental to patients and most noticeable to clinicians."
Their findings weren't particularly surprising. The DI was inversely related to tidal volume, and APC generally allowed a reduction in the DI at any given tidal volume target. The severe DI followed the same pattern. At the same tidal volume target, patients on APC achieved higher expiratory volumes than those on VC, but this difference was rarely > 1 mL/kg.
The researchers concluded that APC can reduce the DI with minimal increase in risk for volutrauma and ventilator-induced lung injury.
Implications and Limitations
This study is a welcome addition to the literature, and the authors should be commended for their work. It's not easy to control for all of the variables that influence patient/ventilator interactions. Nor is it easy to quantify dyssynchrony and gauge its effects.
The DI, and particularly severe DI, are subjective, however, because they rely on an individual's inspection of the ventilator's flow and pressure tracings. The validity of the study could have been increased by evaluating the tracings and statistically assessing interevaluator agreement. Only one investigator measured dyssynchrony.
In addition, the investigators weren't blinded to mode or volume settings. Granted, blinding would have been difficult to achieve—visual inspection of flow and pressure tracings would provide information on mode, and volume could be calculated from flow. Nonetheless, the absence of blinding is a study limitation. It helps that neither author has received money from the company that markets the Puritan Bennett ventilator (according to the funding disclosures in the manuscript).
A review of the statistics and visual inspection of the figures and tables show that the DI wasn't normally distributed across the 19 patients. Table 2 shows that the median percentage occurrence was zero for most types of dyssynchrony. In Figure 2, it is evident that patients were clustered at opposite ends of the DI. They were either close to 100% or below 20%, with no "in between." This implies that patients either tolerated the settings well, or not at all. The patients who didn't clearly drove the difference between volume settings and mode, and they should receive special attention.
There is a difference in the median DI between modes and volumes, but there is also a difference in exhaled volumes between VC and APC. Are the same patients who achieved a DI reduction also achieving the largest increase in exhaled tidal volume? If so, perhaps volume is driving all of the dyssynchrony.
Other issues, such as restricting all patients in the VC group to a flow rate of 50 L/min, also limit generalization. Most clinicians would set the flow rate higher at baseline, or simply increase it to reduce the severe flow dyssynchronies seen in this group. An increase in tidal volume or change in mode would not be necessary.
The Richmond Agitation-Sedation Scale scores and PaO2/FiO2 varied enough that respiratory drive probably differed significantly across patients. Whenever ventilator settings are standardized without allowing for individual requirements, some patients will be dyssynchronous. It may be that the patients with DI indices close to 100% simply had higher respiratory drives, making compliance with low tidal volumes and fixed flow rates difficult. Such is life when your sample size is only 19 patients and you are trying to control for multiple physiologic variables that can influence dyssynchrony rates.
Limitations aside, the study has value. This is not the first group to draw attention to the effect of tidal volume on synchrony, but in today's world of low tidal volume ventilation, the relationship deserves emphasis. The ARDSNet investigators recognized the effects that the settings they advocated could have on dyssynchrony. They even included a dyssynchrony measure in their protocol and advised adjustments for breath stacking.[2,9,10]
No matter what, clinicians should expect dyssynchrony with severe ARDS when trying to limit pressure and volume (unless you are going to blunt respiratory drive with narcotics or paralyze your patient). In fact, this may be why neuromuscular blockade has the most benefit for those with severe ARDS: Dyssynchrony is eliminated when it would otherwise be present.
On the basis of this study's results, APC is a reasonable mode to start with if your patient needs ventilatory support. For those with severe ARDS, however, I would assume that adjustments will need to be made. I would also watch the tidal volume to ensure that it isn't excessive. We have yet to find a ventilator mode that can mimic the patient's respiratory centers and replace the need for a physician at the bedside.
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Any views expressed above are the author's own and do not necessarily reflect the views of WebMD or Medscape.
Cite this: Achieving Patient/Ventilator Synchrony -- Good Luck - Medscape - Dec 13, 2016.