Respiratory Failure

Hypoxemic Respiratory Failure (Type I)

Hypercapneic Respiratory Failure (Type II)

Marc Valera, RTRP

 Objectives
• De ne respiratory failure type I & II

• Di erentiate between hypoxemic respiratory failure (type I) and hypercapnic

respiratory failure (type II)

• Discuss the causes of acute respiratory failure.

ff
fi
Respiratory failure
The “inability to maintain either:

(a) the normal delivery of O2 to the tissues or

(b) the normal removal of carbon dioxide (CO2) from the tissues”

and often results from an imbalance between respiratory workload and

ventilatory strength or endurance.
 Respiratory failure
De nition
• Arterial partial pressure of
oxygen (PaO2) less than 60
mm Hg (also referred to as
hypoxemic or type I respiratory
failure),
• Alveolar partial pressure of
carbon dioxide (PaCO2)
greater than 50 mm Hg
(hypercapnic or type II
respiratory failure), or both,
fi
Criteria for respiratory failure
based on arterial blood gases
(ABGs)
“Although ABG analysis is helpful in
distinguishing hypoxemic (type I) and
hypercapnic (type II) respiratory failure,
many patients in acute respiratory failure
develop both hypoxemia and
hypercapnia.“
Respiratory failure
can be an acute or a
chronic process.
respiratory failure develop both hypoxemia and hypercapnia. PaO2 = 100
B CaO2 = 20 B
HYPOXEMIC RESPIRATORY
HYPOXEMIC RESPIRATORY FIGURE
effect of
44-1 Hypoxemia
supplemental O . !
caused
!
V/Q
by ! ! mismatch
FIGURE
V/Q
is normal on the left sid
FAILURE (TYPE I) 2
effect of su
FAILURE (TYPE I) idealized lung unit and low on the right. Only O2 exchan
The primary causes of hypoxemia are the following: shown, and P(A − a)O2 is assumed to be idealized
zero. A, Withlu
! ! ) mismatch not enough O2 reaches the poorly ventilated alveolus to
• Ventilation/perfusion ( V/Q
The primary causes of hypoxemia are the following: shown,
capillary blood fully. B, With 40% O2, PaO 2 in this an
alveo
• Shunt
• Ventilation/perfusion
• Alveolar hypoventilation ! !
( V/Q ) mismatch increased enough to make capillary PO2not nearlyenough
normal.
mixed blood from the two capillaries is determined by t
• Diffusion impairment capillary
of the O2 contents of the two streams of blood, not by bl
• Shunt
• Perfusion/diffusion impairment increased
values. (Modified from Pierson DJ, Kacmarek RM: Foun
• Alveolar
• Decreased inspired Ohypoventilation
2
respiratory care, New York, 1992, Churchill Livingstone
mixed bloo
• Diffusion
• Venous admixture impairment of the O2 c
These entities are briefly discussed here and are discussed in
• Perfusion/diffusion
more detail in Chapters 11 and 12. impairment values.
compromised despite adequate blood flow. Obstr
(Mo
• Decreased inspired O2 diseases are frequent causes. The respiratory
bronchospasm, m
Ventilation/Perfusion Mismatch ging, inflammation, and premature airway closure
• Venous admixture
There are regions in healthy lungs where ventilation and perfu- asthmatic or emphysematous exacerbations worsen
These entities are briefly discussed here and are discussed
sion are not evenly matched, so it seems logical that this is the and create !
V/Q ! mismatch. in
Infection, heart failure,
most common cause of hypoxemia. RTs are familiar with this tion injury may lead to partially collapsed or fluid-fi
more detail in Chapters5 11 and 12.
concept through the work of West, which described a high V/Q ! ! comprom
also resulting in decreased ventilation and reduce
ratio at the apex of the lungs and a low ratio at the bases. This levels. diseases a
conceptVentilation/Perfusion Mismatch
can be oversimplified and stated as there being more air
ging, infla
 respiratory failure develop both hypoxemia and hypercapnia.
Respiratory Failure and the Need for Ventilatory Support • CHAPTER PaO2 44
= 100 973
B CaO2 = 20
HYPOXEMIC RESPIRATORY FIGURE 44-1 Hypoxemia caused by ! ! mismatch
V/Q
ratory failure is a clinical problem that all respira- PIO2 = 150
effect of supplemental O . !
V/Q ! is normal on the left sid
FAILURE must
care practitioners (TYPE I) at identifying,
be skilled 2
idealized lung unit and low on the right. Only O2 exchan
ssing, and treating. The mortality of patients re- · · · ·
normaland P(A − a)O2V/Q to be zero. A, With
nsive careV/Q mismatch
The primary causes of hypoxemia are the following: V/Q shown, is assumed
low
unit (ICU) admission ! !with respiratory not enough O2 reaches the poorly ventilated alveolus to
• Ventilation/perfusion ( V/Q ) mismatch
44% in 1995, and only marginally improved to capillary blood fully. B, With 40% O2, PaO2 in this alveo
1,2• Shunt
• •Alveolar hypoventilation
10. The Obstructive
need for oxygen lung
(O 2) diseases
delivery, are
mechani- increased enough to make capillary PO2 nearly normal.
Pmixed
O = blood
100 from the P two
O capillaries
= 50 is determined by t
frequent
on, •andDiffusion
other modalitiescauses.
impairment
in the management A 2 A 2
of the O2 contents of the two streams of blood, not by
ients • makes the respiratory therapist’s (RT) role PO2 = 40 values. (Modified from Pierson DJ,
Perfusion/diffusion impairment PO2Kacmarek
= 40 RM: Foun
e. • •Decreased
Bronchospasm,
inspired O2 mucous O2 Content = 15respiratory care, New York, 1992, Churchill Livingstone
O2 Content = 15
ry failure is the
plugging, “inability to maintain
in ammation, and either the
• Venous admixture 50

