Arterial Blood gas Analysis(ABG)

Reference ranges

• pH: 7.35 – 7.45
• PaCO₂: 4.7 – 6.0 kPa || 35.2 – 45 mmHg
• PaO₂: 11 – 13 kPa || 82.5 – 97.5 mmHg
• HCO₃–: 22 – 26 mEq/L
• Base excess (BE): -2 to +2 mmol/L

Oxygenation(PaO2) :

Your first question when looking at the ABG should be “Is this patient hypoxic?” as hypoxia is the most immediate threat to life.

PaO₂ should be >10 kPa (75mmHg) when oxygenating on room air in a healthy patient.

If the patient is receiving oxygen therapy their PaO₂ should be approximately 10kPa less than the % inspired

concentration FiO₂ (so a patient on 40% oxygen would be expected to have a PaO₂ of approximately 30kPa /225mmHg).

Oxygen delivery devices and flow rates:

A common question is “What percentage of oxygen does this device deliver at a given flow rate?”. Below is a quick reference guide,

providing some approximate values for the various oxygen delivery devices and flow rates you’ll come across in practice.

Nasal cannulae

As with all oxygen delivery devices, there is a significant amount of variability depending on the patient’s breathing rate, depth and how

well the oxygen delivery device is fitted. Below are some guides to various oxygen flow rates and the approximate percentage of oxygen delivered:

1L / min – 24%

• 2L/ min – 28%
• 3L/ min – 32%
• 4L / min – 36%

Simple face mask

The oxygen delivery of simple face masks is highly variable depending upon oxygen flow rate, the quality of the mask fit, the

patient’s respiratory rate and their tidal volume. Simple face masks can deliver a maximum FiO₂ of approximately 40%-60% at a

flow rate of 15L/min. These masks should not be used with flow rates less than 5L/min.

Reservoir mask (also known as a non-rebreather mask)

Reservoir masks deliver oxygen at concentrations between 60% and 90% when used at a flow rate of 10–15 l/min.

The concentration is not accurate and will depend on the flow of oxygen as well as the patient’s breathing pattern.

These masks are most suitable for trauma and emergency use where carbon dioxide retention is unlikely.

Venturi masks

A Venturi mask will give an accurate concentration of oxygen to the patient regardless of the oxygen flow rate (the minimum suggested

flow rate is written on each). Venturi masks are available in the following concentrations: 24%, 28%, 35%, 40% and 60%.

They are suitable for all patients needing a known concentration of oxygen, but 24% and 28% Venturi masks are particularly

suited to those at risk of carbon dioxide retention (e.g. patients with chronic obstructive pulmonary disease).

Hypoxaemia

If PaO₂ is <10 kPa (75mmHg) on air, a patient is considered hypoxaemic.

If PaO₂ is <8 kPa (60mmHg) on air, a patient is considered severely hypoxaemic and in respiratory failure.

Type 1 & 2 respiratory failure:

Type 1 respiratory failure involves hypoxaemia (PaO₂ <8 kPa / 60mmHg) with normocapnia (PaCO₂ <6.0 kPa / 45mmHg).

Type 2 respiratory failure involves hypoxaemia (PaO₂ <8 kPa / 60mmHg) with hypercapnia (PaCO₂ >6.0 kPa / 45mmHg).

Type 1 respiratory failure

Type 1 respiratory failure involves hypoxaemia (PaO₂ <8 kPa /60mmHg) with normocapnia (PaCO₂ <6.0 kPa / 45mmHg).

It occurs as a result of ventilation/perfusion (V/Q) mismatch; the volume of air flowing in and out of the lungs is not matched with the

flow of blood to the lung tissue. As a result of the VQ mismatch, PaO₂ falls and PaCO₂ rises. The rise in PaCO₂ rapidly triggers an increase in

a patient’s overall alveolar ventilation, which corrects the PaCO₂ but not the PaO₂ due to the different shape of the CO₂ and

O₂ dissociation curves. The end result is hypoxaemia (PaO₂ < 8 kPa /60mmHg) with normocapnia (PaCO₂ < 6.0 kPa / 45mmHg).

