Vol. 21, No.
7 July 1999 V 20TH ANNIVERSARY
CE Refereed Peer Review
FOCAL POINT
★ Oxygen (O ) therapy optimizes
2
blood O2 content, helps increase
O2 delivery to tissue, and
decreases the ventilatory and
myocardial work necessary to
maintain adequate tissue
oxygenation.
KEY FACTS
■ The five causes of hypoxemia
are low fraction of inspired O2
(FIO2), hypoventilation, diffusion
barrier impairment, shunt, and
ventilation/perfusion mismatch.
■ As a general rule, the delivered O2
concentration should not exceed
an FIO2 of 50% for more than
24 hours or complications
associated with O2 toxicity
may develop.
■ Delivered O2 should be humidified
when supplementation is
required for more than a few
hours or if the upper respiratory
airways are bypassed.
■ Arterial blood gas analysis,
alveolar–arterial O2 tension
difference, arterial partial
pressure of O2:FIO2 ratio, and
pulse oximetry are ancillary tests
that support the need for and
help to monitor response to O2
therapy.
Small Animal
Oxygen Therapy
Louisiana State University
Maria A. Camps-Palau, DVM
Steven L. Marks, BVSc, MS, MRCVS
Janyce L. Cornick, DVM, MS
ABSTRACT: Oxygen (O2) therapy is easy to administer, readily available, and relatively safe if
used judiciously. Optimizing O2 delivery to tissue is imperative in clinical conditions character-
ized by hypoxia. It is important to understand the physiology of O2 uptake and delivery to rec-
ognize those patients that will benefit from O2 supplementation. Several O2 administration
techniques are available and can be adapted to every clinical situation and patient condition. O2
therapy is an important adjunctive therapy but is not without complications and thus must be
closely monitored.
H
ypoxia is a broad term that means decreased levels of oxygen (O2) in air,
blood, or tissue.1 Clinically, hypoxia is defined as inadequate supply of
O2 to the body’s tissue and can result from insufficient blood oxygena-
tion (i.e., hypoxemia), reduced O2-carrying capacity of erythrocytes, decreased
tissue blood flow, increased tissue demand for O2, or impaired tissue extraction
of O2.2,3
Oxygen is easy to administer, readily available, and relatively safe. Supple-
mentation with O2 increases blood O2 content, minimizes detrimental effects
of hypoxemia, and decreases ventilatory and myocardial work necessary to
maintain tissue O2 delivery.4,5 Therapeutic considerations in animals with ab-
normalities that increase O2 demand or decrease O2 delivery to tissue include
correction of the underlying problem and maintenance of adequate tissue oxy-
genation.
When evaluating patients that may benefit from O2 therapy, understanding
respiratory and O2-transport physiology is necessary to formulate a rational diag-
nostic and therapeutic plan. When O2 delivery to tissue is inadequate, cells must
use alternate anaerobic pathways to maintain their metabolism. Anaerobic
metabolism causes rapid depletion of energy and accumulation of lactic acid
within cells, leading to cellular dysfunction and death.4,6 This article discusses
the physiology of respiration and O2 uptake and delivery, indications for O2 sup-
plementation, methods of O2 administration, and criteria to assess response to
O2 therapy.
RESPIRATORY PHYSIOLOGY
The major function of the respiratory system is to exchange O2 and carbon
Small Animal/Exotics 20TH ANNIVERSARY Compendium July 1999

