Venous Blood Gas Interpretation

Assessment of acid-base status gives insight into three physiologic processes: alveolar ventilation (venous), acid-base (venous or arterial), and oxygenation (arterial). Venous blood gas (VBG) analysis is arguably one of the most routinely used point of care tests done in the critical care setting. A VBG is performed when there is a need to know what a patient’s acid-base or ventilation status is. The results of a VBG gives the veterinary team more information about the severity of a critical patient’s disease, so that appropriate interventions (i.e., fluid therapy, electrolyte supplementation, oxygen support) can be provided. Obtaining a venous blood sample is a routine procedure and can be collected either from a peripheral/central vessel or during IV catheter placement. Ideally, the blood sample should be run as soon as possible (within minutes) to ensure accurate results. It is also important to note that the status of tissues (i.e., well-perfused vs. hypoperfused) from the venous sample site can affect results. While the analyzers used for VBG analysis can vary, the interpretation of results remains constant. When evaluating a patient’s VBG result, the values needed for interpretation are pH, PCO₂, and HCO₃. The pH is a measurement of acidity or alkalinity of the blood (how many hydrogen molecules are present in the blood). An excess of hydrogen ions causes a decrease in pH (acidosis), while a shortage of hydrogen ions causes an increase in pH (alkalosis). PCO₂ is a measurement of the partial pressure of carbon dioxide in the blood. PCO₂ is an indicator of the respiratory component of a blood gas analysis. An excess of CO₂ causes an acidosis, while a shortage of CO₂ causes an alkalosis. HCO₃ is a measurement of bicarbonate (bicarb) in the body. Bicarb is a major buffer and represents the metabolic component of blood gas analysis.

Below is a quick reference chart for general reference ranges of VBG analysis

A simple acid-base disturbance is when there is one primary disorder (metabolic vs. respiratory), and the appropriate compensation for that disorder. The four primary acid-base disturbances that occur in the body are metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis.

When you approach interpretation of a VBG result, go through the following steps:

1.  Is there an acid-base disturbance? Evaluate pH—is it acidotic or alkalotic?

2.  Identify the primary disturbance—is it respiratory (PCO₂) or metabolic (HCO₃)?

3.  Is the compensatory response as expected?

4.  Consider the underlying disease process(es) that may be responsible for the acid-base disturbance.

One method for helping determine the acid-base status is to memorize the pneumonic ROME, which stands for respiratory opposite metabolic equal. This helps quickly identify the primary acid-base disorder. For primary respiratory disturbance, the pH and PCO₂ are opposite (↓pH + ↑PCO₂ = respiratory acidosis, ↑pH + ↓PCO₂ = respiratory alkalosis). For primary metabolic disturbance, the pH and HCO₃ are equal (↓pH + ↓HCO₃ = metabolic acidosis, ↑pH + ↑HCO₃ = metabolic alkalosis). Whatever the primary disturbance is, the body compensates for the acid-base imbalance. This means a change in the respiratory or metabolic component will induce a change in the other in an effort to get the pH back to the normal range. A respiratory compensation is expected in metabolic acid-base disturbances. The respiratory system responds within minutes by adjusting ventilation (i.e., changes respiratory rate, changes tidal volume, or changes both). A metabolic compensation is expected in respiratory acid-base disturbances. The metabolic system responds more slowly (hours to days) via the kidneys by adjusting the absorption or excretion of ions (i.e., bicarbonate, ammonia).

