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Blood gas analysis for metabolic disorders in practice

Blood gas analysis can help guide appropriate therapies, especially with patients with complex co-morbidities or those not responding as you might expect

The minute blood gas analysis gets mentioned, many vets glaze over and feel that it is a theoretical entity that isn’t of value to their patients and won’t change what they do as veterinary surgeons. I am the first to admit that blood gas analysis is not relevant to all patients, but for those that have complex co-morbidities or simply are not responding as you might initially expect, it can guide appro­priate therapies. The principles of blood gas evaluation can be applied to all species. However, to practically use blood gases, a basic and more complex understanding of physiol­ogy behind the numbers is required. The aims of this article are to recap prior knowledge of blood gas analysis and then move on to more complex concepts you can apply to clinical cases.


No discussion regarding blood gas evaluation would be complete without discussing lactate concentrations and for the purposes of this article will be confined to measurement in the blood. Lactate is produced by anaerobic metabolic processes and its subsequent quantitative assessment pro­vides the opportunity to gain an insight into the presence and severity of tissue hypoperfusion (or hypoxia) in the majority of our clinical patients. Point-of-care laboratory tests have allowed more rapid assessment of patient lactate status and increased its clinical usefulness. They work best on plasma, but you can get an idea of trends using whole blood. Normal lactate concentrations in plasma of normal animals should be less than 1.5 to 2.0mmol/l. Although absolute values correlate with the severity of the disease process, survival in many diseases is better correlated to reduction in lactate concentrations in response to therapy. Hyperlactataemia can be split into two types: A and B. A is the most common, but in patients that do not respond to standard therapies (fluid, oxygen or blood administration depending on the underlying cause), understanding causes of type B hyperlactataemia is required (Brunori, 2020).

Practical points regarding blood gas analysis

Venous blood gas analysis is performed to evaluate acid-base status and jugular venous oxygen analysis can be of value to assess tissue oxygen uptake. Compared with arterial samples, pH will be slightly lower and PCO2 slightly higher.

When collecting samples, try to avoid excessive preparation of the sampling site. Samples should be collected into hep­arin only – citrate or EDTA will alter pH and make measure­ments of K and Ca unreliable. Samples should be analysed as quickly as possible.

Basic physiology behind blood gas evaluation

The basic knowledge many of us have of acid-base disturbances are centred around the relationship of pH to partial pressures of CO2 and bicarbonate. These factors are related by the Henderson-Hasselbalch equation:

pH = pK + log[HCO3]x 0.03[PaCO2]
This can be simplified as: pH ~HCO3/PaCO2

Normal ranges do vary between species. In a very basic sense for mammals, we can use the rule of fours: normal pH=7.4, PCO2=40mmHg and HCO3=24mmol/l. This rule does not work well for cats, but works adequately for other species (Table 1).

TABLE (1) Normal ranges of pH, PCO2 and HCO3- vary between animals, but in a very basic sense for mammals we can use the rule of fours

The initial basic evaluation of a blood gas is to deter­mine whether the patient is acidaemic or alkalaemic and whether the primary derangement is respiratory, metabolic or mixed. Initially the primary disorder is identified as being either respiratory or metabolic depending upon the changes seen in PCO2 and HCO3. The next step is to consider whether there is any compensation that is a result of the primary event (Table 2). For respiratory disorders, this can provide us with information regarding chronicity of disease as it requires changes in HCO3concentration. Calculations are available in order to quantify expected compensation (Table 3). The main limitation of this approach is that if you have a metabolic derangement, it does not help you to categorise the underlying cause.

TABLE (2) Evaluation of basic blood gas analysis
TABLE (3) Ways to quantify degree and extent of compensation

Base excess (BE)

This is the difference between the normal concentration of buffer bases (Hb, proteins, phosphate, etc) and the measured concentration. It should more accurately identify the meta­bolic component of any disturbance, but can also identify a compensatory metabolic abnormality in chronic respiratory disorders. Please also note that the terminology is confusing as it is possible to have a negative base excess.

Anion gap (AG)

The number of measured cations in the body is usually greater than the number of measured anions (this includes proteins, phosphates and sulphates) hence the nor­mal AG is positive (8 to 25 for dogs and 10 to 27 for cats).

