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Small Animal Oxygen Therapy

Small Animal Oxygen Therapy

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Vol. 21, No. 7July 199920TH ANNIVERSARY
Refereed Peer Review
FOCAL POINTKEY FACTS
5
Oxygen (O
2
) therapy optimizesblood O
2
content, helps increaseO
2
delivery to tissue, anddecreases the ventilatory andmyocardial work necessary tomaintain adequate tissueoxygenation.
Small AnimalOxygen Therapy 
Louisiana State University 
Maria A. Camps-Palau, DVMSteven L. Marks, BVSc, MS, MRCVS Janyce L. Cornick, DVM, MS
ABSTRACT:
Oxygen (O
2
) therapy is easy to administer, readily available, and relatively safe ifused judiciously. Optimizing O
2
delivery to tissue is imperative in clinical conditions character-ized by hypoxia. It is important to understand the physiology of O
2
uptake and delivery to rec-ognize those patients that will benefit from O
2
supplementation. Several O
2
administrationtechniques are available and can be adapted to every clinical situation and patient condition. O
2
therapy is an important adjunctive therapy but is not without complications and thus must beclosely monitored.
H
 ypoxia 
is a broad term that means decreased levels of oxygen (O
2
) in air,blood, or tissue.
1
Clinically, hypoxia is defined as inadequate supply of O
2
to the body’s tissue and can result from insufficient blood oxygena-tion(i.e., hypoxemia), reduced O
2
-carrying capacity of erythrocytes, decreasedtissue blood flow, increased tissue demand for O
2
, or impaired tissue extractionof O
2
.
2,3
Oxygen is easy to administer, readily available, and relatively safe. Supple-mentation with O
2
increases blood O
2
content, minimizes detrimental effectsof hypoxemia, and decreases ventilatory and myocardial work necessary tomaintain tissue O
2
delivery.
4,5
Therapeutic considerations in animals with ab-normalities that increase O
2
demand or decrease O
2
delivery to tissue includecorrection of the underlying problem and maintenance of adequate tissue oxy-genation. When evaluating patients that may benefit from O
2
therapy, understandingrespiratory and O
2
-transport physiology is necessary to formulate a rational diag-nostic and therapeutic plan. When O
2
delivery to tissue is inadequate, cells mustuse alternate anaerobic pathways to maintain their metabolism. Anaerobicmetabolism causes rapid depletion of energy and accumulation of lactic acid within cells, leading to cellular dysfunction and death.
4,6
This article discussesthe physiology of respiration and O
2
uptake and delivery, indications for O
2
sup-plementation, methods of O
2
administration, and criteria to assess response toO
2
therapy.
RESPIRATORY PHYSIOLOGY
The major function of the respiratory system is to exchange O
2
and carbon
CE
V
s
The five causes of hypoxemiaare low fraction of inspired O
2
(FI
O
2
), hypoventilation, diffusionbarrier impairment, shunt, andventilation/perfusion mismatch.
s
As a general rule, the delivered O
2
concentration should not exceedan FI
O
2
of 50% for more than24 hours or complicationsassociated with O
2
toxicitymay develop.
s
Delivered O
2
should be humidifiedwhen supplementation isrequired for more than a fewhours or if the upper respiratoryairways are bypassed.
s
Arterial blood gas analysis,alveolar–arterial O
2
tensiondifference, arterial partialpressure of O
2
:FI
O
2
ratio, andpulse oximetry are ancillary teststhat support the need for andhelp to monitor response to O
2
therapy.
 
