Introduction to Mechanical Ventilation
Prepared by EK Buzbee 2/08
Revised 2/12/09
The need for mechanical ventilation
Reading assignment:


Chang, Mechanical Ventilation Ch. 1
Egan’s Fundamentals, Ch. 41
Basic definitions for mechanical ventilation:
The need for mechanical ventilation
Spontaneous breathing is the act of using the patient’s primary and accessory muscle of inspiration to
create a driving pressure to move gas into the lungs. The intrapulmonary pressure will be less than zero and
inspiration will be triggered by changes in the patient’s CSF pH or low Pa02 in the periphery.
With normal compliance of 100 ml/cmH20 pressure and normal RAW of .5 to 2.5 cm H20/L/second the
WOB is easy because the driving pressure is low. [Egan’s pp. 215] With lowered compliance or increased
RAW, the driving pressure needed for adequate alveolar ventilation may rise to the point where the patient
needs help. The RAW of the intubated patient rises to about 6 cm H20/L/second [Pilbeam pp. 21]
Most [not all] forms of mechanical ventilation will result in the creation of positive pressure in the airway
to create the driving pressure needed to move air along. This driving pressure will result in positive
pressure inside the thorax for at least part of the breath in contrast to the negative intrathoracic pressures
achieved by spontaneous breathing.
The need for mechanical ventilation is usually due to a person’s problem with the ability of the patient to
create the driving pressure required to move gas into the alveoli so that diffusion can occur.
 The driving pressure might be excessive due to decreased compliance or increased R AW,
 or the patient may lack the ventilatory muscles to initiate a normal driving pressure.
 The patient may lack the ventilatory drive so that changes in pH or Pa02 have little or no effect on the
brain stem.
In this unit we will discuss these problems with spontaneous ventilation. You may need to review your
pathology notes for the specific effects of disease states on spontaneous breathing.
Respiratory Failure [Egan’s pp.950-962 & Chang pp. 1-23]
1. Define respiratory failure [Egan’s pp. 950]
 Inability to oxygenate the tissues and/or to remove C02
 Frequently both hypoxemia and hypercapnia are present, but we can have situations in which the
patient’s problem is refractory hypoxemia without hypercapnia
 Specifically, if the Pa02 is less than 60 torr and/or the PaC02 is more than 50 torr in a healthy
person breathing room air, we can have respiratory failure.
 A person with chronic hypercapnia can have both moderate hypoxemia and hypercapnia, but the
pH will be WNL-thus this person is not in respiratory failure-- until the hypercapnia rises making
the pH is only partially compensated.
2. List and differentiate the 3 different types of respiratory failure [Egan’s pp.950-962]
 Acute hypoxemic respiratory failure- Type I in which there is refractory hypoxemia secondary
to a number of causes: shunts, V/Q mismatch, alveolar hypoventilation, diffusion issues and
decreased Pi02
 Acute hypercapnia respiratory failure- type II: in which the patient is having problems
removing C02.
 This patient will have acute [uncompensated respiratory] acidosis. This can be due to a number of
causes: decreased alveolar ventilation, increased VD ventilation [VD physiological], decreased
ventilatory drive, respiratory fatigue & increased WOB.
 Fatigue and increased WOB can be due to compliance and/or RAW issues

Chronic respiratory failure [hypoxemia and hypercapnia] - Type III, This person will have an
acute onset on a chronic problem.
 They will have a baseline ABG that shows chronic moderate hypoxemia with compensated
respiratory acidosis, but acute illness will drop the Pa02 and raise the C02 so that the pH is now
partially compensated respiratory acidosis
 This patient could have increased RAW or compliance problems associated with a chronic problems
such as COPD, chronic restrictive defects such as pulmonary fibrosis or neuromuscular or
neurological disorder
3. Define the V/Q mismatch. [Egan’s pp. 950-951]
 One of the causes of acute hypoxemic respiratory failure.
 As we remember from A & P there are different zone of alveolar ventilation [V] and
pulmonary perfusion [Q] in the normal lung.
