An introduction to ABGs
Arterial Blood Gas (ABG) sampling is a commonly performed test. It involves obtaining a sample of arterial blood taken from the radial, femoral or brachial arteries for testing in a blood gas analysis machine.
This is a test that senior medical students and foundation level doctors are asked to perform. It can be quite a daunting prospect initially. However, with practice and confidence can be performed with (hopefully) relative ease.
Why do ABGS?
ABGs are useful in a number of clinical scenarios. The most useful results an ABG sample gives us are:
- Acid-base balance
- Ventilatory efficiency
ABGs are taken for a number of reasons, below are some common situations where ABGs may be required:
In the following clinical scenarios:
- Any unexpected deterioration in an ill patient
- Anyone with an acute exacerbation of a chronic chest condition- most commonly COPD
- Anyone with impaired consciousness
- Anyone with impaired respiratory effort
In the presence of the following signs/symptoms
- Bounding pulse, drowsy, flapping tremor, headache, pink palms, papilloedema (all signs of CO2 retention)
- Confusion, cyanosis, visual hallucinations (all signs of hypoxia)
To monitor treatment of a critically ill patient
- Monitoring treatment of known respiratory failure
- Anyone ventilated in ITU
- After majory surgery
- After major trauma
Acid-base balance- Definitions
An acid donates H+ ions while a base accepts H+. An alkali is a soluble base. Therefore, the central theme of acid-base balance is regulation of H+, primarily within plasma but also wihtin interstitial and intracellular fluid.
The normal plasma concentration is only 40nmol/l-1, normal range of 35-45nmol/l-1
This is the same as 40 X 10-9 M
which is 4 X 10-8 M
or 10-7.4 M
or a pH of 7.4, since pH = -log10[H+]
H+ ion regulation is essential since inappropriate binding of H+ ions by amino acid groups of polypeptides may lead to adverse changes in protein structure, active transport, enzymatic function, hormone function and receptor function.
The human body operates effectively within a very narrow pH range and is very sensitive to change outside the normal vaues. The body ceases to function if overwhelmed with H+ ions, and therefore adequate acid-base balance is essential.
Regulation of acid-base is acheived in the short term by buffering and in the long-term by excretion by the body.
This is mediated by partly ionised compounds termed weak acid or weak bases. The types of buffers can be broadly classified into (i) inorganic compounds and (ii) amino acid groups of peptide chains.
The actions of buffers can be divided into (i) regulation of pH at 7.4 and (ii) absorption of H+ when the ph falls below 7.4
Regulation of pH at 7.4
1 Plasma inorganic phosphate.
HPO4(2-) + H+ <------> H2PO4(-)
This reaction is of modest importance, though HPO4(2-) is also linked to plasma Ca2+ levels.
2. Imidazole group of histidine residues of peptides, especially haemoglobin.
His-N + H+ <------> His-NH+
This reaction is very important. Note also that the binding of H+ ions promotes dissociation of oxygen from haemoglobin into the tissues (the Bohr effect)
Absorption of H+ ions
The main buffer used to absorb H+ when pH begins to fall is plasma inorganic bicarbonate, in the following reaction:
HCO3- + H+ <-----> H2CO3
Examining levels of bicarbonate on an ABG result is important as a greatly reduced bicarbonate level indicates that the buffering system is saturated with H+ ions and is no longer buffering effectively. This is one of the key indicators of a metabolic acidosis.
This reaction is also very important due to its link with H+ excretion via respiration, which is explained in the next section. (You lucky devils)
Excretion of excess hydrogen
The two main routes for excreting excess hydrogen from the body are via ventilation in the lungs or renal excretion in the kidney. Ventilation is a acute, short-term response to an immediate rise in H+ levels within the body. Renal excretion and bicarbonate recylcing is a chronic, long-term response.
Remember the role of bicarbonate ions in buffering excess hydrogen in plasma? In the lungs the H2CO3 dissociates to release CO2, which is expired:
HCO3- + H+ <-----> H2CO3 <-----> H20 + CO2
CA= Carbonic anhydrase enzyme.
Increased ventilatory effort cause more CO2 to be expired thus shifting the entire equation to the right. This facilates continued absorption of H+ ions so long as there is sufficient plasma bicarbonate to buffer it.
This is a process that can be quite hard to get your head around with words alone, so hopefully the diagram below will help to put things into context. The main concept to keep in mind is that renal excretion occurs through the preffered reabsorption of HCO3- ions, leaving H+ ions in the renal filtrate to be excreted in the urine. The principal site is in the proximal convoluted tubule (PCT) of the nephron with further fine-tuning of the regulation occuring within the collecting duct.