dioxide (CO
2
) between bloodand inspired air to maintainnormal arterial partial pres-sures of O
2
(Pa
O
2
) and CO
2
(Pa
CO
2
). The O
2
pathway canbe divided into four majorfunctions
pulmonary gasexchange, diffusion of gasesbetween alveoli and blood,transport of gases to and fromcells, and regulation of venti-lation.
2,4
Despite the variable demands of the body, the respi-ratory control system maintains Pa
O
2
and Pa
CO
2
 withina narrow homeostatic range. The basic components of the respiratory control system are the central and pe-ripheral chemoreceptors, medullary respiratory center,and muscles of respiration.
2
Under normal conditions,the primary driving forces for alveolar ventilation arehypercapnia (sensed by the central chemoreceptors inthe brain stem) and, to a lesser degree, hypoxemia(sensed by the peripheral chemoreceptors in the aorticarch and carotid bodies).
2,4
The respiratory system consists of the anatomic deadspace and the respiratory zone. The anatomic dead space(i.e., respiratory airways)includes the upper airways and aseries of branching tubes from the trachea to the termi-nal bronchioles that lead inspired air to the gas-exchang-ing regions of the lungs. The respiratory zone (i.e., alveo-lated regions) of the lungs is where gas exchange occurs. Alveolated regions that are ventilated but not perfusedconstitute the physiologic dead space.
2,4
 At the blood
gas interface, the pulmonary capillariesform a dense network in thealveolar walls and have diame-ters just large enough for a sin-gle erythrocyte to pass.
2
Therate and direction of gas move-ment are based on pressuregradients and follow Fick 
s law, which states that the amountof gas moving through a sheetof tissue is proportional to thearea of that sheet and inversely proportional to its thickness.
2
The blood
gas barrier com-prises a large surface area of capillaries wrapping aroundthe alveoli and is extremely thin, thus maximizing exchangeof O
2
and CO
2
between alveoliand capillary blood by simplediffusion.
2,4
PHYSIOLOGY OFOXYGEN UPTAKEAND DELIVERY
Oxygen is carried in theblood in either the dissolvedstate or bound to hemoglo-bin (oxyhemoglobin).
2,4
 Arte-rial O
2
content (Ca
O
2
) is theamount of oxyhemoglobinplus the O
2
dissolved in plas-ma (see Arterial OxygenContent Formula).
6
The contribution of dissolved O
2
tooverall Ca
O
2
is relatively small because most O
2
travels asoxyhemoglobin.
2,4
Tissue hypoxia can result from de-creased Ca
O
2
even in patients that maintain normalPa
O
2
values. Causes of decreased Ca
O
2
include anemiaand hemoglobin abnormalities.
2,4
The sigmoid shape of the oxyhemoglobin dissocia-tion curve (Figure 1) demonstrates that the amount of O
2
bound to hemoglobin increases rapidly up to a par-tial pressure of O
2
(P
O
2
) of approximately 50 mm Hg;however, the rate of O
2
uptake decreases at higher P
O
2
values. Arterial hemoglobin saturation (Sa
O
2
) at a Pa
O
2
of 100 mm Hg is 97.5%, whereas mixed venous blood with a P
O
2
of 40 mm Hg has a hemoglobin saturation(S
O
2
) of approximately 75%.
2,4
The plateau portion of the oxyhemoglobin dissocia-tion curve illustrates that a decrease in Pa
O
2
results inminimal changes in the oxygenation of erythrocytes. Incontrast, the steep lower part of the curve indicates thatsmall drops in capillary P
O
2
allow peripheral tissue toreceive large amounts of O
2
from erythrocytes. A right shift of the oxyhemoglobin dissociation curvedecreases the affinity of hemo-globin for O
2
, thereby facilitat-ing O
2
release because a higherPa
O
2
is necessary to load hemo-globin with O
2
. Right shifts areseen with acidosis (Bohr effect),hypercapnia, hyperthermia, orincreases in erythrocyte 2,3-diphosphoglycerate (2,3-DPG)concentration.
2,4
 A left shift of the curve increases the affinity of hemoglobin for O
2
, whichmeans the Pa
O
2
must drop low-er for hemoglobin unloading of O
2
to occur. Left shifts occur with alkalosis, hypocapnia, hy-pothermia, methemoglobine-mia, or 2,3-DPG deficiency.
2,4
 According to Fick 
s law, O
2
and CO
2
move between sys-
Small Animal/Exotics20TH ANNIVERSARY
Compendium 
July 1999
RESPIRATORY SYSTEM
s
FICK
S LAW
s
OXYHEMOGLOBIN DISSOCIATION CURVE
Ca
O
2
= Oxyhemoglobin + Dissolved O
2
Ca
O
2
(ml O
2
 /dl) =(Sa
O
2
[%]
×
Hemoglobin [g/dl]
×
1.34 [ml O
2
 /g]) +(Pa
O
2
[mm Hg]
×
0.003 [ml O
2
 /dl/mm Hg])
Ca 
= arterial oxygen content;
= oxygen;
Pa 
= arterialpartial pressure of oxygen;
Sa 
= arterial hemoglobinsaturation.
Arterial Oxygen Content Formula
100755025255075100
Oxygen Tension (P
O
2
; mm Hg)
Steep PhasePlateau Phase
    H   e   m   o   g    l   o    b    i   n    S   a   t   u   r   a   t    i   o   n    (    S
    O
    2
   ;    %    )
Figure 1—
The oxyhemoglobin dissociation curve dem-onstratesthe relationship between partial pressure of oxy-genand hemoglobin saturation.
 