dioxide (CO2) between blood PHYSIOLOGY OF

and inspired air to maintain Arterial Oxygen Content Formula OXYGEN UPTAKE
normal arterial partial pres- CaO2 = Oxyhemoglobin + Dissolved O2 AND DELIVERY
sures of O2 (PaO2) and CO2 CaO (ml O /dl) = Oxygen is carried in the
2 2
(PaCO2). The O2 pathway can blood in either the dissolved
(SaO2 [%] × Hemoglobin [g/dl] × 1.34 [ml O2/g]) +
be divided into four major state or bound to hemoglo-
functions—pulmonary gas (PaO2 [mm Hg] × 0.003 [ml O2/dl/mm Hg]) bin (oxyhemoglobin).2,4 Arte-
exchange, diffusion of gases CaO2 = arterial oxygen content; O2 = oxygen; PaO2 = arterial rial O2 content (CaO2) is the
between alveoli and blood, partial pressure of oxygen; SaO2 = arterial hemoglobin amount of oxyhemoglobin
transport of gases to and from saturation. plus the O2 dissolved in plas-
cells, and regulation of venti- ma (see Arterial Oxygen
lation.2,4 Content Formula).6 The contribution of dissolved O2 to
Despite the variable demands of the body, the respi- overall CaO2 is relatively small because most O2 travels as
ratory control system maintains PaO2 and PaCO2 within oxyhemoglobin.2,4 Tissue hypoxia can result from de-
a narrow homeostatic range. The basic components of creased CaO2 even in patients that maintain normal
the respiratory control system are the central and pe- PaO2 values. Causes of decreased CaO2 include anemia
ripheral chemoreceptors, medullary respiratory center, and hemoglobin abnormalities.2,4
2
and muscles of respiration. Under normal conditions, The sigmoid shape of the oxyhemoglobin dissocia-
the primary driving forces for alveolar ventilation are tion curve (Figure 1) demonstrates that the amount of
hypercapnia (sensed by the central chemoreceptors in O2 bound to hemoglobin increases rapidly up to a par-
the brain stem) and, to a lesser degree, hypoxemia tial pressure of O2 (PO2) of approximately 50 mm Hg;
(sensed by the peripheral chemoreceptors in the aortic however, the rate of O2 uptake decreases at higher PO2
arch and carotid bodies).2,4 values. Arterial hemoglobin saturation (SaO2) at a PaO2
The respiratory system consists of the anatomic dead of 100 mm Hg is 97.5%, whereas mixed venous blood
space and the respiratory zone. The anatomic dead space with a PO2 of 40 mm Hg has a hemoglobin saturation
(i.e., respiratory airways) includes the upper airways and a (SO2) of approximately 75%.2,4
series of branching tubes from the trachea to the termi- The plateau portion of the oxyhemoglobin dissocia-
nal bronchioles that lead inspired air to the gas-exchang- tion curve illustrates that a decrease in PaO2 results in
ing regions of the lungs. The respiratory zone (i.e., alveo- minimal changes in the oxygenation of erythrocytes. In
lated regions) of the lungs is where gas exchange occurs. contrast, the steep lower part of the curve indicates that
Alveolated regions that are ventilated but not perfused small drops in capillary PO2 allow peripheral tissue to
constitute the physiologic dead space.2,4 receive large amounts of O2 from erythrocytes.
At the blood–gas interface, the pulmonary capillaries A right shift of the oxyhemoglobin dissociation curve
form a dense network in the decreases the affinity of hemo-
alveolar walls and have diame- globin for O2, thereby facilitat-
Hemoglobin Saturation (SO2; %)

ters just large enough for a sin- Plateau Phase ing O2 release because a higher
gle erythrocyte to pass.2 The 100 PaO2 is necessary to load hemo-
rate and direction of gas move- globin with O2. Right shifts are
ment are based on pressure seen with acidosis (Bohr effect),
gradients and follow Fick’s law, 75
hypercapnia, hyperthermia, or
which states that the amount increases in erythrocyte 2,3-
of gas moving through a sheet 50 diphosphoglycerate (2,3-DPG)
of tissue is proportional to the concentration.2,4 A left shift of
area of that sheet and inversely Steep Phase the curve increases the affinity
proportional to its thickness.2 25 of hemoglobin for O2, which
The blood–gas barrier com- means the PaO2 must drop low-
prises a large surface area of er for hemoglobin unloading of
capillaries wrapping around 25 50 75 100 O2 to occur. Left shifts occur
the alveoli and is extremely Oxygen Tension (PO2; mm Hg) with alkalosis, hypocapnia, hy-
thin, thus maximizing exchange pothermia, methemoglobine-
of O2 and CO2 between alveoli Figure 1—The oxyhemoglobin dissociation curve dem- mia, or 2,3-DPG deficiency.2,4
and capillary blood by simple onstrates the relationship between partial pressure of oxy- According to Fick’s law, O2
gen and hemoglobin saturation.
diffusion.2,4 and CO2 move between sys-