Metabolic acidosis is the most common acid-base disturbance in veterinary medicine. It is characterized by a low pH, low HCO₃, and compensatory low PCO₂. Metabolic acidosis occurs due to an increase in the amount of acid in the body. The body responds to metabolic acidosis by implementing buffering systems (renal excretion of ammonia) and hyperventilation (to increase alveolar ventilation) in an effort to raise the pH. Primary causes that contribute to metabolic acidosis include a loss of bicarbonate-rich fluids (i.e., small intestinal diarrhea), addition or production of an acid (i.e., toxin ingestion, lactic acidosis, diabetic ketoacidosis), or failure of renal excretion of an acid (i.e., hypoadrenocorticism, renal failure). Metabolic alkalosis is characterized by a high pH, high HCO₃, and compensatory high PCO₂. The body responds to metabolic alkalosis by converting buffers, increasing renal excretion of alkali, and hypoventilation (to decrease alveolar ventilation) in an effort to lower the pH. Primary causes that contribute to metabolic alkalosis include loss of chloride-rich fluid (i.e., vomiting), severe potassium or magnesium deficiency, hypoalbuminemia, refeeding syndrome, impaired renal function, post-hypercapnia syndrome, pyloric obstruction, chronic administration of an alkali, or diuretic treatment. Respiratory acidosis is characterized by low pH, high PCO₂, and compensatory high HCO₃. The body responds to respiratory acidosis by buffering and renal absorption of HCO₃, in an effort to raise pH. Primary causes that contribute to respiratory acidosis include hypoventilation, gas exchange disorders (i.e., diffusion impairment, ventilation-perfusion mismatch, shunt), or increase in CO₂ production. Respiratory alkalosis is characterized by high pH, low PCO₂, and compensatory low HCO₃. The body responds to respiratory alkalosis by buffering and renal excretion of HCO₃, in an effort to lower pH. Primary causes that contribute to respiratory alkalosis include hypotension, fever/heat-induced illness, systemic inflammatory response syndrome, sepsis, pulmonary thromboembolism, pulmonary parenchymal disease, or hyperventilation.

Below is a quick reference chart of the primary acid-base disturbances

Another method for helping determine the acid-base status of a critical patient based on VBG results is by doing acid-base tic-tac-toe. Acid-base tic-tac-toe is where you input your values (pH, PCO₂, HCO₃) into the boxes of a tic-tac-toe chart based on if the value is acidotic, normal, or alkalotic.

Figure 1

Before “playing” tic-tac-toe, remember what the acid and base parameters are for pH, PCO₂, and HCO₃:

• Acid pH <7.35
• Base pH >7.45
• Acid PCO₂ >45
• Base PCO₂ <35
• Acid HCO₃ <18
• Base HCO₃ >24

Once you have a VBG result, look at the pH, PCO₂, and HCO₃ values and mark which box they fall into. For example, a patient has the following VBG values:

• pH = 7.15
• PCO₂ = 65
• HCO₃ = 27

For this VBG result, mark pH in the acid box, mark PCO₂ in the acid box, and mark HCO₃ in the base box.

Figure 2

From the pH, it’s clear this is an acidosis, with the primary disturbance being respiratory since it’s also in the acid box. It’s also clear there’s the appropriate compensatory response since the metabolic disturbance in the opposite base box. For another example, a patient has the following VBG values:

• pH = 7.5
• PCO₂ = 50
• HCO₃ = 27

For this VBG result, mark pH in the base box, mark PCO₂ in the acid box, and mark HCO₃ in the base box.

Figure 3

From the pH, it’s clear this is an alkalosis, with the primary disturbance being metabolic since it’s also in the base box. It’s also clear there’s the appropriate compensatory response since the respiratory disturbance in the opposite acid box.

It is important for the veterinary technician/nurse to be familiar in their understanding of venous blood gas values. Doing so empowers them to not only contribute to the interpretation, but also to apply critical thinking skills by looking at how the lab values correlate with the patient’s condition.

Arterial Blood Gas Interpretation

Assessment of arterial blood gases gives insight into three physiologic processes: alveolar ventilation, acid-base, and oxygenation. Arterial blood gas (ABG) analysis differs from venous blood gas analysis in that it’s specifically indicated in patients with respiratory compromise, as all aspects of pulmonary function can be assessed. While a venous blood gas (VBG) can be a screening tool for ventilation status and an acid-base baseline, ABG should be used whenever pulmonary parenchymal disease is suspected.

