MECHINICAL VENTILATION
S. Kache, MD
Spontaneous respiration vs. Mechanical ventilation
Natural spontaneous ventilation occurs when the respiratory muscles, diaphragm
and intercostal muscles pull on the rib cage open, creating a negative inspiratory
pressure. This leads to lung expansion and the pulling of air into the alveoli
allowing gas exchange to occur. Therefore, spontaneous respiration occurs by
negative inspiratory force.
Once a patient is intubated, the endo-tracheal tube (ETT) is connected to the
ventilator. Depending on the type of ventilator, positive pressure ventilation is
provided either by a pneumatic or electric device. The compressed air entering
at the alveolar level allows for gas exchange.
The significant difference between spontaneous respiration and mechanical
ventilation is that during spontaneous respiration, air is pulled into the lungs
where as during mechanical ventilation, air is pushed into the lungs. This
difference impacts cardio-pulmonary dynamics, as well as the integrity of lung
tissue with the potential for long-term injury.
Initiating Mechanical Ventilation
(See previous chapter for specifics of intubating a patient.)
There are essentially three reasons patients require endo-tracheal intubation and
initiation of mechanical ventilation
• Hypoxia
• Hypercarbia
• Inability to protect their airway
• (To decrease the demand created by the work of breathing in patients
with poor cardiac output – e.g. cardiomyopathy. Note that this is the only
non-respiratory reason to intubate a patient.)
Pulmonary Compliance
Compliance = Volume
Pressure
This simple formula is worth memorizing since it provides the basis of
understanding pulmonary and ventilator interactions. By tracking some simple
ventilator parameters, this equation allows the physician to monitor patient
progression or recovery from the primary disease process.
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Conventional Ventilation
Parameters of the Ventilator
Important terms regarding conventional ventilation are listed below.
Abbreviation Term
PIP
Peak inspiratory pressure
PEEP
Positive end expiratory
pressure
Delta Pressure
∆P
Vt
Tidal Volume
It
Et
MAP
Inspiratory time
Expiratory time
Mean airway pressure
R
Rate
Definition
Point of maximal airway pressure
Pressure maintained in airways at
end of exhalation
Difference between PIP – PEEP
Volume of gas entering patient’s
lung during inspiration
Duration of time in inspiration
Duration of time in expiration
An average of the airway pressure
throughout the respiratory cycle
Respiratory rate as set on the
ventilator
Modes of Ventilation
There are several ways the modes of ventilation can be divided. One method is
by assessing the amount of support the ventilator is providing for the patient.
•
Assist control (AC): This mode provides the maximal support for the
patient. Every breath, whether mechanical or spontaneous, is fully
supported. Each breath has the same PIP or Vt and It. Pressure support
is unnecessary in this mode.
•
Synchronized intermittent mandatory ventilation (SIMV): This mode can
provide minimal to moderate amounts of ventilatory support. The
ventilator breaths as determined by the set respiratory rate are fully
supported breaths. These ventilator breaths deliver the set PIP or Vt and
the set It. All spontaneous breaths above the set ventilator rate only
receive the set pressure support. As the set ventilator rate is weaned, the
patient is forced to do more of the work of breathing. Should the patient
tolerate a minimal rate without developing respiratory distress, s/he may
be ready for extubation.
•
Continuous positive airway pressure (CPAP): In this mode, no ventilator
breaths are provided; only the CPAP or PEEP and pressure support are
set. Note that the amount of support provided is determined by the level
at which the pressure support is set. With a minimal pressure support,
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this mode provides the minimal amount of support and the patient is
forced to do all the work of breathing. This is an ideal mode to test for an
adequate respiratory drive, particularly in patients with impaired
neurologic status, either from an underlying disorder or from oversedation.
A second method of dividing modes of ventilation is by the mechanism that the
ventilator actually provides support for the patient.
•
Pressure Mode: In this mode, the operator sets the PIP and the machine
determines the volume delivered to the patient based on the patient’s
pulmonary compliance (Compliance = Volume / Pressure). As the
patient’s compliance improves, the tidal volume delivered by the ventilator
per breath will increase; conversely as compliance worsens the tidal
volume delivered decreases. This mode can be used both in AC or SIMV.
The greatest advantage of the pressure mode is that it provides greater
ventilatory support by using a decelerating flow pattern, and for stiff, noncompliant lungs, this is the preferred mode of ventilation. The
disadvantage is the minute ventilation is not guaranteed.
•
Volume Mode: The operator sets the tidal volume and the ventilator
determines the pressure required based on the pulmonary compliance
(Compliance = Volume / Pressure). As the compliance improves, the PIP
required to deliver the set tidal volume decreases; conversely as the
compliance worsens the PIP required increases. The volume mode can be
used both in AC or SIMV. The advantage of the volume mode is that a
minute volume is guaranteed. The drawbacks are that it cannot be used
in a patient with a large leak around the ETT and it is not optimal for
poorly compliant lungs.
Hypoxia
There are six major causes of poor oxygen delivery to tissues:
• Decreased alveolar PaO2
• Shunts
• Diffusion impairment
• V/Q mismatch
• Hemoglobin abnormalities
• Poor cardiac output
Decreased alveolar PaO2 can occur secondary to poor patient respiratory effort as
seen in over-sedated patients with hypoventilation. It may also occur because of
decreased ambient oxygen as observed at high altitudes (i.e. the top of Mt.
Everest at 29,035ft has an oxygen level 33% of that at sea level due to the
change in barometric pressure from 760 mm Hg to 253 mm Hg.)
