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15
15 Respiratory Acidosis
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The Fluid, Electrolyte and Acid-Base Companion
HCO3– HCO3–
pH | pH |
CO2 CO2
HCO3– HCO3–
pH | pH |
CO2 CO2
One could imagine that O C2 levels could rise from increased production. But,
healthy lungs
are so adept at removing CO , that no matter how fast CO is produced, the lungs are able
to clear it. Only if lung disease is already present can increased production 2ofcauseCO
2 2
respiratory acidosis. For example, in patients with chronic pulmonary disease and chroni-
cally elevated levels of carbon dioxide, increased metabolic production 2of(e.g.,
CO sepsis)
can further increase CPO2.
400
S. Faubel and J. Topf 15 Respiratory Acidosis
O2
CO2
CO2 O2
CO2
O2
The process of respiration contains four steps: sensing and _________, signaling
muscles and motion, free _______ and gas exchange. flow
401
The Fluid, Electrolyte and Acid-Base Companion
C
C
PCO2 (mmHg) C C
C C
C C C
C C C
C C C C
C C C C C
Tidal volume is the amount of Physiologic dead space is the Respiratory rate is the num-
air inspired in a single breath. volume of air in the lungs which ber of breaths per minute and
Normal tidal volume is be- does not participate in gas ex- is normally between 12 and 16
tween 6 and 8 mL/kg (about change. Physiologic dead space breaths/min.
500 mL in a 70 kg man). is normally 30% of tidal volume,
or about 150 mL.
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S. Faubel and J. Topf 15 Respiratory Acidosis
CO2
O2
CO2
O2
O2
Physiologic dead space refers to all the areas of the lung where air is
delivered, but gas exchange does not occur. Physiologic dead space is the
sum of the anatomic and alveolar dead spaces.
Anatomic dead space. The air passages which bring air into
and out of the alveoli, the conducting airways, are not capable of
gas exchange. The conducting airways are made up of the tra-
chea, bronchi and bronchioles. The volume of anatomic dead
space is constant.
Alveolar dead space. Some alveoli receive air but do not par-
ticipate in gas exchange because they are not perfused with blood.
The volume of alveolar dead space varies with disease and body
position.
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The Fluid, Electrolyte and Acid-Base Companion
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S. Faubel and J. Topf 15 Respiratory Acidosis
carotid body
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The Fluid, Electrolyte and Acid-Base Companion
O2 O2
O2 O2
O2 O2 O2 O2 O2 O2
O2
O2 O2 O2 O2
O2 O2 O2
C C
C C C
C C C
C C
When PO2 decreases, the carotid bodies trigger the respiratory control center
to increase minute ventilation. Increased minute ventilation causes a decrease
in PCO2. The fall in PCO2 is detected in the medulla which suppresses respiration
in order to return PCO2 to normal. Only when hypoxemia becomes critical, PO2
below 60 mmHg, does the respiratory control center sacrifice tight regulation of
carbon dioxide in order to increase oxygenation. Thus, carbon dioxide main-
tains primary control over minute ventilation unless hypoxia is life-threatening.
_______ maintains primary control over minute ventilation until the PCO2
partial pressure of oxygen falls below ______ mmHg. 60
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S. Faubel and J. Topf 15 Respiratory Acidosis
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The Fluid, Electrolyte and Acid-Base Companion
O2 CO2
408
S. Faubel and J. Topf 15 Respiratory Acidosis
Z
Z
Z
Z
pH, CO2 and O2 Apnea occurs at night; CO2 Z
are normal dur- increases while pH and O 2
ing the day. decrease.
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The Fluid, Electrolyte and Acid-Base Companion
Inspiration Expiration
Chest wall moves out; air moves in. Chest wall moves in; air moves out.
Step two of respiration is muscles and motion which refers to the mechanical
process of inspiration and expiration. Inspiration is an active process and expi-
ration is a passive process. Inspiration and expiration are controlled by the
contraction and relaxation of the muscles of respiration.