Examples of VQ mismatch include:

• Reduced ventilation and normal perfusion (e.g. pulmonary oedema, bronchoconstriction)
• Reduced perfusion with normal ventilation (e.g. pulmonary embolism)

Type 2 respiratory failure 

Type 2 respiratory failure involves hypoxaemia (PaO₂ is <8 kPa / 60mmHg) with hypercapnia (PaCO₂ >6.0 kPa / 45mmHg).

It occurs as a result of alveolar hypoventilation, which prevents the patient from being able to

adequately oxygenate and eliminate CO₂ from their blood.

Hypoventilation can occur for a number of reasons including:

• Increased resistance as a result of airway obstruction (e.g. COPD).
• Reduced compliance of the lung tissue/chest wall (e.g. pneumonia, rib fractures, obesity).
• Reduced strength of the respiratory muscles (e.g. Guillain-Barré, motor neurone disease).
• Drugs acting on the respiratory centre reducing overall ventilation (e.g. opiates).

Seemingly small abnormalities in pH have very significant and wide-spanning effects on the physiology of

the human body. Therefore, paying close attention to pH abnormalities is essential.

So we need to ask ourselves, is the pH normal, acidotic or alkalotic?

• Acidotic: pH <7.35
• Normal: pH 7.35 – 7.45
• Alkalotic: pH >7.45

pH scale 

We need to consider the driving force behind the change in pH. Broadly speaking the causes can be either metabolic or respiratory.

The changes in pH are caused by an imbalance in the CO₂ (respiratory) or HCO₃– (metabolic). These work as buffers to keep

the pH within a set range and when there is an abnormality in either of these the pH will be outside of the normal range.

As a result, when an ABG demonstrates alkalosis or acidosis you need to then begin considering what is driving this

abnormality by moving through the next few steps of this guide.

PaO_{2 :}

At this point, prior to assessing the CO₂, you already know the pH and the PaO₂. So for example, you may know your patient’s pH is

abnormal but you don’t yet know the underlying cause. It could be caused by the respiratory system (abnormal level of CO₂) or

it could be metabolically driven (abnormal level of HCO₃-).

Looking at the level of CO₂ quickly helps rule in or out the respiratory system as the cause for the derangement in pH.

Underlying Biochemistry:

CO₂ binds with H₂O and forms carbonic acid (H₂CO₃) which will decrease pH. When a patient is retaining CO₂ the

blood will, therefore, become more acidic from the increased concentration of carbonic acid. When a patient is ‘blowing

off’ CO₂ there is less of it in the system and, as a result, the patient’s blood will become less acidotic and more alkalotic.

The idea of ‘compensation’ is that the body can try and adjust other buffers to keep the pH within the normal range.

If the cause of the pH imbalance is from the respiratory system, the body can adjust the HCO₃– to counterbalance

the pH abnormality bringing it closer to the normal range. This works the other way around as well; if the

cause of a pH imbalance is metabolic, the respiratory system can try and compensate by either retaining

or blowing off CO₂ to counterbalance the metabolic problem (via increasing or decreasing alveolar ventilation).

So we need to ask ourselves:

1. Is the CO₂ normal or abnormal?
2. If abnormal, does this abnormality fit with the current pH (e.g. if the CO₂ is high, it would make sense that
3. the pH was low, suggesting this was more likely a respiratory acidosis)?
4. If the abnormality in CO₂ doesn’t make sense as the cause of the pH abnormality (e.g. normal or  ↓ CO₂ and ↓ pH),
5. it would suggest that the underlying cause for the pH abnormality is metabolic.

HCO₃– :

We now know the pH and whether the underlying problem is metabolic or respiratory in

nature from the CO₂ level.

Piecing this information together with the HCO₃– we can complete the picture:

• HCO₃– is a base, which helps mop up acids (H+ ions).
• So when HCO₃– is raised the pH is increased as there are less free H+ ions (alkalosis).
• When HCO₃– is low the pH is decreased as there are more free H+ ions (acidosis).

So we need to ask ourselves:

1. Is the HCO₃– normal or abnormal?
   
2. If abnormal, does this abnormality fit with the current pH (e.g. ↓HCO₃– and acidosis)?
3. If the abnormality doesn’t make sense as the cause for the deranged pH, it suggests the cause is more likely
4. respiratory (which you should have already known from your assessment of CO₂).

