mech vent

In medicine, mechanical ventilation is a method to mechanically assist or replace
spontaneous breathing. This may involve a machine called a ventilator or the breathing may be
assisted by a registered nurse, physician, respiratory therapist, paramedic, or other suitable
person compressing a bag or set of bellows. There are two main divisions of mechanical
ventilation: invasive ventilation and non-invasive ventilation.
[1]
There are two main modes of
mechanical ventilation within the two divisions: positive pressure ventilation, where air (or
another gas mix) is pushed into the trachea, and negative pressure ventilation, where air is, in
essence, sucked into the lungs.
Contents
[hide]
 1 Medical uses
 2 Associated risk
o 2.1 Complications
 3 Application and duration
o 3.1 Negative pressure machines
o 3.2 Positive pressure
 3.2.1 Transairway pressure
 4 Types of ventilators
o 4.1 Mechanical ventilators
 5 Breath delivery
o 5.1 Trigger
o 5.2 Cycle
o 5.3 Limit
 6 Breath exhalation
 7 Dead space
 8 Modes of ventilation
 9 Modification of settings
o 9.1 Weaning from mechanical ventilation
 10 Respiratory monitoring
 11 Artificial airways as a connection to the ventilator
 12 Ventilation formulas
o 12.1 Alveolar Ventilation
o 12.2 Arterial PaCO2
o 12.3 Alveolar volume
o 12.4 Estimated physiologic shunt equation
 13 History
 14 References
 15 External links
Medical uses[edit]


Respiratory therapist examining a mechanically ventilated patient on an Intensive Care Unit.
Mechanical ventilation is indicated when the patient's spontaneous ventilation is inadequate to
maintain life. It is also indicated as prophylaxis for imminent collapse of other physiologic
functions, or ineffective gas exchange in the lungs. Because mechanical ventilation serves only
to provide assistance for breathing and does not cure a disease, the patient's underlying
condition should be correctable and should resolve over time. In addition, other factors must be
taken into consideration because mechanical ventilation is not without its complications (see
below)
Common medical indications for use include:
 Acute lung injury (including ARDS, trauma)
 Apnea with respiratory arrest, including cases from intoxication
 Chronic obstructive pulmonary disease (COPD)
 Acute respiratory acidosis with partial pressure of carbon dioxide (pCO
2) > 50 mmHg and pH < 7.25, which may be due to paralysis of the diaphragm due
to Guillain-Barré syndrome, myasthenia gravis, spinal cord injury, or the effect
of anaesthetic and muscle relaxant drugs
 Increased work of breathing as evidenced by significant tachypnea, retractions, and other
physical signs of respiratory distress
 Hypoxemia with arterial partial pressure of oxygen (PaO
2) < 55 mm Hg with supplemental fraction of inspired oxygen (FiO
2) = 1.0
 Hypotension including sepsis, shock, congestive heart failure
 Neurological diseases such as muscular dystrophy and amyotrophic lateral sclerosis
Associated risk[edit]
Barotrauma — Pulmonary barotrauma is a well-known complication of positive pressure
mechanical ventilation.
[2]
This includes pneumothorax, subcutaneous
emphysema,pneumomediastinum, and pneumoperitoneum.
[2]

Ventilator-associated lung injury — Ventilator-associated lung injury (VALI) refers to acute
lung injury that occurs during mechanical ventilation. It is clinically indistinguishable from acute
lung injury or acute respiratory distress syndrome (ALI/ARDS).
[3]

Diaphragm — Controlled mechanical ventilation may lead to a rapid type of
disuse atrophy involving the diaphragmatic muscle fibers, which can develop within the first day
of mechanical ventilation.
[4]
This cause of atrophy in the diaphragm is also a cause of atrophy in
all respiratory related muscles during controlled mechanical ventilation.
[5]

Motility of mucocilia in the airways — Positive pressure ventilation appears to impair
mucociliary motility in the airways. Bronchial mucus transport was frequently impaired and
associated with retention of secretions and pneumonia.
[6]

