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S. Faubel and J.

Topf 15 Respiratory Acidosis

15 Respiratory Acidosis

The Fluid, Electrolyte and Acid-Base Companion

Introduction!Respiratory acidosis is due to respiratory in-



pH | pH |


pH | pH |

Respiratory acidosis is characterized by an increased PCO2 and a decreased

pH. After buffering and renal compensation, the bicarbonate is increased.
Increased carbon dioxide, hypercarbia, is always the result of inadequate
Carbon dioxide is a waste product of cellular metabolism. Each day, the
body produces approximately 15,000 millimoles of CO2 which needs to be
eliminated by the lungs. If the lungs are unable to completely eliminate
carbon dioxide, it accumulates and causes respiratory acidosis.
The study of respiratory acidosis is the study of respiratory insufficiency.

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.

Respiratory acidosis is characterized by an increase in ________ PCO2

which decreases _____. pH

An increase in the arterial carbon dioxide level is _________ due to always

inadequate respiration.

S. Faubel and J. Topf 15 Respiratory Acidosis

Overview: Respiration is a four-step process.

Sensing and signaling Muscles and motion

The respiratory control center in the medulla The muscles of respiration expand the
responds to changes in CO2, O2 and pH by chest which lowers intrathoracic pressure
sending signals via nerves to the muscles and draws air into the lungs.
of respiration.

CO2 O2

Free flow Gas exchange

A patent airway is necessary for air to flow Exchange of CO2 and O2 occurs in the al-
into the alveoli. veoli. Oxygen enters the blood and CO2 en-
ters the alveoli.

To fully understand the development of respiratory acidosis, it is important to

have an understanding of respiration. Respiration is the process by which the
lungs carry out their primary function of eliminating CO2 and oxygenating the
Respiration occurs in four steps: 1) sensing and signaling 2) muscles and
motion 3) free flow and 4) gas exchange. Inadequate respiration causing respi-
ratory acidosis may occur from a defect in one or more of the steps of respira-
The delivery of air to the alveoli is called ventilation. Ventilation encompasses
the first three steps of respiration. Hypoventilation is the inadequate deliv-
ery of air to the alveoli resulting in the accumulation of carbon dioxide.

The process of respiration contains four steps: sensing and _________, signaling
muscles and motion, free _______ and gas exchange. flow

Gas exchange occurs in the _________. alveoli

Ventilation encompasses the first _______ steps of respiration. three

The Fluid, Electrolyte and Acid-Base Companion

Introduction to terms used by pulmonologists, part one.

PCO2 (mmHg) C C

alveolar minute ventilation (L/ min)

minute tidal physiologic respiratory

ventilation volume dead space rate

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.

Alveolar minute ventilation (minute ventilation) is the amount of air

delivered to functioning alveoli each minute. This process is accomplished
in the first three steps of respiration (sensing and signaling, muscles and
motion, and free flow). Normal minute ventilation for an adult ranges from
four to six liters per minute.
Minute ventilation and PCO2 are inversely related. Increased minute ven-
tilation causes carbon dioxide to fall and decreased minute ventilation
causes carbon dioxide to rise.

S. Faubel and J. Topf 15 Respiratory Acidosis

Introduction to terms used by pulmonologists, part two.

Anatomic dead space

Trachea, bronchi and bronchi-
oles are all examples of ana-
tomic dead space.

Alveolar dead space

Alveoli which are ventilated
but not perfused are alveolar
dead space.


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

The Fluid, Electrolyte and Acid-Base Companion

On the following pages, we introduce each of the steps of respiration (sens-

ing and signaling, muscles and motion, free flow and gas exchange). Following
each description, there is a page that lists several diseases associated with that
step. This is followed by one or two grey pages discussing a specific disorder
associated with that step.
When reading through this for the first time, you may not want to spend too
much time reading through the details of each disorder. The lists and definitions
are provided primarily as examples and are not exhaustive.
Additionally, keep in mind that respiratory diseases which cause respiratory
acidosis commonly involve a defect in more than one of the steps of respiration.
When more than one defect is at fault, we typically list the disorders under the
primary and/or inciting event.

S. Faubel and J. Topf 15 Respiratory Acidosis

Sensing and signaling!The first step of respiration is sensing

CO2 and O2 and signaling the muscles of respiration.
nerves muscles of respiration
phrenic diaphragm
medulla intercostal intercostal
accessory sternocleidomastoid
O2 C3, C4 scalene

carotid body

The unconscious control of breathing resides in the respiratory control

center of the medulla. Here, information about CO2 and O2 levels are pro-
cessed (sensed) and signals are sent, via nerves, to the muscles of respira-
tion. CO2 and O2 are the primary stimuli affecting respiration. Surprisingly,
increased CO2 is a stronger stimulus for respiration than decreased O2.
Intracellular alterations in pH, induced by changes in CO2, are sensed by
chemoreceptors in the medulla (separate from the respiratory control cen-
ter). An increase in PCO2 of only 1 mmHg is sufficient to stimulate respira-
tion. Because of this exquisite sensitivity to CO2, arterial PCO2 is normally
kept within the narrow range of 36 to 44 mmHg.
Oxygen levels are sensed by chemoreceptors in the carotid bodies located
at the bifurcation of the internal and external carotid arteries. Hypoxia does
not stimulate respiration until the PO2 falls below 60 mmHg.
Sensing defects causing respiratory acidosis are typically due to disorders
which affect the ability of the respiratory control center to respond to increases
in carbon dioxide. Signaling defects are due to diseases which affect the nerves
of the respiratory muscles. Specific disorders of sensing and signaling are re-
viewed on the following pages.

Breathing is controlled in the _________ control center. respiratory

The respiratory control center regulates ventilation by integrating

information about _______ _______ levels and O2 levels. carbon dioxide

The Fluid, Electrolyte and Acid-Base Companion

Sensing and signaling!Carbon dioxide is the primary regulator

of respiration unless oxygen is too low (PO2 < 60 mmHg).

O2 O2
O2 O2
O2 O2 O2 O2 O2 O2
O2 O2 O2 O2
O2 O2 O2


Decreased P O2 is sensed at Increased ventilation increas- Decreased ventilation returns

the carotid bodies and a signal es PO 2 but decreases PCO2. P CO2 to normal, but returns
is sent to the respiratory con- Decreased PCO2 is detected in oxygen to the initial low level.
trol center which increases the medulla and ventilation is
ventilation. decreased.