10 20
very of O 2 to the tissues or the normal removal of

0
Thesepremature airway
entities are briefly
3 closure
discussed herethat
and are discussed in 1 7
ide (CO 2) from the tissues” and often results from
moresignal
detail inasthmatic
Chapters 11 and or
ce between respiratory workload and ventilatory
12. compromised despite adequate blood flow. Obstr
endurance. emphysematous
Ventilation/Perfusion exacerbations
Criteria for respiratory failure Mismatch
based on
diseases are frequent causes. The bronchospasm, m
ging, PaO2 = 64 and premature airway closure
inflammation,
4
d gases (ABGs) were established by Campbell and
There are regions in healthy lungs where ventilation and perfu- A CaO2 = 18.5
asthmatic or emphysematous exacerbations worsen
fine sion
failure as arterial partial pressure of oxygen
are not evenly matched, so it seems logical that this is the and create V/Q ! ! mismatch. Infection, heart failure,
than most
60 mm Hg (also referred to as hypoxemic or
common cause of hypoxemia. RTs are familiar with this A, With room
tionair, Pmay
IO2 =O
not enough
injury 285
2 reaches
lead the poorly
to partially collapsed or fluid-fi
ratory failure), alveolar partial pressure 5 of carbon
concept through the work of West, which described a high V/Q ! !
ventilated alveolus to saturate its capillary blood fully.
also resulting in decreased ventilation and reduce
CO2) ratio
greater than 50 mm Hg (hypercapnic or type
at the apex of the lungs and a low ratio at the bases. This ·levels.
· · ·
V/Q normal V/Q low
ry failure), or both, in otherwise healthy individuals
concept can be oversimplified and stated as there being more air
fl
ECTION VI • failure
respiratory Acute andboth
develop Critical Care
hypoxemia and hypercapnia. PaO2 = 100
B CaO2 = 20
44-1, B). Hypoxemia commonly manifests with PIO2 = 150 ! ! mismatch
HYPOXEMIC RESPIRATORY FIGURE 44-1 Hypoxemia caused by V/Q
hycardia, and tachypnea, but these are very non- effect of supplemental O . !
V/Q! is normal on the left sid
FAILURE (TYPE I) 2
ngs. However, patient observation is extremely idealized lung unit and low onNo the right. Only O2 exchan
shown, and P(A − a)O2 is assumed ventilationto be zero. A, With
use The Shunt
primary
of accessory causes
muscles of hypoxemia
of respiration
! !
are the following:
(scalene,
not enough O2 reaches the poorly ventilated alveolus to
Ventilation/perfusion ( V/Q ) mismatch
jor, and sternomastoid) is an important sign that
•
capillary blood fully. B, With 40% O2, PaO2 in this alveo
• Shunt
hragmatic inspiration is inadequate. In an elderly,
• Normal anatomic shunt (2-3%) increased enough to make capillary PO2 nearly normal.
• Alveolarindividual
barrel-chested hypoventilation
who is leaning forward mixed
PAO2 blood
= 100 from the two capillaries is determined by t
• • Pathologicimpairment
Diffusion anatomic shunt
arms, COPD is the likely diagnosis. Nasal flaring of the O2 contents of the two streams of blood, not by
• Perfusion/diffusion impairment PO = values.
40 (Modified from Pierson DJ, Kacmarek
PO = 40 RM: Foun
nt. Lower• extremity
ASD; VSD; edemapulmonary arteriovenous
is more indicative of 2 2
malformations
• Decreased inspired O O 2 Content = respiratory care, New York, 1992, O
15 Churchill
2 ContentLivingstone
= 15
e as the cause of hypoxemia. Cyanosis may be
2
• Venous admixture 0

