top of page
  • Writer's pictureChristie Roberts

Blood Gases (the theory- part 2)

Hello and welcome to part 2 of 3! Hopefully you've come from part 1, but if not, you can check it out here. After this post, you can head onto blood gases (the practice) for some real life examples.

As before, this goes through the vague A-E approach that I use to systematically scan through a gas.

This second part covers C and D in my ABCDE approach (there actually is no E, but you can just assume that E is everything else and overall impressions).

Causes are highlighted in pink, treatments in orange.

4. Haemodynamics- C

Haemoglobin (Hb) is probably the most relevant figure under cardiovascular in an ABG. Haemoglobin is a protein used for carrying oxygen round the body via red blood cells, in a molecule called oxyhaemoglobin. A normal Hb will sit somewhere around 120-150g/L, and a low Hb is seen in anaemia- there are different types of anaemia which will all present with low Hb, but these can be differentiated by Mean Cell Volume (MCV will be low in iron deficiency, normal in blood loss, and high in folate and B12 deficiency). Anaemia can cause symptoms of oxygen lack- lethargy, shortness of breath, weakness, palpitations, angina and light-headedness. Causes of anaemia can include renal failure, in which the kidneys do not produce enough erythropoietin (EPO), a hormone which signals the bone marrow to produce red blood cells, dietary deficiency of iron and active bleeding (acute or chronic, for example in trauma or GI bleeds).

Mild anaemia treatment will be with iron replacement tablets- this is an easy, safe and cheap treatment option. In cases of anaemia associated with chronic renal failure, EPO injections will be given as an erythropoiesis stimulating agents (ESAs).

In acute and severe anaemia, blood transfusions are used. Often in ICU, the trigger point for giving a unit of packed red blood cells (PRBC) is 70g/L, but a higher trigger of 80g/L will be used in certain scenarios. In non bleeding patients, only one unit should be given at a time and it can generally be assumed that one unit will increase Hb by 10g/L.

Having a higher transfusion trigger point is somewhat contentious in terms of risk vs benefit (given that blood transfusion does come with risks of allergic/immune modulated reactions, ABO incompatible reactions, TACO and TRALI, but anaemia can also contribute to poor outcomes) but a higher trigger point is being considered for cancer patients (research shows up to a 65% higher mortality in oncology patients with anaemia compared to those without, alongside marked decreases in quality of life), trauma patients, patients with severe septic shock (where demand for tissue oxygenation is higher, so presence of sufficient oxyhaemoglobin is critical) and cardiac patients with

active ischaemic changes like high troponin and unstable angina- see the ongoing 2017 phase 3 Myocardial Ischaemia and Transfusion (MINT) trial, referenced below.

As stated earlier, the presence of higher transfusion triggers and what exactly those triggers should be remains unclear, with a distinct dearth of evidence. Generally, transfusion and other treatments for anaemia should be dictated by symptoms, rather than numbers.

***a quick note about Hb values. The old way of reporting these, which is still occasionally used, was g/dL rather than g/L. So a Hb of 70g/L would be written as 7.0g/dL, 115 g/L would be 11.5g/dL. This usually doesn't cause any problems, unless you're getting down to really low values. For example, the lowest Hb I ever saw was 12g/L, and some clinicians initially thought I meant the Hb was 120g/dL and that I was using the old scale but no, I really meant 12g/L. If in doubt, clarify or check the gas yourself to see which units are being used***

Haematocrit (Hct) is the other useful value in this section, and can be used to assess fluid status and dehydration. Hct is the percentage of RBCs in whole blood (made up of RBCs, WBCs, platelets and plasma), In a lab, this is calculated by spinning down whole blood in a centrifuge, then calculating the proportion of RBCs to total blood volume. Then multiply by 100 to get a % Hct.

Example- If the column of RBCs measures 20 mm and the whole blood column measures 50 mm, the haematocrit is 20/50 = 0.4- 0.4 × 100% = 40%.

A higher or lower plasma volume/total blood volume will skew the results. More plasma (so potentially fluid overloaded, or anaemic) means fewer RBCs, so a lower Hct. Less plasma (in a dehydrated state) means more RBCs, so a higher Hct. I remember this by saying that 'high is dry' (so a high Hct indicates dehydration- get that 250mL fluid bolus going).