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

Oxygen is essentially ignored by the respiratory __________ center control

until hypoxia is life-____________. threatening

Carbon dioxide levels are detected by pH detectors in the _______, medulla

while oxygen is detected by ______________ in the carotid bodies. chemoreceptors

S. Faubel and J. Topf 15 Respiratory Acidosis

Sensing and signaling!The causes of sensing and signaling

defects are both central and peripheral.
Sensing defects Signaling defects
Apnea of prematurity is an almost uni- Amyotrophic lateral sclerosis (ALS) is a
versal problem associated with premature motor neuron disease characterized by mo-
birth. In this disorder, low oxygen and high tor neuron destruction. ALS is characterized
carbon dioxide suppress respiration rather by ascending paralysis, muscle atrophy and
than stimulate it. While this is maladaptive loss of deep tendon reflexes. Involvement of
for an infant, it is an appropriate response the respiratory nerves results in respiratory
for the fetus. insufficiency.
In utero, the fetus practices breathing to Lou Gehrig was a baseball player in the early
strengthen its respiratory muscles in anticipa- twentieth century. He played with Babe Ruth
tion of life after birth. In utero, however, oxy- for the New York Yankees. Mr. Gehrig set a
gen is supplied by the placenta. When oxygen major league record by playing in over 2000
levels fall, the fetus stops wasting oxygen by consecutive games. He died in his thirties of
breathing, shunting oxygen to essential organs ALS which is now commonly referred to as Lou
and processes. Gehrig’s disease.
Apnea of prematurity resolves with brain stem Diaphragmatic paralysis can be caused
maturation and is treated with caffeine. by thoracic trauma, thoracic surgery, multiple
Brain stem injury from infarction, hemor- sclerosis and muscular dystrophy.
rhage, trauma, demyelination or degeneration Guillain-Barré syndrome is a rapidly pro-
can cause respiratory failure by direct damage gressive paralysis which typically follows an
to the respiratory control center. acute viral illness by 1 to 3 weeks. It is charac-
Central sleep apnea: see page 409. terized by ascending muscle weakness, loss
of reflexes and a lack of sensory involvement.
Drugs such as narcotics, ethanol, benzodi- Respiratory insufficiency and failure occur from
azepines and inhaled anesthetics (with the involvement of the muscles of respiration.
exception of nitrous oxide) all decrease the About a third of patients require mechanical
sensitivity of the respiratory control center to ventilation. Complete recovery is the norm and
CO2, inhibiting respiration. mortality is low. Patients may be treated with
Hypothyroidism, when severe, can cause plasmapheresis or gamma globulins.
hypoventilation from decreased sensitivity of Guillain-Barré is also known as acute demy-
the respiratory control center to CO2. elinating polyneuropathy.
Oxygen therapy in patients with chronic CO2 Post-polio syndrome is characterized by the
retention. See page 408. degradation of motor neurons which can oc-
Obesity hypoventilation syndrome cur 20 to 30 years after paralytic polio. Involve-
(Pickwickian syndrome) is due to a defect ment of the nerves of respiration can occur.
which prevents the increase in respiratory ef- Spinal cord injury at or above the level of
fort needed to overcome obesity. the origin of the phrenic nerve can cause res-
Primary alveolar hypoventilation (On- piratory insufficiency or failure. The phrenic
dine’s curse) is a rare condition in which pa- nerve is composed of nerves from C3, C4 and
tients do not have an unconscious respiratory C5 (3,4 and 5 keep the diaphragm alive).
drive. Since conscious control of respiration is
intact, the disorder reveals itself only during
sleep. Primary alveolar hypoventilation can be
treated with nighttime mechanical ventilation.

The Fluid, Electrolyte and Acid-Base Companion

Clinical correlation: In chronic respiratory acidosis, hypoxia is the

primary stimulus for respiration.

Chronic respiratory acidosis

O2 CO2

carotid body medulla

Oxygen is the primary stimu- RESPIRATORY The respiratory control cen-

lus for respiration. CONTROL CENTER ter is insensitive to CO2.

The control of respiration is altered in patients with chronically elevated

carbon dioxide levels and chronic respiratory acidosis (e.g., COPD). In
these patients, hypoxemia is the primary stimulus for respiration while in-
creases in CO2 have little effect.
In chronic respiratory acidosis, the pH is nearly normal despite a grossly
elevated PCO2. The respiratory control center of the medulla is less sensi-
tive to increases in CO2 because of the near-normal pH. If CO 2 increases
further, the change in pH is less dramatic and produces little change in
respiration. Because the sensitivity to CO2 is lost in patients with chronic
respiratory acidosis, hypoxemia is the primary stimulus for respiration.
The hypoxic drive of respiration is clinically important. The administra-
tion of large amounts of oxygen (100% oxygen by mask) removes the hy-
poxic respiratory drive and suppresses respiration. The ensuing hypoven-
tilation increases CO2 resulting in acidosis, obtunded mental status and
respiratory failure. Therefore, oxygen must be used with caution in patients
with chronic carbon dioxide retention.

S. Faubel and J. Topf 15 Respiratory Acidosis

Clinical correlation: Sleep apnea is a defect in nocturnal res-


pH, CO2 and O2 Apnea occurs at night; CO2 Z
are normal dur- increases while pH and O 2
ing the day. decrease.

Sleep apnea is characterized by arrests in airflow which occur during

sleep. Apneic episodes last at least 10 seconds and occur more than 30
times per night. The characteristic symptoms and signs include daytime
somnolence, hypertension, snoring and obesity. An important characteris-
tic of all types of sleep apnea is that the hypoxia, hypercarbia and respira-
tory acidosis occur only at night. During the day, patients with sleep apnea
have normal O2, CO2 and pH.
There are three types of sleep apnea: central, obstructive and mixed.
Central sleep apnea is a cerebral disorder which affects the normal
respiratory drive in the medulla. Apneic episodes are characterized by a
lack of respiratory effort. During apneic episodes, patients become hypoxic
and hypercarbic, then awaken, restore normal ventilation and return to sleep.
This cycle can recur hundreds of times each night.
Obstructive sleep apnea (OSA) is characterized by collapse of the
soft tissues in the upper airway during sleep. Apneic episodes are charac-
terized by respiratory effort that is unable to overcome the obstruction.
Breathing is restored when the patient arouses and increased muscle tone
clears the obstruction. Loud snoring is an almost universal feature of OSA.
Medical management involves weight loss, and the use of a device that
maintains continuous positive airway pressure (CPAP) in the pharynx and
thus stents the soft tissues open. Surgery is an option for patients who fail
medical management.
Mixed sleep apnea is characterized by components of both central
and obstructive sleep apnea. Apneic episodes are characterized by the
cessation of respiratory effort followed by collapse of the soft tissues and
airway obstruction. Respiratory effort then returns, but cannot overcome
the obstruction.

The Fluid, Electrolyte and Acid-Base Companion

Muscles and motion!The second step of respiration is proper

movement of the chest wall.