10 20
• Physiologic
d primarily due to shuntdecreased blood flow. Central 4

0
These entities are briefly discussed here and are discussed in 1 5
n most easily as a bluish tint around the lips,
more• detail
alveoliincollapse or 11
Chapters lledand
with12.uid or exudate. compromised despite adequate blood flow. Obstr
greater than 5 g/dl of unsaturated hemoglobin is
• atelectasis, pulmonary edema, and diseases are frequent causes. The bronchospasm, m
finding is more common
Ventilation/Perfusion
pneumonia.
in patients with
Mismatchpolycy-
ging, inflammation,PaO2 = 54and premature airway closure
may be subject to wide observer variability. More A perfu- O2 = 17.5
Caemphysematous
There are regions in healthy lungs where ventilation and asthmatic or exacerbations worsen
emia can lead to significant central nervous system ! ! mismatch. Infection, heart failure,
sion are not evenly matched, so it seems logical that this is the and create V/Q
A, With room air, although blood leaving the
nction, ranging from irritability to confusion
most common cause of hypoxemia. RTs are familiar with this normal alveolar-capillary
tion injury
PIisOnormally
unit
may 2 = 285saturated, blood passing
lead to partially collapsed or fluid-fi
the capillary on the right “sees” no O2 because its alveolus is
5
concept through the work of West, which described a high V/Q !
! unventilated,
alsoandresulting in unsaturated.
it leaves the unit decreasedWhen ventilation
the two and reduce
on and percussion are very useful when added to
ratio at the apex of the lungs and a low ratio at the bases. This
streams of blood mix, the resulting PaO2 is determinedNo by the
average oflevels.
the O2 contents, not by the PO2 ventilation
values.
vation. Bilateral
concept can bewheezing, especially
oversimplified in a young
and stated as there being more air
fi
fl
 respiratory failure develop both hypoxemia and A
hypercapnia. CaO2 = 17.5
PaO2 = 100
n lead to significant central nervous system
, ranging from irritability to confusion B PIO2 = 285 CaO2 = 20
HYPOXEMIC RESPIRATORY FIGURE 44-1 Hypoxemia caused by V/Q ! ! mismatch
effect of supplemental O . !
V/Q! is normal on the left sid
FAILURE (TYPE I)
percussion are very useful when added to 2
No
idealized lung unit and low on the right. Only O2 exchan
Bilateral wheezing, especially in a young ventilation
shown, and P(A − a)O2 is assumed to be zero. A, With
V/Q
The primary
ry distress,
mismatch
causes of hypoxemia
often identifies( V/Q
are
!the! )broncho-
the following:
not enough O2 reaches the poorly ventilated alveolus to
• Ventilation/perfusion mismatch
capillary blood fully. B, With 40% O2, PaO2 in this alveo
Upper• airway
Shunt disease or fluid-filled airways increased enough to make capillary PO2 nearly normal.
• Alveolar
heezing. Breath hypoventilation
sounds that are diminished PAmixed
O2 = 225
V/Q mismatch, shunt does not blood from the two capillaries is determined by t
Diffusionon
eased•resonance impairment
percussion are common of the O2 contents of the two streams of blood, not by
•
respond to supplemental
Perfusion/diffusion impairment O 2 PO 2 = 40 values. (Modified from Pierson PO2Kacmarek
DJ, = 40 RM: Foun
ateral abnormalities are significant. Wheez-
because
• Decreased the gas-
inspired exchange
O
identify an endobronchial lesion, whereas
2
unit O2 Content = 15 respiratory care, New York, 1992, O 2 Churchill =Livingstone
Content 15
(the alveolus) is not open 40