RESPIRATORY SYSTEM ■ FICK’S LAW ■ OXYHEMOGLOBIN DISSOCIATION CURVE

Compendium July 1999 20TH ANNIVERSARY
temic capillary blood and cells by simple diffusion just
as they move between the pulmonary capillary blood
and alveolar gas in the lungs.2 O2 delivery is defined as
the amount of O2 delivered to a peripheral tissue each
minute and is the product of CaO2 and cardiac out-
put.2,4 O2 delivery can be maintained in patients with
low CaO2 by increasing cardiac output, assuming car-
diac function is normal.2,4 O2 utilization is the amount
of O2 consumed by tissue per minute and can be calcu-
lated by determining the difference between arterial
and venous O2 contents.2,4 Some toxic substances inter-
fere with the ability of tissue to use available O2; an ex-
ample is cyanide, which prevents the use of O2 by cy-
tochrome oxidase. In this case, the O2 concentrations of
arterial and venous blood are high and the O2 utiliza-
tion by the tissue is extremely low.2
PATHOPHYSIOLOGY OF HYPOXEMIA
Arterial partial pressure of O2 is considered abnor-
mally low if its value is less than 75 mm Hg, which at
37˚C, corresponds to an SaO2 of approximately 95%.2,7
Because of the shape of the oxyhemoglobin dissociation
curve, PaO2 levels of 60 to 75 mm Hg maintain ade-
quate hemoglobin saturation and whole blood O2 con-
tent under normal conditions.5,8 A PaO2 below 60 mm
Hg causes stress to a patient,8,9 and subsequent reduc-
tions in PaO2 will lead to significant decreases in oxyhe-
moglobin.8–10
Inadequate blood oxygenation may result from a low
fraction of inspired O2 (FIO2), hypoventilation, diffu-
sion impairment, shunt, or ventilation/perfusion (V/Q)
mismatch.2,4 Hypoxemia caused by low FIO2 has been
associated with anesthetic equipment failure or mal-
function, nitrous oxide use, and high altitude.3,9–11
Hypoventilation occurs when there is inefficient gas
exchange between the atmospheric air and the alveoli.4
Causes of hypoventilation include those related to cen-
tral respiratory depression and abnormalities affecting
the respiratory apparatus.9,12 Central nervous system
(CNS) depression has been associated with CNS and
cervical spinal cord trauma; anesthetic drug overdose;
and tumors, granulomas, or abscesses of the brain.9,12
Respiratory apparatus abnormalities include upper air-
way occlusion, bronchial spasm (e.g., anaphylaxis, asth-
ma), pleural space disease (e.g., pneumothorax, pleural
effusion, flail chest), thoracic pain, severe abdominal
distention (e.g., gastric dilation, ascites), and neuro-
muscular disease (e.g., myasthenia gravis, botulism,
tetanus, organophosphate toxicity).10,11,13,14 Hypoventi-
lation-induced hypoxemia may be alleviated by O2 sup-
plementation, but ventilatory support and correction of
the underlying cause are necessary to reestablish eucap-
nia.4,15–17
OXYGEN DELIVERY ■ FRACTION OF INSPIRED OXYGEN ■ VENTILATION/PERFUSION MISMATCH
Small Animal/Exotics
Impaired gas exchange results in a PaO2 that is sub-
stantially lower than the PO2 in the alveoli2,4; ventilatory
compensation by the respiratory control system usually
maintains normal or even decreased PaCO2 during such
conditions. 4 The three basic mechanisms of gas ex-
change impairment are diffusion barrier impairment,
shunt, and V/Q mismatch.2,4,9
Diffusion barrier impairment is caused by pulmonary
diseases that decrease the area or increase the thickness
of the alveolar–arterial membrane, such as interstitial
pulmonary edema, pulmonary interstitial fibrosis, and
chronic emphysema.18,19 The physiologic efficiency of
the lungs makes true diffusion barrier impairment an
uncommon cause of hypoxemia because pathologic
changes must be very advanced to significantly decrease
PaO2.9 This disorder is highly responsive to O2 supple-
mentation.9
Shunt occurs when venous blood bypasses gas-ex-
change areas of the lungs and mixes with oxygenated
arterial blood (venous admixture). This cause of hypox-
emia accompanies many types of lung diseases, such as
right-to-left cardiac shunt, pneumonia, cardiogenic and
noncardiogenic alveolar pulmonary edema, and lung
atelectasis.2 Shunts are typically poorly responsive to
O2; however, in patients with severe hypoxemia, small
increases in PaO2 may significantly increase blood O2
content and hence peripheral O2 delivery.19 This occurs
because, at extreme degrees of shunting, PaO2 values
correlate to the rapidly changing portion of the oxyhe-
moglobin dissociation curve.19
Ventilation/perfusion mismatch occurs when alveolar
ventilation and blood flow are not closely matched; this
results in inefficient gas exchange and hypoxemia.2,4
V/Q mismatch is a frequent cause of hypoxemia in ani-
mals with pulmonary thromboembolism, acute respira-
tory distress syndrome, alveolar pulmonary edema,
pulmonary contusions, pulmonary neoplasia, and
pneumonia.10,14,17–19 A high V/Q mismatch (e.g., pul-
monary thromboembolism) is seen when regions of the
lung are ventilated but not perfused, causing an in-
crease in the physiologic dead space of the lung; pa-
tients with high V/Q mismatches typically respond well
to O2 supplementation.2,4,6 In contrast, a low V/Q mis-
match (e.g., pulmonary contusion) occurs when re-
gions of the lung are perfused but not ventilated; the
functional result is a pulmonary shunt. Low V/Q mis-
matches respond poorly to O2 therapy.2,4,6
INDICATIONS
Oxygen therapy is indicated in patients with clinical
conditions associated with hypoxia (see Indications for
Oxygen Therapy). Hypoxia is caused by hypoxemia,
decreased tissue blood flow, reduced O2-carrying capac-
Small Animal/Exotics 20TH ANNIVERSARY Compendium July 1999

