The Veterinary Nurse’s Role in Reading Blood Gases

Obtaining blood samples for serum chemistry panels, complete blood counts, and coagulation panels is a familiar procedure for most veterinary nurses, but samples for blood gases are less commonly collected and analyzed in general practice. Knowing when and how to draw blood gas samples, as well as how to interpret the results, is critical to good patient care, as veterinary nurses are frequently the members of the team reviewing and delivering results. What the veterinary nurse reports back to the clinician has a direct impact on the patient’s treatment and outcome.

Why Measure Blood Gasses?

Blood gas measurement allows assessment of 3 primary parameters: the patient’s oxygenation, ventilation, and acid–base status. Blood gases can also be used to assess blood glucose, electrolytes, ionized calcium, and/or lactate levels. 

When used alone or in conjunction with a serum chemistry profile and a complete blood count, blood gas analysis aids in the diagnosis and treatment of many disease processes that are directly related to metabolic or respiratory dysfunction. Blood gas results are also indicators of how well that patient’s body is compensating for that disease. Being familiar with the dysfunctions that affect blood gases and their causes will help veterinary nurses remind veterinarians that blood gases can play a vital role in diagnosis and treatment. When a blood gas reading is needed, veterinary nurses should understand vessel selection (arterial or venous), collection methods, normal values and reference ranges (TABLE 1), and the physiologic meaning of findings.

Overview of Sample Collection and Processing

Step-by-step descriptions of how to properly obtain and process blood samples for blood gas evaluation are available elsewhere, but a few key considerations are listed here. TABLE 2 lists common sampling and processing errors and their effects.

Obtaining Venous Samples

Venous blood gas samples are commonly collected from the jugular vein, unless a central line is present, in which case they should be collected from the central line. Samples from these locations give a more global picture of the patient’s status than a sample taken from a peripheral vessel (FIGURE 1).

Figure 1. Process of obtaining a venous blood gas sample from a lateral saphenous central venous catheter. (A) Catheter in place with necessary supplies.

Figure 1. Process of obtaining a venous blood gas sample from a lateral saphenous central venous catheter. (B) Tapping out all air from syringe.

Figure 1. Process of obtaining a venous blood gas sample from a lateral saphenous central venous catheter. (C) Syringe sealed against air contamination.

Obtaining Arterial Samples

For arterial sampling, the area surrounding the collection site should be clipped and scrubbed. Hands should be sanitized and gloves donned. A prepared heparin (1000 IU/mL)-coated 3-mL syringe, a fresh 25-gauge needle, and a rubber stopper or tightly fitted syringe cap are needed.

TIP: Obtaining an arterial blood gas sample from a conscious patient can be challenging and cause pain. If the patient is anxious, panting, and/or shaking, this activity could alter the results. A local infusion of 2% lidocaine or a topical application of EMLA cream (a eutectic mixture of 2.5% lidocaine and 2.5% prilocaine) can aid in pain management of arterial punctures along with sedation to relieve stress.

Handling Samples

Once the blood sample is collected, every effort should be made to quickly remove any air bubbles from the syringe. Flicking the syringe and expelling air will help keep the integrity of the sample. The sample should be capped or the needle put in a rubber stopper. This prevents further contamination of the sample with air. Rolling the sample between the palms helps combine the sample with the anticoagulant, avoiding the common error of sample clotting.

Processing Samples

The sample should be analyzed directly after collection. If this is not possible, then the sample should be immersed in ice water.¹ At room temperature, if the sample is not analyzed within 20 minutes, continued cell metabolism starts to increase the PCO₂ and decrease the pH. The sample can be stored for up to 2 hours in an ice water bath; otherwise, a new sample must be obtained.

Evaluation of Blood Gas Findings

When assessing metabolic function, obtaining a venous sample is appropriate. Respiratory function can be assessed from venous blood gas findings; however, obtaining an arterial sample to assess whether respiratory dysfunction is affecting oxygenation (PaO₂) is ideal in clinical treatment. TABLE 3 lists the findings for metabolic and respiratory acidosis and alkalosis. 

Metabolic Dysfunction

Maintaining a balanced pH is vital to overall cellular function. The lungs and kidneys have synergistic roles in maintaining pH, which, along with chemical buffers, is constantly monitored and regulated by the brain. The body uses multiple mechanisms to correct acid–base imbalances, some of which work faster than others. For example, the process in which the lungs aid in pH balance takes effect in minutes to hours, unlike the process by which the kidneys compensate, which takes hours to days. Like the lungs, chemical buffers can assist rapidly in maintaining acid–base balance.