Complications[edit]
Mechanical ventilation is often a life-saving intervention, but carries many potential complications
including pneumothorax, airway injury, alveolar damage, and ventilator-associated
pneumonia.
[7]
Other complications include diaphragm atrophy, decreased cardiac output, and
oxygen toxicity. One of the primary complications that presents in patients mechanically
ventilated is acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). ALI/ARDS are
recognized as significant contributors to patient morbidity and mortality.
[8]

In many healthcare systems, prolonged ventilation as part of intensive care is a limited resource
(in that there are only so many patients that can receive care at any given moment). It is used to
support a single failing organ system (the lungs) and cannot reverse any underlying disease
process (such as terminal cancer). For this reason, there can be (occasionally difficult) decisions
to be made about whether it is suitable to commence someone on mechanical ventilation.
Equally many ethical issues surround the decision to discontinue mechanical ventilation.
[9]

Application and duration[edit]
It can be used as a short-term measure, for example during an operation or critical illness (often
in the setting of an intensive-care unit). It may be used at home or in a nursing or rehabilitation
institution if patients have chronic illnesses that require long-term ventilatory assistance. Due to
the anatomy of the human pharynx, larynx, and esophagus and the circumstances for which
ventilation is needed, additional measures are often required to secure the airway during positive
pressure ventilation in order to allow unimpeded passage of air into the trachea and avoid air
passing into the esophagus and stomach. The common method is by insertion of a tube into the
trachea, which provides a clear route for the air. This can be either an endotracheal tube,
inserted through the natural openings of mouth or nose, or a tracheostomy inserted through an
artificial opening in the neck. In other circumstances simple airway maneuvres, an oropharyngeal
airway or laryngeal mask airway may be employed. If the patient is able to protect his/her own
airway and non-invasive ventilation or negative-pressure ventilation is used then an airway
adjunct may not be needed.
Negative pressure machines[edit]


An iron lung
Main article: Negative pressure ventilator
The iron lung, also known as the Drinker and Shaw tank, was developed in 1929 and was one of
the first negative-pressure machines used for long-term ventilation. It was refined and used in the
20th century largely as a result of the polio epidemic that struck the world in the 1940s. The
machine is, in effect, a large elongated tank, which encases the patient up to the neck. The neck
is sealed with a rubbergasket so that the patient's face (and airway) are exposed to the room air.
While the exchange of oxygen and carbon dioxide between the bloodstream and the pulmonary
airspace works by diffusion and requires no external work, air must be moved into and out of
the lungs to make it available to the gas exchange process. In spontaneous breathing, a negative
pressure is created in the pleural cavity by the muscles of respiration, and the resulting gradient
between the atmospheric pressure and the pressure inside the thorax generates a flow of air.
In the iron lung by means of a pump, the air is withdrawn mechanically to produce a vacuum
inside the tank, thus creating negative pressure. This negative pressure leads to expansion of
the chest, which causes a decrease in intrapulmonary pressure, and increases flow of ambient
air into the lungs. As the vacuum is released, the pressure inside the tank equalizes to that of the
ambient pressure, and the elastic coil of the chest and lungs leads to passive exhalation.
However, when the vacuum is created, the abdomen also expands along with the lung, cutting
off venous flow back to the heart, leading to pooling of venous blood in the lower extremities.
There are large portholes for nurse or home assistant access. The patients can talk and eat
normally, and can see the world through a well-placed series of mirrors. Some could remain in
these iron lungs for years at a time quite successfully.
Today, negative pressure mechanical ventilators are still in use, notably with the polio wing
hospitals in England such as St Thomas' Hospital in London and the John Radcliffe inOxford.
The prominent device used is a smaller device known as the cuirass. The cuirass is a shell-like
unit, creating negative pressure only to the chest using a combination of a fitting shell and a soft
bladder. Its main use is in patients with neuromuscular disorders that have some residual
muscular function. However, it was prone to falling off and caused severe chafing and skin
damage and was not used as a long-term device. In recent years this device has re-surfaced as
a modern polycarbonate shell with multiple seals and a high-pressure oscillation pump in order to
carry out biphasic cuirass ventilation.
Positive pressure[edit]