temic capillary blood and cells by simple diffusion justas they move between the pulmonary capillary bloodand alveolar gas in the lungs.
2
delivery 
is defined asthe amount of O
2
delivered to a peripheral tissue eachminute and is the product of Ca
O
2
and cardiac out-put.
2,4
O
2
delivery can be maintained in patients withlow Ca
O
2
by increasing cardiac output, assuming car-diac function is normal.
2,4
utilization 
is the amountof O
2
consumedby tissueper minute and can be calcu-lated by determining the difference between arterialand venous O
2
contents.
2,4
Some toxic substances inter-fere with the ability of tissue to use available O
2
; an ex-ample is cyanide, which prevents the use of O
2
by cy-tochrome oxidase. In this case, the O
2
concentrations of arterial and venous blood are high and the O
2
utiliza-tion by the tissue is extremely low.
2
PATHOPHYSIOLOGY OF HYPOXEMIA
 Arterial partial pressure of O
2
is considered abnor-mally low if its value is less than 75 mm Hg, which at37
˚
C, corresponds to an Sa
O
2
of approximately 95%.
2,7
Because of the shape of the oxyhemoglobindissociationcurve, Pa
O
2
levels of 60 to 75 mm Hg maintain ade-quate hemoglobin saturation and whole blood O
2
con-tent under normal conditions.
5,8
 A Pa
O
2
below 60 mmHg causes stress to a patient,
8,9
and subsequent reduc-tions in Pa
O
2
 will lead to significant decreases in oxyhe-moglobin.
8
10
Inadequate blood oxygenation may result from a low fraction of inspired O
2
(FI
O
2
), hypoventilation, diffu-sion impairment, shunt, or ventilation/perfusion (V/Q)mismatch.
2,4
Hypoxemia caused by low FI
O
2
has beenassociated with anesthetic equipment failure or mal-function, nitrous oxide use, and high altitude.
3,9
11
Hypoventilation occurs when there is inefficient gasexchange between the atmospheric air and the alveoli.
4
Causes of hypoventilation include those related to cen-tral respiratory depression and abnormalities affectingthe respiratory apparatus.
9,12
Central nervous system(CNS) depression has been associated with CNS andcervical 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, pleuraleffusion, flail chest), thoracic pain, severe abdominaldistention (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 O
2
sup-plementation, but ventilatory support and correction of the underlying cause are necessary to reestablish eucap-nia.
4,15
17
Impaired gas exchange results in a Pa
O
2
that is sub-stantially lower than the P
O
2
in the alveoli
2,4
; ventilatory compensation by the respiratory control system usually maintains normal or even decreased Pa
CO
2
during suchconditions.
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 thicknessof the alveolar
arterial membrane, such as interstitialpulmonary edema, pulmonary interstitial fibrosis, andchronic emphysema.
18,19
The physiologic efficiency of the lungs makes true diffusion barrier impairment anuncommon cause of hypoxemia because pathologicchanges must be very advanced to significantly decreasePa
O
2
.
9
This disorder is highly responsive to O
2
supple-mentation.
9
Shunt occurs when venous blood bypasses gas-ex-change areas of the lungs and mixes with oxygenatedarterial blood (venous admixture). This cause of hypox-emia accompanies many types of lung diseases, such asright-to-left cardiac shunt, pneumonia, cardiogenic andnoncardiogenic alveolar pulmonary edema, and lungatelectasis.
2
Shunts are typically poorly responsive toO
2
; however, in patients with severe hypoxemia, smallincreases in Pa
O
2
may significantly increase blood O
2
content and hence peripheral O
2
delivery.
19
This occursbecause, at extreme degrees of shunting, Pa
O
2
valuescorrelate to the rapidly changing portion of the oxyhe-moglobindissociation curve.
19
Ventilation/perfusion mismatch occurs when alveolarventilation and blood flow are not closely matched; thisresults 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, andpneumonia.
10,14,17
19
 A high V/Q mismatch (e.g., pul-monary thromboembolism) is seen when regions of thelung 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 wellto O
2
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; thefunctional result is a pulmonary shunt. Low V/Q mis-matches respond poorly to O
2
therapy.
2,4,6
INDICATIONS
Oxygen therapy is indicated in patients with clinicalconditions associated with hypoxia (see Indications forOxygen Therapy). Hypoxia is caused by hypoxemia,decreased tissue blood flow, reduced O
2
-carrying capac-
Compendium 
July 199920TH ANNIVERSARYSmall Animal/Exotics
OXYGEN DELIVERY
s
FRACTION OF INSPIRED OXYGEN
s
VENTILATION/PERFUSION MISMATCH

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