You are on page 1of 10

Vol.18, No.

10 October 1996 V

Continuing Education Article

Respiratory Monitoring
FOCAL POINT
During Anesthesia:
★Continuous, noninvasive
monitoring of oxygenation and
Pulse Oximetry and
ventilation with a pulse oximeter
and capnometer, respectively,
can greatly improve patient
Capnography
management and safety during
anesthesia.
Colorado State University
Bonnie Wright, DVM
KEY FACTS
Peter W. Hellyer, DVM, MS
■ An anemic animal may not have
enough hemoglobin to exhibit
The general public had, at any rate, sufficient sense to realize
signs of cyanosis, even when
that although the percentage of deaths might be statistically
critically hypoxemic.
and numerically small, each fatality was 100% dead.1
■ Opioid analgesics, α2 agonists,

A
lthough the incidence of anesthesia-related deaths seems to be low in
anesthetic induction drugs, and
veterinary medicine, the unexpected death of an animal due to anes-
inhalant anesthetics may produce
thesia-related complications can be devastating for both the owner and
respiratory depression.
the veterinary staff. Death can be the result of an idiosyncratic reaction by the
animal, mechanical failure of anesthetic equipment, or human error. Human
■ At very high and very low
patients subjected to prolonged hypercapnia and hypoxemia from inadequate
oxygen saturation, pulse
ventilation seem to be at greater risk of secondary complications and death, not
oximetry readings may be
only during anesthesia but also in the postoperative period.2,3 Information re-
different from actual arterial
garding the risks of inadequate ventilation is scarce in the veterinary literature;
hemoglobin saturation.
however, it is likely that hypoxemia and hypercapnia during anesthesia place
the small animal patient at increased risk of secondary complications.
■ Capnography is an excellent and
In humans, the combination of pulse oximetry and capnography has been
objective technique for assessing
postulated to detect between 60% and 93% of all anesthetic complications be-
ventilation and determining if
fore they are noted by a trained clinician.2,3 Continuous monitoring of end-
ventilation needs to be assisted
tidal carbon dioxide (ETCO2) and arterial oxygen saturation (SaO2) has been
in anesthetized patients.
considered the minimal standard of care in human anesthesia since 1985 when
Harvard Medical School established a set of basic monitoring standards for the
practice of anesthesia.3
Veterinarians often do not have access to new medical technology until it is
well established and subsequently less expensive. Therefore, evaluation of respi-
ratory system function during anesthesia is frequently based, at present, on
subjective parameters. Such methods as counting the respiratory rate and eval-
uating the color of mucous membranes are commonly used.
Small Animal The Compendium October 1996

Mucous membrane color piratory center as well as re-


and capillary refill time can laxation of respiratory mus-
provide some information cles.
about oxygenation and per- 98%–99% Some animals have an in-
fusion. However, unless the creased vulnerability to respi-
mucous membranes are cya- ratory compromise (see the
notic (i.e., blue), evaluating box). Health status, age, po-
color change can be mislead- 1%–2% sitioning for surgery, and
SaO2
ing. For example, greater body condition are some of
than 5 g of reduced hemo- the factors that affect vulner-
globin per deciliter of blood PaO2 ability. For example, some
must be present before mu- animals do not have ade-
cous membrane color ap- quate tidal volume because
pears blue.4,5 Thus, anemic of pressure on the diaphragm
animals and those with poor Figure 1—Percentage of O2 bound to hemoglobin and mea- resulting from obesity, dorsal
tissue perfusion (e.g., an an- sured as O2 saturation (SaO2) and percentage of O2 dissolved recumbency, or sternal re-
imal in shock) may not ex- in plasma and measured as partial pressure of O2 (PaO2). cumbency in a head-down
hibit cyanosis, even when (From Principles of Pulse Oximetry. Pleasanton, CA, Nellcor position. An animal with
critically hypoxemic. Con- Puritan Bennett, 1996. Reprinted with permission.) lung disease may have inade-
versely, an animal with poly- quate gas exchange, even
cythemia may appear cyan- with a relatively normal tidal
otic, even in the presence of volume and respiratory rate.
adequate oxygen delivery. An animal with extreme va- Geriatric animals that are anesthetized and breathing
sodilatation, such as might occur in a state of cardiovas- room air seem to be more prone to hypoxemia than are
cular decompensation (e.g., young animals. Such age-related changes as decreased
cardiopulmonary arrest), lung elasticity, chronic bronchitis, fibrotic vasculitis, stiff-
Risk Factors for may have deceptively pink ened chest wall, less active protective reflexes, neoplasia,
Respiratory mucous membranes, despite decreased ventilatory function, and obesity decrease the
Compromise During severe tissue hypoxia. ability of geriatric animals to respond to hypercapnia or
Anesthesia Respiratory rate can also hypoxemia.6
be misleading. Tidal volume A very young animal or an animal with muscle wast-
often decreases dramatically ing resulting from cachexia or metabolic disease may be
■ Anesthetic-induced
when a patient is under anes- unable to maintain adequate ventilation during anes-
depression of thesia, 4 and this decrease thesia. Finally, any animal that is deeply anesthetized
medullary respiratory may be accompanied by an may lose its ability to ventilate.
centers increase in respiratory fre- The technology to objectively and noninvasively as-
■ Positioning for quency. The increase in fre- sess gas exchange in anesthetized animals has only re-
surgery (i.e., dorsal quency, however, may not cently become readily available to veterinary staff. Arte-
adequately offset the decrease rial blood gas measurements give the most accurate
recumbency or head
in tidal volume. Thus, even information about a patient’s ventilation, oxygenation,
down) at a higher respiratory rate, and acid-base status. Blood gas analysis, however, is sel-
■ Obesity an animal may be physiolog- dom available to veterinarians in private practice. Even
■ Age (i.e., geriatric ically hypoventilating. when a blood gas analyzer is available, obtaining an in-
patients) Respiratory depression, traoperative arterial blood sample from an animal posi-
■ Preexisting pulmonary which may be caused by tioned under surgical drapes may be difficult, if not im-
anesthetic premedications possible. Blood gas analysis provides information about
disease
(particularly opioid anal- gas exchange only at the time the blood sample was
gesics and α2 agonists), anes- drawn. Considering how rapidly oxygenation and ven-
thetic induction drugs, and tilation can change in an anesthetized animal, continu-
inhalant anesthetics, is common during anesthesia. The ous assessment of gas exchange would be more useful
effects of these drugs are dose-dependent and, when than an occasional blood gas evaluation. Capnography
multiple agents are used, additive. Respiratory depres- and pulse oximetry allow for continuous and noninva-
sion results from direct depression of the medullary res- sive monitoring of ventilation and oxygenation, respec-