Inspiration is the process by which air is sucked into the lungs. When the
muscles of respiration contract, the chest cavity expands, lowering intratho-
racic pressure. The difference between the atmospheric and intrathoracic pres-
sures draws air into the lungs.
Expiration is a passive process which occurs when the muscles of respiration
relax, the chest wall falls inward and air is forced out. With increased respira-
tory effort (e.g., exercise), expiration can become an active process as muscles
speed the contraction of the chest.
When the muscles of respiration contract, the size of the intrathoracic AAA
cavity ________ and intrathoracic pressure __________. increases; decreases
410
S. Faubel and J. Topf 15 Respiratory Acidosis
Sternocleidomastoid Scalene
Accessory nerve Third and fourth cervical nerve
(CN XI) (C3, C4)
Diaphragm
Phrenic nerve (C3, C4, C5)
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The Fluid, Electrolyte and Acid-Base Companion
412
S. Faubel and J. Topf 15 Respiratory Acidosis
air
air
air
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The Fluid, Electrolyte and Acid-Base Companion
Free flow!The third step of respiration is the free flow of air into
the alveoli through a patent airway.
nasopharynx
trachea
oropharynx
bronchi
bronchioles
Respiration requires the free flow of air through a patent airway. Obstruction
at any point in the flow of air to the alveoli can cause respiratory acidosis. The
airway is divided into the upper and lower respiratory tracts.
The upper respiratory tract consists of the nasopharynx and oropharynx.
The lower respiratory tract begins at the larynx. In addition to its role in phona-
tion, the vocal cords of the larynx protect against the entry of foreign bodies into
the lower respiratory tract.
The lower respiratory tract consists of conducting airways which begin with
the trachea and end with the terminal bronchioles. In the thorax, the trachea
divides into right and left mainstem bronchi which supply the right and left lung.
Anatomically, the right mainstem bronchus is a nearly straight continuation of
the trachea, while the left mainstem bronchus branches off at an abrupt angle.
Therefore, the right lung is more commonly involved when foreign material
is aspirated.
The mainstem bronchi branch into secondary bronchi which supply the lobes
of the lungs. These bronchi branch into the tertiary bronchi which supply the
segments of each lobe. The tertiary bronchi branch several times into progres-
sively smaller airways known as bronchioles. The terminal bronchioles are the
smallest segments of the conducting system; only beyond this point can gas
exchange occur.
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S. Faubel and J. Topf 15 Respiratory Acidosis
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The Fluid, Electrolyte and Acid-Base Companion
C
C
C C
C C
C C
C
C
C
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S. Faubel and J. Topf 15 Respiratory Acidosis
O2
O2
CO2
CO2 CO2
O2 CO2 CO2 O2
CO2 CO2
CO2 CO2
Diffusion defect Ventilation defect Perfusion defect
Air and blood reach the alveoli Blood reaches the alveoli, but Air reaches the alveoli, but
but defective membranes pre- air does not. blood does not.
vent gas exchange.
Gas exchange occurs exclusively in the alveoli which are specialized lung
tissues surrounded by pulmonary capillaries. Normally, oxygen diffuses from
the alveoli into the capillaries and carbon dioxide diffuses from the capillaries
into the alveoli. There are three types of defects at the alveolar level which
interfere with gas exchange.
Diffusion defect: air and blood both reach the alveoli, but de-
fects in the alveolar membrane prevent efficient gas exchange.
Ventilation defect: blood reaches the alveoli, but air does not.
Perfusion defect: air reaches the alveoli, but blood does not.
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The Fluid, Electrolyte and Acid-Base Companion
+
Sensing and signalling defect CO2
O2
CO2 O2
CO2
O2
The A-a gradient is a useful tool for detecting abnormal gas exchange. The
A-a gradient is the difference between Alveolar oxygen content and arterial
oxygen content. The calculation is explained on the next page.