ity of erythrocytes, or increased de-

mand for O2 by tissue.2–4,9–14 Dimin- Indications for Oxygen Therapy
ished O2 delivery to tissue occurs in
cases of generalized decreased tissue Hypoxemia
blood flow (e.g., congestive heart Low fraction of inspired oxygen Diffusion impairment
failure, shock, cardiopulmonary Anesthesia accident Interstitial pulmonary edema
arrest) or local vascular obstruc-
High altitude Pulmonary interstitial fibrosis
tion.20,21 Anemia and hemoglobin
Chronic emphysema
abnormalities (e.g., carboxyhemo-
Ventilation/perfusion mismatch
globinemia, methemoglobinemia)
Pulmonary thromboembolism Hypoventilation
reduce the ability of hemoglobin to
22–24 Acute respiratory distress Central nervous system depression
carry O2. Increased tissue O2 de-
mand occurs in hyperthermia (e.g., syndrome Upper airway obstruction
fever, heat stroke, malignant hyper- Alveolar pulmonary edema Bronchial spasm (anaphylaxis)
thermia), sepsis, and seizures. 3,25–27 Pulmonary contusion Pleural filling defect
Clinical signs of hypoxia include Pulmonary neoplasia Thoracic pain
cyanosis, tachypnea, dyspnea, tachy- Pneumonia Abdominal distention
cardia, psychomotor incoordina- Neuromuscular disease
tion, gastrointestinal upset, and rest- Shunt
lessness.10,11,13,14 Although cyanosis Right-to-left cardiac shunt
indicates the need for O2 therapy, at Atelectasis
least 5 g/dl of deoxygenated hemo-
globin in the circulating blood is Decreased oxygen delivery
necessary for it to be apparent.2,4,10 Reduced blood flow
Anemia
Patients suffering from anemia or
Congestive heart failure
carbon monoxide poisoning may Hemoglobin malfunction Cardiovascular shock
not appear cyanotic but will usually
Carboxyhemoglobin Vascular obstruction
benefit from O2 therapy.28,29 Ancil-
Methemoglobin
lary tests, such as arterial blood gas
analysis, pulse oximetry, and alveo-
Increased oxygen demand
lar–arterial O 2 tension difference
(i.e., A-a gradient), help support the Hyperthermia Sepsis
presence of hypoxemia or hypoxia.3 Fever
Oxygen therapy is beneficial in Heat stroke Seizures
treating patients with craniocerebral Malignant hyperthermia
trauma,10,11,13,30–33 which may experi-
ence cerebral ischemia caused by in- Head trauma
creased intracranial pressure and
subsequent reduction in cerebral per-
fusion. This results in increased cerebral PCO2 and de- In most clinical situations, an FIO2 of 30% to 40%
creased cerebral PO2, which cause an increase in cerebral provides adequate hemoglobin saturation and is consid-
blood flow and further increases in intracranial pres- ered safe.34,35 As a general rule, the delivered O2 concen-
30,32,33
sure. Although hyperventilation has been the major tration should not exceed 50% for more than 24 hours
therapeutic approach to craniocerebral trauma patients, or complications associated with O2 toxicity may devel-
O2 supplementation is essential to ensure adequate cere- op.2,34,36 However, patients should not be deprived of
31–33
bral O2 delivery. higher concentrations of O2 if necessary to maintain an
adequate PaO2, especially during the initial stabilization
OXYGEN ADMINISTRATION TECHNIQUES period.2,34,36 If 100% inspired O2 fails to increase the
Several techniques for O2 supplementation are avail- PaO2 to a minimum of 60 mm Hg or if the PaCO2 is
able. Selection of the appropriate delivery method de- unacceptably high, mechanical ventilatory support
pends on the animal’s primary problem, desired FIO2, must be incorporated into the therapeutic plan.8,15,16
anticipated treatment duration, available equipment, Humidification is recommended when O2 supple-
and patient size and temperament. mentation is delivered for more than a few hours and is