CYANOSIS ■ HYPOVENTILATION ■ RESPIRATORY COMPROMISE


The Compendium October 1996 Small Animal

tively, in anesthetized patients and can supplement the amount of hemoglobin present. Therefore, the
blood gas evaluation that may be available. quantity and binding capacity of hemoglobin is vitally
important to tissue oxygenation. A hemoglobin
RESPIRATORY PHYSIOLOGY molecule is capable of binding four oxygen molecules,
Gas Exchange at which point the saturated molecule is referred to as
The purpose of ventilation is gas exchange, and the oxyhemoglobin (HgbO2). Deoxyhemoglobin and reduced
primary gases of interest are CO2 and O2. The partial hemoglobin (Hgb) are the terms used to describe a
pressure difference between alveolar gas and blood gas hemoglobin molecule that is not carrying any oxygen.
determines the direction and rate of gas diffusion. After the first oxygen molecule binds to a hemo-
Thus, O2 diffuses into pulmonary capillary blood from globin molecule, the structure of the hemoglobin
the alveoli, whereas CO2 diffuses from the pulmonary molecule changes so that the remaining three oxygen
capillary bed into the alveolar gas. molecules bind very easily. The relationship between
The alveolar membrane is exceedingly thin in a the partial pressure of O2 (PO2 or PaO2) and hemo-
healthy lung and is therefore well suited to gas ex- globin saturation is represented by the sigmoidal shape
change. In general, CO2 diffuses across the alveolar of the oxyhemoglobin dissociation curve (Figure 2). After
membrane 20 times as rapidly as does O2. Thickening the plateau of the curve is reached (usually a PaO2 > 70
of the alveolar membrane (as occurs with pulmonary mm Hg), increasing PaO2 has very little effect on oxy-
edema) interferes more with O2 diffusion than with gen saturation. Concomitantly, even slight decreases in
CO2 diffusion.7 PaO2 below 60 mm Hg can have profound effects on
oxygen desaturation.
Dissolved and Bound Oxygen in Blood
When oxygen diffuses into capillary blood, 98% is Hypoxemia
bound to hemoglobin and 1% to 2% is dissolved in Possible causes of hypoxemia (PaO2 < 80 mm Hg)
plasma (Figure 1). The bound portion is represented by and reduced oxygen saturation are decreased inspired
the measurement of oxygen saturation (SaO2), and the oxygen concentration (low FIO2), hypoventilation, ven-
1% to 2% dissolved in plasma is represented by the tilation-perfusion (V/Q)
partial pressure of arterial oxygen (PaO2). SO2 and PO2 mismatching, intrapulmon-
Causes of
are general terms indicating saturation and partial pres- ary shunt (V/Q = 0, right-to-
sure, respectively, whereas the lower case a is more spe- left shunting of blood), dif- Hypoxemia
cific, denoting saturation (SaO2) or partial pressure fusion impairment, and ■ Hypoventilation
(PaO2) of arterial blood. decreased mixed venous oxy-
■ Ventilation–perfusion
The partial pressure of O2 in the alveoli (PAO2) for a gen content (from increased
normal adult animal can be estimated based on the metabolic rate or decreased mismatch
barometric pressure (Patm) exerted on the partial pres- cardiac output). Although ■ Intrapulmonary shunt
5

sure of gases present in inspired air (FIO2) and in the not common, severe decreas- ■ Diffusion impairment
alveolus and is described by the following equation8: es in cardiac output during ■ Decreased inspired O2
anesthesia may result in hy- concentration
PAO2 = FIO2 (Patm – PH2O) – (PaCO2 × 1.2) poxemia. In an anesthetic
■ Decreased mixed
setting, where 100% oxygen
Alveolar CO2, which is usually estimated from the pa- is often delivered, ventila- venous O2 content
tient’s partial pressure of arterial CO2 (PaCO2), is approx- tion-perfusion mismatches
imately 40 mm Hg, and the partial pressure of water va- and intrapulmonary shunts are the most common caus-
por (inspired air is humidified before it reaches the es of hypoxemia. Hypoventilation may be a significant
lungs) is 47 mm Hg. Therefore, in a dog or cat that is cause of hypoxemia in the anesthetized animal breath-
ventilating normally (PaCO2 = 40 mm Hg) and breath- ing room air (see the box).
ing room air (FIO2 = 0.21) at sea level (barometric pres- Ventilation-perfusion mismatches (V/Q < 1), such as
sure = 760 mm Hg), a normal PaO2 would be approxi- atelectasis, alveolar pneumonia, and loss of negative in-
mately 100 mm Hg, which corresponds to greater than trathoracic pressure, occur when areas of lung are per-
98% SaO2. An animal breathing 100% oxygen (FIO2 = fused but not ventilated. These types of ventilation-per-
1.0) would have a PaO2 of approximately 660 mm Hg, fusion mismatches create right-to-left intrapulmonary
which also corresponds to an SaO2 of greater than 98%.8 shunts, such that deoxygenated blood passes through
Neither PaO2 nor SaO2 measures the exact oxygen the lungs without becoming oxygenated. When venti-
content of blood; this measurement depends largely on lated lung is not perfused (V/Q > 1), the amount of

OXYHEMOGLOBIN ■ DEOXYHEMOGLOBIN ■ HYPOXEMIA


Small Animal The Compendium October 1996

dead-space ventilation in- chemoreceptors include in-


creases (no gas exchange oc- creases in PaCO2 (primarily
curs). Pulmonary embolism detected at the medullary
and severely compromised chemoreceptors), decreases
cardiac output can increase in PaO2 (primarily detected
the amount of dead-space at the carotid bodies), de-