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

Muscles and motion is step ______ in the process of respiration. two

S. Faubel and J. Topf 15 Respiratory Acidosis

Muscles and motion!The diaphragm, chest wall muscles and

muscles in the neck expand the lungs.

Sternocleidomastoid Scalene
Accessory nerve Third and fourth cervical nerve
(CN XI) (C3, C4)

Intercostal muscles Intercostal muscles

Intercostal nerves Intercostal nerves
(T1 - T12) (T1 - T12)

Phrenic nerve (C3, C4, C5)

The major muscles of respiration are the sternocleidomastoid, scalene,

intercostals and diaphragm. When contracted, all serve to expand the intratho-
racic cavity and facilitate the movement of air into the lungs.
The sternocleidomastoid and scalene are located in the neck and attach to
the clavicle and first rib. When contracted, these muscles lift the clavicles and
the first ribs to expand the chest cavity upward. The sternocleidomastoid and
scalene are accessory muscles of respiration which means they are not essen-
tial to the process of respiration, but are important when breathing becomes
labored. The sternocleidomastoid is innervated by the accessory cranial nerve
(CN XI) and the scalene muscles are innervated by the inferior cervical nerve
plexus (C3, C4).
Intercostal muscles are located between the ribs and join a set of upper and
lower ribs. The intercostal muscles raise the chest up and out and are inner-
vated by the intercostal nerves (T1-T12).
The diaphragm separates the thoracic and abdominal cavities and is the pri-
mary muscle of respiration. It attaches to the lower ribs and moves inferiorly
when it contracts to expand the chest cavity downward. Innervation is via the
phrenic nerve (C3, C4, C5).

The __________ is the primary muscle of respiration. diaphragm

The sternocleidomastoid and scalene muscles are known as

____________ muscles of respiration. accessory

The Fluid, Electrolyte and Acid-Base Companion

Muscles and motion!There are many causes of respiratory

muscle dysfunction.
Anatomic abnormalities and trauma Genetic disorders
Flail chest is due to multiple consecutive Acid maltase deficiency is a disorder of
fractured ribs on a single side of the chest, an enzyme involved in the metabolism of gly-
causing the chest wall to become unstable. cogen into glucose (type 2 glycogen storage
During inspiration, the unstable chest wall disease). This disorder is associated with the
collapses inward instead of moving outward. accumulation of glycogen in muscle cells
Kyphoscoliosis is a deformity of the spine which interferes with contraction. This dis-
which restricts chest wall expansion during in- ease presents in infancy with respiratory in-
spiration. sufficiency, cardiomegaly and hepatomegaly.
Pneumothorax: see page 413. Death usually occurs by two years of age.
Childhood and adult onset is less common.
The childhood form resembles muscular dys-
trophy and is associated with elevated CK
Botulinus toxin is produced by the bacte-
ria Clostridium botulinum, a gram positive enzymes. The responsible gene has been
rod. There are three forms of the disease: mapped to chromosome 17.
• food-borne: direct ingestion of toxin due Duchenne’s and Becker’s muscular dys-
to improperly canned foods. trophy are X-linked recessive disorders which
• wound infection: spores enter a wound cause progressive muscle weakness. Patients
and germinate, releasing toxin; it is associ- are usually asymptomatic at birth but gross
ated with trauma. motor control is delayed until late in the first
year of life. Muscle weakness is progressive
• infantile: ingestion and germination of
and ultimately compromises respiration.
spores in an immature GI tract; it is associ-
Duchenne’s is more severe with death usually
ated with giving infants honey.
occurring by the third decade of life. Because
Botulism toxin irreversibly blocks the release Becker’s causes less severe disease, patients
of acetylcholine from the neuromuscular junc- can live into their forties. The responsible gene
tion. Death is due to respiratory failure. See has been localized to Xp21.
The Microbiology Companion for details.
Periodic paralysis is a genetic disorder (au-
Drugs tosomal dominant in ⅔ of cases and sporadic
Aminoglycoside antibiotics, such as gen- in ⅓) associated with intermittent episodes of
tamicin and tobramycin, can cause muscular severe hypokalemia and muscle weakness.
weakness at high doses. Muscle weakness is Respiratory involvement is rare, but can be
exacerbated by hypermagnesemia. Treatment fatal. See page 495.
consists of stopping the drug and giving cal-
Myasthenia gravis
Myasthenia gravis is an autoimmune dis-
Succinyl choline / vecuronium are depo-
order characterized by the production of anti-
larizing agents used for paralysis during sur-
bodies against the acetylcholine receptors at
gical and medical procedures. These agents
the neuromuscular junction. Prevalence is 1
act at the neuromuscular junction.
in 10,000. The male:female ratio is 2:3 with
men affected in the 50-70 age range and fe-
males in early adulthood. Myasthenia crisis oc-
Hypokalemia, hypophosphatemia or hy-
curs when weakness affects the muscles of
permagnesemia, when severe, can cause
respiration. Crises are treated with anticho-
muscle weakness and respiratory acidosis.
linesterases (pyridostigmine) and plasmapher-

S. Faubel and J. Topf 15 Respiratory Acidosis

Clinical correlation: Pneumothorax can cause respiratory ac-

idosis by affecting muscles and motion.


visceral pleura parietal pleura second intercostal space

midclavicular line

In order to understand how a pneumothorax develops, it is important to

understand how the lung and chest wall work together. The lung is like a
Nerf® ball: elastic walls surrounding millions of tiny air pockets which can
be compressed or stretched open. The Nerf® lung has a smooth, shiny sur-
face called the visceral pleura. The chest wall, which surrounds the Nerf®
lung, is lined by the parietal pleura. Between the visceral and parietal
pleurae is a small amount of fluid. Although there is no solid connection
between the visceral and parietal pleurae, surface tension seals the lung to
the chest wall. The surface tension is strong enough that during inspira-
tion, when the chest wall expands outward, it also expands the lung.
In a pneumothorax, air gets into the space between the two pleurae
breaking the surface tension which adheres the lung to the chest wall.
When the seal between the visceral and parietal pleurae is broken, expan-
sion of the chest wall during inspiration does not expand the lung. Without
the chest wall to expand it, the lung collapses due to its elasticity. The
collapse of the lung can shift the trachea toward the pneumothorax.
A tension pneumothorax is more life-threatening than a pneumothorax
because the size of the air-filled space between the pleurae enlarges with
each inspiration. During expiration, the air is unable to escape due to a
one-way valve effect of the pleural defect. This results in continued air
entrapment in the pleural space. The complications of the increasing pleu-
ral air are ineffective respiration, hypoxia and decreased venous return
resulting in hemodynamic collapse. In a tension pneumothorax, the struc-
tures of the mediastinum (e.g., trachea, heart) shift to the opposite side of
the pneumothorax. Tension pneumothorax is a medical emergency which
requires immediate decompression. A 14-gauge needle should be inserted
into the air-filled pleural space in the second or third intercostal space at
the midclavicular line.

