How to interpret arterial blood gas results

pharmaceutical-journal.com/article/ld/how-to-interpret-arterial-blood-gas-results-2

Understanding acid-base balance and interpreting arterial blood gas results can be complex,
but they are useful skills for clinical pharmacists.

Haemotologic disorders

08 February 2023
By Nicola Corkhill & Olivia Moswela

Shutterstock.com

After reading this article, you should be able to:

Understand the basics of acid-base balance;

Interpret arterial blood gas results;
Make treatment decisions, including where drug treatment may be required to correct
acid-base imbalance.

Maintaining the pH of blood is essential for normal bodily function; however, several clinical
scenarios can result in disruption of the body’s acid-base balance. Monitoring of acid-base
balance is done by testing patients’ arterial blood gases (ABGs). The results of ABG testing
will often influence the treatment that patients receive.

Monitoring ABGs can be useful to:

Assess the effectiveness of pulmonary gas exchange;

Identify the presence of metabolic acidosis and alkalosis;
Identify critically unwell patients requiring urgent intervention;

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 Guide treatment and monitor response​[1–5]​.

A basic understanding of how to interpret ABG results can therefore be useful for
pharmacists to help them to clarify the clinical picture.

The basics of acid-base balance

The optimal physiological pH of extracellular fluid is 7.35–7.45. A pH outside this range can
cause protein denaturation and enzyme inactivation​[6]​​. Because pH is a logarithmic scale, a
small change in pH reflects a large change in hydrogen ion (H+) concentration​[6]​. The
following equilibrium equation is crucial to understanding acid-base balance:

H2O + CO2 ↔ H2CO3 ↔ HCO3– + H+

This equation shows that carbon dioxide (CO2) in blood dissolves to form carbonic acid
(H2CO3), which dissociates to form acidic H+ (which can then combine with physiological
bicarbonate to push the equation back to the left). Blood pH depends on the balance of
carbon dioxide and bicarbonate (HCO3–). A change in the amount of carbon dioxide will not
lead to a change in pH if it is accompanied by a change in the amount of bicarbonate that
preserves the balance (and vice versa)​[2]​. It is the renal and respiratory systems that are
responsible for maintaining the pH of the blood.

The following equation can be used to estimate pH:

Respiratory mechanisms
Carbon dioxide behaves as an acid in aqueous solution. One way that the body controls the
pH of extracellular fluid is by increasing or decreasing the rate and depth of respiration and
thereby the amount of carbon dioxide expelled. The partial pressure of carbon dioxide in
arterial blood (PaCO2) reflects the amount of carbon dioxide in arterial blood. PaCO2 is
determined by alveolar ventilation​[2,4]​. Chemoreceptors located in the medulla sense pH
changes in extracellular fluid and changes in arterial carbon dioxide, altering ventilation to
maintain normal pH. In patients with chronically high PaCO2 (chronic hypercapnia); for
example, owing to severe chronic obstructive pulmonary disease (COPD), chemoreceptors
may become desensitised. The body then relies on PaO2 to detect inadequate ventilation
(hypoxic drive)​[2,7]​. In chronic hypercapnia, supplemental oxygen in emergency settings
should be given in a controlled manner with ABG monitoring to avoid respiratory depression
[3]​.

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Renal (metabolic) mechanisms
Another way that the body can control pH is through the kidneys, by:

Excretion of hydrogen ions;

Renal tubular reabsorption of bicarbonate ions.

The kidneys can adjust the amount of hydrogen and bicarbonate that is excreted in the urine
in response to metabolic acid production. However, kidneys also preserve electroneutrality
by maintaining stable concentrations of major electrolytes, such as potassium and sodium.
This function can sometimes take priority over pH regulation. Normally, sodium (Na+) ions
are retained in exchange for potassium (K+) or hydrogen ions. When potassium ions are in
short supply, more hydrogen ions are excreted, which can interfere with pH regulation.
Another kidney function which can affect acid-base balance is the maintenance of negatively
charged chloride (Cl–) and HCO3– ions to balance positively charged ions. When chloride
ions are in low supply, more bicarbonate is retained and vice versa​[2]​.