SaO2 (%)
ventilation. Some degree of PcO2 creases in arterial pH, and
ventilation-perfusion mis- sympathetic stimulation. 7
matching is almost always Arterial PCO2 reflects the bal-
seen when blood flow to de- ance between the amount of
pendent lung lobes increases CO 2 produced (metabo-
and when ventilation of lism) and eliminated (alveo-
elevated lobes increases. In PaO2 (mm Hg) lar ventilation). Because CO2
addition to the anesthesia- tension is inversely propor-
induced hypoventilation Figure 2—Oxyhemoglobin dissociation curve and factors that tional to alveolar ventilation,
mentioned previously, pneu- shift the curve to the right. (From Principles of Pulse Oxime- the adequacy of ventilation is
mothorax, diaphragmatic try. Pleasanton, CA, Nellcor Puritan Bennett, 1996. primarily determined by the
hernia, pleural effusions, Reprinted with permission.) arterial PaCO2.
muscle wasting, and any Tidal volume is the vol-
disease that occupies thoracic space can compromise ume of air inhaled in a normal breath and is generally
ventilation. considered to be 10 to 15 ml/kg in small animals. This
volume is multiplied by the number of breaths in a
Oxyhemoglobin Dissociation Curve minute to calculate the minute volume. Some of this
The oxyhemoglobin dissociation curve describes the volume represents the physiologic dead space, or gas
relationship between the partial pressure of oxygen from airways that do not participate in gas exchange
(Pa O 2) and the saturation of hemoglobin and O 2 (e.g., trachea and communicating bronchi). The
(SaO2). Arterial blood gas analysis measures the partial amount of dead space is influenced by size of the pa-
pressure of dissolved oxygen in blood (PaO2) and then tient, anesthetic agents (including anticholinergic
extrapolates the hemoglobin saturation based on a nor- drugs), posture and head positioning, age, intubation,
mal, human oxyhemoglobin dissociation curve. How- hypoventilation, mechanical ventilation, species, and
ever, hemoglobin is a dynamic molecule that is capable breed.7 The exhaled gas toward the end of expiration
of changing its affinity for oxygen in different physio- usually consists predominantly of alveolar gas. There-
logic situations. For example, in the presence of fore, the ETCO2 is nearly identical to the PaCO2 in a
acidemia, increased temperature, increased CO2, or in- normal patient.8 The ratio of dead space volume (VD)
creased protein 2,3-diphosphoglycerate (2,3-DPG), and tidal volume (VT ) can be calculated as described
the oxyhemoglobin dissociation curve shifts to the by the Bohr equation:
right. The affinity of hemoglobin for oxygen decreases
with a rightward shift of the oxyhemoglobin dissocia- VD PaCO2 – ETCO2
5
=
tion curve. A rightward shift indicates that a higher VT PaCO2
PaO2 is required in order for hemoglobin to remain sat-
urated. Because PaO2 is lower at the tissue levels, a Thus, an animal with a large amount of dead-space
rightward shift of the oxyhemoglobin dissociation ventilation would be expected to have a large gradient
curve favors the off-loading of O 2 from the between ETCO2 and PaCO2.8
hemoglobin molecule. Conversely, the oxyhemoglobin
dissociation curve shifts to the left when acidemia is PULSE OXIMETRY
not present or when temperature, CO2, or 2,3-DPG is Technology
decreased. The result is a higher hemoglobin satura- A pulse oximeter is designed to noninvasively calcu-
tion with oxygen (SaO2) at a given PaO2 (Figure 2). late oxygen saturation of hemoglobin using light ab-
sorption in tissue. Hemoglobin saturation detected by a
Control of Ventilation pulse oximeter is often referred to as SpO2. A probe
Ventilatory rhythm is controlled by the medullary from the oximeter emits red (660 nm) and infrared
respiratory centers and modulated by central and pe- (920 nm) lights, which are detected by a photode-
ripheral chemoreceptors.7 The strongest stimulants to tector that is placed across an arterial bed.9 Reduced

