Respiratory Monitoring: Arterial Blood Gas

Analysis, Pulse Oximetry, and End-tidal

Carbon Dioxide Analysis
Jeffrey Proulx

The use of arterial blood gas analysis, pulse oximetry, and patient status. Repeated blood gas analysis may also be
capnography has become commonplace in the assessment of necessary to evaluate the response to treatment.
vetennary patients. Blood gas analys~s allows for the quahtat~ve
and quantitative assessment of both metabolic and respiratory
acid-base problems, including the interrelationships between Arterial Blood Gas Sampling
ventilation, oxygenation, and metabohc conditions. Blood gas
analys~s is a useful adjunct to clinical patient assessment and To accurately assess respiratory function, especially oxygen-
other diagnostms in determining appropriate therapy for specific ation, arterial sampling is necessary. The ease of arterial blood
and complex conditions. Both pulse oximetry and capnography gas sampling depends on operator experience and patient size
are useful monitoring tools. However, they have technical and stability. Patients requiring supplemental oxygen should
hmitations and cannot comprehensively evaluate patient never be held off oxygen to collect a better sample. Evaluation
oxygenation and ventilation. Pulse oxlmetry and capnography are is sull possible regardless of oxygen supplementation. Obtain-
not replacements for arterial blood gas analysis, but rather serve mg a blood gas sample should never supersede stability in a
as adjunctive monitoring tools. strugghng or markedly dyspneic patmnt.
Copyright © 1999 by W.B. Saunders Company
In dogs, the site of arterial puncture usually includes the
femoral or dorsal pedal arteries, although the radial artery or
digital palmar arches may be used. In cats, the femoral artery is
bjective evaluation of the respiratory system is helpful m
O the medical management of small animal patients with
critical illnesses. Monitoring is useful for following trends m
usually the only vessel large enough to be successfully sampled.
After arterial puncture, direct pressure should be applied to the
site for 2 to 5 minutes. Patients with low platelets and/or
individual ammals, as well as for assessing the severity of a coagulopathy should not undergo arterial puncture. The pa-
&sease. Available methods include arterial blood gas analysis, tient should be restrained, and the site of the puncture should
pulse oximetry, and end-tidal carbon dioxide monitoring be wiped with 70% isopropyl alcohol. A 45 ° to 90 ° angled
(capnography). arterial puncture is usually adequate. The vessel is palpated to
envision its location. The needle should be withdrawn to the
Arterial Blood Gas Analysis subcutaneous level before redirecting after a negative punc-
ture. Patients requiring repeated arterial blood gas sampling
With the advent of portable and relatively inexpensive blood may benefit from arterial catheterization to minimtze the stress
gas analyzers, analysis of blood gases has become common- of repeated arterial samples. To prevent sample clotting, the
place in the evaluation of veterinary patients. With correct syringe should be preheparmized. The sample should be
interpretation, blood gas analysis permits the quantification of capped with nongas-permeable material to prevent equilibra-
clinical metabohc acid-base and respiratory disorders. It also tion with room air. Samples not processed within 5 to I0
permits differentiation of metabolic, ventilation (carbon diox- minutes should be refrigerated to decrease white cell and red
ide), and oxygenation (oxygen) problems, enabling specific cell metabolism with consequent changes in blood gas values.
decisions to be made regarding appropriate diagnosis and
therapy. Although nonlnvasive monitoring devices such as
pulse oximetry and end-tidal carbon dioxide analysis will often Oxygenation
decrease the need for multiple arterial blood gas sampling,
Discussion about arterial blood gas analysis centers on an
these noninvasive methods have several limitations and cannot
understanding of oxygenation and ventilation. In the ideal
replace blood gas analysis. Thmr use is meant to complement
lung, oxygenation of arterial blood would occur by uninhibited
blood gas analysis and involves monitoring for changes in
diffusion, perfectly matched ventilation and pulmonary perfu-
slon (WQ) at all alveoli, the absence of shunt, and complete
equilibration of alveolar gas with pulmonary capillary blood.
From Critical Care Services, Dove Lewis Emergency Animal Hospital, The P02 of the inspired air at sea level is 150 mmHg. However,
Portland, OR. the actual alveolar pamal pressure of oxygen (Pa02) is depen-
Address reprint requests to Jeffrey Proulx, DVM, Cntical Care Services, dent on other factors including alveolar ventilation and the
Dove Lewis Emergency Animal Hospital, 1984 NW Pettygrove, Portland,
OR 97209. rate of the removal of 02 by the pulmonary capillary bed. The
Copyright © 1999 by W.B. Saunders Company alveolar gas equation may be used to calculate the apprommate
1096-2867/99/1404-0006510 00/0 Pa02.