You may note that in each of these tables HCO₃– and CO₂ are both included, as it is important to look at each in the context of the other.

Base Excess:

The base excess is another surrogate marker of metabolic acidosis or alkalosis:

1.A high base excess (> +2mmol/L) indicates that there is a higher than normal amount of HCO₃– in the blood,

which may be due to a primary metabolic alkalosis or a compensated respiratory acidosis

2.A low base excess (< -2mmol/L) indicates that there is a lower than normal amount of HCO₃– in the blood,

suggesting either a primary metabolic acidosis or a compensated respiratory alkalosis.

Compensation:

Compensation has been touched on already in the above sections, to clarify we have made it simple below:

1.Respiratory acidosis/alkalosis (changes in CO₂) can be metabolically compensated by increasing or

decreasing the levels of HCO₃– in an attempt to move the pH closer to the normal range.

2.Metabolic acidosis/alkalosis (changes in HCO₃-) can be compensated by the respiratory

system retaining or blowing off CO₂ in an attempt to move the pH closer to the normal range.

Role of compensation:

Respiratory compensation for a metabolic disorder can occur quickly by either increasing or decreasing

alveolar ventilation to blow off more CO₂ (↑ pH) or retain more CO₂ (↓ pH).

Metabolic compensation for a respiratory disorder, however, takes at least a few days to occur as it requires the

kidneys to either reduce HCO₃– production (to decrease pH) or increase HCO₃– production (to increase pH).

As a result, if you see evidence of metabolic compensation for a respiratory disorder (e.g. increased HCO₃-/base excess

in a patient with COPD and CO₂ retention) you can assume that the respiratory derangement has been ongoing for at least a few days, if not more.

It’s important to note that ‘over-compensation’ should never occur and, therefore, if you see something that resembles

this you should consider other pathologies driving the change (e.g. a mixed acid/base disorder).

mixed acidosis or alkalosis:

It’s worth mentioning that it is possible to have a mixed acidosis or alkalosis

 (e.g. respiratory and metabolic acidosis/respiratory and metabolic alkalosis).  

In these circumstances, the CO₂ and HCO₃– will be moving in opposite directions

(e.g. ↑ CO₂ ↓ HCO₃– in mixed respiratory and metabolic acidosis).

Treatment is directed towards correcting each primary acid-base disturbance.

You can see some causes of mixed acidosis and alkalosis below.

mixed respiratory and metabolic acidosis:

A mixed respiratory and metabolic acidosis would have the following characteristics on an ABG:

• ↓ pH
• ↑CO₂
• ↓HCO₃–

Causes of mixed respiratory and metabolic acidosis include:

• Cardiac arrest
• Multi-organ failure

mixed respiratory and metabolic alkalosis:

mixed respiratory and metabolic alkalosis would have the following characteristics on an ABG:

• ↑ pH
• ↓ CO₂
• ↑ HCO₃–

Causes of mixed respiratory and metabolic alkalosis:

• Liver cirrhosis in addition to diuretic use
• Hyperemesis gravidarum
• Excessive ventilation in COPD

Acid/Base Disturbance causes:

So far we have discussed how to determine what the acid-base disturbance is, once we have this established

we need to consider the underlying pathology that is driving this disturbance

Respiratory Acidosis:

Respiratory acidosis is caused by inadequate alveolar ventilation leading to CO₂ retention.

A respiratory acidosis would have the following characteristics on an ABG:

• ↓ pH
• ↑ CO₂

Causes of respiratory acidosis include:

• Respiratory depression (e.g. opiates)
• Guillain-Barre: paralysis leads to an inability to adequately ventilate
• Asthma
• Chronic obstructive pulmonary disease (COPD)
• Iatrogenic (incorrect mechanical ventilation settings)

Respiratory Alkalosis:

Respiratory alkalosis is caused by excessive alveolar ventilation (hyperventilation) resulting in more

CO₂ than normal being exhaled. As a result, PaCO₂ is reduced and pH increases causing alkalosis.