Compensation
When acidosis or alkalosis occurs (either through respiratory or renal mechanisms; see
Table 1), the opposite system will attempt to rectify this imbalance; this is termed
‘compensation’. For example, if the kidneys fail to excrete metabolic acids, ventilation is
adjusted to eliminate more carbon dioxide​​[2]​.

It is important to note that compensatory changes in respiration can occur over minutes to
hours, whereas metabolic processes take hours or days to respond​​[2,8]​.

Buffers
The body has three main buffers that minimise any changes in pH that occur when acids or
bases are added: haemoglobin, bicarbonate and proteins. Haemoglobin is six times more
powerful as a buffer than proteins​[6]​. Bicarbonate is the most important buffer in the blood
and is the dominant buffer in the interstitial fluid. The intracellular fluid uses proteins and
phosphate to buffer pH​​[8]​​. At an intracellular level, buffering occurs instantly but the effect is
small.

Arterial blood gas sampling

Commonly reported parameters of ABG results (see Table 2 for the normal reference ranges​
[2]​) include:

pH — to determine whether a patient’s blood pH is within physiological range;

PaCO2 and PaO2 — the partial pressures of CO2 and oxygen in arterial blood,
respectively;

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 Bicarbonate — indicates how much bicarbonate is in the blood and is therefore
available as a buffer;
BE (base excess or deficit) — a measure of the excess or deficiency of base in the
blood; by definition, it is the amount of base (in mmol) that would correct one litre of
blood to a normal pH of 7.4. If an excess, this is the amount of base needed to be
removed for a normal pH, or, if a deficit, the amount required to be added.
Lactate — the product of anaerobic glycolysis. A rise in lactate indicates poor
oxygenation and perfusion of tissues.

Other parameters commonly found on ABG reports are haemoglobin, glucose and
electrolytes (sodium, potassium, chloride and ionised calcium).

Assess pulmonary gas exchange

In type one respiratory impairment there is defective oxygenation despite adequate
ventilation, characterised by a low PaO2 with a low or normal PaCO2. In patients receiving
supplemental oxygen, the PaO2 may be within normal range but inappropriately low for the
fraction of inhaled oxygen (FiO2). Common causes of type one respiratory failure include:
pneumonia; COPD; acute respiratory distress syndrome; pulmonary embolism;
pneumothorax; acute asthma; and pulmonary oedema​[2,4]​.

In type two respiratory impairment there is inadequate ventilation (pumping air in and out of
the lungs), characterised by a high PaCO2 and low PaO2. In patients receiving supplemental
oxygen, the PaO2 may be within normal range. Common causes of type two respiratory
impairment include: COPD; opioid or benzodiazepine toxicity; obstructive sleep apnoea; flail
chest injury; neuromuscular disorders; and exhaustion following type one respiratory
impairment​[2,4]​.

Hyperventilation is characterised by a low PaCO2. Accompanying low HCO3– indicates

hyperventilation secondary to metabolic acidosis or, rarely, chronic hyperventilation with
metabolic compensation​[2]​.

Interpreting the results

ABGs can be interpreted using a stepped approach.

Step 1 — check the pH

The pH should be assessed first. A pH of less than 7.35 indicates acidaemia — acid in the
blood, and a pH greater than 7.45 indicates alkalaemia — alkali in the blood.

Step 2 — check the HCO3– and PaCO2

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Having determined if the patient is acidotic or alkalotic, check the bicarbonate and the
PaCO2 (refer to Table 3) to classify the results as follows:

Metabolic acidosis: patients who are acidotic and have a low bicarbonate and
increased base deficit. There is usually a compensatory increase in alveolar ventilation
to lower PaCO2. A high chloride indicates hyperchloremic acidosis;
Respiratory acidosis: patients who are acidotic with a high PaCO2. Because
metabolic compensatory response takes longer to develop, acute respiratory acidosis
is almost always uncompensated;
Metabolic alkalosis: patients who are alkalotic with a high bicarbonate and an
increase in base excess. Respiratory compensation (increase in PaCO2) occurs but is
limited by the need to avoid hypoxaemia;
Respiratory alkalosis: patients who are alkalotic with a low PaCO2. Metabolic
compensatory response takes longer to develop​[2]​.