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.




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.

Because of the downward angle of the ________ mainstem bron- right

chus, aspirated material is more likely to affect the _______ lung. right

S. Faubel and J. Topf 15 Respiratory Acidosis

Free flow!Factors which cause airway obstruction interfere with

the free flow of air into the alveoli.
Anatomic obstruction Obstructive lung disease
Laryngomalacia and tracheomalacia are Asthma attacks are characterized by bron-
congenital malformations of the airway; both choconstriction and increased production of
are characterized by floppy airways which secretions in the airways. Narrowed airways
collapse on inspiration. The malformation and the increased work of breathing can tire
typically presents in infancy as noisy breath- the respiratory muscles leading to respira-
ing. These disorders can also be a complica- tory failure. Note that muscle fatigue,
tion of prolonged intubation. Laryngo- and muscles and motion, is ultimately the cause
tracheomalacia typically resolve without in- of respiratory acidosis, but obstruction of the
tervention. For severe cases, CPAP or tra- airway is the inciting event. (See page 416.)
cheostomy may be necessary. Chronic bronchitis is characterized by ob-
struction of airflow from increased mucus
secretion and airway destruction. Expiration
Aspiration of foreign bodies can obstruct
is more difficult than inspiration which leads
the airway at the pharynx, larynx or bron-
to air trapping and hyperinflation. (See page
chial level. Foreign bodies are more likely to
enter the right lung due to the anatomy of
the mainstem bronchi. Emphysema is characterized by the loss of
elastic tissue in the lung. Without this sup-
Infections portive framework to maintain airway ten-
Croup (laryngotracheobronchitis) is an in- sion, the distal airways collapse. (See page
fection of the lower respiratory tract which 422.)
can lead to airway swelling, edema and ob-
struction. The etiology is typically viral, al- Seizures
though it can be caused by mycoplasma. Grand mal seizures typically cause occlu-
Treatment is with cool mist oxygen and ra- sion of the upper airway which can result in
cemic epinephrine. hypoxia and hypercarbia.
Epiglottitis is a medical emergency caused
by an infection of the epiglottis. Haemophi-
Smoke inhalation
Smoke inhalation can increase the mor-
lus influenza type B is the most common eti- tality for burns by ten-fold. Burning poly-
ology. Inflammation of the epiglottis can lead mers (e.g., carpets, insulation) release alde-
to complete airway obstruction. Epiglottitis hydes such as acrolein which damage the
is rare in the U.S. due to universal Haemo- airway. Injury to the large airways can cause
philus vaccination (HiB) in infancy. swelling and occlusion; injury to the alveoli
can cause pulmonary edema.

The Fluid, Electrolyte and Acid-Base Companion

Clinical correlation: Acute asthma exacerbations can occur

in two stages.


Respiratory alkalosis Respiratory acidosis

Increased respiratory effort Fatigue results in decreased
causes an increase in ventila- ventilation. PCO 2 is high and
tion. PCO2 is low and PO 2 is PO 2 is low.

Asthma is a disorder characterized by reversible attacks of airway

obstruction. During an acute asthma exacerbation, there are two types
of obstruction: bronchoconstriction, which narrows the airways and
mucus plugging (secondary to inflammation), which occludes the air-
An acute asthma exacerbation can be described in two stages. In the
first stage, bronchoconstriction and mucus plugging increase the work
of breathing, and oxygenation is difficult to maintain. To maintain oxy-
genation, ventilation increases. Increased ventilation lowers the PCO2
causing respiratory alkalosis.
The second stage, if a patient does not improve, occurs when the
muscles of respiration fatigue. The combination of airway obstruction
and fatigue results in inadequate ventilation, CO2 retention and respi-
ratory acidosis.
A normal or increased PCO2 in the face of an asthma exacerbation is
always a bad sign which can herald complete respiratory collapse and
the need for mechanical ventilation.
Note that respiratory failure from asthma is ultimately due to a failure of step two in
respiration:muscles and motion. Although respiratory failure is due to respiratory muscle
fatigue, the primary inciting event is obstruction of the airways, a defect in step three
of respiration:free flow.

S. Faubel and J. Topf 15 Respiratory Acidosis

Gas exchange!The fourth step of respiration is the exchange of

gasses in the alveoli.



O2 CO2 CO2 O2
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.

Gas exchange occurs exclusively in the _________. alveoli

There are three types of defects which prevent gas exchange in

the alveoli: perfusion, ventilation and ___________. diffusion

A ___________ defect is characterized by adequate perfusion and ventilation

inadequate ventilation.

The Fluid, Electrolyte and Acid-Base Companion

Gas exchange!The A-a gradient identifies abnormal gas exchange.

A-a gradient is normal A-a gradient is high

Sensing and signalling defect CO2
CO2 O2

Gas exchange defect

Muscles and motion defect

Free flow defect

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.

If respiratory acidosis is secondary to a defect in ventilation, then aaa

the A-a gradient is _________. normal

S. Faubel and J. Topf 15 Respiratory Acidosis

Gas exchange!Calculation of the A-a gradient is important in

evaluating disorders of respiration.

Alveolar O2 – Arterial O2 = A-a gradient

Partial pressure of oxygen – Resp. quotient

( barometric partial pres.

pressure – of H O vapor ) × %FiO 2
– (1.25 × PCO )
– PO2

(760 mmHg – 47 mmHg) × 0.21 – (1.25 × 40 mmHg) – 90 mmHg = 10 mmHg

Barometric pressure at sea level ... 760 mmHg

Normal water vapor pressure ................ 47 mmHg
Room air FiO2 ........................................................................ 21%
Normal PCO2 ........................................................... 40 mmHg
Normal PO2 ................................................................ 90 mmHg
Normal Aa-gradient ........................................... 10 mmHg

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.

As people age, the normalA-a gradient increases.The normalA-a gradient is estimated by

the following formula: (Age
÷4) + 4.
A-a gradient of(80÷4) + 4 = 20 + 4 or 24;
Therefore, an 80 year old will have a normal
A-a gradient of(20÷4) + 4 = 5 + 4 or 9.
a 20 year old will have a normal

The A-a gradient is the alveolar _______ content minus the oxygen
________ oxygen content. arterial

Alveolar oxygen is calculated from the FiO2, PCO2 and barometric

pressure, while the arterial oxygen is measured by the ____. ABG

The Fluid, Electrolyte and Acid-Base Companion

Gas exchange!Many disorders interfere with gas exchange.