VENTILATION-PERFUSION MISMATCHES ■ OXYHEMOBLOBIN DISSOCIATION CURVE ■ TIDAL VOLUME


The Compendium October 1996 Small Animal

hemoglobin (deoxyhemo- poor signal. Repositioning


globin) does not absorb a the sensor, improving car-
significant amount of in- diac output, or warming the
frared light, but it absorbs patient may help to improve
red light well and produces the signal. Some light sour-
a large plethysmographic ces (e.g., heat lamps) can
signal. Conversely, oxyhe- also interfere with the sig-
moglobin absorbs infrared nal, and the probe site may
light and generates a strong need to be covered by a dark
signal, whereas the red light material.
passes through and gener-
ates a weak signal. In this Clinical Uses
way, pulse oximeters can Studies have been con-
calculate, according to a pre- ducted with many oximeter
set nomogram, the amount Figure 3—Infrared and red light absorption by deoxyhemo- probes, including human
of each form of hemoglobin globin (Hgb) and oxyhemoglobin (HgbO2). Red light (660 earlobe probes, finger
present in arterial blood 10 nm) is absorbed to a greater extent by deoxyhemoglobin, and probes, and specific veteri-
(Figure 3). infrared light (920 nm) is absorbed to a greater extent by nary probes. 13,14 Jacobson
Oximeters are designed oxyhemoglobin. (From Principles of Pulse Oximetry. Pleasan- found the human probes to
ton, CA, Nellcor Puritan Bennett, 1996. Reprinted with per-
to restrict readings to areas mission.) be equally efficacious for
modulated by the pulsating measuring oxygen satura-
flow of fluids. In a still pa- tion in dogs, and Matthews
tient, only arteries should be pulsating; therefore, only and Fairman found that neonatal sensors were the most
arterial hemoglobin saturation is calculated.11 In con- effective in critically ill small animal patients.12–14 Varia-
trast to arterial blood gas analysis, SpO2 measured on a tions occur in the performance of different oximeters,
pulse oximeter reflects the amount of oxygen bound to and each oximeter should be evaluated for accuracy by
hemoglobin at any given time, thus accounting for comparing it with blood gas analysis data or co-oxime-
changes that have occurred in the oxyhemoglobin dis- try results (when available).14 A variety of probes de-
sociation curve. signed for use in veterinary medicine may be particular-
Pulse oximetry, like all monitoring techniques, is also ly useful in very small animals.a
susceptible to inaccuracies. For example, adult In small animals and horses, the most effective loca-
hemoglobin may actually exist in one of four forms: tion for oximeter probe placement is the tongue. Other
oxyhemoglobin, deoxyhemoglobin, carboxyhemo- locations that have been shown to be fairly accurate in
globin, and methemoglobin. Because the percentage of small animals are the lip, ear, toe, prepuce, vulva,
methemoglobin and carboxyhemoglobin is usually neg- metacarpus, digits, and tail; these areas can be used if
ligible, these two forms are ignored by the pulse oxime- there is not excessive pigmentation in the area and if
ter. any haired areas have been clipped and cleaned.12–15
A more accurate device to measure hemoglobin satu- Hemoglobin molecules vary in structure and oxygen-
ration is the co-oximeter, a spectrophotometer that di- binding capacity in each species, but oximetry readings
rectly measures all four forms of hemoglobin present in do not seem to be dramatically altered by these differ-
blood. Co-oximeters, like blood gas analyzers, require a ences.16,17
sample of arterial blood. Although pulse oximeters are Many studies have shown pulse oximetry to be effec-
not as accurate as co-oximeters, pulse oximeters are tive in measuring oxygen saturation in animals and hu-
more readily available and easier to use than co-oxime- mans. 12–18 At an oxygen hemoglobin saturation of
5
ters. greater than 90%, pulse oximetry saturation tends to be
The probe of the pulse oximeter is sensitive to pulsat- slightly lower than actual arterial oxygen hemoglobin
ing motion; therefore, an animal must remain still for saturation; and at saturation of less than 70%, pulse
accurate readings. Accurate results have been obtained, oximetry saturation tends to be higher than actual arte-
however, in awake, critically ill patients during times of rial oxygen hemoglobin saturation.13 For a reading to
12
minimal movement. In patients with low perfusion, be considered acceptable, the probe must be in place
such as those with hypothermia, hypovolemia, vasocon- for at least 30 seconds. The palpable pulse rate should
striction, and poor cardiac output, reduced pulsating aEmme B: Personal communication, Sensor Devices, Wauke-

activity may fail to modulate absorption, resulting in a sha, WI, 1996.

OXIMETERS ■ CO-OXIMETERS ■ PROBES


The Compendium October 1996 Small Animal

correspond to the pulse rate of the dicrotic notch).15 A


measured by the oximeter valid pulse wave must be de-
(except in horses, in which tected on the monitor, and
the pulse rate may be double the signal must be of high
on the oximeter). If a pul- quality before the saturation
sating signal is displayed, readings can be considered
the strength of the signal valid.
should exceed 40% and the Additional clinical uses
wave form should be smooth, of pulse oximetry include
wide-based, and consistent.16 management of critical care
patients that need repeated
Interpretation of SpO2 oxygenation monitoring as
Oximetry data should be an adjunct to periodic blood
interpreted in conjunction gas analysis, assessment of
with other monitored pa- Figure 4—Mainstream (A ) and sidestream (B ) capnometers. intestinal viability during
rameters and the status of (From Stock MC: Capnography for adults. Crit Care Clin surgery, assessment of oxy-
the entire animal. For exam- 11(1):224, 1995. Reprinted with permission.) gen status of patients with
ple, severely anemic animals pneumothorax, assessment
may have low SpO2 readings of the safety of weaning a
despite a normal PaO2; therefore, hematocrit is an im- patient from oxygen, and measurement of fetal oxy-
portant consideration when interpreting oximetry re- genation during dystocia.10,18,19
sults. Animals in shock may have extremely poor perfu- Possible concerns about the use of pulse oximetry fo-
sion, which can produce a falsely low oximeter reading. cus on interpretation of the results. As mentioned pre-
Aside from these exceptions, when there is an accept- viously, a high oxygen saturation does not guarantee
able signal and wave form, oximeter readings are reli- adequate ventilation. In addition, oximeter readings
able estimates of arterial oxygen saturation in the satu- can be transiently incorrect when intravenous dyes are
ration range from 80% to 100%.19 Even at very high administered and can be incorrect when probes are
and very low saturations, trends in oxygen saturation placed in areas of excessive skin pigmentation.12,20 Car-
are predicted with adequate precision, and the knowl- diac dysrhythmias, fetal hemoglobin concentration, ele-
edge that desaturation is occurring is more important vated bilirubin, changes in body temperature, and
than an exact number or the degree of desaturation. Pe- blood pH should have minimal effects on oximetry
riodic confirmation by blood gas analysis, especially readings. In anemic animals, a low SpO2 reading from
when trends are noted on the oximeter, is ideal. an oximeter should be checked against an arterial blood
Oxygen saturation should be maintained between gas measurement because the SaO2 may be normal.18
95% and 100%, particularly if the animal is breathing Nevertheless, an exaggerated warning of hemoglobin
100% oxygen. Saturation readings of 90% or less in the desaturation in anemic animals may be beneficial be-
presence of a strong, pulsating signal can indicate sig- cause anemic animals are already at an increased risk of
nificant desaturation and hypoxemia, severe shock, or inadequate oxygen delivery.
anemia. Prompt intervention by the anesthetist is re-
quired. Oxygen supplementation, intermittent positive- CAPNOGRAPHY
pressure ventilation, removal of the inciting causes of Technology
hypoventilation, and attempting to correct ventilation- Capnography is the graphic display of the partial
perfusion mismatches with positioning, lung inflation, pressure of CO2 over time. Capnography provides a
and diuretics should be considered. It is important to means to assess ventilation, integrity of airway and
note that normal oxygen saturation is often achieved in breathing circuit, and cardiopulmonary function. It
a hypoventilating patient, especially when high inspired provides early warning of problems in the intubated pa-
oxygen concentrations are being used. Therefore, a tient that could lead to disastrous outcomes if left un-
pulse oximeter is not a reliable sentinel for hypoventila- treated. A capnometer is a gas analyzer that measures
tion or hypercapnia.10 CO2 concentration in respiratory gases. Two methods
Most pulse oximeters also give an accurate reading of are used to perform capnography: infrared light absorp-
heart rate unless the rate exceeds 250 beats/min. 13 tion and mass spectrometry. Capnometers may either
Horses are the exception, as oximeters often detect two be mainstream or sidestream, terms used to describe the
pulse waves for each cardiac contraction (due to the size location of the CO2 sensors (Figure 4). Only infrared