Proximal convoluted tubule (PCT)
Inward movement of Na+ ions into the PCT cell (down its electrochemical gradient) causes an outward movement of H+ ions via an antiporter. These combine with bicarbonate to form H2CO3, which then dissociates as illustrated. The CO2 from this reaction readily enters the PCT cell down a concentration gradient, where it recombines with H2O to form H2CO3.
This H2CO3 then dissociates again and the HCO3- leaves the PCT cell at its basal surface to enter the extracellular fluid, and so into the peritubular capillaries. Approximately 80% of renally filtered HCO3- is reabsorbed from the PCT.
The processes are much the same as within the PCT except that H+ ion extrusion from the collecting duct cell is acheived by an active H+ ion pump which requires ATP. This facilitates the removal of H+ ions against a substantial electrochemical gradient for H+ ions.
A note on ammonia....
With the continued removal of bicarbonate ions from the tubular fluid, there is a potential for H+ ions to accumlate in high concentrations which can be very damaging. This problem is met by the production of NH3 by the collecting duct cells from the deanimation of glutamine. The NH3 diffuses readily into the lumen of the collecting duct where it binds to, and buffers, the H+ ions to give a less harmful NH4+ ion.
NH3 + H+ ----> NH4+
Buffering by phosphate within the tubular fluid is also important.
HPO4(2-) + H+ -----> H2PO4-
However, excessive amount of HPO4(2-) can bind with calcium ions to form kidney stones.
The significance of lactate
Everytime ATP is metabolised to ADP, a HPO4(2-) and a H+ are generated. In normal ventilation and perfusion the H+ generated in the normal metabolism is excreted via the processes mentioned above.
However, when tissues are inadequately perfused, anaerobic respiration occurs. This causes the hydrogen ions produced to form lactic acid (lactate), the principle product of anaerobic respiration. If this lactate builds up, it can cause a lactic acidosis due to its H+ ion content.
Therefore, when examining an ABG result, the lactate value can be a useful indication of tissue perfusion as it will indicate the level of anaerobic respiration occuring within the body.
How to take an ABG
What you need before going to the patient:
- Sharps tray
- Alcohol wipes
- Gauze/cotton wool
- ABG kit
What is inside an ABG kit?
- Heparinsed syringe
- Syringe cap
- Rubber cube for disposing of needle or syringe cap, depending on the kit
Taking the ABG
- Introduce yourself to the patient with your full name and level of study/practice
- Identify the patient with their full name and D.O.B
- Explain the reason for taking an ABG sample
- Explain to the patient that taking an ABG sample is different from normal venepuncture and may be painful
- Check patient understanding and obtain full consent
- Wash hands
- At this point you may wish to don gloves. Personally I prefer to wait unitl I have palpated the radial artery, as sometimes it is difficult to feel whilst wearing gloves.
- Adequately position the patient, with their arm exposed and wrist slightly extended
- Anything around the wrist such as a patient ID tag or wristwatch removed
- Perfom Allen's test to ensure good collateral flow to the wrist via the ulnar artery
- Palpate the radial pulse to be sure of the area you are inserting the needle, and wipe down thoroughly with an alcohol swab
- Expel excess heparin from within the syringe, and attach the needle
- Hold the syringe like a pen, with the needle bevel facing upwards
- Inform the patient you are about to take the sample
- Advance the needle into the radial artery at an angle of 45 degrees, whilst feeling for the pulse with your other hand, aiming beneath the finger you are feeling with
- The syringe should fill up in a pulsatile manner. The majority of ABG sampling syringes will stop filling when a sufficient sample is obtained (1-2ml)
- Remove the needle and syringe as one from the patient's arm and immediately place the needle into the rubber cube. The rubber cube should remain in the sharps tray when you do this, do not pick it up with your other hand. This avoids the chance of a needle-stick injury. It is ok to leave the syringe attached at this point
- Apply firm pressure to the puncture point for at least 3 minutes. This will avoid any bruising or swelling
- Make small talk with the patient, no one likes awkward silences!
- Remove the syringe from the needle and dispose of the needle
- Expel any air from the syringe, being wary of spilling blood. Immediately cap the syringe
- Make a note of whether the patient was on room air or any supplementary oxygen, and take the sample to the nearest analysis machine
Allen's test is performed to assess the arterial supply to the distal hand. In clinical practice, many doctors will tell you that it is a waste of time, and it is not often that you will perform it on the ward before taking an ABG, as convention is to take it from the radial artery.