Normal pulmonary function involves the movement of air (78% nitrogen, 21% oxygen, trace gases) via inspiration and expiration. Air moves into the lungs, through the conducting pathways until it reaches the alveoli. The alveoli are the primary site of gas exchange within the lungs; gas exchange occurs across a blood-gas barrier. Oxygen (O₂) diffuses from the alveoli to the capillary blood supply across the barrier via passive diffusion. Carbon dioxide (CO₂) diffuses from the capillary blood supply to the alveoli across the barrier via passive diffusion. When thinking about diffusion of gases, it can be described by Fick’s law: “The diffusion of a gas across a membrane is directly proportional to the area of the tissue membrane and the pressure gradient, and inversely proportional to the thickness of the membrane.” When we consider normal respiration, there are three different partial pressures of oxygen (PO₂) and partial pressures of carbon dioxide (PCO₂): inspired, alveolar, and arterial. During inspiration of air, PO₂ is at its highest at 150 mm Hg and PCO₂ is 0 mm Hg. Once air has reached the alveoli, PO₂ drops slightly to 100 mm Hg and PCO₂ rises to 40 mm Hg; this is because O₂ and CO₂ rapidly diffuse across the blood-gas barrier (O₂ in, CO₂ out). Once diffusion occurs and the gases are at the level of the arterial capillaries, PO₂ and PCO₂ equal out to the systemic arterial circulation. It’s important to understand the normal physiologic process of respiration, as ventilation and oxygenation are two different processes, despite often being used synonymously. Ventilation is the process of appropriate gas exchange within the alveoli (O₂ is inhaled, CO₂ is exhaled). Once ventilation has occurred, we become concerned with oxygenation and the patient’s oxygenating ability. Oxygenation refers to how well O₂ is diffused from the alveoli, then bound to hemoglobin, dissolved into the bloodstream, and delivered to bodily tissues.

When it comes to measuring oxygenation in a patient, the options are pulse oximetry (SpO₂) or ABG. SpO₂ is an easy, noninvasive means to measure the oxygen saturation of hemoglobin. Each hemoglobin molecule within a red blood cell contains four oxygen binding sites; when all four sites are bound, the hemoglobin molecule is said to be “saturated.” The SpO₂ reading occurs by the pulse oximeter collecting data from passing red blood cells. Pulse oximetry uses infrared light to scan capillaries to assess if red blood cells are saturated or unsaturated; the degree of saturation can vary. The pulse oximeter then averages these findings in order to produce a percentage of saturation, which should be >95%. This means that a normal patient breathing room air (21%) oxygen and an anesthetized patient breathing 100% oxygen can have the same SpO₂ value. A SpO₂ reading of <90% is indicative of hypoxemia, or low levels of oxygen in the bloodstream. While pulse oximetry is a useful tool, it does pose certain limitations, making it a less than ideal monitor when dealing with respiratory compromised patients. Factors such as probe position, patient perfusion, and even ambient light can all affect the SpO₂ value.

While pulse oximetry is a reasonable option, the “gold standard” for measuring a patient’s oxygenation status is through ABG. An ABG allows us to directly assess the partial pressure of O₂ dissolved in the bloodstream (P_aO₂) since arterial blood is oxygen rich (compared to venous blood which is oxygen depleted). P_aO₂ is also a good indicator of a patient’s oxygenation status as it relates to the diffusion ability and perfusion properties of the lungs; it’s a measure of the lungs’ ability to transport oxygen from the atmosphere to the blood. A healthy patient that is breathing room air (FiO₂ 21%) should have a P_aO₂ between 85–110 mm Hg. In normal patients, their P_aO₂ should be roughly five times their FiO₂ (i.e., a patient breathing room air would have P_aO₂ of 105 mm Hg). In patients with pulmonary disease or respiratory compromise who are receiving oxygen supplementation, their P_aO₂ would be higher to account for the increased FiO₂ (there is no limit to P_aO₂ values). In patients who are anesthetized and receiving 100% O₂, their P_aO₂ should be >500 mm Hg. A P_aO₂ value of <80 mm Hg is indicative of hypoxemia, and a value of <60 mm Hg is indicative of severe hypoxemia. Causes of hypoxemia include hypoventilation (P_aCO₂ >60 mm Hg), decreased inspired oxygen (FiO₂) content, ventilation/perfusion (V/Q) mismatch, intrapulmonary shunting, and diffusion impairment. Addressing hypoxemia is very important, as it can lead to hypoxia, or inadequate oxygen delivery (DO₂) to meet tissue oxygen demand (VO₂).