Normal ranges vary between men and women, and it's difficult to find a consensus on reference ranges- general consensus is something like 35-45% for women and 40-55% for men, but from my experience it rarely gets anywhere near 55%. I use 30-45% as my general range.

5. Electrolytes- C/D

A blood gas gives 4 ionized electrolytes values- sodium (Na+), potassium (K+), calcium (Ca2+) and chloride (Cl-). In this section, I'm giving you a (hopefully) succinct of the causes and treatments for high and low values.

Sodium- 135-145 mmol/L

Sodium forms part of the sodium-potassium pump, which helps to regulate electrolyte levels in blood, and is a key electrolyte in managing fluid balance and blood pressure. The general rule is that 'where sodium goes, water will follow'- if more sodium is reabsorbed by the kidneys, more water will be reabsorbed from filtrate, less urine is produced and overall fluid balance/blood volume increases. This is why sodium changes should be managed slowly, as aggressive correction can lead to changes in cerebral fluid content. Most sodium is extracellular (i.e. it is found in the plasma, not in cells).

High sodium is hypernatraemia- >145

  • Causes centre around a deficit of water compared to sodium, so includes water losses (e.g. polyuria- particularly with glucosuria, severe D+V, insensible losses), inadequate fluid intake (e.g. hypodipsia) and occasionally sodium overload (e.g. dietary intake of salt)

  • Be cautious with rapid correction as rapid changes can affect cerebral fluid balance. Monitor for neuro symptoms including seizures and confusion.

  • Treatment involves replacing fluids- ideally oral/NG water, or normal saline. Dietary salt restriction.

Low sodium is hyponatraemia- <135. Mild 125-134 Moderate 120-124 Severe <120

  • Causes include polyuria, D+V, burns, peritonitis, pancreatitis, Syndrome of Inappropriate Antidiuretic Hormone (SIADH- a deranged feedback loop causes excessive ADH/vasopressin release, leading to high urine osmolarity and low serum osmolarity/sodium levels with increased water reabsorption from kidneys which can cause hypervolaemia), dilutional states (where oedema causes dilution of sodium, e.g. renal failure, heart failure, cirrhosis) and extreme polydipsia.

  • Monitor for signs of severe acute hyponatraemia (vomiting, cardiorespiratory distress, coma/low GCS, seizures). Be cautious of rapid correction of Na+ levels- ensure sodium does not rise by more than 6mmol/L in first 6 hours, or 10mmol/L in first 24 hours. Rapid correction can cause osmotic demyelination syndrome/ central pontine myelinolysis.

  • Treatment of symptomatic hyponatraemia is hypertonic saline- 150mL Sodium chloride 2.7% via central access over 15mins. If no clinical improvement, repeat dosage. Check sodium at 6, 12, 24 and 48 hours to monitor for over correction (increase of 10+mmol/L in 24 hours). Only correct to the point of symptom alleviation, the serum sodium does not need to be normalised and symptoms will often resolve after an increase of 4-6mmol/L.

Potassium- 3.5-5.0mmol/L

Potassium is involved in the sodium potassium pump, and contributes to muscle contraction, particularly in cardiac myocyte contraction . Most potassium is intracellular (i.e. it is found in cells, not in the blood) and is excreted by the kidneys. Potassium is inversely related to pH (for each 0.1 increase in pH, K+ decreases by 0.3- alkalosis moves K+ intracellularly, dropping serum potassium) Both low and high K+ can be life threatening due to arrhythmias and ECG changes (see video below). Often in critical care, 4.0 is used as the lower target- particularly if patient has any cardiac risk factors.

High potassium is hyperkalaemia- >5.0

  • Causes include renal impairment/renal failure, burns or severe injury (causes K+ to leave cells), excessive supplementation.