ANCILLARY TESTS ■ CRANIOCEREBRAL TRAUMA ■ OXYGEN CONCENTRATION

Compendium July 1999 20TH ANNIVERSARY Small Animal/Exotics

particularly important when mately 2 cm from a patient’s

the upper respiratory tract is nose creates an area of in-
bypassed (e.g., O2 delivery creased O 2 concentration
via intratracheal catheter or around the animal’s muz-
tracheostomy tube). 10,11,36 zle.37 Although wasteful, this
Administration of dry gases technique offers the advan-
dehydrates mucosae, in- tage of being an easy method
creases mucosal secretion for immediate O2 adminis-
viscosity, degenerates respi- tration and is well tolerated
ratory epithelium, impairs by most patients (Figure 3).
mucociliary apparatus func- Clinical studies have shown
tion, and increases the risk that O2 flow rates of 2 to 3
of infection.4,11 Humidifica- Figure 2—The face mask technique is used for emergencies L/min can achieve an FIO2
tion can be accomplished by and short-term oxygen administration. of 25% to 40%.37
delivering O2 through a poly-
ethylene tube submerged in Elizabethan Collar
a bottle partially filled with Canopy
sterile saline solution. The The Elizabethan collar
humidified O 2 from the canopy is created by placing
space above the solution is an Elizabethan collar snugly
collected by a second poly- around the neck and secur-
ethylene tube and delivered ing an O2 line along the ani-
to the patient. mal’s neck, with the tip
placed inside the collar. The
Face Mask front of the collar is then
Oxygen administration via covered with cellophane, and
a face mask is well suited for a small vent hole is made in
short-term O 2 delivery in the cellophane to help elim-
emergency situations and inate the warm, humid ex-
for evaluation of the effec- pired air (Figure 4). The
tiveness of supplemental O2 Figure 3—The flow-by technique provides emergency oxygen FI O 2 achieved inside the
in equivocal cases. Tank O2 administration for critically ill, stressed patients. canopy depends on a variety
regulated through a flow of factors, including the
meter may be used as an O2 source. Alternatively, an tightness of the collar, size of the vent hole, size of the
anesthetic machine with either a circle rebreathing sys- patient, and respiratory rate. Although this method is
tem or nonrebreathing circuit can provide a method for effective, economic, and easy to set up, disadvantages
O2 delivery. The nonrebreathing circuit allows CO2 re- include O2 leakage, hyperthermia, high humidity, CO2
moval if adequate O2 flow is used. Ophthalmic oint- retention, and lack of patient cooperation. Clinical
ment should be applied periodically to prevent corneal studies in healthy, anesthetized dogs using an O2 flow
desiccation. The face mask technique can be initiated rate of 0.75 to 1 L/min have documented an FIO2 of
immediately, requires minimal set up and equipment, is 30% to 40%.38 In clinical situations, however, an ini-
easy to use, and allows convenient access to patients. tially high O2 flow rate is recommended to quickly fill
Many animals may not tolerate the mask, and constant the canopy with O2, followed by an O2 flow rate of 2 to
supervision is required (Figure 2). Clinical studies in 5 L/min to ensure adequate O2 delivery.
healthy, anesthetized dogs using well-fitting masks with
an O2 flow rate of 0.5 L/min have documented an FIO2 Nasal Catheter Delivery
of 40% to 50%.37 However, a loose-fitting mask and an To use a nasal catheter O2 delivery system, topical
O2 flow rate of 2 to 5 L/min will ensure minimal re- anesthetic (e.g., 2% lidocaine, proparacaine) is instilled
breathing of exhaled CO2 and entrainment of room air into one nostril and a lubricated, soft rubber catheter
if needed to meet peak inspiratory demands of the patient. (5 to 10 Fr, depending on the size of the animal) with
multiple fenestrations at the distal end is introduced
Flow-By through the naris into the ventral meatus. The catheter
Holding the end of an O2 delivery source approxi- is advanced to the level of the carnassial tooth, and the

