Notes supplied by Nadja Sigrist, DrMedVet, FVH(Small Animals), DACVECC.

Introduction

Blood gas analysis allows interpretation of acid-base status as well as respiratory function, including both oxygenation and respiration. This lecture focuses on the practical approach of blood gas analysis and refers to the literature for a more in-depth discussion of acid-base balance and (patho)physiology of respiratory function.

Sample Taking

Both arterial and (central) venous blood samples can be used to interpret acid-base status and ventilation, but only arterial blood gases will provide true information regarding oxygenation. Arterial blood gas samples can be derived from any superficial artery, but commonly the femoral artery or the dorsal pedal artery are used. If continuous arterial blood monitoring is required, an arterial catheter in the dorsal pedal artery is more convenient. Arterial samples should be collected easily (without excessive negative pressure or significant venous stasis) and without air contamination and should ideally be analysed immediately. If not they may be kept at 4°C (ice water) for a maximum of 2 hours.

Normal Values

Normal values for blood gas results have been published (Figure 1); however, validated normal ranges of each individual blood gas machine should be used whenever available.

Figure 1. Normal blood gas values in dogs and cats.

Interpretation of Acid-Base Balance

Interpretation of acid-base balance includes identification of the primary problem (acidosis vs. alkalosis), calculation of compensation, identification of mixed problems and clinical interpretation. Other means of analysis are calculation of the anion gap and Stuart's approach to acid-base disorders.

Acid-base disorders have an underlying primary problem. As the animal tries to maintain a physiological pH, compensatory changes will occur that are typical for each underlying problem (Figure 2).

The following five steps will allow interpretation of the primary problem and identification of mixed problems.

 pH change?

 2 > 7.4 alkalosis

 2 < 7.4 acidosis

 PCO₂ or HCO₃ change:

 Same direction as pH metabolic

 Opposite direction to pH respiratory

 Adequate compensation? Use Figure 3 to calculate expected compensatory changes in PCO₂ (for metabolic acidosis/alkalosis) or HCO₃ (for respiratory acidosis/alkalosis).

 Identification of a mixed problem. The following findings are associated with a mixed problem:

 Normal pH despite abnormal PCO₂ or HCO₃

 Overcompensation

 Insufficient compensation

 Anion gap (AG). Calculation of AG allows identification of metabolic acidosis due to unmeasured anions.

 AG = Na - Cl - HCO₃ Normal < 20 (dog), < 27 (cat)

 Increased AG: metabolic AG acidosis (methanol, uraemia, diabetes/diabetic ketoacidosis (DKA), paraldehyde, isopropyl alcohol, lactate, ethylene glycol, rhabdomyolysis, salicilate (aspirin) MUD PILERS).

 Low AG: hypoalbuminaemia

Once acid-base disorders are identified, the findings should be evaluated in conjunction with clinical signs and differentials of the identified problem.

Figure 2. Primary acid-base problems with compensatory changes.

Figure 3. Expected compensatory changes in PCO₂ (for metabolic acidosis/alkalosis) or HCO₃ (for respiratory acidosis/ alkalosis).

Differentials

Hyperchloraemic Acidosis

 Diarrhoea

 Renal tubular acidosis

 Carbonic anhydrase inhibitors

 Dilutional acidosis (NaCl)

 Addisons disease, aldosterone deficiency

Respiratory Acidosis

Hypoventilation:

 Upper airway stenosis

 Central respiratory depression

 Cardiopulmonary arrest

 Neuromuscular problem

 Severe pulmonary abnormalities

Metabolic Alkalosis

 Loss of Cl^-: vomiting (gastric fluid), diuresis.

 Mineralocorticoid excess: Cushing's, hyperaldosteronism.

 Alkali administration: bicarbonate, phosphorus binder.

 Others, e.g., refeeding syndrome, severe K or Mg deficiency

Respiratory Alkalosis

Hyperventilation:

 Hypoxaemia (anaemia, shock, V/Q mismatch, diffusion problem, shunt)

 Primary lung disease (pulmonary receptor stimulation): pneumonia, embolism, oedema

 Hyperthermia (fever, heat stroke)

 Pain

Therapy

Most metabolic derangements can be corrected by appropriate fluid therapy and will not require drug therapy. Sodium bicarbonate may be indicated in patients with metabolic acidosis associated with renal insufficiency or severe metabolic acidosis despite appropriate fluid therapy (for example patient with DKA). Sodium bicarbonate is contraindicated in patients with respiratory acidosis as it will add to CO₂ concentrations.

Respiratory acid-base abnormalities are treated by eliminating the underlying disease and appropriate ventilation therapy if required.

Interpretation of Oxygenation/ Ventilation

Oxygenation and ventilation are assessed using the following steps.

Oxygenation (PaO₂)

 Normal PaO₂ breathing room air is 80–100 mmHg

 With oxygen supplementation, normal PaO₂ should be 4–5 times FiO₂

Differentials for PaO₂ include:

 FiO₂ (altitude)

 Hypoventilation

 V/Q mismatch

 Pulmonary diffusion problem

 Cardiogenic: Right-to-left shunt

PCO₂

 Increased hypoventilation

 Decreased hyperventilation (see above for differentials)

Signs of V/Q Mismatch or Diffusion Problems

The following equations allow interpretation of pulmonary gas exchange:

 A-a Difference: PAO₂–PaO₂

 PAO₂ = FiO₂ x (barometric pressure - 47) - 1.2 x PaCO₂

 Normal: 0–15 with room air, < 100 with 100% O₂

 PaCO₂ + PaO₂ should be < 120–160 mmHg at room Air

 PaO₂ / FiO₂:

 Normal > 400

 < 300: Acute lung injury

 < 200: Acute respiratory distress syndrome (ARDS)

Therapy

Insufficient oxygenation is treated by eliminating the underlying disease, oxygen therapy and mechanical ventilation in patients where oxygen therapy is not sufficient or increased work of breathing occurs with severely increased respiratory effort. Ventilation problems are treated by eliminating the underlying disease process (analgesia, thoracocentesis, etc.), and mechanical ventilation in patients with hypoventilation.