The Science Journal of the American Association for Respiratory Care

Graphics Corner

February 2002 / Volume 47 / Number 2 / Page 183

Detection of Patient-Ventilator Asynchrony During Low Tidal Volume Ventilation, Using Ventilator Waveform Graphics

Richard H Kallet MSc RRT and John M Luce MD


A 55-year-old woman with pneumonia and septic shock developed acute respiratory distress syndrome (ARDS) and was enrolled into the low tidal volume (VT) ventilation study of the National Heart, Lung, and Blood Institute's ARDS Network.1 The protocol required that VT be reduced to as low as 4 mL/kg (predicted body weight) to minimize ventilator-induced lung injury by maintaining the end-inspiratory plateau pressure (PPLAT) < or = 30 cm H2O. (For further information on the ARDS Network protocol, go to the ARDS Network web site at The patient's breathing was supported with a mechanical ventilator (Dräger E-1, Dräger, Telford, Pennsylvania) in the volume assist/control mode. On ARDS Day 2, the patient required positive end-expiratory pressure (PEEP) of 16 cm H2O and fraction of inspired oxygen (FIO2) of 0.90 to maintain PaO2 of 70 mm Hg. VT of 290 mL (4.9 mL/kg) and respiratory rate of 32 breaths/min were required to keep PPLAT < or = 30 cm H2O and produce pH of 7.33 and PaCO2 of 47 mm Hg. Trigger sensitivity was set at -1 cm H2O below PEEP, and peak inspiratory flow was set at 80 L/min. During periods of controlled mechanical ventilation when spontaneous breathing attempts were absent, intrinsic PEEP measurements were consistently 1 cm H2O above the set PEEP level. Clinicians noted intermittent periods when the measured PPLAT varied between 24 and 40 cm H2O, whereas the exhaled VT often fluctuated by > 100 mL (or 1.7 mL/kg). During these periods, spontaneous breathing attempts were noted and the total respiratory rate was seldom more than 4 breaths above the set respiratory rate. On physical examination the patient appeared to be asynchronous with the ventilator. Her inspiratory efforts appeared to commence at peak inspiration, and intermittently she was able to trigger extra mechanical breaths. Coincidentally, an esophageal balloon had been placed to calculate transmural central venous pressure, and a pulmonary mechanics monitor (Ventrak, Novametrix, Wallingford, Connecticut) attached to the esophageal balloon assessed patient-ventilator interactions (Fig. 1).

Fig 1


  1. Using the negative deflections in esophageal pressure (PES) to locate the patient's inspiratory effort, are there corresponding abnormalities in the appearance of the flow, airway pressure (PAW), and VT scalar waveforms?
  2. Based on the appearance of the flow, PAW, and VT scalar waveforms, can inspiratory efforts that successfully triggered mechanical breaths be distinguished from those that failed to trigger extra breaths?
  3. Based on the difference between the end-expiratory PES and the PES at the point where inspiratory flow and PAW become positive, can the intrinsic PEEP level be estimated?


In Figure 1, Point A represents a “noncaptured” inspiratory effort in which the patient could not trigger a breath from the ventilator. The noncaptured breathing effort can be detected by 3 aspects of the expiratory waveforms. First, there was a premature drop in expiratory flow, to 0 L/min, followed by an additional phase of expiratory flow. Second, early in the expiratory phase there was a sharp drop in PAW to PEEP, followed by the PAW transiently rising back above PEEP at the end of the second expiratory phase. Furthermore, in all ventilator-delivered breaths that were followed by a premature inspiratory effort, there was no stable PPLAT, only a steady downward pressure-slope that paralleled the deflection in PES. Third, the suspension of expiration caused by the noncaptured inspiratory effort resulted in a plateau during the expiratory decay in the VT waveform. Point B represents a patient breathing effort sufficiently strong to trigger the ventilator into inspiration, resulting in a “stacked” breath. This also is noted by 3 features in the waveforms. First, there was an abrupt drop in expiratory pressure below PEEP, followed by an inspiratory phase in which both the peak PEW and the PPLAT were elevated above the preceding controlled breath. This suggested that the end-inspiratory volume and pressure had exceeded the target level for lung protection. Second, the inspiratory effort caused an early disruption in expiratory flow, with an apparently diminished peak expiratory flow. (However, as all breaths in this tracing either have a truncated expiratory flow pattern because of patient effort or an augmented peak expiratory flow as the trapped volume is expelled from the lungs from an elevated driving pressure, it is not possible to determine what the patient's peak expiratory flow would have been in the absence of breathing effort.) Third, there was an abrupt truncation in the expiratory volume tracing after the plateau. On the subsequent volume waveform, the expiratory volume fell below 0 mL, indicating at least partial exhalation of the volume trapped during the previous breath.

On the breath preceding Point B that was captured by the ventilator's trigger system, end-expiratory PES was approximately 15 cm H2O, and the PES nadir at Point B (just preceding the positive change in flow and PAW) was approximately 7 cm H2O. Therefore, a PES change of approximately 8 cm H2O was required to trigger a ventilator breath. Since the trigger sensitivity was set at -1 cm H2, the intrinsic PEEP was approximately 7 cm H2O. On the noncaptured breathing effort (Point A), the estimated PES change was approximately 7 cm H2O.