The disorders of gas exchange are usually characterized by hypoxemia, hy-
perventilation and respiratory alkalosis. Only when these disorders are severe
and/or long-standing does carbon dioxide retention and respiratory acidosis
Diffusion defect Ventilation defect
Alpha1-antitrypsin deficiency is a genetic Adult respiratory distress syndrome
disease which causes emphysema. Alpha1- (ARDS) is a severe pulmonary disease char-
antitrypsin is an enzyme which decreases the acterized by influx of neutrophils, red blood
activity of the proteolytic enzyme trypsin. It cells and proteinaceous fluid into the alveoli.
also decreases the activity of elastase and The influx of fluid and cells prevents gas
other proteases which break down the con- exchange across the alveolar walls. ARDS is
nective tissues of the lung. Lack of this en- usually the result of serious illness (e.g., sep-
zyme allows tissue destruction to continue sis, pancreatitis, trauma, aspiration of gas-
unchecked. tric contents and burns).
Because the disease is genetically recessive, Atelectasis is the absence of air in the al-
two defective alleles must be present for the veoli which causes segmental collapse of lung
disease to occur. In patients who are homozy- tissue.
gotes for a defective allele, emphysema oc- Pulmonary edema is the filling of the al-
curs in the third or fourth decade of life. veoli with fluid. The most common etiology
Emphysema is the destruction of the bron- of pulmonary edema is congestive heart fail-
chioles and alveoli, resulting in large pock- ure. (See page 59.)
ets of air with a relative lack of alveolar Pneumonia is a generic term for infection
walls. Since gas exchange occurs only across and inflammation of the lung parenchyma.
the alveolar wall, emphysema directly pre- The alveolar spaces fill with blood cells and
vents the exchange of carbon dioxide and fibrin (pus). Because the alveoli are filled
oxygen. The most common cause of emphy- with the products of inflammation, gas ex-
sema is smoking. change is impaired.
Interstitial lung diseases are a heteroge-
neous group of disorders characterized by Perfusion defect
acute or chronic infiltration of the alveolar Pulmonary embolism is a blood clot which
walls with cells, fluid and fibrotic tissue. breaks away from a larger clot and flows
There are numerous causes of interstitial through the venous system until it lodges in
lung disease including: the pulmonary arteries of the lung. It pre-
• amiodarone pulmonary toxicity vents blood flow distal to the clot, resulting
• amyloidosis in poor gas exchange. Usually, the source of
• ankylosing spondylitis the embolism is a thrombus in the iliofemo-
• bronchiolitis obliterans organizing ral deep veins. Common presenting symp-
pneumonia (BOOP) toms and signs include dyspnea, tachycar-
• idiopathic pulmonary fibrosis dia, pleuritic chest pain (pain increases with
• organic and synthetic dust exposure breathing) and cough.
(e.g., asbestos)
• radiation therapy
• rheumatoid arthritis
• sarcoidosis
• Wegener’s granulomatosis

S. Faubel and J. Topf 15 Respiratory Acidosis

Clinical correlation: COPD causes abnormalities in all four steps

of respiration.
Respiratory acidosis is commonly due to a defect in more than one
step in the process of respiration. COPD is an excellent example of this,
as there are defects in every step of respiration.

Chronic respiratory acidosis alters the res-

piratory control center so that it becomes less
sensing and signaling

sensitive to changes in carbon dioxide. Pa-

+ tients with chronic hypercarbia are depen-
dent on changes in oxygenation to drive res-
muscles and motion COPD is associated with air trapping and hy-
perinflated lungs due to the destruction of
septal walls and connective tissue. This de-
struction causes the airways to lose tone
which interferes with ventilation. During ex-
halation, the airways collapse, trapping air
in the lungs. The air trapping leads to hyper-
inflated lungs at the end of expiration so that
expansion of the chest during inspiration is
free flow COPD interferes with the free flow of air by
a number of different mechanisms.
Emphysema destroys the elasticity that
holds the bronchioles open, especially dur-
ing expiration. Without the septal walls, the
bronchioles collapse and obstruct the air-
Chronic bronchitis is characterized by
increased mucous production which ob-
structs and narrows the airway.
gas exchange The destruction of the alveolar septa asso-
ciated with COPD interferes with gas ex-
change. The loss of surface area reduces
the area available for the exchange of CO2
and O2.
Interference with gas exchange increases
CO2 O2

the A-a gradient.


The Fluid, Electrolyte and Acid-Base Companion

Clinical correlation: COPD is typically a combination of two

disease processes.
Emphysema Chronic bronchitis
Definition Dilation and air trapping in the distal Excessive sputum production for
alveoli with destruction of alveoli sep- greater than 3 months of the year for
tal tissue at least 2 consecutive years

Mnemonic Pink puffers Blue bloaters

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).

Cough Late in the disease Early in the disease

Dyspnea Early in the disease Late in the disease

Hypoxia Late in the disease Compensation early in the disease by

increasing hematocrit

Infections Less common, but more severe Common, but less severe

Chronic obstructive pulmonary disease (COPD) is a common cause of

respiratory acidosis. Patients with COPD have difficulty completely exhal-
ing which produces an obstructive pattern on pulmonary function tests (?
FEV1, ? FVC and ? FEV1 ⁄FVC ). COPD is the most common cause of chronic
respiratory acidosis. The two types of COPD are chronic bronchitis and
emphysema; usually, patients have a combination of both disorders, al-
though one of the two typically predominates.
Emphysema is defined histologically as dilation of the alveolar air sacs
with destruction of alveolar septa. Chronic bronchitis is defined clini-
cally as an increase in bronchial mucus production sufficient to cause a
cough for at least three months per year for at least two consecutive years.
Smoking is the predominant risk factor for COCOPD
causes hypertrophy of goblet cells, increasing mucus production. Ciga-
rette smoke also inhibits ciliary action which prevents clearing excess mu-
cus and predisposes to chronic bronchitis. Cigarette smoke recruits in-
flammatory cells which release proteolytic enzymes that break down al-
veolar tissue resulting in emphysema.

S. Faubel and J. Topf 15 Respiratory Acidosis

Compensation!The compensation for respiratory acidosis is an

increase in bicarbonate.

Acute Chronic
respiratory acidosis respiratory acidosis
C before renal compensation after renal compensation
C pH | pH |
CO2 3-5 CO2

Examination of the Henderson-Hasselbalch formula reveals that normal-

ization of the HCO3–/CO2 ratio in respiratory acidosis requires an elevation
of plasma HCO3– . Increased plasma HCO3– in respiratory acidosis occurs
through buffering and renal excretion of hydrogen. The buffering response
occurs within hours, but produces only a minimal effect. Renal compensa-
tion produces a large effect, but is not complete for 3-5 days.
Because of the time necessary for renal compensation to occur, two forms
of respiratory acidosis are recognized: acute and chronic. Acute respiratory
acidosis is present before renal compensation is complete, and chronic res-
piratory acidosis is present after renal compensation is complete.