 When there is low V/Q, we have low ventilation with good perfusion
 When there is high V/Q, we have good ventilation with poor perfusion
 A pathological V/Q mismatch can be due to decreased alveolar ventilation or decreased
pulmonary capillary perfusion.
 Pathological V/Q mismatches could be due to airways issues, such as secretions or
bronchospasm or they could be due to alveolar consolidation or inflammation resulting in
decreased alveolar ventilation
4. Discuss the clinical s/s of a V/Q mismatch: [Egan’s pp. 950-951]
 Hypoxemia that will respond to increased Fi02
5. Define and discuss shunts and shunt like effects. [Egan’s pp.951-952]
 One of the causes of acute hypoxemic respiratory failure
 A shunt is an extreme form of V/Q mismatch in which the patient has [refractory] hypoxemia
so that supplementary 02 will not raise the Pa02.
 A normal shunt is 2-3% and is due to the anatomical shunting of right-sided blood into the left
side of the heart due to bronchial circulation and coronary blood return. A physiological shunt
of less than 10% is considered normal
 A Pathological shunt is higher and may not actually be an interface between the right and left
side of the heart. If enough alveoli are collapsed or filled with fluid, the capillaries going to
these nonfunctional areas will be desaturated [right-sided blood.]
i. 10-20% is mild
ii. 20-30% is significant shunt
iii. Over 30% shunt is critical shunt [Chang pp. 15]
 In these circumstances, merely giving supplementary 0 2 will not treat the hypoxemia because
the alveoli are nonfunctional. A means of opening the alveoli is needed. We will discuss these
techniques later.
6. Discuss decreased Pi02 as a cause of acute hypoxemic respiratory failure
 A rare cause of respiratory failure is the phenomenon of decreased Pi02 from situations such
as high altitude barometric pressures, replacement of 02 by other gases [such as during a fire.]
 Obviously, if 02 is given soon enough, before the patient losses consciousness and the ability
to protect his airway, the patient may not require ventilation.
7. Discuss the effect of diffusion problems in acute hypoxemic respiratory failure [Egan’s pp. 952]
 Based on Fick’s law of diffusion through a membrane, the rate of diffusion is inversely
proportional to the thickness of the membrane. As the alveolar-capillary membrane is
thickening from edema or scarring diffusion of 02 is affected adversely.
 As alveolar are destroyed by emphysema, the total surface area for gas exchange is decreased
so that hypoxic respiratory failure can result
8. Using 02 indices to identify V/Q mismatches and shunts. [Egan’s pp.953-954]
 Compare the ratio of Pa02 current and Fi02 current to the Fi02 required to correct the Pa02. Is it possible
to correct the Fi02?
 Use the a/A ratio to determine if there is refractory hypoxemia
 Is the Fi02 more than 50% with a Pa02 of less than 50 torr; if so there is refractory hypoxemia
9. Differentiate between alveolar hypoventilation and diffusion problems. [Egan’s pp.953-954]
 Both are causes of acute hypoxemic respiratory failure
10. Using 02 indices to differentiate between type I and type II respiratory failure [see mini-clinic
Egan’s pp. 954]
 Look at ABG:
 is there hypercapnia?
 Is there respiratory acidosis?
 If so, then part [or all] of the patient’s problem can be solved by reversing the hypercapnia
 Calculate the P[A-a]D02:
1. if the patient is hypoxemic but the P[A-a]D02 is not elevated, the hypoxemia may only be due to
the rise in alveolar C02 replacing the alveolar 02. Once we blow off the C02 with increased VE the
PA02 thus the Pa02 will rise.
11. Discuss the effects of decreased ventilatory drive on respiratory failure. [Egan’s pp.955]
 Another cause of hypercapnia respiratory failure is decreased ventilatory drive due to abnormal
brain stem action from neurological injury, or by CNS depressants.
