MEDSURG NURSING
CE Objectives and Evaluation Form appear on page 86-
Informed Nursing Practice:
The Administration of Oxygen
To Patients with COPD
Prisciiia Simmons
Mark Simmons
Although the Hypoxic Drive
Theory has been a long-time
long-term
M
ore than 1 million patients
worldwide
oxygen
are treated with
(O^) therapy. In
influence on the care of
patients with chronic obstruc- most of these individuals, chronic
obstructive pulmonary disease
tive pulmonary disease (COPD) is the underlying disease
(COPD), in reality a relatively process resulting in hypoxemia
fine line exists between opti- (Zielinski, 2000). For decades, the
mal and excessive oxygen Hypoxic Drive Theory has influ-
therapy. Medical-surgical nurs- enced the care of patients with
es need a clear understanding COPD. Now, however, most experts
in pulmonary disease consider this
of the benefits and the possi- theory obsolete (Whitnack, 2001).
ble complications of oxygen The Hypoxic Drive Theory pro-
therapy in patients with COPD. posed that administering oxygen to
a patient with COPD could result in
apnea, cardiorespiratory arrest,
and subsequent death as a result of
shutting down the patient's hypoxic
respiratory drive (Hoyt, 1997). The
origin of these fallacious ideas is
unclear, but they seem to enter the
information database of clinicians
at an early point in their practice —
"almost like a computer virus cor-
Prisciiia Simmons, EdD, APRN, RN,BC,
rupting the appropriate function of
is a Professor of Nursing, Adult Degree the equipment" (Hoyt, 1997, p.
Completion Prograjii, Eastern Mennonite 1450).
University, Lancaster, PA.
Despite the fact that ample
Maiit Simmons, MSEd, RPFT, RRT-NPS,
research has rendered the theory
is Director. The School of Respiratory defunct (Beachey, 1998; Benditt,
Therapy. York College of Pennsylvania, 2000; Epstein & Singh, 2001). per-
York, PA. petuation of this medical myth and
82
a nurturing of the ensuing clinical
mindset persist. The result is a dan-
ger that misinformed clinicians may
deliver doses of oxygen that are
inadequate for the patient's meta-
bolic needs (Whitnack, 2001).
Clearly, this mindset can adversely
influence the care and ultimate well-
being of patients. In actuality, the
only pharmacologic treatment
shown to increase survival for
hypoxic patients with COPD is long-
term oxygen therapy. For such
patients, long-term oxygen therapy
decreases pulmonary hyperten-
sion, sleep disturbances, nocturnal
dysrhythmias, and their awareness
of dyspnea. It increases exercise
endurance, mental alertness, and
muscle strength (Heffner & Frye,
2002). Accordingly, the purpose of
this article is to review the physiol-
ogy of the respiratory drive in nor-
mal individuals and those with
COPD. Additional discussion will
address the use and treatment
implications of oxygen therapy
along with pertinent nursing assess-
ments.
The Physiology of Breathing
Peripheral chemoreceptors. Breath-
ing, or ventilation, is the movement of
air in and out of the lungs. Blood that
has been oxygenated in the pul-
monary capillary bed provides oxy-
MEDSURG Nursing—April 2004—Vol. 13/No. 2
 Informed Nursing Practice: The Administration of Oxygen to Patients with COPD
gen to all body cells. Ventilation
also removes carbon dioxide (CO.,)
produced in the i^ody's tissue
beds. This mechanism is regulated
by various peripheral chemorecei>
tors, some of which are located on
the arch of the aorta (aortic bodie.s)
and some at the bifurcation of the
common carotid arteries (carotid
bodies). Most of the peripheral
chemoreceptors that help regulate
breathing are located on the
carotid bodies. Aortic body recep-
tors have minimal function in
humans.
Bathed in arterial blood, these
receptors are stimulated by: (a)
changes in blood pH, (b) the partial
pressure of arterial carbon dioxide
(PaCO.,), and (c) the partial pres-
sure of arterial oxygen (PaOj.