Clinical Techmques in Small Animal Practice, Vol 14, No 4 (November), 1999 pp 227-230 227
Alveolar Gas Equation: 4. Hypoventilation: Reduced alveolar ventilation will result in
hypoxemia. Important causes for hypoventilation include
PAO2 = [(PB -- PH20) FIO2] - (Paco2/RQ)
anesthesia, severe neuromuscular disease, pleural space
= [(760 - 47) 0.21] - (40/0.8) = 100 mmHg 02 disease, chest wall disease, among others. The hypoxemia
of hypoventilation will respond to oxygen, though is better
PB = barometric pressure in mmHg; PH20 = water vapor
treated by increasing ventilation.
pressure in mmHg; FIo2 = fraction of inspired oxygen; RQ =
The actual oxygen delivery to tissues depends on several
respiratory quotient (normally 0.8); and Paco2 = partial
factors including cardiac output (dependent on heart rate and
pressure of COz in the alveolus in mmHg.
stroke volume), oxygen-carrying capacity (dependent on the
functional hemoglobin level), and oxygen tension (dependent
However, the normal animal will have arterial oxygenation
on cardiopulmonary function). This can best be illustrated by
occurring to a lesser degree than m the ideal lung. This occurs
the following formulas describing oxygen dehvery and the
because of a small degree of normal bronchial and pleural
oxygen content of blood.
shunting, unmatched ventilation and perfusion, and ventila-
tion of dead space. In the normal animal, with complete
Do 2 = CO X 10 X Cao 2
equilibrauon of pulmonary capillary blood with alveolar gas,
the arterial partial pressure of oxygen (Pa02) is 90 to 100 Cao 2 = (Hb in g/dL X 1.34 mL O2/g Hb X Sa02)
mmHg. The difference between the alveolar and arterial 02 is [Hb bound oxygen]
known as the alveolar-arterial gradient (A-a). The A-a gradient
may be used to assess the degree of pulmonary disease present. + (PaOz X 0.003 mL Oz/dL/mmHg02)
The normal A-a gradmnt is approximately 5 mmHg at an F~02 + [dissolved oxygen]
of 0.21. The A-a gradient will increase with right-to-left shunt,
low mixed venous oxygen saturation, ventilation/perfusion where: D o 2 = delivery of oxygen (mL/min); CO = cardiac
imbalance, and diffusion impairment. However, because the output (Idmin); S a o 2 = arterial hemoglobin saturation (%);
calculation of Pa02 incorporates CO2, hypoventilation will not C a o 2 = arterial content of oxygen (mL O2/dL blood)
affect the calculation of the A-a gradient. The A-a gradient will
be affected by increasing the F~02, and as a result, the A-a Based on the above equation, it is evident that deficient
calculatmn must be made on room air or at least at a consistent oxygen delivery can occur with decreases m hemoglobin and
]=10 2 value to make sequential comparisons of pulmonary cardiac output, as well as deficmncies in pulmonary function.
function in a specific patient. Any deficmncy in oxygenation caused by respiratory failure
The Pao2 may also be interpreted in relation to the inspired must be compensated by increases in cardiovascular work