It is possible for patients to have a mixed respiratory and metabolic alkalosis or acidosis.
This occurs when primary respiratory and primary metabolic disturbances exist
simultaneously. If the two processes oppose each other, pH derangement will be minimised
(see Step 3). However, two processes that cause pH to move in the same direction may lead
to profound acidaemia or alkalaemia​[2]​​.

Step 3 — Check for compensation

Check to see if the patient is compensating for their acid-base imbalance. Patients may
partially or fully compensate for an acid-base imbalance by the “opposite” mechanism; for
example, metabolic acidosis will be compensated for with respiratory alkalosis. This may
create some apparently normal results among some deranged ones. Compensation is
greater in chronic disorders. Overcompensation does not occur​[2,4]​.

When interpreting acid-base status, it is important to always take the clinical context into
account. For example, if presented with ABG results showing a normal pH, low PaCO2 and
low bicarbonate in a diabetic patient with high levels of ketones in the urine, the most likely
primary disorder is metabolic acidosis (diabetic ketoacidosis), rather than respiratory
alkalosis (see Table 3)​[2,5]​.

Step 4 — Calculate the anion gap

For a patient with metabolic acidosis, it can be useful to calculate the anion gap as this can
give some indication of the underlying cause of the acid-base imbalance.

The anion gap is the difference between the measured positively charged cations Na+ and
K+ and the negatively charged anions Cl– and HCO3–[6]​. The following equation can be used
to estimate the anion gap:

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([Na+] + [K+]) – ([Cl–] + [HCO3–])

Some laboratories do not include potassium in the calculation, which affects the accepted
range. An increased anion gap indicates excess acid from the anions that are unmeasured
(e.g. ketones or lactate)​[4]​. These may be endogenous (e.g. ketones or lactate) or
exogenous (e.g. ethylene glycol, aspirin overdose). It is also worth noting that a drop in a
patient’s albumin lowers the anion gap. A deranged phosphate level can also affect the anion
gap, but to a lesser extent​[5,9]​.

Treatment
If possible, the underlying cause of the acid-base derangement should be treated because,
without doing so, the problem can recur. Depending on the cause, this may include: treating
infection; switching intravenous fluid (e.g. to reduce chloride load); managing diarrhoea or
high stoma output; reversal of respiratory depressant drugs; or managing drug overdose. In
some instances, it may not be possible to treat the underlying cause and drug treatment may
be required to correct the acid-base imbalance.

Drugs used to treat metabolic acidosis include sodium bicarbonate and trometamol (THAM).

Sodium bicarbonate is most commonly used in patients with chronic kidney disease, with
National Institute for Health and Care Excellence guidance recommending oral
supplementation in patients with an estimated glomerular filtration rate <30mL/minute and a
bicarbonate of <20mmol/L​[10]​. It increases the patient’s bicarbonate concentration as well as
reduces the potassium concentration. Intravenous infusions of sodium bicarbonate may be
given for severe metabolic acidosis, particularly associated with hyperkalaemia, including
peri-arrest situations. The dose is calculated according to base deficit and care should be
taken not to over-correct the imbalance, causing an alkalosis. The following calculation is
used to calculate the required extracellular buffer:

Body weight (kg) x 1/5 x base deficit = sodium bicarbonate (mmol) dose

In practice, twice the dose is required to facilitate intracellular buffer activity. As over-
correction may have adverse effects on potassium and calcium concentration, it is safer to
achieve a pH of 7.2 and reassess whether there is clinical need for more​[11]​.

Intravenous solutions of sodium bicarbonate come in concentrations ranging from a 1.26%

iso-osmolar preparation to the hyperosmolar 8.4% preparation. Hyperosmolar preparations
are very irritant to veins and should usually be administered through a central line, with the
exception of a peri-arrest situation. Sodium bicarbonate is also used as a buffer in dialysate
and replacement fluid for renal replacement therapy in patients with acute kidney failure and
liver failure and/or lactic acidaemia/or circulatory shock​[12]​.