Neonatal mechanical ventilator
The design of the modern positive-pressure ventilators were based mainly on technical
developments by the military during World War II to supply oxygen to fighter pilots in high
altitude. Such ventilators replaced the iron lungs as safe endotracheal tubes with high-
volume/low-pressure cuffs were developed. The popularity of positive-pressure ventilators rose
during the polio epidemic in the 1950s in Scandinavia and the United States and was the
beginning of modern ventilation therapy. Positive pressure through manual supply of 50%
oxygen through a tracheostomy tube led to a reduced mortality rate among patients with polio
and respiratory paralysis. However, because of the sheer amount of man-power required for
such manual intervention, mechanical positive-pressure ventilators became increasingly popular.
Positive-pressure ventilators work by increasing the patient's airway pressure through an
endotracheal or tracheostomy tube. The positive pressure allows air to flow into the airway until
the ventilator breath is terminated. Then, the airway pressure drops to zero, and the elastic recoil
of the chest wall and lungs push the tidal volume — the breath-out through passive exhalation.
Transairway pressure[edit]

 P
TA
=Transairway pressure
 P
AO
= Pressure at airway opening
 P
ALV
= Pressure in alveoli
Types of ventilators[edit]


SMART BAG MO Bag-Valve-Mask Resuscitator
Ventilators come in many different styles and method of giving a breath to sustain life. There
are manual ventilators such as bag valve masks and anesthesia bags that require the users
to hold the ventilator to the face or to an artificial airway and maintain breaths with their
hands. Mechanical ventilators are ventilators not requiring operator effort and are typically
computer-controlled or pneumatic-controlled.
Mechanical ventilators[edit]
Mechanical ventilators typically require power by a battery or a wall outlet (DC or AC) though
some ventilators work on a pneumatic system not requiring power.
 Transport ventilators — These ventilators are small and more rugged, and can be
powered pneumatically or via AC or DC power sources.
 Intensive-care ventilators — These ventilators are larger and usually run on AC power
(though virtually all contain a battery to facilitate intra-facility transport and as a back-up
in the event of a power failure). This style of ventilator often provides greater control of a
wide variety of ventilation parameters (such as inspiratory rise time). Many ICU
ventilators also incorporate graphics to provide visual feedback of each breath.
 Neonatal ventilators — Designed with the preterm neonate in mind, these are a
specialized subset of ICU ventilators that are designed to deliver the smaller, more
precise volumes and pressures required to ventilate these patients.
 Positive airway pressure ventilators (PAP) — These ventilators are specifically
designed for non-invasive ventilation. This includes ventilators for use at home for
treatment of chronic conditions such as sleep apnea or COPD.
Breath delivery[edit]
Trigger[edit]
The trigger is what causes a breath to be delivered by a mechanical ventilator. Breaths may
be triggered by a patient taking their own breath, a ventilator operator pressing a manual
breath button, or by the ventilator based on the set breath rate and mode of ventilation.
Cycle[edit]
The cycle is what causes the breath to transition from the inspiratory phase to the exhalation
phase. Breaths may be cycled by a mechanical ventilator when a set time has been reached,
or when a preset flow or percentage of the maximum flow delivered during a breath is
reached depending on the breath type and the settings. Breaths can also be cycled when an
alarm condition such as a high pressure limit has been reached, which is a primary strategy
in pressure regulated volume control.
Limit[edit]
Limit is how the breath is controlled. Breaths may be limited to a set maximum circuit
pressure or a set maximum flow.
Breath exhalation[edit]
Exhalation in mechanical ventilation is almost always completely passive. The ventilator's
expiratory valve is opened, and expiratory flow is allowed until the baseline pressure (PEEP)
is reached. Expiratory flow is determined by patient factors such as compliance and
resistance.
Dead space[edit]
Mechanical dead space is defined as the volume of gas re-breathed as the result of use in a
mechanical device.
Example of calculation for mechanical dead space