A respiratory alkalosis would have the following characteristics on an ABG:

• ↑ pH
• ↓ CO₂

Causes of respiratory alkalosis include: ³

• Anxiety (i.e. panic attack)
• Pain: causing an increased respiratory rate.
• Hypoxia: resulting in increased alveolar ventilation in an attempt to compensate.
• Pulmonary embolism
• Pneumothorax
• Iatrogenic (e.g. excessive mechanical ventilation)

Metabolic acidosis:

Metabolic acidosis can occur as a result of either:

• Increased acid production or acid ingestion.
• Decreased acid excretion or increased rate of gastrointestinal and renal HCO₃– loss.

A metabolic acidosis would have the following characteristics on an ABG:

• ↓ pH
• ↓ HCO_3-
• ↓ BE

Anion gap :

Blood plasma is an aqueous solution containing a variety of chemical species, some of which have a net electrical charge

as a result of the dissociation of salts and acids in the aqueous medium. Species that have a net positive charge are called 

cations (e.g. Na+, K+)and those with a net negative charge are called anions (chloride & HCO₃–). 

The anion gap is an artificial measure that is calculated by subtracting the total number of anions (chloride & HCO₃–) from

the total number of cations (Na+). There are lots of other anions and cations, however, those shown in brackets have the most

significant influence, which is why other cations (e.g. K+) and anions (e.g. albumin, phosphate) are not used in the calculation of the anion gap.

Anion gap formula: Na+ – (Cl– + HCO₃–)

The anion gap (AG) is a derived variable primarily used for the evaluation of metabolic acidosis to determine

the presence of unmeasured anions (e.g. albumin is the main unmeasured anion). The normal anion gap

varies with different assays but is typically between 4 to 12 mmol/L.

Causes of a high anion gap metabolic acidosis (typically relate to increased production/ingestion or

reduced excretion of H+ by the kidneys):

• Diabetic ketoacidosis
• Lactic acidosis 
• Aspirin overdose
• Renal failure

Causes of a normal anion gap metabolic acidosis (typically due to loss of bicarbonate which is

subsequently replaced by chloride in the plasma, resulting in a stable overall anion concentration):

• Gastrointestinal loss of HCO₃– (e.g. diarrhoea, ileostomy, proximal colostomy)
• Renal tubular disease
• Addison’s disease 

Vignette

A 17-year-old patient presents to A&E complaining of a tight feeling in their chest, shortness of breath and some tingling in their fingers and around their mouth. They have no significant past medical history and are not on any regular medication. An ABG is performed on the patient (who is not currently receiving any oxygen therapy).

An ABG is performed and reveals the following:

• PaO₂: 14 (11 – 13 kPa) || 105 mmHg (82.5 – 97.5 mmHg)
• pH: 7.49 (7.35 – 7.45)
• PaCO₂: 3.6 (4.7 – 6.0 kPa) || 27 mmHg (35.2 – 45 mmHg)
• HCO₃–: 24 (22 – 26 mEq/L)

Answer:

Oxygenation (PaO₂)

A PaO₂ of 14 on room air is at the upper limit of normal, so the patient is not hypoxic.

pH

A pH of 7.49 is higher than normal and therefore the patient is alkalotic. 

The next step is to figure out whether the respiratory system is contributing the alkalosis (e.g. ↓ CO₂).

PaCO₂

The CO₂ is low, which would be in keeping with an alkalosis, so we now know the respiratory system is

definitely contributing to the alkalosis, if not the entire cause of it.

The next step is to look at the HCO₃– and see if it is also contributing to the alkalosis.

HCO₃–

HCO₃– is normal, ruling out a mixed respiratory and metabolic alkalosis, leaving us with an isolated respiratory alkalosis.

Compensation

There is no evidence of metabolic compensation of the respiratory alkalosis (which would involve a lowered HCO₃-)

suggesting that this derangement is relatively acute (as metabolic compensation takes a few days to develop).

Interpretation

Respiratory alkalosis with no metabolic compensation.

The underlying cause of respiratory alkalosis, in this case, is a panic attack, with hyperventilation in addition

to peripheral and peri-oral tingling being classical presenting features.