The A-a gradient can be thought of as the difference between how much
oxygen can enter the blood (the alveolar oxygen content) and how much oxy-
gen does enter the blood (the partial pressure of arterial oxygen measured on
the ABG). If gas exchange between the alveoli and pulmonary capillaries were
perfect (all of the alveolar oxygen crossed into the blood), the A-a gradient
would be zero. However, due to normal physiologic impediments to gas ex-
change, the A-a gradient is normally about 10 in a healthy young adult. An
increased A-a gradient indicates that an abnormality in gas exchange has inter-
fered with the transfer of oxygen into blood.
The A-a gradient can be used clinically to identify disorders of gas exchange.
If impaired gas exchange is the sole or a contributing cause of respiratory aci-
dosis, then the A-a gradient is increased. If, however, respiratory acidosis is
due to a ventilation defect (one or more the first three steps of respiration), then
the A-a gradient is normal.
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S. Faubel and J. Topf 15 Respiratory Acidosis
The A-a gradient is the alveolar oxygen content minus the arterial oxygen
content. The calculation is shown above. The example above calculates the
normal A-a gradient for someone at sea level, breathing room air.
The alveolar oxygen content is dependent on many factors: the barometric
pressure, partial pressure of water vapor, percentage of oxygen in inspired
air (FiO2) and the partial pressure of CO2 in the alveoli. Barometric pres-
sure is dependent on elevation. Water vapor pressure is a constant. Room
air contains 21% oxygen.
The presence of CO2 in the alveoli reduces the alveolar oxygen content.
The effect of CO2 is factored in by calculating the respiratory quotient and
subtracting it from the partial pressure of oxygen. The PCO2 needed to de-
termine the respiratory quotient is obtained from the ABG.
The arterial oxygen is the measured value obtained from the ABG.
The A-a gradient is the alveolar _______ content minus the oxygen
________ oxygen content. arterial
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The Fluid, Electrolyte and Acid-Base Companion
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The Fluid, Electrolyte and Acid-Base Companion
What the These patients are dyspneic and These patients do not experience
mnemonic breathe heavily (puffers) in order to dyspnea until end-stage disease but
means maintain adequate ventilation and are hypoxic (blue). These patients are
oxygenation (pink). edematous due to right-sided heart
failure (bloaters).
Infections Less common, but more severe Common, but less severe
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S. Faubel and J. Topf 15 Respiratory Acidosis
Acute Chronic
respiratory acidosis respiratory acidosis
C before renal compensation after renal compensation
C
C HCO3– HCO3–
C pH | pH |
CO2 3-5 CO2
C
days
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The Fluid, Electrolyte and Acid-Base Companion
HCO3 H+ HCO3 H+ C
C –
C PO4
C
C
C
–
HCO3 is an ineffective buffer in res- Intracellular buffers (phosphate, hemoglobin) and
piratory acidosis because CO2 can- bone are the primary buffers in respiratory acido-
not be eliminated. sis.
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S. Faubel and J. Topf 15 Respiratory Acidosis
sis
36
c i do
ya
34
tor
pira
32
res
Bicarbonate (mEq/L)
ic
ron
30
ch
cidosis
28
piratory a
acute res
26
24 normal
22
20
18
16
14
35 40 45 50 55 60 65 70 75
PCO2 (mmHg)
Due to relatively ineffective buffering and the lack of a renal response, acute
respiratory acidosis is characterized by only a modest elevation in HCO3–. As
represented in the graph above, the concentration of HCO3– changes very little
for a given elevation of CO2. (Note how flat the acute respiratory acidosis
zone is on the graph.)
Although small, the non-bicarbonate buffers do effect a relatively consistent
change in the concentration of HCO3 for a rise in CO2. The change in bicarbon-
–
ate relative to the change in PCO2 is 1:10. For every 10 mmHg rise in PCO2, the
HCO3– rises by 1 mEq/L. For example, if the PCO2 increases from 40 mmHg to
60 mmHg, then the HCO3 should increase from 24 mEq/L to 26 mEq/L.