Metabolic Acidosis

In patients with metabolic acidosis, blood gas analysis will reveal decreased pH, normal to low-normal PCO₂, and decreased HCO₃. Metabolic acidosis can be seen when there is a loss of bicarbonate, an increased production or addition of acids, or failure of excretion of acids. Electrolytes, lactate, ketones, base excess, anion gap analysis, and urinalysis can help determine the type of metabolic acidosis present.

• Bicarbonate loss is typically through gastrointestinal losses that lead to hypovolemia and electrolyte imbalance.
• Patients with increased production of acids include those with diabetic ketoacidosis, lactic acidosis, or uremic acidosis.
• Excess acids from external sources come from ingestion of acidic toxins such as ethylene glycol or aspirin-containing medications.
• Kidney dysfunction or Addison’s disease causes an inability to excrete acids, leading to metabolic acidosis.

Metabolic Alkalosis

In patients with metabolic alkalosis, blood gas analysis will reveal increased pH, normal to increased PCO₂, and increased HCO₃. As with metabolic acidosis, other parameters to consider include an electrolyte panel and urinalysis. Metabolic alkalosis is seen when there are acid losses or base gains. 

• Acid losses from the digestive tract are caused by gastrointestinal disturbance (vomiting and diarrhea), obstruction, or torsion. 
• Acids can also be lost through potassium loss in urine. This can be associated with the administration of loop diuretics such as furosemide. 
• Excess bases are typically gained iatrogenically through administration of bicarbonate or metabolism of citrate during blood transfusions.

Respiratory Dysfunction

Carbon dioxide (CO₂) is an acidic compound and waste product of cellular metabolism. CO₂ is carried by red blood cells to the lungs, where it is released during exhalation. Changes in PCO₂ therefore reflect changes in ventilation and vice versa.

TIP: A patient’s PaO₂ depends on the FiO₂. This is known as the P/F ratio (PaO₂ to FiO₂) and is normally 5:1 (otherwise known as the 5× rule). For example, if a patient is inhaling “room” air, which has a FiO₂ of 21% (i.e., contains 21% oxygen), the PaO₂ should be ~100 mm Hg (5 × 21). If oxygen supplementation is given, FiO₂ increases, thereby changing the PaO₂. Therefore, if a patient is inhaling 100% oxygen, the PaO₂ should be ~500 mm Hg. These values vary depending on the method of oxygen administration (TABLE 4).

Respiratory Acidosis

In patients with respiratory acidosis, blood gas analysis will reveal decreased pH, increased PCO₂, and increased HCO₃. Respiratory acidosis occurs when there is an accumulation of acid (CO₂) in the blood that cannot be expelled appropriately by the lungs. Increased CO₂ is also called hypercarbia or hypercapnia and is a marker of hypoventilation.

• Neurologic diseases/dysfunction and anesthetic drugs such as opioids, gas inhalants, sedatives, neuromuscular blocking agents, and induction agents can all cause hypoventilation.
• Common restrictive airway processes that cause hypercapnia or CO₂ buildup include pleural effusion, thoracic trauma, pneumothorax, and diaphragmatic hernias.
• Airway obstructions or obstructive processes such as brachycephalic syndrome, occlusion of an endotracheal tube, and laryngeal paralysis are also common causes of respiratory acidosis.

TIP: Monitoring end-tidal CO₂ is vital to detecting respiratory emergencies or complications during anesthesia. Physical parameters such as mucous membrane color, capillary refill time, heart rate, and blood pressure should also be monitored. Hyperdynamic states that produce hyperemic gums, tachycardia, and hypoxia can all be associated with hypercapnia and are all signs of respiratory acidosis.

Respiratory Alkalosis

In patients with respiratory alkalosis, blood gas analysis will reveal increased pH, decreased PCO₂, and normal to decreased HCO₃. Respiratory alkalosis occurs when blood contains low amounts of CO₂ (hypocapnia/hypocarbia). Clinically, respiratory alkalosis is common in veterinary patients that are panting excessively, such as those exhibiting anxiety, stress, and/or pain. 

• Hypocapnia and, therefore, respiratory alkalosis can be caused iatrogenically by using an excessive respiratory rate or tidal volume when mechanically or manually ventilating a patient.
• Other causes of respiratory alkalosis include shock, sepsis, fever, and hypoxemia. 
• Respiratory alkalosis can also be secondary to metabolic acidosis. This response occurs when a decrease in pH leads chemoreceptors in the body to trigger an increase in respiratory rate and/or volume to compensate and balance pH.

TIP: Addressing conditions that cause panting, such as anxiety and pain, before an anesthetic event will help control the patient’s ventilation status. 

Recommended Reading

Day TK. Blood gas analysis. Vet Clin North Am Small Anim Pract. 2002;32(5):1031-1048.