DATA INTERPRETATION ■ INFRARED LIGHT ABSORPTION ■ MASS SPECTROMETRY


Small Animal The Compendium October 1996

Share Your capnometers are available as mainstream analyzers; side-


Knowledge stream analyzers can use infrared absorption or mass
spectrometry.21
Mass spectrometry measures the unique ions that are
We invite you to impart your clinical knowledge released when a gaseous substance is bombarded with
an electron beam. These ions produce an electric current
by discussing your interesting cases, unusual
that a computer can assimilate into a numeric value for
presentations, or procedures for clinical solutions the concentrations of the substances in the sample.22
Mass spectrometry has a long delay period and is too
for the following features: expensive to be devoted to the use of only one patient;
E
thus, it is impractical for use in most veterinary situa-
IC CHALLENG
DIAGNOST

rn on a Rat Po
isoning tions.
Unexpected Tu
DIAGNOSTIC CHALLENGE By Marjory
Brooks, D.V.M
.
., Dipl. A.C.V.
I.M.,
Infrared capnometers measure the absorption of light
(wavelength of 4.28 µm) by CO2. Infrared radiation
on, D.V.M
and Jeff Jacobs
was exam-
d male Beagle,
r-old, neutere Con-
ugsy, a four-yea n of the rat poison
M ined within one
hour of ingestio l placement

A detailed account of a clini- trac® . Initial


of apomorphine
treatment consiste
and 30 mL of
d of subconjunctiva
oral hydrogen
peroxide to induce
, Mugsy vomited
a large

passes through a sample chamber of respiratory gases,


this therapy
response to the rat bait.
Addi-
vomiting. In identified as
of green-b lue material d charcoa l by gas-
amount mL of activate
nt included 200 neously (SC).
tional treatme 2.5 mg/kg subcuta

cal dilemma takes readers from


and vitamin K1 supply of
tric intubation with a 10-day
ed to his owners
Mugsy was discharg

and the remaining radiation is projected onto a detec-


hours orally.
mg every 24
vitamin K1 50

SEALING ry
NS BY LES
blood chemist
nation. All
ILLUSTRATIO

for PT determi PT at recheck

specific patient presentation


hours later limits. The
d for 48 hours within normal because cor-
values were ted finding

tor. The concentration of CO2 is directly proportional


tion was schedule confirm , an unexpec K deficiency
A recheck examina vitamin K regimen to was 65.9 seconds al PT due to vitamin
ion of the owners report- initiating an
after complet Although his rection of abnorm 48 hours of
coagulopathy. and Mugsy within 24 to
resolution of K1 as directed should resolve K1. of
had given vitamin re to rat poison, clotting appropriate
dose of vitamin persistent prolongation
ed that they y the cause of
nity for reexposu was markedl To determine al vitamin
had no opportu time (PT) assay whether addition for more
prothrombin finding in the PT and
time in the : 9.5-12.5). This clotting time was sent

through the steps leading to the to the amount of light absorbed.22


(normal pre- a sample
57 seconds that his early was needed, was drawn
prolonged at it appeared K therapy . Whole blood
ted because prevented ion analyses 3.8 percent
was unexpec ive vomiting had detailed coagulat anticoagulant (one part
product Contrac, how- citrate ged, and the
sentation with of rodenticide. directly into and centrifu
a toxic dose poison. parts blood) to a vet-
absorption of iolone, a long-acting K citrate to nine shipped on cold packs
s bromad vitamin 1 plasma was Coagulation
ever, contain at the same supernatant (Comparative
therefore resumed e laboratory University,
Treatment was erinary referenc ory, Cornell

Infrared sidestream capnometers are practical for vet-


two weeks. completion tic Laborat
dosage for another recheck, 48 hours after Section, Diagnos

ultimate diagnosis in 1000-1500


ed and d
At Mugsy’s next was still markedly prolong York). d of activate
Ithaca, New ion panel consiste
, the PT sample. A thrombin
of vitamin K1 from the previous The initial coagulattime (aPTT), PT, and g
unchanged vita-
essentially submitte d, parenteral partial thrombo
plastin
aPTT and
TCT screenin
ry profile was were (TCT). The
owners clotting time
blood chemist SC, and the
given 50 mg and recheck
48
min K1 was vitamin K1

erinary use. Gas is continuously sampled from the end


oral August 2000
resume
instructed to
ed
Peer Review

words. 76 Veterinary
Forum

THERAPEUTIC
of the endotracheal tube through a narrow-bore tube at
a rate of 150 to 300 ml/minute. When a sidestream
CHALLENGE

THERAPEUTIC CHALLENGE capnometer is used in a patient under inhalant anesthe-


KAREN WILSON

Intussuscep
While the course of therapy is of- tio
In a Yearlin n
g
sia, however, the continuous loss of gas from the anes-
ten clear-cut, some patients pre-
By Linnea Lentz,
D.V.M.

thetic breathing system can pose several problems—


B eau, a 15-mont
when the owners
h-old colt, had been
colicky for about
scavenging of waste gases as well as increasing the O2
sent true challenges to medical
called the referring four hours
veterinarian. The and no other
described as mild, colic was
abnormali-
and Beau was treated ties. An initial
IV injection
nixine) administe with 10 cc Banamin ® of xylazine appeared
red intravenously e (flu-

flow requirements in very small patients or any patient


(IV), 10 cc of control the pain to
approximately 1 dipyrone IV, and for only 20
⁄2 gallon of mineral minutes before
tube. Within the oil administered a second
hour, Beau was via nasogastric dose was necessary.
University of Minneso again colicky and Rectal
was referred to the palpation revealed

skills. In 1000-1500 words, these


ta. many
distended loops
of small
testine. After placemen in-

that is anesthetized using a closed (low O2 flow) circuit.