fraction of oxygen (FIO2). In human medicine the ratio of Pao2 (increased heart rate and stroke volume) to maintain oxygen
to FIo~ is considered useful in assessing the seventy of the lung delivery and tissue oxygenation.
injury. The normal value is greater than 400, whereas a value of
less than 300 is considered to represent acute lung injury Ventilation
(ALl). A value of less than 200 represents acute respiratory
distress syndrome (ARDS). The carbon dioxide tension ( P c o 2 ) IS a value representing a
Hypoxemia refers to abnormally low values of Pao2. There balance between CO2 production and CO2 excretion at the
are four physiological causes of arterial hypoxemia. These alveolus; it also represents the mean alveolar COa tension
include the following: (Pac02). Carbon dioxide production increases with exercise
and increases in metabolic rate, and will also change according
1. True shunt: Blood enters the left side of the heart without to anabolic and catabolic states depending on the ratio of fat
any gas exchange occurring in the lungs. This results in versus carbohydrate metabolism and storage. To maintain
essentially venous blood being added directly to arterial respiratory acid-base balance, ventilation must be matched to
blood. Examples include extrapulmonary shunts such as the production of carbon dioxide. This occurs with increases
patent ductus artenosus (PDA), ventricular septal defect or decreases in alveolar minute ventilation.
(VSD), or intrapulmonary shunts such as occurs in atelectic Ventilation refers to the movement of gas into and out of the
or consolidated lung lobes. Chnically, this type of hypox- pulmonary conducting system and alveoli, with the primary
emia varies in seventy depending on the actual shunt purpose of carbon dioxide excretion and oxygen absorption.
fraction. Hypoxemia caused by true shunt is often not The determinant of carbon dioxide excretion depends on the
responsive to oxygen therapy. quantity of carbon dioxide delivered to the alveolus, alveolar
2. Ventilation/Perfusion mismatch: This indicates an imbal- ventilation, and amount of dead space not contributing to gas
ance between ventilation and perfusion in various regions
of the lung resulting in inefficient gas exchange. This is a
common cause of hypoxemia; it may result from all forms of
TABLE 1. The Normal Values for Arterial Blood Gases at
pulmonary disease. Hypoxemia from ventilation/perfusion
Sea Level
mismatch is responsive to oxygen therapy.
3. Diffusion impairment: This is reflected in a failure of pH 7.36-7.44
PO2 90-100 mmHg
equilibration between the pulmonary capillary blood and PCO2 36-40 mmHg
the alveolar gas. Diffusion impairment is relatively uncom- HCO3- 20-24 mEq/L
mon in veterinary patients but might be important in BE +4 mEq/L
pulmonary fibrosis. It will respond to oxygen supplementa- Abbreviations: mEq/L, milhequwalents/Dter;mmHg, millimetersof mer-
tion. cury; BE, base excess.