In respiratory acidosis the PCO2 is ________ (increased/decreased). increased

The compensation for respiratory acidosis is an

__________ (increase/decrease) in HCO–3. increase

Acute respiratory acidosis exists before ________ compensation is renal


The Fluid, Electrolyte and Acid-Base Companion

Compensation!Acute!Buffering by bicarbonate in respiratory

acidosis is ineffective.
Normal buffering


Normally in acidemia, bicarbon- carbonic acid water and CO2. Excess

ate combines with excess hy- which breaks CO2 is eliminated by
drogen ion to form... down into... the lungs.

Buffering in respiratory acidosis

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.

Although buffering is the initial compensatory response in acute respiratory

acidosis, the effect is minimal because bicarbonate, the primary acid buffer, is
ineffective. Normally in acidemia, excess hydrogen ion combines with bicar-
bonate to produce carbonic acid which breaks down into water and carbon
dioxide. The excess carbon dioxide produced by this reaction is then eliminated
by the lungs via respiration. As carbon dioxide is eliminated, the reaction con-
tinues forward and more acid can be buffered.
In respiratory acidosis, the primary defect is ineffective respiration which re-
sults in the retention of carbon dioxide. Thus, bicarbonate cannot serve as a
buffer because the carbon dioxide produced by the buffering reaction cannot
be eliminated. Only non-bicarbonate buffers such as protein, phosphate and
hemoglobin can effectively absorb excess hydrogen ions.

The major hydrogen ion sponge in the body is ___________. bicarbonate

In respiratory acidosis, _________ is an ineffective buffer because bicarbonate

the CO2 produced in the buffering reaction cannot be eliminated.

S. Faubel and J. Topf 15 Respiratory Acidosis

Compensation!Acute!The bicarbonate increase in acute res-

piratory acidosis is small.


c i do
Bicarbonate (mEq/L)

piratory a
acute res
24 normal
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.


expected HCO3– = 24 + (PCO – 40) 2

BHCO3– : BPCO2 .................................................... 1 : 10

The small increase in bicarbonate concentration in respiratory AAA

acidosis is secondary to the effect of non-bicarbonate _________. buffers

In acute respiratory acidosis, the bicarbonate concentration in-

creases by ___ mEq/L for every 10 mmHg elevation in PCO2. one

The Fluid, Electrolyte and Acid-Base Companion

Compensation!Chronic!Respiratory acidosis is referred to as

chronic when renal compensation is complete.
– days –
pH | pH |

! C


H+ +
H+ H

Respiratory acidosis is defined as chronic only after renal compensation

is complete. The renal compensation for respiratory acidosis involves en-
hanced excretion of hydrogen.
In respiratory acidosis, the bicarbonate buffer equation is shifted to the
left. Carbon dioxide and water combine to form carbonic acid which breaks
down into hydrogen ion and bicarbonate. The excess hydrogen ion is then
excreted by the kidney. As hydrogen ion is excreted by the kidney, new bi-
carbonate is added to the plasma. The increase in plasma bicarbonate bal-
ances the increase in PCO2, lowering the pH toward normal.

Renal compensation in respiratory ________is the increased ex- acidosis

cretion of hydrogen ion which results in the production of
____________. bicarbonate

Renal compensation in respiratory acidosis takes ___ to ___ 3;5

days to complete.

S. Faubel and J. Topf 15 Respiratory Acidosis

Clinical correlation: Renal excretion of hydrogen increases

urinary chloride loss. intercalated cell

ATP water (H2O)

Acidemia increases the se-

cretion of H . H+ H+ OH

When H+ is secreted, Na+ is HCO3
resorbed to maintain elec- Na+


– +
Normally, Cl and Na re- Na+
sorption occur together. Be-
cause Na is resorbed in Cl–

exchange for H+, less Na+ is
available for Cl– resorption.

Increased urinary chloride

losses result in a low plasma

The creation of new bicarbonate and excretion of hydrogen ion occurs in

the intercalated cells of the collecting ducts.
Water (H2O) in the tubular cells breaks down into H+ and OH–. Hydrogen
ion is secreted into the tubular lumen by the H+- ATPase pump. To maintain
electroneutrality, sodium ions flow down their concentration gradient into
the cell. The increased resorption of sodium leaves fewer sodium ions avail-
able to be resorbed with chloride. Chloride excretion in the urine is increased
with increased hydrogen excretion.
In the tubular cell, OH– combines with CO2 to form bicarbonate which
enters the plasma. The formation of bicarbonate from OH– and CO2 is cata-
lyzed by the enzyme carbonic anhydrase.
The renal excretion of hydrogen results in loss of chloride and formation
of additional bicarbonate for the plasma. Plasma chloride is decreased
and plasma bicarbonate is increased.

The Fluid, Electrolyte and Acid-Base Companion

Compensation!Chronic!Renal compensation for chronic res-

piratory acidosis causes a more dramatic increase in bicarbonate
than buffering alone.


c i do
ic r pirato
Bicarbonate (mEq/L)

hro es
28 r
piratory a
acute res
26 Chr
24 normal
35 40 45 50 55 60 65 70 75
PCO2 (mmHg)

Chronic respiratory acidosis is characterized by a more significant com-

pensatory rise in plasma HCO3– than occurs in acute respiratory acidosis. As
represented in the graph above, the change in plasma HCO3– for a given
change in PCO2 is much greater in chronic than in acute respiratory acido-
sis. In chronic respiratory acidosis, the change in bicarbonate relative to the
change in PCO2 is 3:10. For every 10 mmHg rise in PCO2, the HCO3 rises by

3 mEq/L. For example, if the PCO2 increases to 60 mmHg from 40 mmHg,

then the HCO3– should increase from 24 mEq/L to 30 mEq/L.


expected HCO3– = 24 + 3 × ( 40 –10P ) CO2

B HCO3– : B PCO2 ...................................................... 3 : 10

Renal compensation for respiratory acidosis produces a larger aaa

increase in __________ concentration for a given change in P CO2 bicarbonate
than buffering alone.

In acute respiratory acidosis, for every 10 mmHg _______ in car- increase

bon dioxide the bicarbonate increases by _______ . one

In chronic respiratory acidosis, for every 10 mmHg _______ in increase

carbon dioxide the bicarbonate increases by _______ . three
S. Faubel and J. Topf 15 Respiratory Acidosis

Clinical correlation: Identifying the presence of other acid-

base disorders requires calculation of the expected bicarbon-

ate concentration.