Initial Treatme t of
nt on Referra a nasogastric
Clinical signs l reflux were obtained. tube, 6-7 L of
on presentation Abdominocen-
included profuse tesis results were
sweating, numerous normal.
attempts to lie Because of the
down, and a distended severity of the
abdomen. Physical colic, the small
examination re- intestinal distention

cases describe the steps that


vealed a pulse and nasogastr ,
of 84 beats per ic reflux, we
minute,

These problems can be solved by rerouting the aspirat-


decreased gastrointe mended explorato recom-
stinal motility ry laparotomy
all four quadrants in diagnose the cause to
, slightly toxic of the colt’s colic.
cous membran mu- The owners quickly
es, a capillary agreed, and pre-
time of 2.5 seconds refill operative antibiotic
(normal: 1-2),
and a normal
temperature. potassium penicillin s, including
work revealed Blood 22,000 units/kg
a packed cell IV and Gentocin
volume (gentamicin) 6.6

eventually lead to case resolu- ed gas back into the anesthetic circuit. Problems can
of 48 percent mg/kg IV,
(normal: 32-48), were administe
protein of 7.2 g/dL total preparing the colt red before
(normal: 5.7-7.9), for surgery. During
surgery, a jejunocec
August 2000 al intussuscep-➔
Peer Reviewed
Veterinary Forum
73

tion. also arise with sidestream capnometers when prolonged


MONTH
anesthesia is required. The sampling tube can occlude
CASE OF THE

is with condensation from expired respiratory gases.


Canine Hemipares , D.V.M.

CASE OF THE MONTH


By Donivan Hudgins

Some case presentations are so J asmine, a four-year-


kg, spayed Golden
old, 29-
Retriev-
to the clinic
activity levels
and vaccinations
for distemper,
had been normal,
were current
hepatitis, lep-
nza, par-
Estimation of PaCO2
er, was presented tosporosis, parainflue

The amount of expired CO 2 depends on cellular


of lameness. irus, Lyme
for sudden onset vovirus, coronoav

confounding that both diagnosis


found a stray
The owner had and sus- disease, and rabies.
given Solu
goat in the backyard The patient was
goat may have ® (prednisolone)
pected that the Delta Cortef
On presenta- usly (IV) and
butted Jasmine. ry 100 mg intraveno 2.5 cc in-
was ambulato
tion, the dog amoxicillin injectable
The owner was

metabolism, transport of CO2 to the lungs via the cir-


uncoordi nated,
but obviously tramuscularly.
n revealed the provide cage rest
and observatio instructed to

and therapy are perplexing. Often,


deficit was in and return
primary walking over the weekend
dog’s condition
the right rear leg. ion re- Monday if the
Physical examinat .
had not improved
re of 101.6˚F, week, Jas-
vealed a temperatu The following

culation, and diffusion of gases along pressure gradients


es, capil- to improve, and
pink mucous membran (normal:
CORBIS

mine appeared
of 1 sec she did have
lary refill time whatever problems
heart and Over the next
1-2 sec), normal seemed subtle.

a patient may return again and


sign of pain. The weeks, her prob-
lungs, and no two to three
did knuckle over, but not as pro-
right rear foot proprio- lems recurred the
indicating decreased indicat- before, and
nounced as

in the alveoli. Readings for ETCO2 are generally lower


pinch that the dog
ception, but toe owner reported
were intact. to her deficits.
ed sensory nerves seemed to adjust
of the affected next few weeks,
Temperatures Then, over the
no different of coördination
foot and leg were Jasmine’s lack

again with continuously changing


other three feet
than that of the seemed to worsen.
and flexion 21, Jasmine
and legs. Extension On October

than those for PaCO2, as exchange is not perfect across


hip joints were for examina-
of the stifle and reflex on was re-presented
on a leash
normal, but patellar tion. When followed appeared
exaggerated,
the right was in the lawn, Jasmine
upper motor ated, with
which suggested to be very uncoördin
Appetite and
neuron disease.

signs. Word count: 1000-2000. 66 Veterinary Forum


Peer Reviewed
August 2000

the alveolar wall. The normal range for PaCO2 is 35 to


45 mm Hg. At a PaCO2 of approximately 80 mm Hg,
an animal that had a normal blood pH at the begin-
ning of anesthetic maintenance will become severely
acidemic (pH <7.20) and cardiac function may begin
SEND YOUR ARTICLES TO: to decline. Some elevation of PaCO2 is expected during
anesthesia because of the respiratory depression in-
Editor, Veterinary Forum
duced by anesthetic drugs. However, an ET CO 2 of
275 Phillips Blvd. greater than 60 mm Hg should serve as a warning and
Trenton, NJ 08618 prompt either a blood gas assessment or the induction
of intermittent positive-pressure ventilation. If ventila-
Fax: (609) 882-6357
tion is already being assisted, the respiratory rate and/or
E-mail: lmiller.vls@medimedia.com tidal volume may need to be increased and the poten-

INFRARED CAPNOMETRY
The Compendium October 1996 Small Animal

tial for such complications shunt).4 The difference be-


as tension pneumothorax 40 C D tween ETCO2 and PaCO2 is
should be explored. widened by the amount of
Because the alveoli are the physiologic dead space and