Simplified version

Modes of ventilation[edit]
Main article: Modes of mechanical ventilation
Mechanical ventilation utilizes several separate systems for ventilation referred to as the
mode. Modes come in many different delivery concepts but all modes fall into one of three
categories; volume-cycled, pressure-cycled, spontaneously cycled. In general, the selection
of which mode of mechanical ventilation to use for a given patient is based on the familiarity
of clinicians with modes and the equipment availability at a particular institution.
[10]

Modification of settings[edit]
In adults when 100% FiO
2 is used initially, it is easy to calculate the next FiO
2 to be used and easy to estimate the shunt fraction. The estimated shunt fraction refers to
the amount of oxygen not being absorbed into the circulation. In normal physiology, gas
exchange (oxygen/carbon dioxide) occurs at the level of the alveoli in the lungs. The
existence of a shunt refers to any process that hinders this gas exchange, leading to wasted
oxygen inspired and the flow of un-oxygenated blood back to the left heart (which ultimately
supplies the rest of the body with unoxygenated blood).
When using 100% FiO
2, the degree of shunting is estimated by subtracting the measured PaO
2 (from an arterial blood gas) from 700 mmHg. For each difference of 100 mmHg, the shunt
is 5%. A shunt of more than 25% should prompt a search for the cause of this hypoxemia,
such as mainstem intubation or pneumothorax, and should be treated accordingly. If such
complications are not present, other causes must be sought after, and PEEP should be used
to treat this intrapulmonary shunt. Other such causes of a shunt include:
 Alveolar collapse from major atelectasis
 Alveolar collection of material other than gas, such as pus from pneumonia, water and
protein from acute respiratory distress syndrome, water from congestive heart failure, or
blood from haemorrhage
Weaning from mechanical ventilation[edit]
Withdrawal from mechanical ventilation—also known as weaning—should not be delayed
unnecessarily, nor should it be done prematurely. Patients should have their ventilation
considered for withdrawal if they are able to support their own ventilation and oxygenation,
and this should be assessed continuously. There are several objective parameters to look for
when considering withdrawal, but there are no specific criteria that generalizes to all patients.
Trials of spontaneous breathing have been shown to accurately predict the success of
spontaneous breathing.
[11]

Respiratory monitoring[edit]
Main article: respiratory monitoring


Respiratory mechanics monitor
One of the main reasons why a patient is admitted to an ICU is for delivery of mechanical
ventilation. Monitoring a patient in mechanical ventilation has many clinical applications:
Enhance understanding of pathophysiology, aid with diagnosis, guide patient management,
avoid complications and assessment of trends.
[12]