 A person with chronic hypercapnia whose chronic hypoxia has been over-corrected by
supplementary 02 is also suffering CNS depression
“The clinical manifestations of acute hypercapnia are primarily neurological. Acute elevations of
PaCO2 greater than 60 mm Hg cause confusion and headache. PaCO2 more than 70 mm Hg
produces……CO2 narcosis manifesting as drowsiness, depressed consciousness, or coma. “
http://www.emedicine.com/PED/topic16.htm
12. Situations that contribute to respiratory failure. [Chang pp.1-23]
 Conditions that result in increased WOB due to need for excessive driving pressures
i. increased RAW
ii. decreased lung compliance
iii. Persons at risk for muscle fatigue would be persons with long-term increased
WOB, or persons who are malnourished
iv. Persons with severe muscle fatigue need to rest on mechanical ventilation for 24
– 48 hours
2. V/Q mismatch:
i. Can be corrected by increasing Fi02
3. Shunts: because the hypoxemia is unresponsive to Fi02, we may need to mechanically ventilate to
increase alveolar ventilation or increase baseline pressure. This may or may not include intubation.
i. Acute lung injury or ARDS
ii. Shock or other severe decreased C
4. Situation that result in ineffective ventilator muscle action
i. Dis-coordination / paralysis from neuromuscular or myopathic disorders
 VC of less than 20 ml/kg IBW requires some ventilator support. VC of less than 25
ml/kg IBW is associated with decreased ability to cough effectively.
 inspiratory max pressure measures weakness of inspiratory chest wall
muscles and diaphragm. a need for mechanical ventilation is seen with a
[PI max] less -30 cmH20
o expiratory max pressure measures weakness of the abdominal muscles. a
need for mechanical ventilation is seen with a [PE max] less than + 40
cmH20
o be aware that facial weakness can result in false values for these two figures if
the patient cannot seal properly—needless to say, that alone tells us we
have problems
ii.
Chest trauma such as flail chest
iii.
Electrolyte imbalance such as hyperkalemia that affects muscle action: Go here for a
cases study of a patient who suffered prolonged paralysis from hyperkalemia
http://www.aana.com/uploadedFiles/Resources/Publications/AANA_Journal__Public/2005/December_2005/p437-441.pdf
iv.
High doses of steroids particularly with persons in sepsis, who have been sedated &
paralyzed & ventilated for a period of time resulting in myopathy
v.
Persons at risk for muscle fatigue would be persons with long-term increased WOB,
or persons who are malnourished.
5. Situations that result in increased VD ventilation
i. anatomical VD
1. conducting airways. Comprises about 30% of the VD of the body.
2. is equal to 1 ml / pound of IBW
3. Is always present, but can be reduced by tracheostomy which bypasses
upper airways
4. VD/VT ratio will change, as the patient’s VT varies but the VD will
stay the same
If the patient’s IBW is
His VD anatomical is
If his VT is
his VD/VT ratio is
100/500 = .20 20% of his VT is VD
100 pounds
100 ml
500
88 pounds
600
135 pounds
800
180 pounds
900
ii. alveolar VD
1. when an alveoli gets ventilation but no perfusion, it is considered
alveolar VD
2. as CO drops or there are problems with pulmonary blood flow the
alveolar VD will rise above baseline
iii. physiological VD
1. is the sum of the anatomical VD + the alveolar VD
2. VD /VT in normal circumstances, will be more or less equal to the
anatomical VD/VT
3. rises in the physiological VD are usually due to rises in the alveolar V D
4. the normal VD /VT is about .3 or 30%. It is not uncommon for
mechanically ventilated persons to have VD /VT of .6 and higher.
5. VT - VD = alveolar ventilation
6. Alveolar ventilation results in gas exchange
7. if physiological VD is excessive, we can increase the VT to get the
alveolar ventilation back to an effective level
8. Failure to get the VD /VT below .6 will prevent successful weaning of a
patient from mechanical ventilation.
His VD anatomical is
50 ml
125 ml
88 ml
120 ml
If his VT is
500
600
800
900
his VD/VT ratio is:
Is this
excessive?
