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10 October 1996 V
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
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
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
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
SEALING ry
NS BY LES
blood chemist
nation. All
ILLUSTRATIO
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
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.
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
mine appeared
of 1 sec she did have
lary refill time whatever problems
heart and Over the next
1-2 sec), normal seemed subtle.
INFRARED CAPNOMETRY
The Compendium October 1996 Small Animal