ETCO2 (mm Hg)


site of gas exchange, the can normally be up to 10%
highest concentration of CO2 20
in an anesthetized patient.
should occur at the end Thus, the Pa CO 2 will nor-
of an expiration (ET CO 2), mally be 1 to 10 mm Hg
when the diluted gases from higher than the ETCO2.
the trachea and primary B E During prolonged anes-
A
bronchi are no longer being 0 thesia in horses, dependent
sampled. Therefore, a nor- lung lobes may become in-
mal capnographic wave Time (seconds) creasingly collapsed and
form will have a sharp rise there may be decreased pul-
from zero at the beginning Figure 5—A normal pattern of exhaled PCO2 on a capnogram. monary capillary perfusion,
of exhalation to a smooth Segment A to B is inspiration; the inspired gas should have a increased dead space ventila-
plateau and then to a sharp PCO2 of 0. Segment B to C marks the beginning of exhala- tion, and widening of the
drop back to zero at the be- tion, with a steady rise in CO2 as the dead space gases are ex- differential between ETCO2
pelled and alveolar gases reach the sensor. Segment C to D
ginning of inhalation (Fig- must be a plateau shape, representing alveolar CO . The and PaCO2.25 Therefore, the
2
ure 5). Changes in the stan- reading at point D is the ETCO . If the C-to-D segment is longer the procedure, at
2
dard wave form should alert not a smooth plateau, the ETCO2 may not be accurate. Seg- least in very large animals,
the anesthetist to a problem ment D to E is the beginning of inspiration, which should the less accurate an ETCO2
with the patient, the airway, again have a PCO2 of 0. reading is likely to be.26 The
or the anesthetic circuit same phenomenon can be
(Figure 6). noted during a thoracotomy
Sampling errors can occur with tachypnea, hypoven- in small animal patients. During this procedure, the
tilation, and nonrebreathing anesthetic systems using loss of negative intrathoracic pressure changes the ven-
high O2 flow rates. All sampling errors provide a falsely tilation and perfusion ratios, increasing the ETCO2 and
low ETCO2 reading as compared with PaCO2. In other PaCO2 gradient.
words, sampling errors tend to underestimate the
PaCO2. Tachypnea may falsely decrease the ETCO2 be- Other Clinical Uses Causes of Abrupt
cause of incomplete exhalation of alveolar gases, dilu- If an abrupt change in Changes in ETCO2
tion of alveolar gas by gas from areas of physiologic ETCO2 is noted, several pos-
dead space (air that does not contain CO2), and a delay sibilities should be investi- ■ Apnea
in the response time of the analyzer. A manual ventila- gated (see the box). The first ■ Patient extubation
tion, or sigh, in a tachypneic patient may clear more is endotracheal tube acci- ■ Endotracheal tube
alveolar CO2 and give a transiently accurate ETCO2 dents. If a patient is extubat- occlusion
reading. Hypoventilation may allow the capnometer to ed or if the tube is suddenly
aspirate gases that do not contain CO2 during the expi- occluded, the ETCO2 will fall ■ Cardiac arrest
ratory pause, thus providing low readings during this to zero. Either of these situa- ■ Cardiac or pulmonary
time. Anesthetic breathing systems with high flow rates tions can be life threatening. embolism
may have the effect of washing out the end-tidal gases In addition, esophageal intu- ■ Capnometer
with fresh gas flow. A right-angle adapter on these bation should be suspected if disconnection from
breathing circuits may minimize admixture of gases.21 the capnometer does not endotracheal tube
record CO2 in a ventilating
PaCO2-to-ETCO2 Gradient animal. The stomach is usu- ■ Sampling tube
Normal ventilation is defined as a PaCO2 of 40 mm ally void of CO2. Detection occlusion from
Hg; the ETCO2 should closely approximate the PaCO2 of any CO2 by the capnome- a sidestream
under most circumstances.3 The relationship between ter confirms endotracheal in- capnometer
ETCO2 and PaCO2 has been documented in horses,23 tubation.
dogs,24 and other species. However, 2% to 5% of blood Another potential reason for an abrupt change in CO2
flow from the right ventricle bypasses the lungs via is cardiac arrest. As blood flow to the alveoli stops, there
bronchial vessels and cardiac veins (i.e., physiologic is no longer a gradient of CO2 to exchange with alveolar

SAMPLING ERRORS ■ DEAD SPACE ■ ETCO2 CHANGES


Small Animal The Compendium October 1996

gases. Although the animal Figure 6—Examples of abnor-


may be manually ventilated, mal capnogram wave forms.
ETCO2 will be zero. (A) A single wave form show-
Capnography can be in- ing hypoventilation based on
dispensable once cardiopul- 40 an elevated CO2 reading with
a normal shape. This could be
monary resuscitation has seen in animals with brady-
been initiated.27 The better pnea, low tidal volume, or ma-
the pulmonary blood flow, lignant hyperthermia. (B) This
the higher the amount of wave form shows hyperventila-
CO 2 that should be deliv- tion, again with a normal
ered to and cleared from the shape but with a low ETCO2.
Figure 6A
lungs. Therefore, the higher (C) The flattened expiratory
the CO 2 readings that are slope, lacking a smooth plateau,
achieved during cardiopul- indicates dilution of the CO2
monary resuscitation, the 40 from a leak in the respiratory
more effective the chest system or a system with high
oxygen flow. (D) The gradual
compressions will be. Fur- incline in both baseline and
thermore, an increase in ET C O 2 levels indicates re-
ET CO 2 during cardiopul- breathing of CO2 from satura-
monary resuscitation can be tion of the CO 2 absorbent
the first indication of a pa- (such as soda lime) or inade-
tient’s return to spontaneous Figure 6B quate flow rates in a nonre-
circulation.3 An abrupt drop breathing system. (E) When
in CO2 can occur with an respiratory rate is slow, cardio-
embolism in the heart or 40 genic oscillations (caused by
pulmonary vasculature. the heart beating against the
The magnitude and dura- lungs) may create spikes in the
wave form. ETCO2 is measured
tion of the decrease in in mm Hg. (From Ohmeda
ETCO2 depends on the size Inc., Madison, WI. Modified
and location of the embo- with permission.)
lus. However, if the patient
is doing well in all other re- Figure 6C
spects (i.e., stable vital signs) 1980s. During this period,
and a sidestream capnome- the number of intraoperative
ter is being used, the sam- accidents and subsequent
40
pling tube may have become lawsuits dropped dramatical-
occluded with respiratory ly.2,18,21 Clearly, both moni-
secretions. This situation is toring techniques are simple,
especially prevalent in rumi- noninvasive, provide excel-
nants and in patients with lent information, seldom
respiratory disease that are provide false-negative results,
undergoing prolonged anes- Figure 6D and remove the dependence
thesia. Replacement of the on subjective interpretations
sampling tube and some- of cyanosis or hypercapnia.
times the filter (on machines Beyond their direct clinical
that have them) should re- 40 usefulness, pulse oximetry
solve the occlusion. and capnography provide in-
formation that tends to pro-
CONCLUSION mote a greater awareness and
New monitoring stan- vigilance in the individual
dards, including pulse oxime- monitoring anesthesia, there-
try and capnography, emerged by indirectly improving pa-
Figure 6E
in human medicine in the tient outcome.