  • Monitor for ECG changes (like, I cannot emphasize this enough. Get a a continuous monitor, maybe get a doctor depending on how high it is)

  • Treatment is dependent on severity. Mild- treated by increasing excretion in urine with diuretics (NOT potassium sparing diuretics, like spironolactone). Consider IV fluid boluses to improve renal perfusion, therefore enhance excretion. Moderate-severe (especially if symptomatic with ECG changes)- shifting K+ out of the blood using insulin and dextrose (insulin causes the potassium to move intracellularly, and dextrose is used to avoid hypoglycaemia) or salbutamol nebuliser or IV injection. Final option is starting haemofiltration/dialysis (concentration gradients in dialysate fluid will decrease plasma potassium). Severe hyperkalaemia (>6.5) is a medical emergency due to the high risk of cardiac arrhythmias and death- 10% calcium gluconate IV injection can be given to protect against myocardial excitability, dosage titrated to ECG improvements.

Low potassium is hypokalaemia- <3.5. Mild 3-3.5 Moderate 2.5-3 Severe <2.5

  • Causes include polyuria (too much K+ excreted in urine, including in diuretic use), chronic diarrhoea/overuse of laxatives, severe vomiting, insulin use and corticosteroid use.

  • Monitor for ECG changes. If supplementing, be conscious of rebound hyperkalaemia particularly in patients with renal impairments. Check magnesium levels, as low Mg increases renal K+ loss.

  • Treatment for mild deficiency involves supplementation enterally, using oral agents like Sando K. For moderate, give IV using low concentration (40mmol in 1L KCl 0.3% in dextrose or NaCl, given peripherally at a maximum rate of 20mmol/hour) or if severe, high concentration (20mmol/L KCl in 50mL NaCl, given centrally over 1 hour- generally only available in critical care). Should be given slowly due to risk of cardiac complications and risk of phlebitis. If on diuretics, consider switching to potassium sparing (usually preferred over active replacement of K+). Top up Mg if needed.

Chloride- 95-105mmol/L

In all honesty, I've never seen a low or high chloride actually actively treated. I'm sure it does happen, I've just never seen it. There are no direct symptoms associated with a high or low chloride- symptoms are generally associated with the underlying pathology causing dysregulation (usually pH abnormalities) and for the most part, chloride concentrations will mirror sodium, as they go hand in hand as NaCl (salt).

High chloride is hyperchloraemia- <105

  • Causes include dehydration, metabolic acidosis and hyperparathyroidism, high serum sodium, renal failure (leading to decreased excretion), IV NaCl replacement, and increased salt intake (this may present with hypertension)

  • Treatment involves addressing underlying cause- give enteral/IV fluids (NaCl), reducing D+V and other sources of fluid loss, correcting acidosis.

Low chloride is hypochloraemia- >95

  • Causes include metabolic alkalosis, bicarbonate administration (inversely proportional to chloride) dilutional states (where oedema causes dilution of chloride e.g. renal failure, heart failure, cirrhosis), excess fluid losses (polyuria, D+V, insensible losses), SIADH and aldosterone deficiency.

  • Treatment involves addressing underlying cause- fluid removal with diuretics/renal filtration, correcting alkalosis.

Calcium- 1.15-1.29mmol/L

Calcium is needed for cardiac (with ATP and troponin) and smooth muscle contraction, blood coagulation and hormone regulation (particularly vitamin D and PTH). Calcium is stored in bones and teeth, and can be released from here (potentially causing weakening of the bones, in chronic insufficiency) or from the intestines when required. Calcium is excreted by the kidneys, and plays a central role in mineral bone disease in renal failure (more on that in this post). Important to recognise that there is a difference between total and ionised calcium- blood gas is ionised.

High calcium is hypercalcaemia- >1.29

  • Causes include hyperparathyroidism (high PTH leads to ongoing increased renal and intestinal absorption, and higher rates of bone resorption/osteoclastic activity to take calcium from bones), prolonged immobility (which leads to accelerated rates of bone resorption), excessive vitamin D and renal failure (with decreased excretion).

  • Monitor for ECG changes due to decreased neuromuscular excitability leading to arrhythmias, cardiac arrest and skeletal muscle weakness. In prolonged or severe hypercalcemia, monitor kidneys for kidney stones (made of calcium oxide) and irreversible nephrocalcinosis.

  • The main symptoms have a mnemonic- 'painful bones, renal stones, abdominal groans and psychic moans'- abnormal bone remodelling, nephrolithiasis, ileus and depression.