22 0.5
• Venous admixture
h sounds and decreased resonance on one

5
15

2
These entities are briefly discussed here and are discussed in
y reflect collapse, infection, edema, or effu-
more! detail in Chapters 11 and
! mismatch. Discordant exam 12. compromised despite adequate blood flow. Obstr
uses of V/Q
diseases are frequent causes. The bronchospasm, m
Ventilation/Perfusion
sed resonance on percussion and decreased Mismatch PaO2 = 57 and premature airway closure
ging, inflammation,
he same
Thereside
are may
regionssignal a pneumothorax.
in healthy B and perfu-
lungs where ventilation asthmaticCaOor2 =emphysematous
17.75 exacerbations worsen
and sion
decreased resonance
are not evenly matched,on so percussion
it seems logical that this is the and create
FIGURE 44-2 Alveolar-capillary diagram
!
V/Q ! mismatch. Infection, heart failure,
of intrapulmonary
n alveolar filling process (mass, infection,
most common cause of hypoxemia. RTs are familiar Addition
with
(capillary)
of 40%
this showing
shunting
O2 fails
tion injury
why may
to correct the
lead to partially
supplemental
hypoxemia
O2 failscollapsed
to corrector fluid-fi
because
hypoxemia. ! O2
! content is not signi cantly increased in
− a)O2 is and reduce
5
concept through the work of West, which described a high Only
V/Q O2 exchange is shown,
also resulting and P(A ventilation
in decreased
! !ratio the
assumed
normal
to This
unit, and capillary blood in the
A, With room air, although blood leaving the
be zero. levels.
V/Q mismatch canofmanifest
at the apex the lungsasand
a “black”
a low ratio at the bases.
unventilated unit still “sees” no O2.
ge orconcept can be oversimplified
hyperinflated and case
lungs as in the normal alveolar-capillary unit is normally saturated, blood passing
statedofas there being more air
fi
respiratory failure develop both hypoxemia and hypercapnia. PaO2 = 100
B CaO2 = 20
HYPOXEMIC RESPIRATORY FIGURE 44-1 Hypoxemia caused by V/Q ! ! mismatch
effect of supplemental O2. V/Q! ! is normal on the left sid
FAILURE (TYPE I)
idealized lung unit and low on the right. Only O2 exchan
shown, and P(A − a)O2 is assumed to be zero. A, With
Alveolar Hypoventilation
The primary causes of hypoxemia are the
! ! ) mismatch
following:
not enough O2 reaches the poorly ventilated alveolus to
• Ventilation/perfusion ( V/Q
capillary blood fully. B, With 40% O2, PaO2 in this alveo
• Shunt
increased enough to make capillary PO2 nearly normal.
• Alveolar hypoventilation mixed blood from the two capillaries is determined by t
• Diffusion impairment of the O2 contents of the two streams of blood, not by
• Perfusion/diffusion impairment values. (Modified from Pierson DJ, Kacmarek RM: Foun
• Decreased inspired O2
Discussed subsequently in the section respiratory
on care, New
hypercapnic York, 1992, Churchill Livingstone
respiratory
• Venous admixture failure (Type II)
These entities are briefly discussed here and are discussed in
more detail in Chapters 11 and 12. compromised despite adequate blood flow. Obstr
diseases are frequent causes. The bronchospasm, m
Ventilation/Perfusion Mismatch ging, inflammation, and premature airway closure
There are regions in healthy lungs where ventilation and perfu- asthmatic or emphysematous exacerbations worsen
sion are not evenly matched, so it seems logical that this is the ! ! mismatch. Infection, heart failure,
and create V/Q
most common cause of hypoxemia. RTs are familiar with this tion injury may lead to partially collapsed or fluid-fi
5
concept through the work of West, which described a high V/Q ! ! also resulting in decreased ventilation and reduce
ratio at the apex of the lungs and a low ratio at the bases. This levels.
concept can be oversimplified and stated as there being more air