HUMIDIFICATION ■ NONREBREATHING CIRCUIT ■ FLOW RATES

Small Animal/Exotics 20TH ANNIVERSARY Compendium July 1999

remainder is attached to the attached to a humidified O2

dorsum of the nose and head source.39 This method is in-
with sutures or an adhesive expensive, efficient, and well
agent (e.g., cyanoacrylate).35 tolerated; provides continu-
To avoid inflammation of ous O2 administration; and
the mucosa, nasal catheters allows easy access to the pa-
should be changed every 24 tient. Intratracheal catheters
to 48 hours and replaced in are invasive and more diffi-
alternate naris.35 cult to place than are in-
This mode of O2 adminis- tranasal catheters and, al-
tration allows free access to though less irritating than
the patient and is one of the nasal catheters, have been
most efficient, convenient, associated with tracheitis.36,39
cost-effective, and well-tol- Other potential disadvan-
erated methods available Figure 4—The Elizabethan collar canopy is used for tempo- tages include kinking of the
(Figure 5). Nasal catheteri- rary oxygen therapy. catheter at the skin entry
zation is primarily used for site and subcutaneous insuf-
prolonged O 2 therapy, but flation of O2 caused by cath-
ease of application makes it eter misplacement. An O 2
a suitable short-term option flow rate of 50 ml/kg/min
for animals that will not tol- has been recommended to
erate a face mask. The FIO2 achieve an FIO2 of 40% to
achieved by this method 60%.36
varies considerably depend-
ing on the patient’s size, res- Oxygen Cage
piratory rate, and extent to The oxygen cage method
which the animal is mouth of delivery requires a sealed
breathing. Disadvantages in- compartment with mecha-
clude serous nasal discharge nisms to regulate O2 concen-
production, jet damage tration and ambient tem-
(caused by high flow of O2) perature and humidity as
to the nasal mucosa, and Figure 5—The nasal catheter delivery system is suitable for well as to eliminate expired
lack of patient tolerance. In prolonged oxygen therapy. CO2. This is a noninvasive
one report, a small dog de- system that allows accurate
veloped signs of gastric dila- monitoring and control of
tion secondary to high O2 flow rates.35 An O2 flow rate the environment (Figure 6). Major disadvantages in-
of 0.75 L/min reportedly produces an FIO2 of 30% to clude expense, O2 waste, and isolation of the patient
70% in healthy, anesthetized dogs.38 In clinical situa- from the clinician. Ambient temperature should be
tions, O2 flow rates of 100 to 150 ml/kg/min have been maintained at 22˚C (70˚F) with a relative humidity of
recommended to achieve an FIO2 of 30% to 50%.35,36 40% to 50%.10,13 It is generally difficult to maintain FIO2
concentrations greater than 40% to 50% when using
Intratracheal Catheter Delivery an oxygen cage.10,13
The area over the cricothyroid ligament, or the area
between two tracheal rings in larger dogs (i.e., those Mechanical Ventilation
weighing more than 10 kg [20 lb]), is clipped and sur- Ventilatory support is indicated in the presence of
gically prepared for intratracheal catheter placement. hypoventilation, high FIO2 requirements for extended
Local anesthesia of the skin is recommended, and asep- periods, respiratory fatigue or arrest, comatose states,
tic technique must be followed. A large-gauge, long, and increased intracranial pressure as well as when pas-
flexible catheter with a fenestrated distal end is inserted sive O 2 delivery fails to adequately correct hypox-
via a large-bore needle; the needle is withdrawn; and emia.15,16,30,31 A review of ventilatory techniques, such as
the catheter is advanced until the tip lies just cranial to positive end-expiratory pressure ventilation, continuous
the carina (at approximately the fifth intercostal space). positive-pressure ventilation, and intermittent positive-
The catheter is secured in place with a neck wrap and pressure ventilation, may be found in the literature.15,16