Most of modern ventilators have basic monitoring tools. There are also monitors that work
independently of the ventilator, which allow to measure patients after the ventilator has been
removed, such as a T tube test.
Artificial airways as a connection to the ventilator[edit]
Main article: Artificial airway
There are various procedures and mechanical devices that provide protection against airway
collapse, air leakage, and aspiration:
 Face mask — In resuscitation and for minor procedures under anaesthesia, a face mask
is often sufficient to achieve a seal against air leakage. Airway patency of the
unconscious patient is maintained either by manipulation of the jaw or by the use
of nasopharyngeal or oropharyngeal airway. These are designed to provide a passage of
air to the pharynx through the nose or mouth, respectively. Poorly fitted masks often
cause nasal bridge ulcers, a problem for some patients. Face masks are also used
for non-invasive ventilation in conscious patients. A full face mask does not, however,
provide protection against aspiration.
 Tracheal intubation is often performed for mechanical ventilation of hours to weeks
duration. A tube is inserted through the nose (nasotracheal intubation) or mouth
(orotracheal intubation) and advanced into the trachea. In most cases, tubes with
inflatable cuffs are used for protection against leakage and aspiration. Intubation with a
cuffed tube is thought to provide the best protection against aspiration. Tracheal tubes
inevitably cause pain and coughing. Therefore, unless a patient is unconscious or
anaesthetized for other reasons, sedative drugs are usually given to provide tolerance of
the tube. Other disadvantages of tracheal intubation include damage to the mucosal
lining of the nasopharynx or oropharynx and subglottic stenosis.
 Supraglottic airway — a supraglottic airway (SGA) is any airway device that is seated
above and outside the trachea, as an alternative to endotracheal intubation. Most
devices work via masks or cuffs that inflate to isolate the trachea for oxygen delivery.
Newer devices feature esophageal ports for suctioning or ports for tube exchange to
allow intubation. Supraglottic airways differ primarily from tracheal intubation in that they
do not prevent aspiration. After the introduction of the laryngeal mask airway (LMA) in
1998, supraglottic airway devices have become mainstream in both elective and
emergency anesthesia.
[13]
There are many types of SGAs available including
the Esophageal-tracheal Combitube (ETC), Laryngeal tube (LT), and the
obsolete Esophageal obturator airway (EOA).
 Cricothyrotomy — Patients requiring emergency airway management, in whom tracheal
intubation has been unsuccessful, may require an airway inserted through a surgical
opening in the cricothyroid membrane. This is similar to a tracheostomy but
a cricothyrotomy is reserved for emergency access.
[14]

 Tracheostomy — When patients require mechanical ventilation for several weeks, a
tracheostomy may provide the most suitable access to the trachea. A tracheostomy is a
surgically created passage into the trachea. Tracheostomy tubes are well-tolerated and
often do not necessitate any use of sedative drugs. Tracheostomy tubes may be inserted
early during treatment in patients with pre-existing severe respiratory disease, or in any
patient expected to be difficult to wean from mechanical ventilation, i.e., patients with
little muscular reserve.
 Mouthpiece — Less common interface, does not provide protection against aspiration.
There are lipseal mouthpieces with flanges to help hold them in place if patient is unable.
Ventilation formulas[edit]
Alveolar Ventilation[edit]

Arterial PaCO2[edit]

Alveolar volume[edit]

Estimated physiologic shunt equation[edit]










Indications
The major indication for mechanical ventilation is acute respiratory failure, of which there are
two basic causes:
1. Ventilatory (Hypercapnic respiratory failure)
o Reduced respiratory drive
o Chest wall abnormalities
o Respiratory muscle fatigue
2. Inefficient Gas Exchange (Hypoxic respiratory failure)
o Intrapulmonary shunt
o Ventilation-perfusion mismatch
o Decreased FRC

Goals of Mechanical Ventilation
1. Relieve respiratory distress
2. Decrease work of breathing
3. Improve pulmonary gas exchange
4. Reverse respiratory muscle fatigue
5. Permit lung healing
6. Avoid complications

Minimizing the Work of Breathing (WOB)
Reduce Ventilatory Demand
1. Decrease C02 production
2. Decrease deadspace
3. Decrease ventilatory drive
a. Correct metabolic acidosis
b. Reduce psychogenic stress
c. Maintain adequate oxygenation
d. Consider sedation
Improve Respiratory Impedance
1. Decrease airflow resistance
a. Improve secretion clearance
b. Reverse bronchospasm
c. Reduce circuit resistance
2. Increase thoracic compliance
a. Diuresis
b. Apply PEEP/CPAP
3. Synchronize machine output to patient demand
Improve Breathing Efficiency
1. Decrease auto-PEEP
2. Appropriate positioning

Negative Pressure Ventilators
1. Iron lung
2. Chest cuirasse

Positive Pressure Ventilators
Almost all modern ventilators employ the principle of intermittent positive-pressure
ventilation (IPPV), which produces lung inflation by generating and applying positive
pressure to the airways.
Pressure-cycled ventilators:

Gas is allowed to flow into the lungs until a present airway pressure limit is reached, at which
time a valve opens allowing exhalation to ensue. The volume delivered by the ventilator
varies with changes in airway resistance, lung compliance, and integrity of the ventilatory
circuit.
Volume-cycled ventilators:

Gas flows to the patient until a preset volume is delivered to the ventilator circuit, even if this
entails a very high airway pressure.