However, saying that you would perform Allen's test is a specific marking point in OSCEs, and is a very easy one to gain for yourself. It takes two seconds to mention and you will want every point you can get!
- Hold the patient's hand as pictured, using your fingers to occlude the ulnar and radial arteries.
- Ask the patient to make a fist a number of times, until their hand becomes white and starts to feel a little sore.
- Release the ulnar artery, if the hand immediately becomes red and looks well perfused, the artery is patent
- Perform the test again, releasing the radial artery to check its patency.
Some useful tips
- Taking an ABG sample can be sore for the patient. Good communication skills from the outset to give them prior warning of this can avoid giving the patient a nasty surprise
- When advancing the needle, do it with confidence. The first time I took an ABG, I went for the slowly-slowly approach as I was nervous, and almost received a smack round the head for my trouble, as it caused the patient more pain.
- Practice! ABGs can be quite daunting at first but the only way to get better is to put yourself forward and keep doing them. Sometimes practicing doctors find them tricky so don't be disheartened if you don't always get them first time!
Interpreting ABG results
Interpreting ABGs can be a nightmare. Below is a simple stepwise system which hopefully makes the process a logical one.
- 8-12 kPa on room air
- pH 7.35-7.45
- H+ 35-45
Interpreting ABG results continued
Interpreting the ABG
First, look at the report and determine whether the patient is on room air or supplementary oxygen. Then examine the ABG results in the following order:
1. Look at the p02 level. Is the patient hypoxic? If the patient's p02 falls within the normal range for their oxygen intake, then they are fully compensated.This doesn't mean that you can disregard the patient, as the other results can show the compensatory mechanisms involved.
2. Next, examine the H+/pH. If H+ is >45m the patient is acidaemic. If H+ is <35 the patient is alkalaemic. The H+/pH value indicates whether the patients compensatory mechanisms have allowed them to keep a normal acid-base balance.
3. Move on to the pC02. If the pC02 is above 6.0kPa, the patient has a respiratory acidosis. If the pC02 is below 4.7kPa, they have a respiratory alkalosis.
4. Finally, look at the HCO3. If the HCO3 is <22mmols/l, the patient has a metabolic acidosis. If the HCO3 is >26 mmols/l, the patient has a metabolic alkalosis.
Mr B, a 22 year old male, was admitted to A&E by ambulance with a GCS of 5/15. Passers-by reported he was stabbed in the left chest with a knife. Inspection reveals an incised wound in the left thorax which makes a sucking noise on inspiration. The patient is breathing at 30 breaths per min, has a heart rate of 150 bpm and a BP of 150/100mmHg. Analysis of an ABG showed the following:
- pCO2: 12.4 kPa
- pO2: 8.7 kPa
- H+: 126 nmol/l
- pH 6.9
- HCO3-: 23 nmol/l
Interpreting the results
1. Mr T's pO2 of 8.7 kPa indicates that he is acutely hypoxic.
2 . The H+ level is massively raised in this scenario, reflected by the greatly lowered pH. Mr T has become fiercely acidaemic.
3. The pCO2 value is raised to above the normal range. This indicates that Mr T is suffering from a respiratory acidosis
4. As the bicarbonate ion level is within the normal range, this indicates there has not been time for any metabolic compensation for the acidosis, indicating that the problem is acute in nature.
- Ruh roh! Mr T is currently suffering from a tension pneumothorax. The wound is acting as a one way valve, bringing air into the pleural space.
- This collapses one lung and compresses the other
- This results in hypoxia and hypercapnia with corresponding respiratory acidosis and acidaemia.
- Since the normal mechanism of clearance of excess H+ in the acute setting is via breathing, and Mr T has lost >50% of his surface area for gas exchange due to the lung being compromised, the situation is critical and death will result unless treatment is given rapidly.
