Page 107 - Basic Monitoring in Canine and Feline Emergency Patients

also include renal values and hemoglobin levels, they calculated from arterial blood gas data to help the
can provide quick additional point-of-care informa- clinician trend improvement or deterioration of lung
VetBooks.ir tion about the patient’s disease processes. function over time. Any major change in mechanical
Venous analysis can also be used as a reasonable
ventilator settings or patient stability should prompt
surrogate for PaCO in most patients. For example,
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if the PvCO is 70 mmHg, one can reasonably infer reassessment of oxygenation and ventilation.
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that the PaCO is likely to be around 65 mmHg and
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the patient is severely hypoventilating. Venous pH is
generally 0.02–0.05 units lower than arterial because 5.4 Interpretation of Findings
of the slightly higher PCO content of venous blood.
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Assessment of PvCO or PaCO is important any- Blood gas analysis: Acid–base
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time a patient’s ventilation status is in question. The Traditional acid–base analysis
ventilation status of a patient cannot be accurately
determined by physical examination alone. For 1. Evaluate the pH. An elevated pH is an alkalemia,
example, many clinicians will refer to animals with and a low pH an acidemia.
elevated respiratory rates (tachypnea) as ‘hyperventi- 2. Determine what is causing the change in pH by
lating.’ However, it is important to remember that looking at the PCO and HCO . Remember that
−
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ventilation is a function of both respiratory rate and PCO acts as an acid, so increased PCO will cause
2
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tidal volume. Therefore, patients with diseases that a respiratory acidosis and decreased PCO a respira-
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−
impair respiratory strength or drive (e.g. excessive sed- tory alkalosis. The HCO acts as a base, so its influ-
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ation, see Table 5.1) can have inadequate ventilation ence will be opposite; increases in HCO will cause
−
3
(elevated PCO values) even with a fast and shallow metabolic alkalosis, and decreases in HCO meta-
−
2
3
respiratory rate. Assessment of the PaCO level is the bolic acidosis. The combination of these two forces
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gold standard method to quantify ventilation. will create the final ‘-emia’ of the blood.
Arterial blood gas analysis is also commonly per- 3. The third step is to determine if compensation is
formed either to rule in/out hypoxemia as a true occurring. Compensation means the opposite process
cause of a patient’s underlying clinical signs or to is trying to antagonize the pH change caused by the
assess severity and response to therapy in cases of primary problem. For example, if the primary prob-
respiratory disease. For example, if a patient pres- lem is a respiratory acidosis (increased PCO ), the
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ents on an emergency bases with an increased compensation will be a metabolic alkalosis (increased
−
−
respiratory rate, this could be due to hypoxemia, or HCO ). If the PCO and HCO change in oppo-
2
3
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could be hyperventilation due to a ‘lookalike’ for site directions, the disorder is considered a mixed
respiratory distress, such as pain, compensation for disorder.
a metabolic acidosis, hyperthermia, etc. (see Table 4. If it appears that compensation is occurring, the
5.1). If initial screening tests and examination do next step is to determine if compensation is appropri-
not reveal an alternate explanation and/or pulse ate or not. This is determined by the calculations in
oximetry is not reliable in the patient, arterial Table 5.4. If compensation is not adequate, the disor-
blood gas analysis can be used to establish if hyp- der is considered a mixed disorder (see Box 5.4).
oxemia is truly the cause of tachypnea. 5. If there is a metabolic acidosis, use the AG to fur-
In general, serial blood gas analysis (at least every ther classify metabolic acidosis as ‘high gap’ or ‘normal
8–12 hours) should be considered in patients requir- gap.’ See Box 5.3, Case study 2, and Fig. 5.1 for further
ing oxygen and/or ventilator support. This data information about application of the anion gap.
helps determine if oxygen supplementation levels are # # An elevated gap implies the presence of
adequate, and assures adequate blood levels of PaO additional anions not measured with the
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and PaCO as oxygen/ventilation support is weaned. standard electrolytes. Common differentials
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However, due to increased cost and invasiveness as for an elevated AG are shown in Table 5.2.
compared to SpO and end tidal carbon dioxide # # If the AG is normal, the chloride must be
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(ETCO ), arterial blood gas readings are typically elevated to cause the metabolic acidosis.
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performed intermittently and the results corrobor- This is called either a ‘normal gap’ or ‘hyper-
ated with those monitors (see Chapters 4 and 6) in chloremic’ metabolic acidosis. Common dif-
each patient. In addition, methods such as the A–a ferentials for a hyperchloremic metabolic
gradient and P/F ratio (see Section 5.4) can be acidosis are shown in Table 5.2.
Venous and Arterial Blood Gas Analysis 99