A key concept to understand that relates to a patient’s oxygenation status is the oxyhemoglobin dissociation curve. The oxyhemoglobin dissociation curve depicts the relationship between oxygen hemoglobin saturation (SpO₂) and partial pressure of oxygen (P_aO₂). What’s unique about this curve is that it isn’t linear, but rather sigmoid, meaning SpO₂ and P_aO₂ are directionally, but not linearly, related. The curve is determined by hemoglobin’s affinity for oxygen (how readily hemoglobin acquires and releases oxygen molecules). Factors that affect the curve are CO₂, temperature, and pH. During periods of hypocapnia, hypothermia, and alkalosis, the curve shifts left; this increases hemoglobin’s affinity for oxygen, making it easier for oxygen to bind to hemoglobin but harder for oxygen to be released. During periods of hypercapnia, hyperthermia, and acidosis, the curve shifts right; this decreases hemoglobin’s affinity for oxygen, making it harder for oxygen to bind to hemoglobin but easier for oxygen to be released. The most important clinical manifestation of this SpO₂/P_aO₂ relationship is the difference between normoxemia and hypoxemia; small changes in SpO₂ correlate with large changes (roughly 4x) in P_aO₂.

When assessing critical respiratory patients, an ABG also allows us to assess oxygen indices such as the PF ratio and alveolar-arterial (A-a) gradient. The PF ratio is the ratio of arterial partial pressure of oxygen (P = P_aO₂) and fraction of inspired oxygen (F = FiO₂). When calculating FiO₂, the FiO₂ percentage is converted into decimal form (i.e., 21% = 0.21, 100% = 1.0). The PF ratio is a quick and easy calculation that can be helpful in assessing the severity of pulmonary injury and to determine how oxygen responsive the patient is. In a healthy patient breathing room air that has a P_aO₂ of 105 mm Hg, they would have a PF ratio of 105:0.21 (105 ÷ 0.21) = 500. Since it’s a ratio, the calculated value has no units. When supplementing oxygen, the general guidelines for FiO₂ values are flow-by/face mask delivery = 25–30%, nasal cannula delivery = 35–40%, oxygen cage = 40–60%, anesthetic circuit = 100%. A normal PF ratio is ≥400. A PF ratio <300 is suggestive of acute lung injury (ALI), and a PF ratio of <200 is suggestive of acute respiratory distress syndrome (ARDS). The A-a gradient is the difference between the alveolar oxygen concentration (PAO₂) and arterial oxygen (P_aO₂) concentration (a) and is helpful in assessing the efficiency of gas exchange. The equation is as follows:
A-a gradient = PAO₂–P_aO₂

Although at first glance this looks simple, we must first calculate the value of PAO₂, as the P_aO₂ value is provided from an ABG. PAO₂ is calculated from the alveolar gas exchange equation, which is:
PAO₂ = FiO₂(P_atm–P_H20)–(P_aCO₂/RQ)

In order to calculate the PAO₂ value, we need to break down the components of the equation and understand what each represents. The FiO₂ represents the fraction of inspired oxygen, and ideally should be room air (21%). The P_atm is a constant and represents the atmospheric barometric pressure. Sea level is 760 mm Hg and the P_atm value will be dependent on elevation. P_H20 is another constant that represents the water vapor pressure; its value is 47 mm Hg. The P_aCO₂ value is provided from the ABG sample. The RQ (respiratory quotient) is the last constant and accounts for the ratio of oxygen consumption to CO₂ production; its value is 0.8. Once the constant values have been inputted, the full A-a gradient calculation is:
A-a = [FiO₂(P_atm–47)–P_aCO₂/0.8]–P_aO₂

When working out the calculation, it’s important to remember the order of operations (PEMDAS): parentheses, exponents, multiplication/division, addition/subtraction. To practice with a sample problem, let’s have a patient that is breathing room air, is at sea level, and has a P_aO₂ = 90 mm Hg and P_aCO₂ = 50.