Impulses from the carotid bodies
travel via the glossopharyngeal
(9th) cranial nerve to the central
respiratory centers in the brain
stem to stimulate or suppress
breathing as needed.
Increased levels of arterial car-
bon dioxide (hypercarhia) and
decreased arterial pH (acidosis)
stimulate ventilation. Decreased
PaO,, levels also stimulate ventila-
tion. However, hypoxemia does not
become a significant stimulus until
PaO., levels drop below 60 mmHg
(normal PaO,. = 80-100 mmHg). This
means that oxygen plays little role
in control of ventilation in healthy
individuals. Hypoxemia does play a
role, however, in individuals who
ascend into high altitudes where
the total atmospheric pressure and
thus partial pressure of oxygen are
decreased (West, 2000). Hypoxemia
also stimulates ventilation in
patients with lung disease that has
resulted in a low PaO.,. Although
such stimulation of the carotid
bodies is very rapid, its overall
effect for control of normal ventila-
tion is only about 20% to 30% of the
total response.
Central chemoreceptors. Other
receptors known as central
chemoreceptors are found in the
MEDSURG Nursing—April 2004—Vol. 13/No. 2
brain. These chemoreceptors are
located bilaterally on the ventrolat-
eral surfaces of the medulla.
Because CO., from the arterial
blood readily crosses the blood-
brain barrier and influences the pH
of the cerebral spinal fluid (CSF),
the central chemoreceptors are
said to be CO, responsive. This
effect is indirect in that central
chemoreceptors are directly stimu-
lated not by PaCO,, but rather by
the lowered pH of the CSF
Nonetheless, CO., is given credit for
normal control of ventilation via
these central chemoreceptors,
thereby providing the majority of
ventilation control from minute to
minute. Typically, the body's PaCO,,
is maintained within 3 mmHg (+/-)
of normal (40 mmHg). Because
there are no oxygen receptors in
the brain, oxygen level has no
direct effect on the central
chemoreceptors.
Control of Ventilation
In Patients with COPD
COPD has passed accidents,
pneumonia, and diabetes to
become the fourth leading cause of
death in America. Cigarette smok-
ing is responsible for 80% to 90% of
diseases classified under the term
COPD. Most smokers with COPD
have emphysema, chronic bronchi-
tis, or elements of both diseases
(Bunch, 2002; Lenfant, 2002). COPD
is characterized by progressive
deterioration of the airways and a
gradual loss of lung function.
Spirometry (a pulmonary function
test) confirms the diagnosis of
COPD based primarily on the pres-
ence of expiratory airflow limita-
tion (National Heart, Lung. & Blood
Institute, 2003). Some patients with
COPD have normal or near-normal
blood gases, and their control of
ventilation is the same as in the
healthy individual.
However, some patients with
COPD have a chronically increased
PaCO,,. Over time, an Increased
^ (respiratory acidosis) results
sems
in renal retention of bicarbonate
(metabolic alkalosi.'i), thus bringing
the pH of a stable patient with
COPD closer to normal (7.40). At
the same time, bicarbonate
(HC(^,") has crossed the blood-
brain barrier (a slow process) and
adjusted the CSF pH back to nor-
mal (7.33). When the pH of the CSF
has become normal once again in a
stable COPD patient, the central
chemoreceptors do not detect an
elevated PaCO^. Because patients
with COPD have been observed to
have a "blunted" drive to breathe,
the question then is, "What is their
stimulus for ventilation?"
Peripheral chemoreceptor phy-
siology provides this answer The
carotid bodies are stimulated by a
decreased pH, an increased PaCO.,,
and a decreased PaO.,. Because the
stable patient with COPD has a
near-normal arterial pH, the
increased PaCO, is probably not a
major respiratory stimulus. How-
ever, if the PaCO, increases further
(as with hypoventilation in acute
respiratory failure), the PaO., will
decrease because increased CO,,
levels in the blood dilute or replace
oxygen at an approximate 1:1 ratio.
For example, if PaCO, increases 10
mmHg, PaO, will decrease at least
10 mmHg. When this fact is cou-
pled with the reality of gas
exchange problems at the alveolar
level, it is no surprise that the
patient with COPD suffers from
hypoxemia. This low oxygen level
eventually stimulates the peripher-
al chemoreceptors, and the patient
with COPD is said to be breathing
by virtue of the hypoxic drive.
