• pH: 7.35 – 7.45
• pO₂: 10 – 14kPa
• pCO₂: 4.5 – 6kPa
• Base excess (BE): -2 – 2 mmol/l
• Bicarbonate (HCO₃₎: 22 – 26 mmol/l

• Normally the body’s pH is closely controlled at between 7.35 – 7.45.
• Blood pH is controlled through buffering and excretion of acids.
• Buffers include plasma proteins and bicarbonate (extracellular) and proteins, phosphate and haemoglobin (intracellularly).
• Hydrogen ions are excreted via the kidney and carbon dioxide is excreted via the lungs.
• Changes in ventilation are the primary way in which the concentration of H+ ions is regulated.

• Though these terms are often used interchangeably the strict difference is that acidaemia causes a change in the pH whereas an acidosis is something that occurs with accumulation of acids but crucially may not change the pH if compensatory mechanisms are sufficient.
• For example, with metabolic acidosis there may not be an acidaemia if respiratory compensation is  sufficient to maintain a normal pH but this doesn’t mean that there is not an ongoing pathological process.
• Only when the compensatory mechanisms are overwhelmed does an acidaemia develop.
• It is therefore possible to have a significant acidosis without developing an acidaemia.

• Partial pressure is a way of assessing the number of molecules of a particular gas in a mixture of gases.  It is the amount of pressure a particular gas contributes to the total pressure.
• For example, we normally breathe air which at sea level has a pressure of 100kPa, oxygen contributes 21% of 100kPa, which corresponds to a partial pressure of 21kPa.

• Base excess is the amount of strong base which would need to be added or subtracted from a substance in order to return the pH to normal (7.40).
• A value outside of the normal range (-2 to +2 mEq/L) suggests a metabolic cause for the acidosis or alkalosis.

• A high base excess (more than +2 mEq/L) indicates a metabolic alkalosis.
  • A low base excess (less than -2 mEq/L) indicates a metabolic acidosis.

• A low base excess (less than -2 mEq/L) indicates a metabolic acidosis.
  • A high base excess (more than +2 mEq/L) indicates a metabolic alkalosis

• Bicarbonate is produced by the kidneys and acts as a buffer to maintain a normal blood pH. The normal range for bicarbonate is 22 – 26mmol/l.
• If there are additional acids in the blood the level of bicarbonate will fall as ions are used to buffer these acids. If there is a chronic acidosis additional bicarbonate is produced by the kidneys to keep the pH in range.
• Raised bicarbonate may therefore be seen in chronic type 2 respiratory failure where the pH remains normal despite a raised CO₂.

• Lactate is produced as a by-product of anaerobic respiration.
• A raised lactate can be caused by any process which causes tissue to use anaerobic respiration.
• Lactate is therefore a good indicator of poor tissue perfusion.

• If a metabolic acidosis develops the change is sensed by chemoreceptors centrally in the medulla oblongata and peripherally in the carotid bodies.
• The body responds by increasing depth and rate of respiration therefore increasing the excretion of CO2 to try to keep the pH constant.
  • The classic example of this is ‘Kussmaul breathing’ the deep sighing pattern of respiration seen in severe acidosis including diabetic ketoacidosis.
  • Here you will see a low pH and a low pCO2 which would be described as a metabolic acidosis with partial respiratory compensation (partial as a normal pH has not been reached).

• In response to a respiratory acidosis, for example in CO2 retention secondary to  COPD, the kidneys will start to retain more HCO3 in order to correct the pH.
• Here you would see a low normal pH with a high CO2 and high bicarbonate.
  • This process takes place over days.
• It is important to ensure that the compensation that you see is appropriate, i.e. as you would expect. If not then you should start to think about mixed acid base disorders.

Though there are various systems to interpret ABGs. This one is systematic, practical and ensures nothing is missed.

1. Look at the patient! Review history and examination findings.
2. What is the pO2? How much oxygen was your patient on when the gas was taken?
3. What is the pH?  Is the patient acidaemic or alkalaemic.
4. What is the pCO2?
5. What is the HCO3 and base excess?
6. Is the patient compensating?
7. What are the other values? Ensure that you look at all other figures on the gas.

1. State that this is an arterial blood gas sample (rather than venous).
2. State the patients name and outline history/pertinent examination findings.
3. State the time the sample was taken and how much oxygen the patient was on at the time.
4. Present your findings: e.g. “This showed type one respiratory failure with a PO2 of 7.0.”
5. Present any abnormal findings or important negatives from the rest of the values.
6. A one line summary of your findings.

For example:

• “This is an arterial blood gas sample taken from Mrs Smith, a 70 year old lady who presented this morning with shortness of breath. She has a back ground of heart failure and diabetes and on auscultation of her chest she has bibasal crackles.
• This gas was taken at 10 a.m. today when Mrs Smith was on 15l per minute of oxygen via a non rebreathe mask.
• It showed type one respiratory failure with a p02 of 10.0 and a pCO2 of 4.1.
• There is no acid base disturbance although her glucose was noted to be 15.
• In summary this lady has type 1 respiratory failure.”

• Type one respiratory failure is diagnosed when there is a PO2 less than 8 and a PCO2 which is low or normal.
• T1RF is caused by pathological processes which reduce the ability of the lungs to exchange oxygen, without changing the ability to excrete CO2.

• Causes of T1RF include pulmonary embolus, pneumonia, asthma and pulmonary oedema.

• T2RF is defined as a PaO2 of less than 8 and a raised PaCO2.

T2RF can be caused by:

1. A problem with the lungs.
2. A problem with the mechanics of respiration.
3. A problem with the control of respiration.