 respiratory failure develop both hypoxemia and hypercapnia. PaO2 = 100

B CaO2 = 20
HYPOXEMIC RESPIRATORY FIGURE 44-1 Hypoxemia caused by V/Q ! ! mismatch
effect of supplemental O2. V/Q! ! is normal on the left sid
FAILURE (TYPE I)
idealized lung unit and low on the right. Only O2 exchan
shown, and P(A − a)O2 is assumed to be zero. A, With
Di usion Impairment
The primary causes of hypoxemia are the
! ! ) mismatch
following:
not enough O2 reaches the poorly ventilated alveolus to
• Ventilation/perfusion ( V/Q
capillary blood fully. B, With 40% O2, PaO2 in this alveo
•• Shunt
Rarely a cause of signi cant “Pulmonary
increased enough to makevascular
capillary PO2 nearly normal.
hypoxemia
• Alveolar at rest,
hypoventilation mixed blood from the twoalso
capillaries
abnormalities can leadis to
determined by t
• Diffusion impairment of the O2 contents of the two streams of blood, not by
•• Perfusion/diffusion
E ects becomeimpairmentmore pronounced diffusion impairment.
values. (Modified from Pierson Anemia,
DJ, Kacmarek RM: Foun
with exercise,
• Decreased inspiredwhich
O2 limits the time pulmonary
respiratory care,hypertension, and Livingstone
New York, 1992, Churchill
for gasadmixture
• Venous exchange. pulmonary embolus all may
These entities are briefly discussed here and are discussed in reduce capillary blood ow,
• Caused
more detail inby interstitial
Chapters 11 andlung
12. disease compromised despite adequate
resulting in diminished gas blood flow. Obstr
(e.g., pulmonary brosis, asbestosis, diseases are frequent causes. The bronchospasm, m
Ventilation/Perfusion
sarcoidosis) Mismatch transfer.”
ging, inflammation, and premature airway closure
There are regions in healthy lungs where ventilation and perfu- asthmatic or emphysematous exacerbations worsen
• Thickening
sion are not evenlyand scarring
matched, of thelogical that this is the
so it seems ! ! mismatch. Infection, heart failure,
and create V/Q
mostinterstitium
common cause undermine normal
of hypoxemia. gas
RTs are familiar with this tion injury may lead to partially collapsed or fluid-fi
exchange, 5
concept through the work of West, which described a high V/Q ! ! also resulting in decreased ventilation and reduce
ratio at the apex of the lungs and a low ratio at the bases. This levels.
concept can be oversimplified and stated as there being more air
ff
ff
fi
fi
fl
respiratory failure develop both hypoxemia and hypercapnia. PaO2 = 100
B CaO2 = 20
HYPOXEMIC RESPIRATORY FIGURE 44-1 Hypoxemia caused by V/Q ! ! mismatch
effect of supplemental O2. V/Q! ! is normal on the left sid
FAILURE (TYPE I)
idealized lung unit and low on the right. Only O2 exchan
shown, and P(A − a)O2 is assumed to be zero. A, With
Perfusion/Di ! usion
The primary causes of hypoxemia are Impairment
the
! ) mismatch
following:
not enough O2 reaches the poorly ventilated alveolus to
• Ventilation/perfusion ( V/Q
capillary blood fully. B, With 40% O2, PaO2 in this alveo
• • Shunt
Cause of hypoxemia in individuals increased enough to make
“Although capillary
shunt is aPO2 nearly normal.
with liver
• Alveolar disease complicated by the
hypoventilation mixed blood from the two capillaries is determined by t
hepato-pulmonary
• Diffusion impairment syndrome ofcomponent
the O2 contents of thetwosyndrome,
of the streams of blood, not by
• Perfusion/diffusion impairment signi(Modified
values. cant from
supplemental O2 RM: Foun
Pierson DJ, Kacmarek
respiratory care, New York, 1992, Churchill Livingstone
• Right-to-left
• Decreased inspiredintracardiac
O2 shunt can overcome the hypoxemia,
• Venous admixture
combines with dilated pulmonary so this is commonly called a
These entities are briefly discussed here
capillaries resulting in impaired gas and are discussed in
more detail in Chapters 11 and 12.
perfusion/diffusion defect. “
compromised despite adequate blood flow. Obstr
exchange because the normal diseases are frequent causes. The bronchospasm, m
alveolar partial pressures
Ventilation/Perfusion of O2 may
Mismatch ging, inflammation, and premature airway closure
beareinsu
There regionscient to drive
in healthy the O2
lungs where ventilation and perfu- asthmatic or emphysematous exacerbations worsen
sionmolecules
are not evenlyto the center
matched, of the
so it seems dilated
logical that this is the ! ! mismatch. Infection, heart failure,
and create V/Q
mostpulmonary
common cause vasculature.
of hypoxemia. RTs are familiar with this tion injury may lead to partially collapsed or fluid-fi
5