50/500 = .10
13. Clinical signs and symptoms of respiratory failure in the adult patient. [Egan’s pp. 921-923]
 inadequate alveolar ventilation: decreased peripheral air movement, crackles, significant
atelectasis or consolidation on X-ray
 inadequate lung expansion: poor chest movement; weak cough decreased peripheral air
movement, crackles, significant atelectasis or consolidation on X-ray
 poor muscle strength: inability to cough or protect airway decreased peripheral air movement,
crackles, significant atelectasis or consolidation on X-ray
 increased WOB: tachypnic, retractions, flaring, muscle tremor, altered LOC
 hypoxemic respiratory failure: s/s of hypoxemia, tachycardia, tachypnea, cyanosis, confusion
14. Parameters associated with a need for mechanical ventilation [Egan’s pp. 950-962]
 s/s of inadequate alveolar ventilation: hypercapnia above 55 torr & pH below 7.20




s/s of inadequate lung expansion: VT less than 5 ml/kg IBW, VC less than 10 ml/kg IBW
requires full ventilator support, and RR over 35 bpm
s/s poor muscle strength : MIP less than -20 cmH20, VC less than 10 ml/kg and MVV less than
2x VE
s/s of increased WOB: VE more than 10 LPM & VD/VT more than .6
s/s hypoxemic respiratory failure: P(A-a)D02 on 100% more than 350 mmHg & Pa0 2/Fi02 less
than 200.
15. Arterial blood gases associated with respiratory failure. [Egan’s pp. 950-952, 953, 955-956]
 Acute respiratory acidosis with moderate/severe hypoxemia
 Partially compensated respiratory acidosis with moderate / severe hypoxemia. Chronic patient is
no longer compensating effectively.
 Panic values on ABG: hypercapnia above 55 torr & pH below 7.20
 Serial ABG in which the trend is to see PaC02 rise each time
16. The effects of decreased compliance or increased RAW on the driving pressure required to
ventilate the patient. [Chang’s pp. 3-10]
 Bedside measurement of the RAW
RAW = P1 - P2
Flow rate in liters/second
See page 8 Figure 1-2 and 1-3 of Chang.
P1 on the mechanical ventilator is the PIP, while P2 is the P plateau
When PIP is --cmH20
Pplateau is --cmH20
flow liter/sec
45
35
1
35
33
.83
35
18
RAW:
When the machine delivers a VT, there is a peak pressure [PIP], when there is a breath-hold the
pressure drops down to the Pplateau before finally returning to the baseline pressure [which may or
may not be zero.]

The flow rate is not necessarily the peak flow set by the machine, but the actual inspiratory flow
rate read from the graphic
Bedside measurement of the lung compliance
Static C = corrected VT
Pplateau – PEEP
PEEP cmH20
Pplateau cmH20
corrected VT
Static C
10
28
600 ml
ml/cmH20
5
18
750 ml
ml/cmH20
15
30
800 ml
ml/cmH20
Basic definitions for mechanical ventilation:
Mechanical ventilation: a machine that can perform bulk transfer of gas into the lung for a patient who
cannot perform this task effectively enough to exchange gases. The ventilator works during inspiration,
while exhalation is usually passive. Based on the mode of ventilation, these machines will have various
parameters the RCP can set to get the required VE, changes in inspiratory time, baseline pressures and Fi02
to normalize ABG.
While some use the term ‘respiratory’, a true respiratory would exchange gas molecules and no ventilator
on the market can do anything but move bulk gases in and out of the lung. [Pilbeam pp. 16]
Inspiratory phase: Breathing involves inspiration in which
gas enters the lung. During the inspiratory phase, the
machine’s settings and the status of the patient’s lungs will
determine parameters such as inspiratory time [TI] and peak
inspiratory airway pressures [PIP] inspiratory holds and
flow patterns during the inspiratory phase.
P
R
E
S
S
U
R
E
The TI is a function of the flow rate, the V T and the patient’s
RAW
TI
TE
T I M E
Expiratory phase: the portion of the breath that is
concerned with the passive flow of gas out of the lung. The
inspiratory phase and the status of the patient’s lungs will determine the expiratory time [TE] The airway
pressure during the expiratory phase will be a function of the patient’s RAW and the baseline pressure set on
the mechanical ventilation.
