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Note also that the lines between pressure and volume controlled methods are being continually blurred by increasingly complex modes.
If alarms and backup modes are properly set, the “disadvantages” of classic modes (e.g. possibility of insufficient minute ventilation in
PCV) can be essentially eliminated
For historical reasons, the following modes will be separated into volume controlled, pressure controlled, and other modes
Volume Modes
Assist-Control Ventilation (ACV)
Also known as continuous mandatory ventilation (CMV). Each breath is either an assist or control breath, but they are all of the same
volume. The larger the volume, the more expiratory time required. If the I:E ratio is less than 1:2, progressive hyperinflation may result.
ACV is particularly undesirable for patients who breathe rapidly – they may induce both hyperinflation and respiratory alkalosis. Note that
mechanical ventilation does not eliminate the work of breathing, because the diaphragm may still be very active.
Pressure Modes
Pressure-Controlled Ventilation (PCV)
Less risk of barotrauma as compared to ACV and SIMV. Does not allow for patient-initiated breaths. The inspiratory flow pattern
decreases exponentially, reducing peak pressures and improving gas exchange [Chest 122: 2096, 2002]. The major disadvantage is that
there are no guarantees for volume, especially when lung mechanics are changing. Thus, PCV has traditionally been preferred for
patients with neuromuscular disease but otherwise normal lungs
Pressure controlled ventilatory mode in which the majority of time is spent at the higher (inspiratory) pressure. Early trials were
promising, however the risks of auto PEEP and hemodynamic deterioration due to the decreased expiratory time and increased mean
airway pressure generally outweight the small potential for improved oxygenation
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Dual Modes
Pressure Regulated Volume Control (PRVC)
A volume target backup is added to a pressure assist-control mode
Interactive Modes
Proportional Assist Ventilation (PAV)
During PAV, the clinician sets the percentage of work of breathing to be provided by the ventilator. PAV uses a positive feedback
loop to accomplish this, which requires knowledge of resistance and elastance to properly attenuate the signal
Compliance and resistance must therefore be periodically calculated – this is accomplished by usingintermittent end-inspiratory and
end-expiratory pause maneuvers (which also calculate auto PEEP). In addition to percent support, the clinician sets the trigger and the
cycle (what actually ends the breath)
The theoretical advantage of PAV is increased synchrony compared to PSV (which provides the same amount of support regardless of
how much effort the patient makes)
Tube Compensation
Positive End Expiratory Pressure (PEEP)
Note: PEEP is not a ventilatory mode in and of itself
Does not allow alveolar pressure to equilibrate with the atmosphere. PEEP displaces the entire pressure waveform, thus mean
intrathoracic pressure increases and the effects on cardiac output are amplified. Low levels of PEEP can be very dangerous, even 5 cm
H20, especially in patients with hypovolemia or cardiac dysfunction. When measuring the effectiveness of PEEP, cardiac output must
always be calculated because at high saturations, changes in Q will be more important than SaO2 – never use SaO2 as an endpoint for
PEEP. The effects of PEEP are not caused by the PEEP itself but by its effects on Ppeak and Pmean, both of which it increases. Risk of
barotrauma is dependent on Ppeak, while cardiac output response depends on Pmean. In fact, in a recent study of ARDS patients, it
was shown that increasing PEEP from 0 to 5 10 and 15 cm H2O was met with corresponding decreases in CO [Crit Care Med 31:
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was shown that increasing PEEP from 0 to 5, 10, and 15 cm H2O was met with corresponding decreases in CO [Crit Care Med 31:
2719, 2003]
PEEP is indicated clinically for 1) low-volume ventilation cycles 2) FiO2 requirements > 0.60, especially in stiff, diffusely injured lungs
such as ARDS and 3) obstructive lung disease. Do NOT use in pneumonia, which is not diffuse, and where PEEP will adversely affect
healthy tissue and worsen oxygenation. One way to gauge the effect of PEEP is to look at peak inspiratory pressure (PIP) – if PIP
increases less than the added PEEP, then the PEEP improved the compliance of the lungs.
A recent phenomena in the understanding of PEEP is the principle of recruitable lung volume: while this cannot be calculated, it can be
estimated by looking at CT scans: atalectasis containing air is recruitable, that devoid of air is not, the idea being only apply PEEP to
recruitable lungs, otherwise you may just be inducing ARDS [NEJM 354: 1775, 2006]. The effects of PEEP can also be monitored by
tracking the PaO2/FiO2 ratio (it should increase).
ARDSnet II: 8.3 vs. 13.2 cm H2O: in patients with acute lung injury and ARDS who receive mechanical ventilation with a tidal-volume
goal of 6 ml per kilogram of predicted body weight and an end-inspiratory plateau-pressure limit of 30 cm of water, clinical outcomes are
similar whether lower or higher PEEP levels are used [NEJM 351: 327, 2004]
PEEP should not be used routinely. It does not reduce lung edema (can cause it) or prevent mediastinal bleeding.
Prone Ventilation
May improve oxygenation by redistributing pulmonary blood flow, however a multicenter, randomized trial of 304 patients showed that
this improved oxygenation is not accompanied by a change in survival [NEJM 345: 568, 2001] – this was corroborated by two smaller,
subsequent randomized controlled trials, which showed an insignificant trend towards improved mortality [J Trauma 59: 333, 2005; Am J
Respir Crit Care Med 173: 1233, 2006]. This may not hold for neurosurgery patients – in a study of 16 SAH (H&H 3 or higher) patients in
ARDS, PaO2 increased from 97.3 to 126.6 mm Hg in the prone position and brain tissue oxygen partial pressure increased from 26.8 to
31.6 mm Hg (both p <.0001), despite the fact that ICP increased from 9.3 to 14.8 mm Hg and CPP decreased from 73.0 to 67.7 (both p
<.0001) [Crit Care Med 31: 1831, 2003]
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