JET DAMAGE ■ TRACHEITIS ■ VENTILATORY SUPPORT

Compendium July 1999 20TH ANNIVERSARY Small Animal/Exotics

MONITORING ing a precise FI O 2 may be

RESPONSE TO THERAPY difficult with some methods
Arterial blood gases and of O2 delivery. In humans,
pulse oximetry are used to as- the Pa O 2:FI O 2 ratio should
sess pulmonary function and be greater than 300 in nor-
the patient’s response to O2 mal patients breathing room
supplementation and to help air.40,41 We consider a PaO2:
determine the lowest concen- FIO2 ratio greater than 200
tration of O 2 delivery that suggestive of a positive re-
prevents hypoxemia. Calcu- sponse to O2 supplementa-
lated A-a gradients and tion.41 Values for PaO2:FIO2
Pa O 2:FI O 2 ratios are useful ratio less than 100 suggest
tools to estimate the gas-ex- poor response to O2 therapy.40,41
change efficiency of the Pulse oximetry, which dis-
lungs.2,3,19 Figure 6—The oxygen cage provides a controlled environ- plays SaO and pulse rate val-
2
Blood gas analysis is the ment and is suitable for prolonged oxygen therapy. ues, provides objective as-
most accurate method to sessment of the need for O2
measure the degree of hypoxemia.9,19 Arterial blood gas supplementation and can be used to continuously mon-
analysis measures the amounts of O2 and CO2 in arteri- itor a patient during O2 administration.3,42 Although
al blood, reflecting the functional efficiency of the SaO2 is not linearly related to PaO2, it is an indirect mea-
lungs and response to O2 therapy.9 Major disadvantages sure of PaO2. As illustrated by the oxyhemoglobin disso-
of this analysis are difficulty in obtaining arterial blood ciation curve, SaO2 provides information about delivery
samples and availability and cost of the necessary tech- of O2 to tissue.3,9,19,42 Factors that interfere with accurate
3,9
nology. In healthy animals breathing room air (FIO2, SaO2 readings include tissue thickness and pigmentation,
21%), values for PaO2 and PaCO2 are 90 to 100 mm Hg decreased tissue perfusion, hypothermia, bilirubinemia,
and 35 to 45 mm Hg, respectively.3,9 anemia, and motion.3,42 Advantages of this method com-
The A-a gradient is calculated from arterial blood gas pared with blood gas analysis include continuous, im-
analysis and is a sensitive measure of gas-exchange effi- mediate, and noninvasive estimation of blood oxygena-
ciency (see Alveolar–Arterial Gradient Formula).2,19 The tion.42 Transmission probes can be placed on the digits,
A-a gradient formula allows clinicians to estimate the tongue, lips, or other nonpigmented mucous mem-
adequacy of O2 transfer from the alveolus to the pul- branes; reflectance probes are placed in the esophagus or
monary capillary blood in animals breathing room air at rectum, increasing the versatility of SaO2 monitoring.3
sea level. If the lung is perfectly homogeneous, there Pulse oximetry can be used in conjunction with arterial
should be no difference between the calculated A-a gra- blood gas measurements in critical patients to reduce
dient and the measured PaO2; any factor making gas ex- the number of blood samples needed.3 In the absence of
change less efficient will lead to a widening of the A-a arterial blood gas analysis, the limitations of pulse
gradient.19 The A-a gradient should be less than 10 mm oximetry must be recognized.3,42
9
Hg in normal animals breathing room air. An A-a gra- Clinical response to O2 administration provides an
dient of 15 mm Hg is indicative of decreased oxygenat- adequate evaluation of therapeutic efficacy in the ab-
ing efficiency of the lungs (venous admixture).2,9 Values sence of ancillary tests. Patients benefiting from O2
greater than 30 mm Hg sug- therapy should show im-
gest clinically significant im- proved mucous membrane
pairment of gas exchange and Alveolar–Arterial (A-a) Gradient Formula color, decreased heart rate,
the need for additional O 2 A-a gradient = P O – PaO decreased respiratory rate
A 2 2
supplementation.9 and effort, and reduced anxi-
Gas-exchange abnormali- = (FIO2 × [PB – PH2O] – 1.2 × PaCO2) – PaO2 ety.10,13
ties can also be reflected in = (0.21 × [760 – 47] – 1.2 × PaCO2) – PaO2 Analyzing arterial blood
the PaO2:FIO2 ratio.40,41 This = (150 – 1.2 × PaCO2) – PaO2 gases and pulse oximetry
ratio provides an assessment recorded while an animal is
of gas exchange similar to the FIO2 = fraction of inspired oxygen; PAO2 = alveolar partial breathing room air may help
pressure of oxygen; PaO2 = arterial partial pressure of
A-a gradient and is more eas- oxygen; PaCO = arterial partial pressure of carbon dioxide;
monitor progress and deter-
2
ily calculated from blood gas PB = barometric pressure; PH2O = vapor pressure of water. mine the ongoing need for
analysis40; however, determin- therapy.8,9 Discontinuation of

P a O 2: F I O 2 R A T I O ■ P U L S E O X I M E T R Y ■ C L I N I C A L R E S P O N S E
 Small Animal/Exotics Compendium July 1999

O2 therapy should be based on improvement of clinical

signs and resolution of the primary disease. It is recom-

CALL mended that patients be slowly weaned off O2 over 24 to

48 hours, using blood gas analysis and pulse oximetry for
objective evaluation.11,13