AG = (Na+ + K+) – (Cl + HCO3)

As acid accumulates in the body, buffering by HCO3 occurs. If the acid is HCl, then there is a mEq for mEq exchange of Cl for HCO3 and the AG remains unchanged. This will also occur if there is a net loss of HCO3(eg diarrhoea). If the reason for the acidosis is due to an unmeasured anion (eg ketoacidosis), the gap increases as the HCO3 falls. Although previously relied upon as a diagnostic aid, its usefulness has been questioned.

The Stewart approach

Unlike Henderson-Hasselbalch (H-H), this approach consid­ers three independent variables as contributors to changes in pH: PCO2, the difference between strong cations and strong anions (strong ion difference [SID]) and total weak acids (albumin, globulins and inorganic phosphate [ATOT]) (Stewart, 1983).

SID = [Na+] + [K+] – [Cl] – [lactate]

This theoretical approach allows detection of the individual contributors to the metabolic component (within reason), which can help to narrow down the primary cause of the acid-base disturbance (Hopper and Haskins, 2008). This approach acknowledges that electrolytes and plasma pro­teins play a significant role in acid-base disturbances and that bicarbonate does not, but instead changes in response to other primary causes. Unlike BE or AG, it can be used to analyse acid-base problems even in the presence of elec­trolyte abnormalities or hypoalbuminaemia.

Due to the cumbersome nature of calculations and assumptions, the development of a modified Fencl-Stew­art approach, designed to be easily applied clinically for evaluating the metabolic contribution to acid-base, provides more detailed information of the various contributors.

The Fencl-Stewart approach

This approach combines BE and the Stewart approach by separating BE into components to assess metabolic changes to the acid-base disorder. These components form five equa­tions, which allow the magnitude and contribution of each parameter to be calculated. These equations are based on: (1) a free water effect (indirectly derived from sodium con­centration); (2) chloride effect; (3) albumin effect; (4) lactate effect; and (5) phosphate effect. These equations are easily applied clinically for evaluating the metabolic contribution to acid-base balance, separating the net metabolic abnormali­ties into components thus allowing easier detection of mixed metabolic acid-base abnormalities. The basic rules are that for each effect, the larger the number is from one, the more impact that effect is having on the metabolic derangements in that animal. If the number is negative, the change is having an acidifying effect and if it is positive, it is having an alkalin­ising effect. When you start to evaluate animals with meta­bolic derangements using this approach, it becomes evident that many have marked acidifying and alkalinising compo­nents, such that the pH in some circumstances is less severe than the changes that are evident and indeed the degree of clinical signs evident in the patient.

Free water effect

Free water effect = 0.22 (cats)-0.25 (other species) x ([Na+] – normal [Na+])

An excess of free water (positive value) causes Na+ concen­tration to decrease (hyponatraemia) which is acidifying. A deficit (negative value) of free water has the opposite effect; it increases Na+ concentration (hypernatraemia) and is alkalinising.

Chloride effect

Chloride = normal [Cl] – corrected [Cl]

Corrected [Cl] = [Cl] x ([Na+normal] / [Na+])

Chloride is the most prevalent anion in the extracellular fluid (ECF). Increased chloride leads to a metabolic acidosis by decreasing SID, whereas decreased Cl causes an alka­losis due to increased SID. Chloride itself is overlooked in the H-H approach, despite playing a pivotal role in acid-base status and is acknowledged here.

Albumin effect

Albumin effect = 0.37 (normal [alb g/l] – patient [alb g/l])

Albumin is the principal weak acid in the body. Hypoalbuminaemia tends to increase pH and cause a metabolic alkalosis and hyperalbuminaemia a metabolic acidosis.

Lactate effect

Lactate effect = –1 x [lactate]

A common abnormality in critically ill patients is lactic aci­dosis. Lactic acidosis results when the anaerobic production of lactate exceeds its utilisation by the liver and kidneys and is usually due to systemic hypoperfusion and tissue hypoxia, but can rarely also be caused by septic shock, rhabdomyolysis and renal failure. Lactate is a large con­tributor to the acid-base status, yet only the Fencl-Stewart approach takes lactate concentration into consideration as an individual parameter when evaluating acid-base status.