  • Aims of treatment are to increase renal excretion (diuretics, or haemofiltration), decrease intestinal calcium absorption (with phosphate restriction, phosphate binders and vitamin D- calcitriol), and decrease bone resorption (bisphosphonates- alendronic acid, and mobilization).

Low calcium is hypocalcaemia- <1.15.

  • Causes include citrate toxicity (if using a citrate anticoagulation on renal filtration or post blood transfusion as citrate is used to prevent clotting), in vitamin D deficiency, renal failure, burns (calcium gets trapped in damaged tissues) low albumin, metabolic acidosis (tumour lysis syndrome, sepsis), hypoparathyroidism and hyperphosphataemia.

  • Monitor for osteopenia- weakening of the bones- in chronic hypocalcaemia. The more calcium is leached form bones to replace dietary calcium, the weaker said bones become. In acute hypocalcaemia, monitor for ECG changes due to decreased excitability of the heart, and monitor for seizure activity due to increased neuromuscular excitability (can cause tingling fingers, tremors, cramps, tetany, and convulsions). When giving IV boluses, monitor HR and ECG.

  • Treatment for mild decreases should be oral/enteral- tabs such as Adcal D3 with calcium carbonate plus colecalciferol. If only IV therapy possible (e.g. no absorbing, or NBM), or for severe, symptomatic deficiency, treat with calcium gluconate 10% via central line or large peripheral vein. Levels will increase immediately, so should be rechecked 2 hours post administration. PTH and vitamin D levels should also be checked and corrected, but treatment of hypocalcaemia should continue regardless. Magnesium levels should be checked and corrected prior to calcium replacement.

6. Other biochemistry- D

Glucose is vitally important, for diabetic and non diabetic patients. Target range is usually 4-8mmol/L (4-12mmol/L in diabetic patients), and each NHS trust should have a protocol to follow for if a reading is low (hypoglycaemia) or high (hyperglycaemia).

Treatment of hypoglycaemia will initially use oral agents (such as HypoStop juice or dextrose tablets, followed by a long acting carbohydrate to prevent further hypos) but will escalate if a patient is unconscious, unable to swallow/NBM, or is conscious but disoriented or aggressive. Then, you should give 1-2 tubes of GlucoGel applied to the patients gums, Glucagon 1mg IM injection or IV 20% dextrose. Make sure to recheck blood glucose 15 mins after treating (can do a fingerstick, rather than another gas) and more frequently for the next 24-48 hours

Prevention is always better than treatment, so consider factors such as if a patient is on insulin, are they eating adequately/on NG feed/on TPN? Is the insulin at the correct rate (if IV insulin)? Often hypos can occur in patients whose NG feed has been suspended pre surgery, but the insulin infusion has not been reduced/stopped.

Hyperglycaemia usually won't be treated unless blood glucose is consistently out of range- for example, 3 readings above 12 in a non-diabetic patient would trigger initiation of insulin. A single high reading could be coincidental, or be a post prandial reading where an increase is expected.. If blood glucose is above 12, ketones should also be checked. Causes of a high blood sugar can include insulin omission in diabetes, use of steroids, critical illness in general (likely from a body under stress) and parenteral nutrition.

In diabetic patients, it's essential to continue any long acting insulin they may be on, alongside short acting subcutaneous or IV insulin, to prevent DKA. T1D patients will usually have an adapted scale for titrating insulin.

For patients on variable rate intravenous insulin infusions (VRIII, aka a sliding scale), continue monitoring blood glucose regularly and be watching out for hypoglycaemia, DKA and hyper/hypokalaemia.

Make the most of your diabetes specialist nurses!! They will be more than happy to answer any questions about blood glucose management.

**to be aware of- euglycaemic DKA is a thing- patients, usually with type 2 diabetes on SGLT2 inhibitors, have a normal blood sugar but profound ketosis and acidaemia**

I think the essential part of these posts isn't actually the reading of the blood gas, but the thought process that follows. There's no point in identifying that your patient has a low PO2/ high lactate/ high potassium, if you then don't increase the FiO2/give a fluid bolus/ watch for arrhythmias. Where possible, I've tried to outline the follow ups to common blood gas findings. Obviously things will vary slightly between NHS trusts, and this is only a brief outline, but the key to this isn't what, but why.