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Shunts can be either intra-cardiac or intra-pulmonary. An intra-cardiac right-toleft shunt causes hypoxia that is unresponsive to oxygen therapy. An intrapulmonary shunt represents a portion of lung that has blood flow without air
exchange, causing a right-to-left shunt of de-oxygenated blood.
A diffusion impairment is an abnormality at the alveolar capillary level preventing
oxygen from entering the blood stream. Examples include fibrotic thickening or
interstitial edema. Large areas of lung with V/Q mismatch can also lead to
hypoxia.
Managing Hypoxia / Hypercarbia
If an intubated patient should develop hypoxia, it can by treated by either
increasing the mean airway pressure or the FiO2. Mean airway pressure is
determined by PIP, PEEP, respiratory rate, I-time, and E-time. Of all these factors,
increasing the PEEP is usually the most effective since it can re-recruit atelectatic
areas. Caution should be taken to not over-distend the lungs while increasing
the PEEP since it can convert normal West zone 2 areas of the lung to zone 1
areas with ventilation and no perfusion. Should the patient have non-compliant
lungs, consider using a lung protective strategy (see section on ARDS).
Increasing the FiO2 can also improve oxygenation. However, FiO2 greater than
60% can be toxic to the lungs due to increased oxygen free radicals. Short-term
oxygen toxicity can lead to reversible pulmonary problems such as edema, which
can worsen pulmonary compliance. Prolonged oxygen toxicity can cause
irreversible pulmonary destruction. Therefore, other vent settings should be
optimized to decrease FiO2 to less than 60% or lower oxygen saturations should
be accepted.
Hypercarbia
Unlike hypoxia, hypercarbia has only a single causative agent: decreased minute
ventilation. A patient’s minute ventilation is determined by the respiratory rate in
a given minute and the tidal volume per breath. Be cautious of patients on
excess carbohydrates since this will increase CO2 production and may prolong
intubation or increase the amount of support required on the ventilator.
Managing Hypercarbia
Elevated CO2 in an intubated patient is treated by increasing minute ventilation,
i.e. increasing the respiratory rate or the tidal volume. If the respiratory rate on
the ventilator is increased, one should monitor for possible air trapping, i.e. not
allowing adequate time to exhale. Air trapping will only amplify the hypercarbia
rather than treating it. Although the tidal volume can be increased to treat
hypercarbia, it should not be increased above 10ml/kg/breath due to the risk of
volutrauma.
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Obstructive Pulmonary Disease
An obstructive disease is defined as any process causing airway obstruction and
increased resistance to airflow. The most common obstructive disease in the
pediatric population is asthma. The obstructed airways make exhalation difficult;
therefore, optimize expiratory time to allow for complete exhalation. The CO2
does not need to be normalized immediately after intubation. Allow for
permissive hypercapnia if required; the CO2 will normalize as the patient’s
primary disease process begins to resolve. At times patients will need an I:E
ratio as high as 1:5. Also be sure to bag the patient slowly immediately after
intubation if you are managing the patient until s/he is transferred to the PICU.
Bagging at a high respiratory rate will exacerbate the air trapping and place the
patient at risk of developing a pneumothorax.
Restrictive Pulmonary Disease
Compromised lung volume secondary to intrinsic lung disease or external
compression is considered a restrictive pulmonary process. A pneumonic
process, focal atelectasis, or a pleural effusion are all examples. Patients should
be managed by optimizing V/Q matching. Assure that a lung protective strategy
is followed particularly while managing a patient with a restrictive process (see
section on ARDS).
High Frequency Ventilation
Theory of Functioning
The lungs have a natural resonant frequency. High velocity inspiratory gas flow
is used to overcome airway resistance in order to oxygenate and ventilate the
patient. Some theories to explain gas exchange with this form of ventilation
include conventional bulk flow, coaxial flow, Taylor dispersion, and the Pendelluft
phenomenon. High frequency ventilation also differs from conventional
ventilation in that it utilizes active exhalation as opposed to passive exhalation.
Parameters of the Ventilator
Some of the terms needed to understand high frequency ventilation are listed
below.
Abbreviation Term
MAP
Mean Airway Pressure
Amp
Amplitude
Hz
I-time
Hertz
Inspiratory time
FiO2
Fraction of inspired oxygen
Definition
Pressure maintained throughout
the respiratory cycle
Rise and fall around MAP
consisting of one cycle
Number of cycles per second
Amount of time spent in inspiration
during a given cycle; usually set at
33%
Can range from 21% to 100%
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Transitioning a patient to high frequency ventilation can be considered either for
difficulty oxygenating or ventilating on conventional ventilation. The MAP usually
is set 2-6 cm H2O above conventional ventilation on the high frequency
ventilator. The amplitude should be based on the patient’s chest “wiggle.” The
hertz can vary from 3 –12 cycles per second. In the PICU population, the hertz
is usually set at 8 or below. If the patient is at 3Hz, a MAP of 20 or lower, and
FiO2 at 50% or lower, transitioning back to conventional ventilation can be
considered.
Managing Hypoxia / Hypercarbia
If a patient is hypoxic, either the MAP or FiO2 can be increased. Use the chest Xray to adjust the MAP. The patient should have a lung expansion of 7-9 ribs on
X-ray. If the FiO2 is increased, be cautious of possible oxygen toxicity as
discussed above. On very rare occasions, one can consider increasing the I-time.
If the patient is hypercarbic, consider either increasing the amplitude or
DECREASING the hertz. Although this seems counter-intuitive, decreasing the
hertz actually treats hypercarbia for patients on high frequency ventilation.
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