When respiratory acidosis is identified, the first step in the evalua-

tion is to assess compensation and determine if another acid-base dis-
order is present. By using the formulas for the predicted bicarbonate,
the presence of an additional acid-base disorder can be determined.
If the bicarbonate does not match the level predicted for either acute or
chronic respiratory acidosis, then a second acid-base disorder is present.
Metabolic acidosis is present when the bicarbonate is below predicted and
metabolic alkalosis is present when the bicarbonate is above predicted.
If the bicarbonate is between the predicted amount for acute and
chronic respiratory alkalosis, then four combinations of acid-base dis-
orders could explain this result:
• chronic respiratory acidosis and metabolic acidosis or
• acute respiratory acidosis and metabolic alkalosis or
• acute-on-chronic respiratory acidosis or
• acute respiratory acidosis becoming chronic
Common scenarios of respiratory acidosis with other acid-base disor-
ders are discussed on the following page.

The Fluid, Electrolyte and Acid-Base Companion

Clinical correlation: Other acid-base disorders commonly

occur with respiratory acidosis.
respiratory acidosis and metabolic acidosis


respiratory failure from sepsis pulmonary edema cardiogenic shock

respiratory acidosis and metabolic alkalosis acute-on-chronic respiratory acidosis

COPD diuretic use pneumonia COPD

Respiratory acidosis and metabolic acidosis. Patients with this

combination of acid-base disorders usually have profound acidemia and
are very sick. This can be seen in a patient with pneumonia and sepsis.
Pneumonia causes respiratory acidosis, and sepsis causes metabolic aci-
dosis. Patients with cardiogenic shock can also have the combination of
respiratory acidosis and metabolic acidosis. Heart failure causes pul-
monary edema and respiratory acidosis while inadequate cardiac out-
put causes metabolic acidosis from accumulation of lactic acid.
Respiratory acidosis and metabolic alkalosis. An example of this
combination of acid-base disorders is the patient with COPD (respira-
tory acidosis) taking diuretics (metabolic alkalosis). Diuretics are fre-
quently prescribed to manage lower extremity edema in patients with
advanced COPD and right-sided heart failure.
Acute-on-chronic respiratory acidosis. Patients with COPD com-
monly develop other causes of respiratory acidosis. These patients of-
ten present with a new, acute cause of respiratory acidosis in addition
to their base-line chronic respiratory acidosis. This is known as acute-
on-chronic respiratory acidosis and is commonly caused by pneumonia.

S. Faubel and J. Topf 15 Respiratory Acidosis

Symptoms and signs!Neurologic symptoms and signs predom-

inate in respiratory acidosis.


increased cerebral hypoxia

flood flow



headaches stupor, coma carbon dioxide


The symptoms and signs of respiratory acidosis are primarily neurologic

due to the effect of cerebral acidosis. Cerebral acidosis stimulates vasodila-
tion which increases cerebral blood flow and intracranial pressure. Initially,
increased cerebral blood flow may cause headaches. As cerebral acidosis
worsens, restlessness and stupor may develop. Carbon dioxide narcosis is
the development of somnolence and depressed consciousness from rising
CO2 levels.
Hypoxia is always present in respiratory acidosis. Hypoxia can cause cy-
anosis and contribute to altered mental status.

CO2 narcosis is the development of __________ from rising CO2 somnolence


Respiratory acidosis ___________ (decreases/increases) cerebral increases

blood flow which may cause headaches.

C3PO! Shut down all of the garbage mashers on the

___________ level! detension

The Fluid, Electrolyte and Acid-Base Companion

Symptoms and signs!The symptoms and signs in COPD are

mainly due to the underlying lung disease.

barrel-shaped chest right-sided heart failure


headaches confusion polycythemia

The clinical picture associated with chronic respiratory acidosis is domi-

nated by the signs and symptoms of chronic lung disease. By far, the most
common cause of chronic lung disease is COPD. The symptoms and signs of
this disease are discussed below.
Due to the underlying pulmonary disease, shortness of breath and cough
are common complaints. Chronic hypoxemia may affect cognitive abilities
and cause cyanosis. To compensate for chronically low oxygen, RBC produc-
tion may increase resulting in an increased hematocrit (known as poly-
cythemia). Chronic CO2 retention can cause somnolence and headaches.
As the disease progresses, the loss of pulmonary blood vessels results in
pulmonary hypertension and right-sided heart failure (cor pulmonale). Right-
sided heart failure can cause lower extremity edema and chest pain.
Physical exam findings in a patient with COPD may include a barrel-
shaped chest, prolonged expiration and wheezing. All of these findings are
caused by air trapping due to obstruction of air flow during exhalation.

Increased hematocrit, also known as _____________, can occur in polycythemia

COPD in order to compensate for chronic __________. hypoxia

In COPD, obstruction of the airways interferes with exhalation causing air

trapping, prolonged exhalation, an enlarged chest cavity (_________- barrel
shaped) and wheezing.

S. Faubel and J. Topf 15 Respiratory Acidosis

Diagnosis!Identifying the underlying cause of respiratory acidosis re-

quires review of the patient data base.

Well, it all
began when
I was sitting
on my front
porch mind-
ing my own
and these
two guys......

History Physical exam Labs and other tests

asthma increased respiratory rate Chest X-ray (CXR)
COPD increased breathlessness ABG
CHF presence of obesity A-a gradient
fever inability to complete sentences potassium
cough use of accessory muscles phosphate
chest pain clubbing magnesium
illicit drug use crackles hematocrit
trauma egophony
dullness to percussion
tactile fremitus

Establishing the cause of respiratory acidosis can be difficult because a

wide range of respiratory diseases exist. Some of the important components
of the history, physical exam and lab tests are discussed below.
History. The history is important to establish if an underlying lung dis-
ease is already present (e.g., asthma, COPD). Patients with COPD com-
monly have exacerbations from infections which cause acute-on-chronic res-
piratory acidosis.
Physical exam. An assessment for breathlessness should be made (e.g.,
can the patient speak in full sentences) and whether accessory muscles of
respiration are being used. A careful lung exam should be done, assessing
for crackles, dullness to percussion, egophony, tactile fremitus and wheezes.
Look at the fingers for clubbing, a sign of chronic hypoxia.
Labs and other tests. The A-a gradient is a useful tool in the evaluation of
respiratory acidosis. The A-a gradient is normal in disorders of ventilation (e.g.,
obesity hypoventilation, narcotic use); it is increased in disorders of impaired
gas exchange (e.g., pneumonia, pulmonary embolism). Because more than one
step in the process of respiration may be affected, an increased A-a gradient
does not exclude a concurrent impairment in ventilation.
A CXR is helpful to identify the presence of infiltrates, pulmonary edema
or pleural effusion.

A most useful tool in the evaluation of respiratory acidosis is the aaa

____ gradient. A-a

The Fluid, Electrolyte and Acid-Base Companion

Diagnosis!Abnormal lab values in respiratory acidosis are found

primarily on the chem-7 and arterial blood gas (ABG).