concept through the work of West, which described a high V/Q ! ! also resulting in decreased ventilation and reduce
ratio at the apex of the lungs and a low ratio at the bases. This levels.
concept can be oversimplified and stated as there being more air
fi
ffi
ff
respiratory failure develop both hypoxemia and hypercapnia. PaO2 = 100
B CaO2 = 20
HYPOXEMIC RESPIRATORY FIGURE 44-1 Hypoxemia caused by V/Q ! ! mismatch
effect of supplemental O2. V/Q! ! is normal on the left sid
FAILURE (TYPE I)
idealized lung unit and low on the right. Only O2 exchan
shown, and P(A − a)O2 is assumed to be zero. A, With
Decreased Inspired
The primary causes of hypoxemia are Oxygen
the
! ! ) mismatch
following:
not enough O2 reaches the poorly ventilated alveolus to
• Ventilation/perfusion ( V/Q
capillary blood fully. B, With 40% O2, PaO2 in this alveo
•• Shunt
Caused by high altitude increased enough to make capillary PO2 nearly normal.
• Alveolar hypoventilation mixed blood from the two capillaries is determined by t
• FiO2impairment
• Diffusion (21%) remains the same of the O2 contents of the two streams of blood, not by
but increased
• Perfusion/diffusion PB a ects PiO2
impairment values. (Modified from Pierson DJ, Kacmarek RM: Foun
• Decreased inspired O2 respiratory care, New York, 1992, Churchill Livingstone
• Venous admixture
These entities are briefly discussed here and are discussed in
more detail in Chapters 11 and 12. compromised despite adequate blood flow. Obstr
diseases are frequent causes. The bronchospasm, m
Ventilation/Perfusion Mismatch ging, inflammation, and premature airway closure
There are regions in healthy lungs where ventilation and perfu- asthmatic or emphysematous exacerbations worsen
sion are not evenly matched, so it seems logical that this is the ! ! mismatch. Infection, heart failure,
and create V/Q
most common cause of hypoxemia. RTs are familiar with this tion injury may lead to partially collapsed or fluid-fi
5
concept through the work of West, which described a high V/Q ! ! also resulting in decreased ventilation and reduce
ratio at the apex of the lungs and a low ratio at the bases. This levels.
concept can be oversimplified and stated as there being more air
ff
respiratory failure develop both hypoxemia and hypercapnia. PaO2 = 100
B CaO2 = 20
HYPOXEMIC RESPIRATORY FIGURE 44-1 Hypoxemia caused by V/Q ! ! mismatch
effect of supplemental O2. V/Q ! ! is normal on the left sid
FAILURE (TYPE I)
idealized lung unit and low on the right. Only O2 exchan
A shown,
decreaseand P(Ain− mixed venous O2zero. A, With
Venous Admixture
The primary causes of hypoxemia are the
! ! ) mismatch
following:
not enough O
a)O2 is assumed
reaches the poorly
to be
ventilated alveolus to
• Ventilation/perfusion ( V/Q increases the gradient by which
2
capillary blood fully. B, With 40% O2, PaO2 in this alveo
•• Shunt
Congestive heart failure with low O2increased
needsenoughto betostepped upPO as2 nearly
it normal.
make capillary
cardiac
• Alveolar output is the most
hypoventilation passes
mixed blood through
from the the lungs and
two capillaries is determined by t
common
• Diffusion cause
impairment of the O2 contents of the two streams of blood, not by
can contribute to the
• Perfusion/diffusion impairment values. (Modified from Pierson DJ, Kacmarek RM: Foun
development
respiratory care, New ofYork,
hypoxemia.
1992, Churchill Livingstone
• Other
• Decreased causes
inspired include
O 2 low
• Venous admixture
hemoglobin concentration and
These entities are briefly
increased O2 consumption.discussed here and are discussed in
more detail in Chapters 11 and 12. compromised despite adequate blood flow. Obstr
diseases are frequent causes. The bronchospasm, m
Ventilation/Perfusion Mismatch ging, inflammation, and premature airway closure
There are regions in healthy lungs where ventilation and perfu- asthmatic or emphysematous exacerbations worsen
sion are not evenly matched, so it seems logical that this is the ! ! mismatch. Infection, heart failure,
and create V/Q
most common cause of hypoxemia. RTs are familiar with this tion injury may lead to partially collapsed or fluid-fi
5
concept through the work of West, which described a high V/Q ! ! also resulting in decreased ventilation and reduce
ratio at the apex of the lungs and a low ratio at the bases. This levels.
concept can be oversimplified and stated as there being more air
 ! !
a V/Q mismatch and shunt can be differentiated by means of
O2 administration (see Figures 44-1 and 44-2). A significant