228 PROULX
 Respiratory Disorder pH Pco2 HCOa" BE
Respiratory Acidosis

Uncompensated $ 1" N N
Fig 1. Blood gas patterns
in respiratory disorders. Compensated SN 1" 1" 1"
The arrows indicate the di-
rection of the expected
change. Respiratory Alkalosis

Uncompensated 1" $ N N

Compensated I"N $ $ $

exchange. This can be expressed mathematically as the follow- excess of metabolic carbon dioxide producuon. Causes of
ing: alveolar hyperventilation include hypoxemIa, a normal re-
sponse to metabolic acidosis (compensation, represents only
ME = VDS --I-VA
hyperventilation and not respiratory alkalosis) and abnormal
VE is the amount of gas expired in one minute; VDS is the control of respiration at the CNS level. Severe hypoxemia or
amount of gas within the nongas exchanging areas of the similar conditions such as severe anemia and cardiovascular
respiratory system (conducting airways-anatomic dead space, shock will produce a similar response because of hypoxemla or
nonperfused alveoli, and areas with unmatched ventilation and acidosis at the tissue level. Finally, anxiety, pain, fear, or
flow [high and low V/Q-alveolar dead space,) and VA represent- excitement may also lead to hyperventllation in otherwise
ing ventilation in alveoli with normal gas exchange. healthy ammals with normal lungs.
Minute ventilation can be increased either by increases m
respiratory rate or volume. Increases in rate will proportion- Interpretation of Blood Gases
ately mcrease the ventilation of dead space areas, whereas
Clinical interpretation of arterial blood gases is dependant on
increases in tidal volume will increase the effective areas of gas
an understanding of the physiology discussed earlier, knowl-
exchange. In the normal animal, the Pco2 is tightly controlled.
edge of normal values (Table 1) and expected changes (Fig 1),
and frequent application of arterial blood gases to patient
Respiratory Acidosis management. As each arterial blood gas sample is obtained it
Ventilatory failure results from the inadequate elimination of should be evaluated systematically for various abnormalities.
carbon dioxide through the pulmonary system. The result is an One simple technique is to first evaluate the pH of the sample.
accumulation of carbonic acid and H+ resulting in respiratory If the pH is too high, an alkalemia is present. If the pH is too
acidosis. The renal response to respiratory acidosis is excretion low an acidemia is present. If the pH is normal, either a mixed
of H + and retention of bicarbonate. There are several causes of acid-base disturbance is present or the patient's acid-base status
ventilatory failure stemming from diseases of the respiratory is normal. Animals with an alkalemia will have either a
center, nerves and muscles of respiration, and also including metabolic or respiratory cause. If the CO2 is low, then the
diseases of the conducting airways, pulmonary parenchyma, alkalemia is induced by a respiratory cause, and the patient
pleural space, and circulation. In addition, any condition that should be evaluated for causes of hyperventilation. If the HCO3
increases the work of breathing (eg, severely hypoxemic is high, then the patient has a metabolic alkalosis. Conversely,
patient, patient with decreased pulmonary compliance) will with the acidemic patient, if the HCO3 is low, a metabolic
cause the patient to tire and develop CO2 retention because of acidosis is present. If the CO2 is high, a respiratory acidosis is
inadequate ventilation. Occasionally, anesthetic drugs and some present.
analgesics (eg, morphine) may promote hypoventilation. Although The patient must also be evaluated for compensatory mecha-
oxygenation failure should be evaluated and considered sepa- nisms by calculating the difference between the actual and the
rately, inadequate ventilation is often accompanied by arterial expected values (Figs 2 and 3). If the values fall outside the
hypoxemia and is directly proportional to the degree of ele- calculated ranges, then a mixed disturbance is present. The
vated carbon dioxide according to the respiratory quotient (RQ). following blood gas illustrates this point: pH, 7.170; Pco2, 71.3
mmHg; HCO3, 26.3 mEq/L; and BE - 3 . 4 mEq/U The pH is
low, indicating an acidemia. The CO2 is quite high which
Respiratory Alkalosis confirms a respiratory acidosis. The expected increase in HCO3
Respiratory alkalosis refers to alveolar hyperventilation leading would be (assuming a chronic respiratory acidosis) 3.5 mEq/L X
to reduction in arterial carbon dioxide. Ventilation occurs in 3.1 (71.3 mmHg to 40 mmHg/10) = 10.8 mEq/L or a final

Acute Respiratory Acidosis 1.5 mEq/LI"HCO3- for each 10 mm Hg 1" in Pc02 Fig 2. Metabolic compen-
sation to respiratory acido-
sis. mEq/L, milliequivalents/
Liter; mmHg, millimeters of
mercury.
Chronic Respiratory Ac=dosis 3.5 mEq/LI"HCO3- for each 10 mm Hg 1" in Pc%

RESPIRATORY MONITORING 229

 Fig 3. Metabolic compen-
Acute Respiratory Alkalosis 2.5 mEq/L4, HCOa- for each 10 mm Hg4, in Pco2 sation to respiratory alkalo-
sis. mEq/L, milliequivalents/
Chronic Respiratory Alkalosis 5.5 m E q / L $ HCO3- for each 10 mm H g $ in Pco2 Liter; mmHg = millimeters
of mercury.