Ventilator Modes
Controlled Mechanical Ventilation
1. The ventilator delivers a present number of breathes/min of a preset volume
2. Additional breathes cannot be triggered by the patient, as in the case of ACV
3. Used in patients who are paralyzed
Assist Control Ventilation
1. Delivers a preset volume
o when patient triggers machine
o automatically if patient fails to trigger within selected time
2. Clinician sets tidal volume, back-up rate, sensitivity, flow rate
3. Set back-up rate about 4 breathes/min below patient's spontaneous rate
4. Delivered volume may be markedly decreased in patients with airway obstruction or
stiff lungs when volume becomes compressed in tubing (usually 2-4 ml/cm H20).
Intermittent Mandatory Ventilation
1. Delivers a preset volume at a preset rate
2. Permits spontaneous breathing (unlike AC)
3. Although it produces a statistically significant decrease in the degree of respiratory
alkalosis, the change is unlikely to be clinically significant
4. Considerable respiratory work may result from demand valve
5. As SIMV rate is decreased, the work of breathing and pressure-time product (a
superior index of energy expenditure) increase for both the spontaneous and assisted
breathes. At any SIMV rate, there is no difference in pressure-time product between
spontaneous and assisted breathes.
6. This indicates that patients display little breath-to-breath adaptation to machine
assistance during SIMV.
Pressure Support Ventilation
1. Fixed amount of pressure (set by clinician) augments each breath
2. Pressure is maintained at preset level until patient's inspiratory flow falls to a certain
level (e.g., 25% of peak flow)
3. Patient has control over rate, inspiratory time, and inspiratory flow rate.
4. Tidal volumes is determined by level of PSV, patient effort, and pulmonary
mechanics.
Other Methods of Mechanical Ventilation
Inverse Ratio Ventilation
Rationale
1. Sustained elevations in airway pressure may more effectively recruit collapsed
alveoli.
2. I:E ratio of > 1:1 may achieve higher mean airway pressure with lower peak alveolar
pressure and lower PEEP than conventional mechanical ventilation (provided that
excessive gas trapping does not occur).
Methods
1. Pressure controlled (preset) ventilation (PCV) with prolonged inspiratory time
2. Most common method
3. Ventilation is a function of mechanics and intrinsic PEEP: the adequacy of the level
of ventilation needs to be carefully monitored
4. Volume controlled ventilation modified by
a. Slow, constant inspiratory flow rate (IFR)
b. Constant IRF, with end-inspiratory pause
c. Decelerating IFR
Problems
1. Marked increase in gas trapping (PEEPi)
a. barotrauma, decreased cardiac output
b. if I:E ratio <2:1, PEEPi is usually <10-15 cm H
2
0)
2. Decreased V
T
with increased PCO
2