When VT was increased to 6.0 mL/kg, the patient quickly ceased all breathing effort and PPLAT stabilized at 33 cm H2O. The appearance and cessation of the patient's breathing effort was reproducible as the VT was adjusted back and forth between 5 and 6.0 mL/kg over several minutes. The level of sedation was increased until the patient ceased all spontaneous breathing efforts. VT was returned to 5 mL/kg to maintain PPLAT < or = 30 cm H2O. Because the patient's oxygenation status was precarious, we did not attempt to measure her spontaneous VT demand to confirm patient-ventilator VT mismatching. Alternatively, the asynchrony may be explained, in part, by a “deflation” or “gasp reflex” that is believed to aid inflation during progressive lung collapse.2 However, 3 aspects of this case suggest that VT mismatching was a likely source of her asynchrony:

  1. The abrupt appearance and cessation of inspiratory efforts with a change in VT.
  2. The peak inspiratory flow was high, the trigger sensitivity was low, and neither variable changed with the appearance and resolution of asynchrony.
  3. Patient effort occurred consistently after the delivery of VT.

Two important points issue from this incident of patient-ventilator asynchrony. First, apparent patient-ventilator VT mismatching may result in asynchrony, despite appropriate settings of peak inspiratory flow, mandatory respiratory rate, and trigger sensitivity. Lung-protective ventilation requires control of the end-inspiratory volume and pressure in order to prevent ventilator-induced lung injury from regional lung over-distention.3 This case illustrates that excessive end-inspiratory lung volume and pressure paradoxically can occur when patient-ventilator asynchrony results in breath-stacking. Second, this patient's breathing efforts occurred at end-inspiration, when her lung volume and alveolar pressure were elevated. Therefore it was more difficult for her to achieve the trigger sensitivity threshold in the ventilator circuit and trigger extra breaths. Mechanically this phenomenon is similar to the “wasted efforts” that typically occur in patients with obstructive lung disease and intrinsic PEEP.4 The esophageal pressure deflections during these uncaptured inspiratory efforts (approximately 7 cm H2O) were similar to the effort level expended during patient-triggered breaths in ARDS when a traditional VT size is used.5

In this case, the clinical importance of an elevated PPLAT might not have been properly elucidated without the aid of graphics analysis. In other words, a plausible explanation for the elevated PPLAT (based on the physical exam) could be transmitted intra-abdominal pressure from expiratory muscle recruitment during asynchrony. The graphics analysis ruled out that interpretation because no airway pressure “spike” appeared during the end-inspiratory pause time. In fact, PAW progressively dissipated during the end-inspiratory pause time on asynchronous breaths. Furthermore, graphics analysis may facilitate detection of this problem when anasarca or abdominal distention obscures the detection of patient effort and asynchrony by physical exam.

Lung-protective ventilation requires strict control over end-inspiratory lung volumes and pressures.3 Therefore, the liberal use of sedation and the possible addition of neuromuscular blocking agents are recommended first to treat asynchrony and dyspnea.3 However, in some situations increasing sedation or using neuromuscular blocking agents must be avoided. Under those circumstances asynchrony can be treated either with airway pressure-release ventilation6 or any other pressure-targeted mode that allows “free-breathing” throughout the ventilatory cycle. Although volume and pressure targets would be violated, the risk of ventilator-induced lung injury probably would be less than allowing breath-stacking to continue in a volume-targeted mode.


  1. 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. N Engl J Med 2000;342(18):1301–1308.
  2. Comroe JH. Physiology of respiration, 2nd ed. Chicago: Year Book; 1974:80–82.
  3. Hickling KG, Walsh J, Henderson S, Jackson R. Low mortality rate in adult respiratory distress syndrome using low-volume, pressure-limited ventilation with permissive hypercapnia: a prospective study. Crit Care Med 1994;22(10):1568–1578.
  4. Nava S, Bruschi C, Rubini F, Palo A, Iotti G, Braschi A. Respiratory response and inspiratory effort during pressure support ventilation in COPD patients. Intensive Care Med 1995;21(11):871–879.
  5. Kallet RH, Campbell AR, Alonso JA, Morabito DJ, Mackersie RC. The effects of pressure control versus volume control assisted ventilation on patient work of breathing in acute lung injury and acute respiratory distress syndrome. Respir Care 2000;45(9):1085–1096.
  6. Cane RD, Peruzzi WT, Shapiro BA. Airway pressure release ventilation in severe acute respiratory failure. Chest 1991;100(2):460–463.

Richard H Kallet MSc RRT and John M Luce MD are affiliated with the National Heart, Lung, and Blood Institute's ARDS Network, University of California, San Francisco, at San Francisco General Hospital, San Francisco, California.

This research was supported by United States National Institutes of Health grant NIH R01-HL51856.

Correspondence: Richard H Kallet MSc RRT, Respiratory Care Services, San Francisco General Hospital, NH:GA-2, 1001 Potrero Avenue, San Francisco CA 94110. E-mail:

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