Na Cl– glucose pH / PCO2 / PO2

K+ HCO3–

Respiratory acidosis is characterized by the following lab abnormalities:

The ABG is characterized by a low pH with a high PCO2. Pulmonary dis-
ease severe enough to cause carbon dioxide retention also causes hypoxia;
thus, the PO2 is low.
The chem-7 is characterized by an increased bicarbonate, representing
compensation by buffering (acute respiratory acidosis) and renal excretion
of hydrogen ion (chronic respiratory acidosis). In chronic respiratory acido-
sis, the bicarbonate can reach as high as 40 mEq/L.
Chloride may be slightly low due to increased renal loss. Renal loss of
chloride increases to maintain electroneutrality with hydrogen loss.
The Alveolar-arterial gradient may be normal or high, depending on
whether an impairment in gas exchange is present. Impaired gas exchange
increases the A-a gradient.

In respiratory acidosis, the bicarbonate is __________ (decreased/ increased

increased) and the chloride is __________ (decreased/increased). decreased

If gas exchange is impaired, the A-a gradient is typically

__________ (normal/high). high

S. Faubel and J. Topf 15 Respiratory Acidosis

Treatment!In respiratory acidosis, treating the underlying disorder

is important.

Treat the underlying disorder.


antibiotics supplemental oxygen diuretics steroids

Mechanically ventilate, if necessary.

The most important aspect in the treatment of respiratory acidosis is to

identify and treat the underlying cause.
Supplemental oxygen should be given to return oxygen levels to normal.
Care must be used when using oxygen in patients with chronic carbon diox-
ide retention. Other important measures include nebulizer treatments with
albuterol for asthma, antibiotics for pneumonia and diuretics for cardio-
genic pulmonary edema. Steroids are used in a number of pulmonary dis-
eases to reduce inflammation (e.g., asthma, BOOP).
If the pulmonary process causing respiratory acidosis cannot be reversed
or is severe, endotracheal intubation and mechanical ventilation may be
required. Mechanical ventilation can be used to support ventilation while
reversible causes of lung injury are treated (e.g., antibiotics are given to
treat pneumonia). The decision to institute mechanical ventilation is a clinical
decision dependent on many factors (e.g., patient fatigue, reversibility of
illness, patient preference, etc.).

Since respiratory acidosis is associated with hypoxia, one of the aaa

mainstays of treatment is to give supplemental _________. oxygen

Albuterol can be helpful in patients with ________. asthma

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.

metabolic acidosis metabolic alkalosis respiratory acidosis respiratory alkalosis

pH | pH | pH | pH |

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.

CO2 O2

sensing and signaling muscles and motion free flow gas exchange

To compensate for the low pH of respiratory acidosis, plasma bicarbonate

increases to balance the increased carbon dioxide. Bicarbonate increases
through intracellular buffering (acute respiratory acidosis) and renal reten-
tion with production of bicarbonate (chronic).
Acute respiratory acidosis exists prior to renal compensation; chronic res-
piratory acidosis exists after renal compensation is complete. Compensa-
tion is assessed by calculating the expected bicarbonate. If the measured
bicarbonate does not match the values predicted by the formulas, then a
second acid-base disorder is present.

expected HCO3– = 24 + (PCO – 40) 2

expected HCO3– = 24 + 3 × ( 40 –10P ) CO2

BHCO3– : BPCO2 .................................................... 1 : 10 B HCO3– : B PCO2 ...................................................... 3 : 10

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
HO ]
)× %O –(1.25 × PCO ) – PO
2 2

normal Aa-gradient = (age

+ 4)

The symptoms and signs of respiratory acidosis are different, depending

on whether it is acute or chronic. The symptoms and signs of acute respira-
tory acidosis are due to hypoxia, hypercarbia and cerebral acidosis. The
presentation can range from tachypnea and headaches to CO2 narcosis with
stupor or even coma.
Since chronic respiratory acidosis is associated with long-standing pul-
monary disease, the symptoms and signs of chronic respiratory acidosis are
dominated by the symptoms and signs of chronic pulmonary disease (COPD).
Lab abnormalities associated with respiratory acidosis include decreased
pH, increased PCO2, decreased PO2, decreased Cl– and increased HCO3 .

The treatment of respiratory acidosis focuses on identifying and treating

the underlying disorder.

Na Cl– glucose pH / PCO2/ PO 2

K+ HCO3–

The Fluid, Electrolyte and Acid-Base Companion

Summary!Clinical review.

pH / PCO2/ PO2 HCO3–

Step 1. Recognize respiratory acidosis.

Step 2. !Compensation, determine acute versus chronic and eval

uate for the presence of other acid-base disorders.

Acute Chronic
expected HCO3– = 24 + (PCO – 40 ) 2
expected HCO3– = 24 + 3 × ( 40 –10P ) CO2

BHCO3– : BPCO2 .................................................... 1 : 10 B HCO3– : B PCO2 ...................................................... 3 : 10

Step 3. ! History, physical, labs and other tests.

History Physical exam Labs and other tests
asthma increased respiratory rate Chest X-ray
COPD increased breathlessness ABG
CHF presence of obesity potassium
fever inability to complete sentences phosphate
cough clubbing magnesium
chest pain crackles hematocrit
illicit drug use egophony
trauma dullness to percussion
tactile fremitus

Step 4. Calculate the A-a gradient.

Normal A-a gradient (Ventilation defect) High A-a gradient*

Anatomic/Trauma Anatomic Diffusion defect

Sensing and signaling Muscles and motion Free flow Gas exchange

apnea of prematurity flail chest laryngomalacia _-antitrypsin deficiency

Sensing defects

brain stem injury kyphoscoliosis tracheomalacia emphysema

central sleep apnea pneumothorax Aspiration interstitial lung disease
Drugs Drugs Infections ankylosing spondylitis
narcotics aminoglycoside croup amiodarone toxicity
alcohol succinyl choline epiglottitis amyloidosis
benzodiazepines vecuronium Obstructive disease BOOP
oxygen therapy in patients Electrolytes asthma dust exposures
with chronic CO retention hypokalemia COPD idiopathic pulmonary
Obesity hypoventilation hypophosphatemia chronic bronchitis fibrosis

Primary hypoventilation hypermagnesemia emphysema rheumatoid arthritis

Genetic disorders Seizures radiation therapy
amyotrophic lateral sclerosis acid maltase deficiency Smoke inhalation sarcoidosis
Signaling defects

diaphragmatic paralysis muscular dystrophy Wegener’s

Guillain-Barré syndrome periodic paralysis granulomatosis
post-polio syndrome Myasthenia gravis Ventilation defect
spinal cord injury ARDS
pulmonary edema
Perfusion defects
* A high A-a gradient does not exclude a concurrent ventilation defect. pulmonary embolism