3. Discomfort (need deep sedation + paralysis)
4. Indications and methodology not well defined
Permissive Hypercapnia
Rationale:
This is based on the notion that high tidal volumes induce or aggravate lung injury.
Study of Hickling et al (Intensive Care Med 1990;16:372)
1. Retrospective study of 50 patients with severe ARDS
2. Aimed for PIP <30 cm H20 (always < 40 cm H20)
a. V
T
as low as 5 ml/kg
b. PaC02 62 torr (as high as 129 torr)
c. pH 7.29 (range, 7.02-7.38)
d. Mortality 16% (vs 40% predict)
Volutrauma in Experimental Animals
1. Alveolar overdistension rapidly produces
a. Detachment of endothelial cells from basement membrane
b. Destruction of type I alveolar cells
c. Increased endothelial and epithelial permeability
2. Increased lung volume, not pressure, is responsible
Study of Dreyfus et al (ARRD 1988;137:1159)
1. Extravascular lung water measurements in rats - Ventilator settings:
HiP-HiV:
Peak airway pressure 45 cm H20
VT 40 ml/kg
LoP-HiV: Negative pressure (iron lung)
VT 44 ml
HiP-LoV:
PIP 45 cm H20 (chest strapping)
VT 19 mVkg
2. Lung water increased with both HiV conditions, whereas HiP-LoV was no different
than findings in control animals
Ventilator Settings
1. Ventilator mode
2. Oxygen concentration
3. Tidal volume
4. Set rate
5. Inspiratory flow rate
6. Inspiration:expiration ratio
7. PEEP
Inspired Oxygen Concentration
1. Initially select high FI02 and adjust when obtain ABGs after 20 min
2. Aim for lowest FI02 that will achieve Pa02 of 60-70 mm Hg (or Sp02 of 92%)
3. PEEP may be required to achieve a decrease in FI02
4. Oxygen toxicity
a. Exposure to FI02 of 1.0 up to 24 hr does not result in a significant clinical risk,
but beyond that time it is clearly toxic.
b. An FI02 of 0.50 is generally considered safe for several weeks if required.
c. For FI02 between 0.5 and 1.0, the duration of safe exposure prior to the onset
of toxicity in humans is unknown.
d. When managing hypoxemic patients, there is more to fear from severe
hypoxemia than the potential threat of oxygen toxicity.
Tidal Volume
1. Tidal volume during normal spontaneous breathing equals 5 ml/kg. Employment of
this volume during mechanical ventilation results in atelectasis which can be avoided
by using intermittent sighs.
2. Large tidal volumes of 10-15 ml/kg may produce alveolar injury.
3. Preferred tidal volume = 7-8 ml/kg
4. Remember that some volume is lost (due to compression) in the circuit (2-3 ml/cm
H20).
Ventilator Rate
1. On bedside chart, record both the rate set on the ventilator and the patient's total
respiratory rate
a. IMV
-Initially, set rate should be close to the patient's total rate
-Slowly decrease set rate with patient's tolerance in order to wean
b. AC
-Back-up rate should be 2-4 breaths below spontaneous rate
-Decreasing set rate does not decrease level of support
Inspiratory Flow Rate
1. An inspiratory flow rate (IFR) OF 60 L/min achieves optimal gas exchange in most
patients.
2. An IFR of 100 L/min achieves better gas exchange in patients with COPD, probably
because the decrease if I:E ratio (with prolongation of expiration) allows more
complete emptying of gas-trapped regions.
3. An inappropriately low IFR can markedly increase the active work of breathing by a
patient.
Inspiration:Expiration Ratio
1. Usually 1:2
2. Inverse ratio ventilation (up to 4:1)
PEEP
Goals
1. Improve oxygenation and minimize risk of oxygen toxicity of excess fluid within the
lung. By recruiting collapsed alveoli, it permits inspiration to occur on the steep
portion of the pressure-volume curve. These changes combined with possible
redistribution of excess fluid within the lungs result in a decrease in shunt.
2. Modify natural course of lung injury; however, prophylactic PEEP does not decrease
the risk of ARDS in patients at risk.
Institution of PEEP
1. Ensure that PEEP is the only variable being altered
2. Use stepwise increments (3-5 cm H20)
3. Minimize interval between change and evaluation
Optimal PEEP
1. Subject of controversy
2. Do not base Pa02 solely (as improvement in P02 may be accompanied by
cardiovascular impairment)
3. As a general rule, optimal PEEP is achieved by maximizing 02 delivery at lowest
FI02 setting.
4. Measurements of shunt fraction and thoracic compliance have been used as a guide to
optimal PEEP; these are no longer commonly employed on routine basis.
Decreasing PEEP
1. Abrupt reduction in PEEP may produce severe hypoxemia that takes days to reverse.
2. Need stable patient with Pa02 > 80 mm Hg and FI02 < 0.40 before decreasing PEEP.
3. Harborview Three-Minute Rule:
a. Measure Pa02 and decrease PEEP by < 5 cm H20
b. Obtain ABG after 3 min and immediately return PEEP to previous setting.
c. If Pa02 falls by > 20%, maintain PEEP at previous setting
d. If Pa02 falls by < 20%, there is a 90% likelihood that PEEP can be
successfully decreased
Monitoring during Mechanical Ventilation
1. Physical examination
2. Respiratory rate (set, spontaneous)
3. Delivered and spontaneous tidal volume
4. Rib cage-abdominal motion
5. Compliance (static, dynamic)
6. Peak inspiratory pressure
7. Auto PEEP
8. Airway pressure waveform
9. Work of breathing
10. Gas exchange (ABG, Sp02)
Compliance
Measurement of delivered tidal volume, peak airway pressure, plateau pressure (during an
end-inspiratory occlusion lasting up to 2 s) and PEEP permits the calculation of static and
dynamic respiratory compliance.
Static compliance (C
st
)
= VT / (Plateau pressure - PEEP)
= 60-100 ml/cm H20
Decreased by pneumonia, edema, atelectasis, pneumothorax, or endobronchial intubation.
Dynamic characteristic (C
dyn
)
= VT / (Peak pressure - PEEP)
= 50-80 ml/cm H2)
Decreased by bronchospasm, mucus plugging, kinked tube, or decreased static compliance.