Administration of Too Much
Oxygen to a CO2 Retainer
Patients with COPD differ.
Some have near normal blood
gases. However, others have chron-
ically elevated PaCO., levels (hyper-
capnia) and decreased PaO, levels.
A subgroup of these individuals is
oxygen .sensitive. That is, when they
are given supplemental O^, their
83
 Informed Nursing Practice: The Administration of Oxygen to Patients with COPD
sems
PaCO,, levels go acutely higher.
Higher levels of carbon dioxide can
suppress the central nervous sys-
tem; if PaCO, levels climb high
enough (>70 mmHg), patients may
become lethargic and difficult to
arouse. This phenomenon is com-
monly known as CO, narcosis,
although it may be better described
as hypercapnic encephahpathy. The
increased PaCO., acts as a sedative,
probably by altering intraceliular
pH and causing derangement of the
metabolic processes of the central
nervous system (Nunn, 1993). This
observation has great clinical sig-
nificance. How can health care
providers know if a patient is sensi-
tive to oxygen therapy or not? In
short, nobody can know for sure
until the patient's response to 0^
therapy has been assessed.
Baseline hypoxia and acidosis
are better predictors of oxygen-
induced hypercapnic encephalopa-
thy than hypercapnia alone
(Epstein & Singh, 2001). Moreover,
current evidence suggests that sev-
eral factors contribute to the devel-
opment of hypercapnia seen when
supplemental oxygen is adminis-
tered to CO., retainers. Three theo-
ries propose an explanation for this
and in all probability, this phenom-
enon results from a combination of
these factors (Epstein & Singh.
2001).
Regulation
Of Respiratory Drive
Theory Number One:
The Hypoxic Drive Theory
A hypoxic drive accounts for
10% to 15% of the total respiratory
drive (Whitnack. 2001). No longer,
however, is it believed that oblitera-
tion of the hypoxic drive serves as
the sole explanation for the rising
hypercarbia that may result when a
chronic CO, retainer is given oxy-
gen (Beachey, 1998). However,
because this hypoxic drive theory
persists as a clinical mindset, its
elements deserve review.
The patient with chronic CO^
84
retention has lost most of the drive
to breathe attributable to elevated
CO,. Thus, it has been commonly
supposed that the patient's breath-
ing must be governed by the hypox-
ic drive. Clinicians have observed
that when some of these patients
are given too much supplemental
0.,, an increased level of CO^ results.
This has led to the assumption that
the hypoxic drive has been obliter-
ated and the movement of air has
diminished.
In reality, however, research
findings have resulted in close
scrutiny of this theory (Beachey,
1998; Crossley McGuire, Barrow, &
Houston, 1997; Epstein & Singh,
2001). Studies have suggested that
even though supplemental 0.^
results in CO^ retention in some
patients, these individuals often
have a minimal decrease in respira-
tory rate, tidal volume, or minute
ventilation (see Table 1 for defini-
tions), in other words, they move as
much air as they did prior to receiv-
ing increased oxygen.
Tfieory Number Two:
The V/Q Mismatch Theory
Normal ventilation (V)-to-perfu-
sion (Q) matching (V/Q matching) is
said to have occurred when alveolar
units receive equal amounts of ven-
tilation and pulmonary capillary
blood flow. In COPD, however, V/Q
mismatch occurs and can lead to
wasted ventilation, increased
PaCO., and decreased PaO,. High
V/Q mismatch results when an alve-
olar unit receives proportionally
more ventilation than perfusion. An
alveolar unit with ventilation but no
perfusion is called dead space (VD).
Conversely, a low V/Q mismatch
takes place when an alveolar unit
receives proportionally less ventila-
tion than blood flow. An alveolar
unit with blood flow but no ventila-
tion is called shunt because blood
flows from the right side of the heart
through the lungs to the left side of
the heart without being oxygenated.