CARDIOPULMONARY RESUSCITATION ■ SAMPLING TUBE OCCLUSION ■ WAVE FORMS


Small Animal The Compendium October 1996

13. Jacobson JD, Miller MW, Hartsfield SM, Knauer KW:


About the Authors Evaluation of accuracy of pulse oximetry in dogs. Am J Vet
Drs. Wright and Hellyer are affiliated with the Department Res 53(4):537–539, 1992.
of Clinical Sciences, College of Veterinary Medicine and 14. Matthews N, Sanders E, Hartsfield S, et al: A comparison of
two pulse oximeters in dogs. J Vet Emerg Crit Care 5(2):
Biomedical Sciences, Colorado State University, Fort
116–120, 1995.
Collins, Colorado. Dr. Hellyer is a Diplomate of the Ameri- 15. Whitehair KJ, Watney GC, Leith DE, Debowes RM: Pulse
can College of Veterinary Anesthesiologists. oximetry in horses. Vet Surg 19(3):243–248, 1990.
16. Ehrhardt W, Hipp LC, von Hegel G, et al: The use of pulse
oximetry in clinical veterinary anaesthesia. J Assoc Vet Anaes-
thesiol 17:30–31, 1990.
REFERENCES 17. Sendak MJ, Harris AP, Donham RT: Accuracy of pulse
1. Sykes W: Essays on the First Hundred Years of Anesthesia. oximetry during arterial oxyhemoglobin desaturation in
London, Churchill Livingstone, 1962. dogs. Anesthesiology 68:111–114, 1988.
2. Eichorn JH: Effects of monitoring standards on anesthesia 18. Severinghaus JW, Kelleher JF: Recent developments in pulse
outcome. Int Anesthesiol Clin 31(3):181–193, 1993. oximetry. Anesthesiology 76:1018–1038, 1992.
3. Saidman LJ, Smith NT: Monitoring in Anesthesia, ed 3. 19. White G, Matthews N, Walker M, Slater M: Pulse oximetry
Woburn, MA, Butterworth-Heinemann, 1993, pp 1–50. for estimation of oxygenation in dogs with experimental
4. Stoelting R: Pharmacology and Physiology in Anesthetic Prac- pneumothorax. J Vet Emerg Crit Care 4(2):69–76, 1994.
tice, ed 2. Philadelphia, JB Lippincott Co, 1991, pp 719– 20. Ralston AC, Webb RK, Runciman WB: Potential errors in
744. pulse oximetry. Anaesthesia 46:202–295, 1991.
5. Shapiro BA, Harrison RA, Cane RD, Templin R: Clinical 21. Bhavani-Shankar K, Mosley J, Kumar AY, Delph Y: Cap-
Application of Blood Gases, ed 4. Chicago, Year Book Medi- nometry and anaesthesia. Can J Anaesthesiol 39:617–632,
cal Publishers, Inc, 1989. 1992.
6. Robinson EP: Pediatric and geriatric anesthetic techniques, 22. Stock MC: Capnography for adults. Crit Care Clin 11(1):
in Slatter D (ed): Textbook of Small Animal Surgery, ed 2. 219–232, 1995.
Philadelphia, WB Saunders Co, 1993, pp 2295–2300. 23. Cribb PH: Capnographic monitoring during anesthesia with
7. Nunn JF: Applied Respiratory Physiology, ed 3. London, But- controlled ventilation in horses. Vet Surg 17(1):48–52,
terworths, 1987. 1988.
8. West JB: Respiratory Physiology—The Essentials, ed 5. Balti- 24. Hightower CE, Kiorpes AL, Butler HC, Fedde MR: End
more, Williams & Wilkins, 1995. tidal partial pressure of CO2 during various ventilatory regi-
9. Principles of Pulse Oximetry. Pleasanton, CA, Nellcor Puritan mens in halothane-anesthetized dogs. Am J Vet Res 41(4):
Bennett, 1996. 610–612, 1980.
10. Lindberg LG, Lennmarken C, Vegfors M: Pulse oximetry— 25. Geiser DR, Rohrbach BW: Use of end-tidal CO2 tension to
Clinical implications and recent technical developments. predict CO 2 values in isoflurane-anesthetized equine
Acta Anaesthesiol Scand 39:279–287, 1995. neonates. Am J Vet Res 53(9):1617–1621, 1992.
11. Ohmeda: 4700 OxiCap® Monitor Pulse Oximeter/Capnome- 26. Meyer RM, Short CE: Arterial to end-tidal CO2 tension and
ter Operator’s Manual. BOC Health Care, 1992, pp 1–3. alveolar dead space in halothane or isoflurane-anesthetized
12. Fairman N: Evaluation of pulse oximetry as a continuous ponies. Am J Vet Res 46(3):597–599, 1985.
monitoring technique in critically ill dogs in the small ani- 27. Weil MH, Bisera J, Trevino RP, Rackow EC: Cardiac out-
mal intensive care unit. J Vet Emerg Crit Care 2(2):50–56, put and end-tidal carbon dioxide. Crit Care Med
1992. 13(11):907–909, 1985.