Airway Pressure Waveform
1. During true passive inflation, the airway pressure tracing shows a smooth rise, it
remains convex upward, and it is highly reproducible from breath to breath.
2. In a patient who is receiving partial ventilator support (e.g., AC, IMV, PSV), the
degree of deformation and scooping of the airway pressure provides a mean of
monitoring the amount of effort expended by a patient
Rapid Shallow Breathing Index
f/VT ration = Frequency (breaths min)

Tidal volume (liter)
If f/VT > 100 breaths per min/L, weaning failure is likely.

Complications
1. Decreased cardiac output
2. Barotrauma
3. Endotracheal tube complications
4. Infection
5. Organ impairment (Renal, GI, CNS)
6. Psychological impairment
Ventilator-Associated Pneumonia
1. Reported incidence, 9-10% (usually, 30%)
2. Mortality, 50-80% (vs 30% is comparable patients without pneumonia)
3. Risk factors
a. Underlying disease
b. Impaired host defenses
c. Depressed mucociliary transport
d. Endotracheal/tracheostomy tube
e. Aspiration
f. Nebulizers
4. Ventilator circuit
Craven (ARRD 1986;133:792)
Pneumonia rate 29% if tubing changed q 24 hr; 14% if tubing changed q 48 hr
Dreyfuss (ARRD 1991;p143)738)
Pneumonia rate (confirmed by bronchoscopy "brush") - same for circuit changes q 48 hr
versus no change (average: 10 days)
5. Clinical diagnosis
a. very unreliable
b. Fagon, Chastre, et al (ARRD 1988;138:110)
 147 ventilator patients with a new pulmonary infiltrate and purulent
secretions, most of whom also had a fever and leukocytosis.
 "Bronchoscopy brush" with quantitative cultures (> 10
3
colony-
forming units per ml) were positive in only 31% of these patients.
 No combination of 16 clinical variables was helpful (stepwise logistic
regression).

Nonconventional Mechanical Ventilation
1. Non-invasive nasal ventilation
2. High-frequency ventilation
3. Prone posture ventilation
4. Pulmonary gas exchange devices
a. Extravascular (ECMO, ECCO
2
removal)
b. Intravascular (IVOX)
5. Tracheal insufflation of oxygen (TRIO)
6. Constant flow ventilation (CFV)