When alveolar units are
exposed to decreased oxygen lev-
els, pulmonary vasoconstriction
occurs. This protective response
helps to redirect blood flow away
from poorly ventilated and hypoxic
parts of the lungs to better-ventilat-
ed and better-oxygenated areas.
One theory suggests that the admin-
istration of oxygen results in vasodi-
latation of those previously vaso-
constricted parts of the lungs.
Consequently, this changes the V/Q
matching. Because COPD patients
with acute respiratory failure can-
not increase minute ventilation to
compensate for this change in V/Q
matching, an increase results in
both the PaO,, and PaCO., levels
(Beachey, 1998; Benditt," 2000;
Epstein & Singh, 2001). As the PaCO.,
level rises, the patient becomes
increasingly somnolent (commonly
known as CO, narcosis).
Theory Number Three:
The Haldane Effect
Hemoglobin is well known for
its ability to carry O^. However,
hemoglobin also carries CO^. The
more 0., hemoglobin carries, the
less CO, it can carry. Conversely,
when hemoglobin carries less 0.,, it
can carry more CO.,. This is known
as the Haldane effect. The patient
with low 0^ levels has an increeise
in the CO., bound to hemoglobin.
However, when supplemental O^ is
administered, increased O,, satura-
tion results. This requires that
more CO., be "dumped off" the
hemoglobin and carried in the
blood in another form — such as
dissolved CO^ or bicarbonate.
Thus, the overall CO^ load Is
increased. If such a patient is
unable to increase ventilation, the
PaCO, will increase.
Significance for Nurses Caring
For Acutely 111 Adults
Oxygen is of life-saving impor-
tance in the treatment of COPD. In
general, low flow rates via nasal
cannula are recommended. Better
yet is the use of an air entrainment
MEDSURG Nursing-April 2004—Vol 13/No. 2
 Informed Nursing Practice: The Administration of Oxygen to Patients with COPD
Table 1.
Definition of Pulmonary Function Ternis
Term Definition
Respiratory rate (RR) Frequency (F) of breathing. Normal for adults is
12 to 16 breaths per minute.
Tidal volume (VT} The volume of air inhaled or exhaled during a
normal breath. Normal adult VT is 400 to 800 mL
depending on body size.
Minute ventilation (V, The volume of air inhaled or exhaled in one
minute. This volume is calculated by multiplying
respiratory rate by tidal volume. The normal V^ is
4 to 8 Uminute.
Deadspace (Vi^) The portion of tidal volume not participating in
gas exchange, also known as "wasted ventila-
tion."
V/Q mismatch Discrepancy between ventilation and perfusion
of alveolar units.
Pulmonary shunt Flow of blood from the right side of the heart
through the lungs to the left side of the heart
without being oxygenated.
device (venturi mask) at low oxy- hypercarbia can be diagnosed only
gen concentrations (24%-28'/i'>). At if it is suspected and communicat-
times, however, even nonrebreath- ed to the physician or respiratory
ing masks with high flow may be therapist, and a blood gas analysis
needed. Regardless of method of obtained. Increasing hypercarbia
administration, oxygen flow rates should be suspected in a patient
(FiO,) should be titrated to achieve with chronic CO, retention who is
the desired PaO,,. becoming increasingly somnolent. If
this is the case, mechanical ventila-
Clearly, the patient must be
closely monitored. Bedside oxygen tion may be necessary. Because the
saturation measurement devices patient may have limited respirato-
are useful in tracking the patient's ry reserve, any acute crisis may pre-
response to therapy. However, cipitate acute respiratory failure.
pulse oximetry does not assess Such deterioration in the
CO,, levels. For this, an arterial patient's condition may be due to a
blood gas is required. Although not change in V/Q matching, which is
sacrosanct, a useful rule is that O,, currently the most popular theory,
therapy for the patient with COPD or to other factors such as the
should be regulated to maintain an
Haldane effect. However, although
O,, saturation around 90X as long the Hypoxic Drive Theory cannot
as there is no sustained increase of be completely discounted in all
PaCO. (Heffner & Frye, 2002). This CO^ retainers (Epstein & Singh,
O,, saturation of 90% is equivalent 2001), well-informed nurses should
to a PaO, of 60 mmHg at a normal
recognize that it is unlikely that ris-
pH. ing PaCO,, levels in most patients
Because a patient's PaCO^ are attributable to obliteration of
the hypoxic drive. This belief may
must be measured by arterial
blood gas analysis, increasing lead to inadequate oxygen therapy.