Thank you SO MUCH for reading this post, especially if you made it all the way through parts 1 and 2! All together, by far the longest post I've attempted but I have tried to keep it succinct and interesting. If you fancy having a practice with some real life examples, head over to this post. Or if you fancy revisiting oxygenation and pH, check out part 1 again.

As always, references below with family favourites in bold.


NHS (2018) 'Iron deficiency anaemia'.

NHS (2018) 'Blood transfusion'

NHS Blood and Transplant (2015) 'Implementation guide- single unit transfusion guide'

  • Based off NICE guidelines for non-actively bleeding patients, this guide helps to clarify the rationale for giving one unit of blood at a time as part of Patient Blood Management (PBM). Considers the impact of unnecessary transfusions from a patient perspective, as well as a blood availability and financial context.

Busti, F., Marchi, G., Ugolini, S., Castagna, A., Girelli, D. (2018) 'Anaemia and iron deficiency in cancer patients: role of iron replacement therapy' in Pharmaceuticals. 11(4), p.94

Wang, J., Klein, H. (2010) 'Red blood cell transfusion in the treatment and management of anaemia: the search for the elusive transfusion trigger' in International Journal of Transfusion Medicine- Vox Sanguinis, 98, p.2-11 (2016) 'Myocardial Ischaemia and Transfusion (MINT)'

Basten, G. (2018) Blood results in clinical practice. M&K Publishing, Cumbria.

Baid, H., Creed, F., Hargreaves, J. (2016) Oxford handbook of critical care nursing. 2nd Edn. Oxford University Press, Oxford

Billett, H. (1990) 'Chapter 151- hemoglobin and hematocrit' in Clinical Methods: the history, physical and laboratory examinations (3rd edn) Butterworths, Boston


BNF (2021) 'Fluid and electrolytes: electrolyte replacement therapy'

Marieb, E., Hoehn, K. (2016) Human Anatomy and Physiology. 10th edn. Pearson, New York.

Geeky Medics (2020) 'Syndrome of inappropriate anti-diuretic hormone (SIADH)'

Oxford University Hospitals NHS Foundation Trust (2017) 'Medicines Information Leaflet: Guidelines for the management of hypokalaemia in adults'

Oxford University Hospitals NHS Foundation Trust (2019) 'Medicines Information Leaflet: Guidelines for the management of acute hypocalcaemia in adults'

Oxford University Hospitals NHS Foundation Trust (2016) 'Medicines Information Leaflet: Guidelines for the management of acute severe symptomatic hyponatraemia in adults'

Appelman-Dijkstra, N., Papapoulos, S. (2015) 'Modulating bone resorption and bone formation in opposite directions in the treatment of postmenopausal osteoporosis' in Drugs. 75(10), pp. 1049-1058

Sam, R., Ing, T. (2020) 'Hypernatraemia' in BMJ Best Practice.

Kim, S. (2006) 'Hypernatraemia: Successful treatment' in Electrolytes and Blood Pressure. 4(2), pp.66-71.,unable%20to%20tolerate%20oral%20water.

Wikipedia (2021) 'Hyperchloraemia'

  • Please no judgement for using Wiki. It's not the demon it's made out to be- everything is fully referenced and I trust it

Salen, P. (2016) 'Hyperparathyroidism in emergency medicine clinical presentation'

LITFL (2020) 'Hypernatraemia'

LITFL (2020) 'Hyponatraemia'

LITFL (2020) 'Potassium'

LITFL (2020) 'Hypokalaemia'

LITFL (2020) 'Hyperkalaemia management'

LITFL (2020) 'Hyperchloraemia'

LITFL (2020) 'Hypochloraemia'

LITFL (2020) 'Hypercalcaemia'

LITFL (2020) 'Hypocalcaemia'


Oxford University Hospitals NHS Foundation Trust (2019) 'Medicines Information Leaflet: the management of hypoglycaemia in adult inpatients'

Oxford University Hospitals NHS Foundation Trust (2015) 'Insulin standards for Adult Intensive Care Unit' (2010) 'Hyperglycaemic control in the ICU'

Recent Posts

See All


Post: Blog2 Post
bottom of page