TABLE 44-1
Differentiating the Cause of Hypoxemia
Cause P(A − a)O2 Response to Increased FiO2
FIG
Hypoventilation Normal Marked rela
Shunt Increased Minimal ven
!V/Q
! mismatch Increased Marked sign
dro
 TABLE 44-2
Causes of Respiratory Failure
Type I (Hypoxemic) Type II (Hypercapnic)
Increased Exposure Impaired Respiratory Control Neurologic Disease Increased Work of Breathing
ARDS Extrinsic Drug overdose Spinal cord trauma Obstructive lung disease
Pulmonary Defective CO2 scrubbers Bilateral endarterectomy Motor neuron COPD
embolism (anesthesia or life- with carotid body
support systems) resection
Pulmonary edema Occupational exposure Central sleep apnea Poliomyelitis Asthma
(miners, spelunkers,
dry-ice workers, firemen)
Septic shock Intrinsic Hypocapnia Amyotrophic lateral sclerosis Upper airway obstruction
Pulmonary infection Fever Cheyne-Stokes Motor nerve Obesity-hypoventilation
Viral Shivering Acromegaly Phrenic nerve Pneumothorax
Bacterial Hypermetabolism Hypothyroid Guillain-Barré Severe burns
Fungal Agitation Brainstem lesions Charcot-Marie-Tooth Chest wall disorders
Inhalation Excess caloric intake Cerebrovascular accident Neuromuscular junction Kyphoscoliosis
Smoke Encephalitis Myasthenia gravis Ankylosing spondylitis
Chemical Multiple sclerosis Botulism
Water Parkinson disease Muscular
Pleural effusion Metabolic alkalosis Muscular dystrophy
Interstitial lung Primary alveolar Myositis
disease hypoventilation
Obstructive lung (Ondine’s curse) Myopathy
disease
Aspiration Congenital central Acid maltase
hypoventilation
Primary pulmonary Carotid body resection Metabolic
hypertension Obesity-hypoventilation