Phosphate effect

Phosphate effect (mmol/l) = 1.8 (normal [phos mmol/l] – measured [phos mmol/l])

Phosphorus is the most abundant intracellular anion and has a large array of functions within the body including acting as a buffer, an enzyme cofactor and aiding in the production of adenosine triphosphate (ATP). Inorganic phosphate, much like albumin, is a non-volatile weak acid in which changes in its plasma concentrations can pro­duce significant acid-base disturbances. Hypophosphatae­mia causes acidosis in the critically ill. If you are unable to measure phosphate, then this can simply become an unmeasured anion.

Unmeasured anion effect (UAE)

UAE = standardised base excess – sum of effects

Sum of effects = free water effect + chloride effect + phos­phate effect + albumin effect + lactate effect

The unmeasured anion effect is calculated by subtracting the sum of the phosphate, free water, chloride, lactate and albumin effects from the standardised base excess. This equation represents unidentified acids or alkalis contribut­ing to the acid-base status. These are usually unidentified acids and include ketoacids, propylene glycol, sulphuric acid, D-lactate, salicylic acid, metaldehyde, ethylene glycol and ethanol. Compared to the anion gap, this equation is of greater use as it takes more of the key factors into consideration when calculating and evaluating metabolic acid-base derangements (Hopper and Haskins, 2008).

TABLE (4) Venous blood was obtained and tested before surgery

Practical application

A 13-year-old Cob gelding is presented following a history of moderate to severe colic signs of 18 hours’ duration. The horse has distended loops of small intestine consistent with a strangulation lesion. The horse’s heart rate is 108 bpm; Table 4 shows the venous blood test results prior to stabili­sation before surgery.

Traditional interpretation

This blood gas doesn’t fit with such a sick animal, nor does the alkalaemia (these patients would normally be markedly acidaemic). The alkalaemia is due to a hypochloraemic metabolic alkalosis (BE 4.6). The difference in bicarbonate from normal is 14mmol/l, so for compensation would expect the PCO2 to be 46.8mmHg and is in fact 47.5mmHg so in the range for a compensatory respiratory acidosis.

In addition, this horse has a low partial pressure of venous oxygen (23.6mmHg; normal range 30 to 40), which is suggestive of a marked increase in tissue oxygen demand/poor tissue oxygenation (assuming that the horse is not hypoxic). This high extraction ratio is suggestive of severe hypovolaemic shock, and so the horse is likely to have refractory hypotension under anaesthesia and will likely benefit from inotropes and vasopressors during and potentially after surgery.

Fencl-Stewart interpretation

This animal has a mixed metabolic component: the meta­bolic alkalosis is due to marked hypoalbuminaemia (this animal is likely to need plasma) and hypochloraemia and the metabolic acidosis is due to the hyperlactataemia (see calculated numbers in Table 5).

TABLE (5) Effect values were calculated following the Fencl-Stewart approach


In this short article, I hope that I have reminded you of what you knew about blood gases and also given you a different and practical approach to allow you to better evaluate and treat your critically ill patients with metabolic derange­ments. If you don’t currently have a blood gas machine, an initial place to start is to begin measuring lactate; the patient-side machines are affordable as is each individual sample. The best way to appreciate the value of blood gases is to start running them on patients and practising interpretation with no time pressure.


Brunori, L.


Clinical use of plasma lactate in the emergency patient: a case-based review. Veterinary Practice, 52, 30-32

Hopper, K. and Haskins, S.


A case-based review of a simplified quantitative approach to acid-base analysis. Journal of Veterinary Emergency and Critical Care, 18, 467-476

Stewart, P.


Modern quantitative acid–base chemistry. Canadian Journal of Physiology and Pharmacology, 61, 1444-1461

Gayle Hallowell

Gayle Hallowell, MA, VetMB, PhD, CertVA, DACVIM, DACVECC, DECVSMR, PFHEA, FRCVS, graduated from the University of Cambridge in 2002 before complet­ing a rotating internship and residency at the RVC. She then moved to the University of Nottingham to undertake a PhD. She is currently a Professor at the University of Nottingham where she still spends 65 percent of her time undertaking clinical work.

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