Modes of Mechanical Ventilation

The Modern Approach to Modes of Mechanical Ventilation

While modes have classically been divided up into pressure or volume controlled modes, a more
modern approach describes ventilatory modes based on three characteristics the trigger (flow
versus pressure), the limit (what determines the size of the breath), and the cycle (what
actually ends the breath). In both VCV and PCV, time is the cycle, the difference being in how the
time to cessation is determined. PSV, by contrast, has a flow cycle.
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.
Synchronized Intermittent-Mandatory Ventilation (SIMV)
Guarantees a certain number of breaths, but unlike ACV, patient breaths are partially their own,
reducing the risk of hyperinflation or alkalosis. Mandatory breaths are synchronized to coincide
with spontaneous respirations. Disadvantages of SIMV are increased work of breathing and a
tendency to reduce cardiac output, which may prolong ventilator dependency. The addition of
pressure support on top of spontaneous breaths can reduce some of the work of breathing. SIMV
has been shown to decrease cardiac output in patients with left-ventricular dysfunction [Crit Care
Med 10: 423, 1982].
ACV vs. SIMV
Personal preference prevails, except in the following scenarios: 1. Patients who breathe rapidly
on ACV should switch to SIMV 2. Patients who have respiratory muscle weakness and/or leftventricular dysfunction should be switched to ACV.
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 Support Ventilation (PSV)
Allows the patient to determine inflation volume and respiratory frequency (but not pressure, as
this is pressure-controlled), thus can only be used to augment spontaneous breathing. Pressure
support can be used to overcome the resistance of ventilator tubing in another cycle (5 10 cm
H20 are generally used, especially during weaning), or to augment spontaneous breathing. PSV
can be delivered through specialized face masks.
Pressure Controlled Inverse Ratio Ventilation (PCIRV)

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.
Airway Pressure Release Ventilation (APRV)
Airway pressure release ventilation is similar to PCIRV instead of being a variation of PCV in
which the I:E ratio is reversed, APRV is a variation of CPAP that releases pressure temporarily on
exhalation. This unique mode of ventilation results in higher average airway pressures. Patients
are able to spontaneously ventilate at both low and high pressures, although typically most (or
all) ventilation occurs at the high pressure. In the absence of attempted breaths, APRV and PCIRV
are identical. As in PCIRV, hemodynamic compromise is a concern in APRV. Additionally, APRV
typically requires increased sedation.
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
using intermittent 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).
Proportional Assist Ventilation: Summary
Independent Variables: % WOB; trigger; cycle
How It Works: positive feedback loop (requires calcluation of resistance and elastance)
Theoretical Advantage(s): better synchrony
Neurally Adjusted Ventilatory Assist (NAVA)
Additional Modes, Strategies, Parameters
Inverse Ratio Ventilation
Inverse Ratio Ventilation (IRV) is a subset of PCV in which inflation time is prolonged (In IRV, 1:1,
2:1, or 3:1 may be use. Normal I:E is 1:3). This lowers peak airway pressures but increases mean
airway pressures. The result may be improved oxygenation but at the expense of compromised
venous return and cardiac output, thus it is not clear that this mode of ventilation leads to
improved survival. IRVs major indication is in patients with ARDS with refractory hypoxemia or
hypercapnia in other modes of ventilation [Am J Surg 183: 151, 2002].
Adaptive Support Ventilation
Calculates the expiratory time constant in order to guarantee sufficient expiratory time and thus
minimize air trapping.
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: 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.
Continuous Positive Airway Pressure (CPAP)
Positive pressure given throughout the cycle. It can be delivered through a mask and is can be
used in obstructive sleep apnea (esp. with a nasal mask), to postpone intubation, or to treat
acute exacerbations of COPD.
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].
High Frequency Oscillatory Ventilation
In one study of 5 patients with TBI and ARDS (390 datasets of ICP, CPP, PaCO2 collected), treated
HFOV with ICP increased in 11 of 390 datasets, CPP was reduced (<70 mmHg) in 66 of 390, and
P(a)CO2 variations (<4.7 kPa; >6.0 kPa) were observed in 8. All these alterations were
responsive to treatment. PaO2/FIO2 improved in four patients [Acta Anaes Scand 49: 209, 2005].

High Frequency Percussive Ventilation

10 severe TBI patients with a Glasgow Coma Score (GCS) < 9, placed on HFPV. There was an
increase in PF ratio (91.8 to 269.7, p < 0.01), PEEP (14 to 16 +/- 3.5), and mean airway pressure
(20.4 to 23.6) 16 hours after institution of HFPV. There was a decrease in ICP (30.9 to 17.4, p <
0.01), PC02 (37.7 to 32.7, p < 0.05), and PIP (49.4 to 41, p < 0.05) at 16 hours [J Trauma 57:
542, 2004].