expected value of 30 to 34 mEq/L. In this patient, the value is markedly compromised perfusion or large increases in central
too low at 26.3 mEq/L. This means that the patient has a venous pressures. In humans, hypothermla, icterus and severe
metabolic and respiratory acidosis. This information should anemia may also compromise pulse oximetry readings. Addi-
prompt the clinician to evaluate the animal for causes of tionally, the pulse oximeter is not able to distinguish abnormal
metabohc acidosis (eg, lactic acidosis, renal failure, diabetic forms of hemoglobin such as methemoglobin or carboxyhemo-
ketoacidosls) in ad&tion to therapy for respiratory acidosis. A globm.
complete understanding of the acid-base status will lead to
better individual patient management. End-tidal Carbon Dioxide Analysis
The final step in blood gas interpretation is the evaluation of (Capnography)
oxygen content. The degree of hypoxemia present may be
Capnographs (CO2 monitors) have also been used in veteri-
simply charactenzed by the value in mmHg, by evaluating the
nary medicine to nomnvasively reflect the arterial PcQ. In
A-a gradient, or the ratio of the PaoJl=~o2. Proper assessment of
theory, the plateau of the C Q at the end of a breath correlates
the PaQ also incorporates knowledge of the CO2 and I=IQ.
with the alveolar CO2, which is very similar to the P¢o2. Most
Arbitrary levels of hypoxemia are mild at 60 to 80 mmHg and
COa monitors depend on either infrared absorption spectropho-
severe at <60 mmHg. Hypoxemia below 60 mmHg becomes
tometry or mass spectrometry. In human medicine, they are
mcreasingly important because the hemoglobin-oxygen disso-
widely used in anesthesia to attempt to reduce the incidence of
ciation curve is very steep below Paoa <60 mmHg, severely
hypoventilation. In veterinary medicine, C Q monitoring is
limiting oxygen delivery below this value.
often used in anesthesia of critically ill patients and also as a
method of monitoring mechanically ventilated patients. An-
Pulse Oximetry other veterinary study, also by Hendncks and King,6 evaluated
Pulse oximetry is a useful technique for evaluating the arterial the usefulness of end-tidal CO~ monitoring in critically ill
oxyhemoglobin saturation. Over the last 15 years the clinical animals. The authors concluded that values from the capno-
use of pulse oximetry has grown immensely in veterinary graph were often lower than the corresponding PcQ value but
medicine. Pulse oximetry works by sensing the difference that capnography was a useful adjunct technique to arterial
between light absorption during pulsations (which are as- blood gas analysis in critically ill veterinary patients.
sumed to be arterial) and the background tissue (ie, venous
blood, interstitial tissues, bone, etc). Pulse oximeters are able Conclusions
to provide an estimate of the hemoglobin saturation (SpQ) as Monitoring respiratory function through arterial blood gases,
well as a heart rate. The hemoglobin saturation is related to the pulse oximetry, and end-tidal CO2 analysis provides useful
Pao2, and the information gained from a pulse oximetry information for the veterinary clinician. Arterial blood gas
reading may be useful for patient monitoring and to decrease analysis will remain the "gold standard" for assessment of
the number of artenal blood samples required. oxygenation as well as acid-base status. Each sample obtained
Many different models of pulse oximeters are available for should be carefully and completely evaluated to obtain the
use in veterinary patients. Most models are equipped with a maximum information possible. Pulse oximetry and capnogra-
probe and a screen which displays the calculated values for phy are useful adjuncts to arterial blood gas analysis, especially
Spoa as well as the heart rate. Some models include a waveform in regard to monitoring trends in oxygenation and ventilation.
of the pulse which many clinicians find particularly helpful in
assuring an accurate signal. Sites for probe placement include
the tongue (particularly useful in anesthetized or heavily Further Reading
sedated patients), ear, lip folds, toe pads, ax]llary or ingumal 1. Shapiro BA, Peruzm WT, Templin R: Clinical Application of Blood
skin fold, or prepuce/vulva. Hair should be removed from the Gases, 5 ed. St. Louis, Mosby, 1994
site. It is helpful to record the site from which the pulse 2. Autran de Morals HS DiBartola SP. VenNatory and metabolic compen-
oximetry value was obtamed. sation in dogs with acid-base disturbances. Vet Emerg Cnt Care
A recent study by Hendricks and King5 evaluated the use of 1(2):39-49, 1991
3. West JB Respiratory Physiology--the essentials. 4th edption, Balti-
pulse oximetry in veterinary patients. The authors conclusions more, MD, Williams and Wilkms, 1990
included that pulse ommetry is a valuable tool in the ICU 4. West JB Pulmonary Pathophyslology--the essentials. 4th edition,
setting. The benefits are a readily obtainable and noninvasive Baltimore, MD, Williams and Wllkins, 1992
estimate of the Spo2. There appeared to be good correlation 5. HendricksJC and King LG. Practicality, Usefulness, and Limits of Pulse
with the oxygen saturation determined by arterial blood gas Oxlmetry in Critical Small Animal Patients. Vet Emerg and Cnt Care
3(1):5-12 1993
analysis in most patients. Some potential caveats in pulse 6. Hendricks JC and King LG: Practicality, Usefulness, and L~m~ts of
oximetry include difficulty in obtaining a value or inaccurate End-t~dal Carbon D~oxideMon~tonng~n Critical Small Animal Patients.
values in some darkly pigmented patients or patients with Vet Emerg and Cnt Care 4(1):29-39, 1994

230 PROULX