MEDSURG Nursing—April 2004—Vol, 13/No, 2
sems
Indeed, recent research suggests
"it may not be so benign to have a
COPD patient — even a real CO.,
retainer — chronically hovering
the boundary of an acceptable
PaO;' (Whitnack, 2001, p. 2).
Because a relatively fine line
between optimal and overzealous
oxygen therapy exists, nurses need
a clear understanding of both the
benefits and the possible complica-
tions of oxygen therapy in patients
with COPD. •
References
Beachey. W. (1998). Respiratory care anato-
my and physiology Philadelphia: Mosby.
Benditt, J.O. (2000). Adverse effects of low-
flow oxygen therapy. Respiratory Care,
45, 54-61.
Bunch, D. (2002, September). A new dawn
breaks for COPD, AARC Times. 37-47,
Crossley, DJ.. McGuire, G.P., Barrow, P.M., &
Houston, RL. (1997). Influence of
inspired oxygen concentration on dead-
space, respiratory drive, PaC02 in intu-
bated patients with chronic obstructive
pulmonary disease. Critical Care
Medicine. 25: 1522-1526.
Epstein, S,K,, & Singh, N, (2001). Respiratory
acidosis. Respiratory Care. 46, 366-383.
Heffner, J.E., & Frye, M.D. (2002). Chronic
obstructive pulmonary disease. In D.R.
Hess, N.R. Maclntyre, S.C Mishoe. W.R
Galvin, A.B. Adams, & A.B, Saposnick
(Eds.). Respiratory care: Principles &
practice (pp. 922-950). Philadelphia:
W.B. Saunders.
Hoyt, J. (1997). Debunking myths of chronic
obstructive pulmonary disease. Critical
Care Medicine, 25. 1450-1451.
Lenfant, C. (2002). AARC Times interviews,
AARC Times. 26(9), 55-57.
National Heart, Lung, and Blood Institute.
(2003, May). Chronic obstructive pul-
monary disease (NIH Publication No,
03-5229). Bethesda, MD: U.S. Govern-
ment Printing Office,
Nunn, J.F. (1993). Nunn's applied respiratory
physioiogy (4th ed,), Cambridge,
England: The University Press.
West, J.B, (2000), Respiratory physiology:
The essentials (6th ed.). Philadelphia:
Lippincott Wiiliams & Wilkins.
Whitnack, J. (2001, September/October).
Notes from the editor: The death of the
hypoxic drive theory. Adult Acute Care
Bulletin, pp. 1-2.
Zielinski, J. (2000). Long-term oxygen therapy
in conditions other than chronic obstruc-
tive pulmonary disease. Respiratory
Care, 45. 172-177.
85
 Informed Nursing Practice: The Administration of Oxygen to Patients with COPD

Answer/Evaluation Form:
Informed Nursing Practice: The Administration of Oxygen
To Patients with COPD MSN J404
This test may be copied for use by others. Objectives
This educational activity is designed
COMPLETE THE FOLLOWING: for nurses and other health care profes-
sionals who care for and educate patients
Name: and their families regarding the adminis-
tration of oxygen to patients with COPD.
Address: For those wishing to obtain CE credit, an
evaluation follows. After studying the
City: State:
information presented in this article, the
Preferred telephone: (Home), (Work). nurse will be able to:
1. Discuss the physiology of breathing.
State where licensed and license number:. 2. Describe control of ventilation in
AMSN Member Expiration Date: patients with COPD.
3. List three theories of regulation of
respiratory drive.
Registration fee: AMSN/ISONG Member: $ 7.00
Nonmember: SIO.OO

Answer Form:

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86 MEDSURG Nursing—April 2004—Vol. 13/No. 2