The TE will be a function of the TI, and to a great part to the patient’s RAW
I:E ratio: comparisons of the TI to the TE. Due to the
problems associated with positive pressure ventilation, the
RCP spends a lot of time manipulating parameters to keep
the I:E ratio at a reasonable level.
P
R
E
S
S
U
R
E
TE = 1 second
Ti = 1 second
I:E ratio = 1:1
Normal I:E ratio during spontaneous breathing is 1:1.5,
but to minimize some of the hazards of mechanical
ventilation, with positive pressure ventilation, this ratio
needs to be 1:2 or more.
T I M E
A patient with significant air-trapping may require much
longer 1:E ratio such as 1:3, 1:4.
Cycle time: the entire time of a full breath which include both TI & TE so the formula for cycle time = T I +
TE
Another formula for the cycle time is used when the RCP doesn’t know the I:E ratio.
cycle time = 60 seconds/BPM
Example60 second/12 BPM = 5 seconds cycle time
If the respiratory rate is
The cycle time is
15
8
6
Airway pressure: Pressures in cmH20 measured in the airways. Usually the pressure is actually measured
at the outlet of the mechanical ventilator. Some may call this the trans-airway pressure
PIP: peak inspiratory pressure is the
highest pressure that is reached. Some
ventilator parameters can be set so that
the patient gets the same PIP with each
breath, while other ventilators will give
a uniform VT in which the PIP varies
based on changes in the patient’s RAW
PIP
P
R
E
S
S
U
R
e
P Plateau
baseline
time
or compliance. In the RAW formula, this PIP is the P1
P plateau: during a breath hold on positive pressure invasive ventilation, the airway pressure drops
from the peak [PIP] down to this pressure. On a graphic, it looks like a flat plateau. This pressure
is the P2 of the RAW formula and the Δ P of the static compliance formula
Baseline pressure: After the positive pressure breath is given, the PIP is reached then the airway
pressure returns to the baseline, which may be zero or a positive number.
PEEP or CPAP are modes in which the baseline is raised over zero. The function of a raised
baseline pressure is to increase alveolar pressure so that Pa02 can rise without increasing Fi02.
PEEP or CPAP are both used to reverse refractory hypoxemia and are required in order to get
toxic levels of Fi02 down.
PAW: the “mean airway pressure” is the average airway pressure. It is a function of the inspiratory
time, the PIP, the baseline pressure and the I:E ratio. There are two formulae for this parameter:
PAW = [PIP ( TI)] + [PEEP (TE)]
(TI + TE)
this is the easiest to calculate, because the RT does not have to calculate the actual TI and TE:
PAW = [PIP ( I )] + [PEEP (E)]
[I + E]
Example
PAW = [10 ( 1 )] + [5 (2)]
[1 + 2]
PAW = [10 + 10]
3
PAW = 20/3 = 6.66 cmH20
If the PIP is
I :E
PEEP
PAW
10
1:2
5
20
1:3
0
30
1:2
10
Positive pressure mechanical ventilation: mechanical ventilators that create positive airway pressure to
create the required driving pressures to fill the alveoli. This can be invasive or non-invasive. Positive
pressure ventilators generally send a flow rate of gas into the airways until a preset pressure or a preset VT
has been reached.
Negative pressure mechanical ventilation: mechanical ventilators that create negative pressure around
the chest wall to create the driving pressure needed to ventilate the patient. Respiratory rates are set and
negative pressures are selected to achieve the VE needed to normalize ABG.
These forms of ventilation are considered non-invasive mechanical ventilation modes because they don’t
need artificial airways. Fi02 adjustments are made by placing masks or nasal cannula on the patient’s face.
Invasive mechanical ventilation: forms of positive pressure ventilation in which the patient must be
intubated or has had a tracheostomy tube placed in order to create a patent airway so that gas can enter and
leave the patient’s lungs.
