Page 82 - Basic Monitoring in Canine and Feline Emergency Patients

VetBooks.ir Box 4.1. The impact of various scenarios on the total oxygen content of arterial blood (CaO ).
2
The total oxygen content of the blood is calculated by the following equation:
×
Hb 134×
PaO ×
.
SaO +)(
.
CaO =(
0 003)
2
2
2
Hb, hemoglobin in g/dL; SaO , the % saturation of arterial Hb as a decimal; and PaO , partial pressure of oxygen
2
2
in arterial blood in mmHg.
1. For a normal canine patient with a normal hemoglobin of 15 mg/dL (equivalent to a PCV of ~45%) breathing
room air (SpO 97%, PaO 100mmHg), we can solve this equation:
2
2
×
×
×
CaO =( 15 1340 97 +( 100 0 003 = 19 .8mLdL
/
)
)
.
.
.
2
/
A normalCaO is geenerally around 20 mL dL
2
2. This normal patient is given 100% O , raising the PaO to 500 mmHg. At this point according to the oxyhemo-
2
2
globin dissociation curve, SaO will be fully saturated at 100%:
2
.
×
/
)
×
)
CaO =( 15 1341×+( 500 0 003 =21 .6mLdL
.
2
While this is certainly a higher number than in point 1, raising the PaO by five times (from 21% room air to
2
100% oxygen) only raised the CaO by 1.2 mL/dL, or about 6%. This is because the Hb was already fully sat-
2
urated at room air. Hemoglobin-bound oxygen contributes the largest volume to the total oxygen content.
Therefore, when the hemoglobin is already saturated, raising the FiO will only increase the dissolved oxygen
2
content of the blood (the PaO ), which has a much smaller impact on the total blood oxygen content than the
2
amount of O bound to Hb.
2
3. For a severely anemic patient with a hemoglobin of 3.3 mg/dL (PCV 10%) breathing room air (SpO 98%, PaO
2
2
100 mmHg):
33 1340 98 +)(
×
.
/
)
CaO =(. × . × . 100 0 003 = .46mL dL ; severelylow
2
4. If we provide the patient in point 3 with 40% oxygen supplementation and raise his PaO to 200 mmHg with a
2
SaO of 100%:
2
×
33 1341×+(
.
CaO =(. × . ) 200 0 003 = .502mLdL ; still severely low
/
)
2
Despite doubling the PaO , the CaO only increased minimally. This is because the minimal amount of hemo-
2
2
globin in this anemic dog is already fully saturated. The oxygen supplementation is only bolstering the
dissolved plasma oxygen content (PaO ) and not greatly improving the total oxygen content. This is why sup-
2
plementing oxygen in a severely anemic animal cannot overcome the need for red blood cell transfusion.
5. In a patient with a normal Hb (15 mg/dL) who is hypoxemic (SpO 90% and PaO 60 mmHg):
2 2
/
CaO =( 15 1340 9 +( 600 003 =18mLdL ; below normal
.
)
×
×
×
.
.)
2
6. Supplementation of the patient in point 5 with oxygen raises the PaO to 80 mmHg, causing a concurrent rise
2
in the SaO to 95%
2
×
×
/
.
CaO =( 15 1340 95 + (80 0 003 =.x ) 19 .3mLdL ; closerto normal
)
.
2
Note that it is not the rise in PaO that caused the majority of this change; the elevation from 60 to 80 mmHg added
2
only 0.06 mg/dL to the total. However, because increasing the PaO also increases the SaO (Fig. 4.3), the total oxy-
2
2
gen content carried by hemoglobin also increased, contributing the most to the increase in the total oxygen content.
when breathing room air. However, as shown in the lungs and breathing 100% O as when under gen-
2
curve, above a PaO of about 100 mmHg, SaO is eral anesthesia, the expected PaO should be
2
2
2
no longer a good surrogate for PaO (and by exten- approximately 400–500 mmHg but the SaO will
2
2
sion lung function). Once the patient’s lungs hit the be 100%. If that same patient loses 50% lung func-
plateau depicted in Fig. 4.3, all the Hb-binding sites tion and the PaO drops to 250 mmHg, the SaO
2
2
are saturated with oxygen and any additional oxy- will still be 100%. In fact, for patients breathing
gen diffusing from the lungs must remain in the higher concentrations of O , a decreasing SaO is a
2
2
dissolved pool. For example, in a patient with normal late indicator of a significant loss of lung function,
74 K.A. Marshall and A.C. Brooks