What can be done
- The immediate treatment of a tension pneumothorax is needle decompression
- A cannula is inserted through the chest wall to allow an escape for air trapped within the thoracic cavity
- This allows the lung to re-expand and for more normal ventilation to occur
- For longer term management, a chest tube may need to be inserted whilst the site of the tension pneumothorx is dealt with
A distressed 12 year old child was brought to A&E by her parents. The child was "unable to catch her breath" and was hyperventilating. ABG analysis revealed:
- p02: 11 kPa
- pCO2: 3.7 kPa
- H+: 25 nmol/l
- pH: 7.6
- HCO3: 27 nmol/l
Interpreting the results
1. The pO2 is within the normal range, suggesting the child is fully compensated
2. The H+ value is below the normal range, suggesting the child is alkalaemic
3. The pCO2 value is below the normal range, showing the child to have a respiratory alkalosis
4. The HCO3 is slightly raised, but not remarkably so
- The child is having an asthma attack with Type 1 respiratory failure
- Broncho-constriction during the attack causes hypoxia
- This stimulates ventilation which drives down [H+] and CO2, giving rise to the respiratory alkalosis
- The hyperventilation also gives rise to the increase in pO2
What can be done
- Administration of a broncho-dilator such as salbutamol should relieve the broncho-constriction
- This will relieve the hypoxia and cause hyperventilation to cease
- This allows the child to breathe normally and return to a normal acid-base balance
A 21 year-old female is found outside a pub unconscious and smelling of alcohol. On admission to hospital, doctors identified the smell as being ketone bodies rather than alcohol. The patient had a respiratory rate of 8 breaths/min, heart rate of 60 bpm, BP 80/60 mmHg and a core temperature of 35 degrees. ABG revealed:
- pO2: 9.3 kPa
- pC02 6.2 kPa
- H+: 126 nmol/l
- HCO3: 9 nmol/l
Interpreting the results
1. The pO2 levels show that the patient has normal levels of oxygenation
2. The massively raised H+ level indicates the patient is acidaemic
3. The realtively normal CO2 value indicates the acidaemia is not respiratory in nature
4. The very low HCO3 value shows that the acidaemia is metabolic in nature. The patient has a metaboloic acidosis
- In an undiagnosed or poorly controlled diabetic, there is elevated plasma glucose which is not driven into cells due to a lack of insulin
- To counter this lack of available energy, there is rapid lipolysis to provide free fatty acids, an alternative energy supply
- These are metabolised in the liver, the end product of which are ketone bodies, which are responsible for the metabolic acidosis
What can be done
- The highest priorites in this case are fluid replacement and insulin treatment
- These therapies together reverse dehydration, help restore normal glucose and electrolyte levels and help reverse the acidosis
- The insulin therapy of choice would be the commencement of sliding scale insulin
Mr A is brought into A&E with a severe bout of vomiting. His vomiting persists despite administration of antiemetic therapy. As his vomiting continues he begins to drop in consciousness, his breathing becomes shallow and his respiratory rate falls. You take an ABG sample and the results are as follows (the results were taken on room air):
- p02: 8 kpa
- pC02: 10 kpa
- H+: 30 nmol/l
- HCO3: 40 mmol/l
Interpreting the results
1. The p02 shows us that Mr A is within the normal limits, but only just. He is on the verge of becoming hypoxic.
2. The H+ value shows us that at this point in time Mr A is alkalaemic. He is not fully compensated.
3. The pCO2 value shows that Mr A is currently experiencing a respiratory acidosis
4. The HCO3 values indicates that Mr A is undergoing a large metabolic alkalosis.
- Mr A has been vomiting profusely, causing large amounts of stomach acid to be evacuated from his system
- This had led to a systemic drop in his H+ levels, allowing his HCO3 levels to rise unapposed. This is why he has a metabolic alkalosis
- In an effort to combat the metabolic acidosis. Mr A is attempting to retain CO2 to buffer the rising HCO3. This has led to a decreased respiratory effort, meaning that Mr A blows off less CO2 with ventilation. The unfortunate by product is that he also receives less oxygen due to his decreased ventilatory effort, therefore causing him to become hypoxic
- The conclusion we can draw from this scenario is that Mr A has a metabolic alkalosis, with a partially compensated respiratory acidosis
- Mr A is judged to be partially compensated as he is not within the normal value for H+/pH
What can be done
- Give oxygen to correct Mr A's hypoxic state.
- Give IV fluids
- Take measures to remove excess base (done in mild metabolic alkalosis with an IV infusion of isotonic NaCl. In severe metabolic alkalosis, IV HCl or dialysis can be given. This requires a specialist nephrology opinion first!)
- Take measures to stop vomiting
2. The Oxford Handbook of Clinical Medicine, 7th Edition
3. Franklin, J. Dawson, P. Pocket Essentials of Clinical Surgery. Kumar and Clarke Family. Elsevier 2008.
4. The Oxford Handbook of Medical Sciences. 2nd Edition