The equation would look like:
A-a = [0.21(760–47)–45/0.8]–90
First calculate the parentheses → 760–47=713
A-a = [0.21(713)–45/0.8]–90
There are no exponents, so next calculate multiplication and division → 0.21(713) and 50/0.8
A-a = [150–56]–50
Lastly, calculate subtraction (there is no addition) → 150–56–90
A-a = 4 mm Hg

In a healthy animal breathing room air, the alveolar oxygen concentration (PAO₂) compared to the P_aO₂ is approximately a 5–15 mm Hg difference. Therefore, the normal A-a gradient value is expected to be around 10 mm Hg. The larger the gradient, the more indicative of the severity of hypoxemia the patient is experiencing; another way to think of this is that there’s a problem with oxygen diffusing from the alveoli to the arterial blood. A-a values greater than 15 mm Hg support the use of supplemental oxygen, while values greater than 20–30 mm Hg become more concerning for severe hypoxemia and development of ARDS. Because the A-a gradient value is based on a FiO₂ of room air (21%), the arterial blood sample should be collected with the patient breathing room air. The A-a gradient can still be calculated with patients receiving supplemental oxygen, however, the reference range for what’s considered normal becomes skewed.

When it comes to measuring ventilation in a patient, the P_aCO₂ should be evaluated. P_aCO₂ is the partial pressure of carbon dioxide dissolved in the bloodstream. P_aCO₂ is determined by a balance between tissue production of CO₂ and the body’s elimination of CO₂. Normal P_aCO₂ should be between 35–45 mm Hg. A P_aCO₂ value of >45 mm Hg is indicative of hypercapnia, and a value of >60 mm Hg is indicative of severe hypercapnia. The most common cause of hypercapnia is hypoventilation or decreased alveolar ventilation. Hypoventilation can be caused by pleural space disease, respiratory muscle fatigue, chest wall injury, upper airway obstruction, CNS disease, neuromuscular disease, and respiratory depressant medications. Addressing hypercapnia is important as it can lead to respiratory acidosis, myocardial depression, vasodilation, and increased intracranial pressure.

Below is a quick reference chart for general reference ranges of ABG analysis

Oxygenation is a vital life process and evaluating an ABG is the best means to assess oxygenation and ventilation status in respiratory patients. Understanding what factors affect a patient’s oxygenation and ventilation status is key to addressing pulmonary pathologies, initiating treatment, and monitoring response to therapy. Veterinary technicians and nurses play an important role in the sample collection and diagnostic testing for ABG analysis and are often the first to have ABG results.

References

1.  Battaglia AM, Steele AM, Battaglia AM, eds. Small Animal Emergency and Critical Care for Veterinary Technicians. St. Louis, MO: Elsevier; 2016.

2.  Creedon JM, Davis H, eds. Advanced Monitoring and Procedures for Small Animal Emergency and Critical Care. Oxford: Wiley-Blackwell; 2012.

3.  DiBartola SR, ed. Fluid, electrolyte, and acid-base disturbances. St. Louis, MO: Saunders; 2012.

4.  Norkus C, ed. Veterinary Technician’s Manual for Small Animal Emergency and Critical Care. Hoboken, NJ: Wiley-Blackwell; 2013.

5.  Randels-Thorp A, Liss D, eds. Acid-Base and Electrolyte Handbook for Veterinary Technicians. Ames, IA: Wiley/Blackwell; 2017.

6.  Scalf R, ed. Study Guide to the AVECCT Examination. San Antonio, TX: AVECCT; 2014.

7.  Silverstein DC, ed. Small Animal Critical Care Medicine. St. Louis, MO: Saunders; 2015.