Authors Siddharth Dugar, MD Critical Care Fellow, Cleveland Clinic, OH
Robert L. Chatburn, MHHS, RRT-NPN, FAARC Professor, Department of Medicine, Lerner College of Medicine of Case Western Reserve University
Case
Consider a 34 year old male with a history of portal hypertension
presented with fever, change in mental status and hypotension. The
patient was intubated for airway protection.
The current ventilator settings are Volume Controlled-Continuous
Mandatory ventilation (VC-CMV) mode with RR 18/min, tidal volume of
460ml, a flow rate of 70L/min with a decelerating flow waveform and PEEP
of 5cm H2O and FiO2 of 40%.
You observe the following flow and pressure waveforms (Figure 1)
Figure 1. Observed waveform showing signs of asynchrony
Question
What form of patient ventilator asynchrony is clearly evident?
A. Delayed inspiratory cycling B. Premature cycling C. Ineffective Triggering D. Auto Triggering
Answer
Answer 2 Premature cycling
Discussion
To interpret this waveform, we need to know what an ideal waveform
would look like for a passive patient given the equation of motion:
Pvent + Pmus = (elastance x volume) + (resistance x flow)
Where Pvent = pressure generated by the ventilator and Pmus is
pressure generated by the ventilatory muscles (zero for a paralyzed
patient). Any deviations from the expected ideal can be evidence of
asynchrony. For a passive patient in this mode of ventilation we would
expect to see the waveform shown in Figure 2.
Figure 2. Idealized waveforms for VC with descending ramp flow
During inspiration
with this flow waveform the initial rise in Paw is due to airway
resistance, with no component due to elastance x volume because volume
is still zero. As volume accumulates, Paw increases but the component
due to elastance x volume becomes larger relative to the component due
to resistance x flow because flow is decreasing. At the end of
inspiration, Paw is lower than the peak value (at mid inspiration)
because flow has dropped to zero. Of course, the actual shape of the Paw
curve depends on the relative values of resistance and elastance. But
for patients with stiff lungs, there is generally a hump in the pressure
waveform.
During exhalation, peak expiratory flow is simply (elastance x
volume)/resistance. Flow then decays according to the time constant
(resistance/elastance or resistance x compliance). Thereafter flow
decreases exponentially to zero, flow waveform depending on product of
resistance and compliance also known as “time constant”.
Given this understanding of the ideal waveforms for a passive
patient, we can now interpret the actual waveform. First, we recall that
for volume control modes, the right hand side of the equation of motion
must remain unchanged in the face of active inspiration (Pmus greater
than zero) because the tidal volume and flow are preset (and we assume
elastance and resistance are constant). Hence, active inspiration must
deform the Paw waveform (i.e., as Pmus increases, Pvent decreases)
Now, we see that Paw dips just prior to the start of inspiratory
flow. This indicates patient triggering and thus the presence of Pmus
(i.e., active inspiration). Next we see a flattening of Paw during
inspiration compared to the expected passive waveform. Again, this
indicates active inspiration. When the ventilator cycles inspiration
off, there is an immediate drop in the total applied pressure because
Pvent goes to zero. As a result there is a short spike in expiratory
flow. However, flow does not decay smoothly as expected for a passive
exhalation. Rather, the flow waveform is distorted toward zero. This
implies a force in the inspiratory direction, which can only be due to
Pmus. Indeed, we can fairly conclude that Pmus continues even though
Pvent stops. Hence, the “neural inspiratory time”, or the duration of
Pmus controlled by the brain, is longer than the set inspiratory time,
which is determined by the preset tidal volume and inspiratory flow.
Hence, we conclude that the asynchrony we see can be classified as
premature cycling.
In summary, premature cycling arises when the ventilator terminates
the breath but the inspiratory muscles continue to contract from patient
effort; as the inspiratory time set on ventilator is shorter than the
neural inspiratory time of the patient. If the patient continues to
generate inspiratory muscle pressure during expiration, this expiratory
flow pattern may be affected in one of the following ways.
Inspiratory (positive) flow for some time after opening of the exhalation valve followed by peak expiratory flow
A sharp decrease from the peak expiratory flow which lasts a few
milliseconds followed by an increase and then decreases gradually to
zero toward the end of expiration (as seen in our patient).
A sharp decrease from the peak expiratory flow to positive flow
causing mechanical ventilator to sense a second effort, resulting in a
second breath causing stacking of breaths, also known as “double
triggering.”
The phenomenon seen in our patient is from the elastic recoil
pressure being higher at end-inspiration than inspiratory muscle
creating an expiratory flow. As volume decreases, the elastic recoil
pressure declines; while inspiratory muscles continue to contract
increasing opposing pressure to expiratory flow causing a corresponding
decrease in expiratory flow. Relaxation of inspiratory muscles
eliminates this opposing pressure and expiratory flow increases.
The most convincing way to confirm patient effort is with a Pes
(Esophageal pressure) or Edi signal (electrical activity of the
diaphragm) but clinical application of such invasive procedure is
limited.
The flow and pressure waveform can be used to determine patient
effort. The dip in the pressure waveform before the start of inspiration
seems to indicate that inspiration was patient triggered. Also there is
small hump in Paw, possibly indicating that Paw was decreased by an
increase in Pmus, again indicating inspiratory effort throughout the
preset inspiratory time and hence the classification of premature
cycling.
Reference
Gentile MA. Cycling of the mechanical ventilator breath. Respir Care. 2011 Jan;56(1):52-60.
Nilsestuen JO, Hargett KD. Using ventilator graphics to identify
patient-ventilator asynchrony. Respir Care. 2005 Feb;50(2):202-34.