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THAM, a proton acceptor, is an unlicensed medicine used in patients unable to tolerate the
high sodium load associated with intravenous sodium bicarbonate. THAM acts as a buffer in
metabolic acidosis. It is rarely used in current clinical practice​[5,13]​. Patients with respiratory
alkalosis may be given acetazolamide, a carbonic anhydrase inhibitor, which promotes the
excretion of bicarbonate in the urine[11]. This is commonly used in the prevention and
treatment of altitude sickness.

Further learning

Test yourself: practice examples

Consider the following patient examples and try to identify which type of disorder is affecting
their blood gases. When you have answered all of the questions, click on ‘Finish quiz’ to see
your results. For any incorrect answers you will have the option to restart the quiz or access
answer guidance from the ‘View questions’ option.

This is an updated version of an article previously published in The Pharmaceutical

Journal in March 2011.

1. 1

Arterial blood gases: a guide to interpretation. BMJ Learning.

2022.https://learning.bmj.com/learning/search-result.html?
channelCode=foundationprogramme&channelFamilyConfig=bmj&moduleId=5004327&
searchTerm=%E2%80%9Cblood%20gas%E2%80%9D&page=0&utm_source=google&
utm_medium=cpc&utm_campaign=usage&utm_content=inst_nhs-
wales&gclid=Cj0KCQiAw8OeBhCeARIsAGxWtUy9OlY0yRPo88n7qp2s1qj3Du9t8h_3D
PJhf6nzHMV6UT1Rq3DrYHsaAliLEALw_wcB (accessed Feb 2023).
2. 2

Hennessey I, Japp A. Arterial blood gases made easy. 2nd ed. Elsevier 2015.

3. 3

O’Driscoll BR, Howard LS, Earis J, et al. British Thoracic Society Guideline for oxygen
use in adults in healthcare and emergency settings. BMJ Open Resp Res.
2017;4:e000170. doi:10.1136/bmjresp-2016-000170

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 4. 4

Burns GP. Arterial blood gases made easy. Clin Med. 2014;14:66–8.
doi:10.7861/clinmedicine.14-1-66
5. 5

Al-Jaghbeer M, Kellum JA. Acid–base disturbances in intensive care patients: etiology,

pathophysiology and treatment. Nephrol. Dial. Transplant. 2014;30:1104–11.
doi:10.1093/ndt/gfu289
6. 6

Baylis C, Till C. Interpretation of arterial blood gases. Surgery 2009;27:470–474.

7. 7

McCartney A, Phillips D, James M, et al. Ventilatory neural drive in chronically

hypercapnic patients with COPD: effects of sleep and nocturnal noninvasive ventilation.
Eur Respir Rev. 2022;31:220069. doi:10.1183/16000617.0069-2022
8. 8

Atherton JC. Acid–base balance: maintenance of plasma pH. Anaesthesia &amp;

Intensive Care Medicine. 2009;10:557–61. doi:10.1016/j.mpaic.2009.08.005
9. 9

Wargo KA, Centor RM. ABCs of ABGs: A Guide to Interpreting Acid-Base Disorders.
Hosp Pharm. 2008;43:808–18. doi:10.1310/hpj4310-808
10. 10

Chronic kidney disease: assessment and management. National Institute for Health
and Care Excellence. 2021.https://www.nice.org.uk/guidance/ng203 (accessed Jan
2023).
11. 11

Waldmann C, Soni N, Rhodes A, et al., editors. Oxford Desk Reference: Critical Care.
Oxford: : Oxford University Press 2019.

12. 12

KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney International
Supplements. 2012.https://kdigo.org/wp-content/uploads/2016/10/KDIGO-2012-AKI-
Guideline-English.pdf (accessed Feb 2023).

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 13. 13

Hoste E, Colpaert K, Vanholder R, et al. Sodium bicarbonate versus THAM in ICU

patients with mild metabolic acidosis. J Nephrol 2005;18:303–
7.https://www.ncbi.nlm.nih.gov/pubmed/16013019

Last updated 9 May 2023 12:07

Citation
The Pharmaceutical Journal, PJ, February 2023, Vol 310, No
7970;310(7970)::DOI:10.1211/PJ.2023.1.172936

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