FOR COMPLICATIONS OF OXYGEN THERAPY

In patients with long-standing respiratory disease and
accompanying chronic hypercapnia, O2 supplementation

PAPERS
may occasionally suppress the respiratory drive. Hypox-

I
emia becomes the main stimulus for ventilation in these
animals because the sensitivity of the central chemore-
ceptors for hypercapnia is lost. In these patients, positive-
pressure ventilation may be required in addition to O2
Are you involved supplementation while attempts are made to diagnose
in research? and treat the underlying cause; however, the prognosis
for this type of condition is generally poor.6,17
Prolonged O2 therapy has been associated with sup-
pression of erythropoiesis, pulmonary vasodilation, and
Announcing a new forum for timely systemic arteriolar vasoconstriction.34,36 In dogs, micro-
publication of research results— scopic changes and initial signs of pulmonary dysfunc-
Veterinary Therapeutics: tion develop within 24 hours of constant exposure to
100% O2, with additional
Research in Applied MP
ENDIU
exposure to 100% O 2 re-
M’

20th

CO

Veterinary Medicine. A quarterly

S

9 - 1
9 9 9
sulting in death from respi-
1 9 7

journal dedicated to rapid ANNIVERSARY ratory failure in 2 to 3 days.34

publication, Veterinary
Therapeutics invites the submission
of clinical and laboratory research
manuscripts in small and large
animal medicine, including
pathophysiology, diagnosis,
treatment, and prognosis.
Prospective, retrospective, and
corroborative studies are all welcome.
Accepted articles are scheduled to be
published 90 to 120 days after
submission. Contact Toni Passaretti,
609-671-2022, email
tpassaretti.vls@medimedia.com.
Another fine publication from the
publisher of Compendium.
A LookBack
An increase in the number of
facilities that are able to
administer oxygen therapy plus
the emergence of noninvasive
and affordable advanced
monitoring equipment have
made oxygen supplementation a
useful and practical therapeutic
tool for general practitioners. prudent approach to O 2
Another important contribution
to the increasing awareness and
management of critically ill pets necessary to provide an ad-
is the recognition and
promotion of emergency and
critical care medicine as a
specialty within veterinary
medicine. (Photo: Drs. Camps-
Palau [left] and Marks.)
Inspiration of 30% to 50%
O2 does not cause perma-
nent changes, but there is
some evidence of increased
permeability of the alveolar
and bronchiolar epithelia.43
Conversely, brain malacia
from hypoxemia reportedly
occurs before the onset of
lung damage induced by
prolonged exposure to high
O2 tensions.30,33,34 The most
supplementation is to use
the lowest possible FI O 2
equate beneficial effect.
SUMMARY
Oxygen therapy is easy
to administer, readily avail-
able, and relatively safe if
used judiciously. Optimiz-
ing O2 delivery to tissue is
imperative in a number of
clinical conditions in which
hypoxia plays an important

DISCONTINUING THERAPY ■ PROLONGED THERAPY

Compendium July 1999 20TH ANNIVERSARY
role. It is important to understand the physiology of O2
uptake and delivery to recognize patients that will ben-
efit from O2 supplementation.
Several techniques for O2 administration are available
and can be adapted to specific clinical situations and
patient conditions. O2 therapy is an important adjunc-
tive therapy but is not without complications and must
be used judiciously.
Arterial blood gases, A-a gradients, PaO2:FIO2 ratio,
and pulse oximetry are used to assess patient response
to O2 supplementation and help determine the lowest
concentration of O2 delivery that prevents hypoxemia.
In the absence of ancillary tests, clinical evaluation of
the patient is an appropriate diagnostic tool to assess re-
sponse to O2 and monitor cessation of therapy.
As a guideline for prolonged supplementation of O2,
administration of 40% to 50% O2 is generally safe, but
patients should not be deprived of higher concentra-
tions of O2 if necessary to maintain adequate PaO2.36
Continual patient assessment is essential; with resolu-
tion of the primary problem, O2 therapy may be dis-
continued gradually.
ACKNOWLEDGMENTS
The authors thank Dr. Jamie Williams for his en-
couragement and critique of the manuscript and Dr.
Giselle L. Hosgood for her help with the figures.
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About the Authors
Drs. Camps-Palau, Marks, and Cornick are affiliated with
the Department of Veterinary Clinical Sciences, School of
Veterinary Medicine, Louisiana State University, Baton
Rouge, Louisiana. Drs. Marks and Cornick are Diplo-
mates of the American College of Veterinary Internal
Medicine; Dr. Cornick is also a Diplomate of the American
College of Veterinary Anesthesiologists.