Non-invasive mechanical ventilation: many positive and negative pressure ventilators can be operated
without the need for artificial airways. A face or nose mask is used to interface with the mechanical
ventilator
Ventilator modes: most modern positive pressure invasive mechanical ventilators have mode selection so
that the clinician can select the level of support a given patient would need. Some modes such as Control or
Assist/control modes are used for full ventilatory support, while other modes such as Intermittent
Mandatory Ventilation [IMV/ SIMV] or are used for partial support. One can pick single modes or dual
modes.
Full-support mechanical ventilation: To rest a patient with respiratory fatigue, mechanical ventilation
assumes all the WOB. This is usually done by positive pressure invasive mechanical ventilation. The
patient is generally sedated, even paralyzed by drugs.
Manipulation of the ventilator parameter will result in very specific, predictable changes in ABGs. Most
fatigued patients need to be rested for 24-48 hours, but a serious complication of full-support is that after a
few days, the patient’s respiratory muscles start to atrophy quickly.
Partial-support mechanical ventilation: also called dual mode ventilation, in which the patient assumes
some of the WOB. There are several types of dual mode ventilators for different needs. SIMV or IMV are
examples of partial-support mechanical ventilation. Frequently patients are started on full support and are
moved to partial support after the mandatory rest period.
Spontaneous modes: When a patient is past the point of needing full or even partial support, we can
challenge the patient by selection of various forms of low level Pressure support ventilation [PSV], or
CPAP modes of ventilation in which the patient controls most, if not all of the parameters of ventilation
with the machine acting only as a monitoring device with/without alarms and mechanical intervention in
case of apnea or hypoventilation.
Patients on spontaneous modes of ventilation must have an intact ventilatory drive, and must be able to
maintain their PaC02 with little or no help from the machine. These modes of ventilation are used for
hypoxemic respiratory failure type I. Frequently, non-invasive positive pressure ventilators are used in their
spontaneous modes.
Wave forms/graphics: electronic devices convert airway pressures, volumes or flows into a graphic with
various parameters being on the x or on the y axis. Interpretation of these wave forms is complex and will
be covered at a later date.
Peak flows /flow rates: All modern positive pressure ventilators have peak flow rates. Some peak flows
are selected while in some modes of ventilation, this parameter can be varied by the patient’s demand. The
actual flow rate may not be the same all the way through the breath. Dependent on the mode selected or the
type of ventilator used, the flow pattern may vary from the constant flow.
Constant flow: The flow rate starts at peak
flow and stays there until it drops to zero flow
Descending ramp: the flow starts at the peak
flow, and then as pressure rises in the system,
it drops down gradually until zero flow is
reached.
F
L
Descending ramp
Constant flow
O
W
Sine wave
Sine wave; the flow starts out slow and
gradually rises to the peak flow then gradually
TIME
drops back to zero. The Sine wave is the closest to spontaneous breathing.
VT
To manipulate the ABG, we need a way to manipulate the V E, we can do this by selection of the
respirator rate or by selection of the VT. Selection of the appropriate VT is determined by the patient’s
disease state. We will go into this selection at great detail at a later date.
Set VT Due to interaction between the patient airways & the ventilator’s circuit, the VT that we select on
the dial may or may not be the same as the VT that the patient gets in his lungs
Corrected VT : the circuit of the mechanical ventilator is a space that can accept a volume of gas and this
circuit can swell in the face of high pressures so that even more volume can be compressed in the circuit.
The more gas compressed into the circuit, the lower the actual VT that reaches the patient’s lungs. The
corrected VT has been corrected for this compressible volume loss. We will discuss this in more detail at a
later date.
Summation
There are many reasons why any patient goes on a ventilator. To optimize the effectiveness of our decision,
we need to select the proper type of ventilation, the appropriate modes and settings that will optimize the
patient’s oxygenation and ventilation while limiting the side effects.
Reference:




Boitano, L.J. Management of Airway Clearance in Neuromuscular Disease in Respiratory Care August
2006, vol 51 (8) pp. 913-921.
Egan’s Fundamentals of Respiratory Care 9th edition
David Chang Clinical Application of Mechanical Ventilation 3rd edition
Susan Pilbeam & JM Cairo Mechanical Ventilation: physiology & Clinical Application. 4th edition