–
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The Fluid, Electrolyte and Acid-Base Companion
NE
HCO3 H+ HCO3 H+ C
W
! C
NE
HCO3
W
C
!
NE
HCO3 C
W
!
C
C
C
H+ +
H+ H
426
S. Faubel and J. Topf 15 Respiratory Acidosis
1
ATP water (H2O)
2
CO2
AMP
When H+ is secreted, Na+ is HCO3
resorbed to maintain elec- Na+
NE
troneutrality.
W
!
– +
Normally, Cl and Na re- Na+
sorption occur together. Be-
+
cause Na is resorbed in Cl–
4
exchange for H+, less Na+ is
available for Cl– resorption.
427
The Fluid, Electrolyte and Acid-Base Companion
sis
36
c i do
ya
34
tor
ira
s
osi
p
32
s
d
e
aci
ic r pirato
Bicarbonate (mEq/L)
n
ry
hro es
30
c
cidosis
28 r
piratory a
nic
acute res
o
26 Chr
24 normal
22
20
18
16
14
35 40 45 50 55 60 65 70 75
PCO2 (mmHg)
?
ate concentration.
C
C
C
C
C
C
C
C
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The Fluid, Electrolyte and Acid-Base Companion
or
R.I
.P.
respiratory failure from sepsis pulmonary edema cardiogenic shock
pneumonia
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S. Faubel and J. Topf 15 Respiratory Acidosis
Oxygen
Z
Z
Z
OUCH!
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The Fluid, Electrolyte and Acid-Base Companion
OUCH!
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S. Faubel and J. Topf 15 Respiratory Acidosis
Well, it all
began when
I was sitting
on my front
porch mind-
ing my own
business,
and these
two guys......
433
The Fluid, Electrolyte and Acid-Base Companion
BUN
Na Cl– glucose pH / PCO2 / PO2
+
K+ HCO3–
Cr
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S. Faubel and J. Topf 15 Respiratory Acidosis
Oxygen
Me
thy
lpr
ed
nis
olo
ne
antibiotics supplemental oxygen diuretics steroids
435
The Fluid, Electrolyte and Acid-Base Companion
Summary!Respiratory acidosis.
Respiratory acidosis is one of the four primary acid-base disorders and is
characterized by a PCO2 greater than 40 mmHg and pH below 7.4. Buffering
and renal compensation cause the bicarbonate to rise above 24 mEq/L.
Respiratory acidosis can be due to a defect in one or more of the four steps
of respiration: sensing and signaling, muscles and motion, free flow and gas
exchange. Ventilation, the delivery of air to the alveoli, occurs in the first
three steps of respiration. Usually, respiratory acidosis is due to a combina-
tion of defects.
O2
CO2
CO2 O2
CO2
O2
sensing and signaling muscles and motion free flow gas exchange
436
S. Faubel and J. Topf 15 Respiratory Acidosis
Summary!Respiratory acidosis.
A useful test in the evaluation of respiratory acidosis is the A-a gradient.
The A-a gradient is the difference between the amount of oxygen in the
Alveoli and the amount of oxygen in the arterial blood. The normal A-a
gradient increases with age. In young healthy adults it is about 10.
A-a gradient
[( barometric
pressure – partialof pressure
2
HO ]
)× %O –(1.25 × PCO ) – PO
2
2 2
BUN
Na Cl– glucose pH / PCO2/ PO 2
+
K+ HCO3–
Cr
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The Fluid, Electrolyte and Acid-Base Companion
Summary!Clinical review.
Acute Chronic
expected HCO3– = 24 + (PCO – 40 ) 2
10
expected HCO3– = 24 + 3 × ( 40 –10P ) CO2
438