The anion gap is a tool used to:

• Confirm that an acidosis is metabolic
• Narrow down the cause of a metabolic acidosis
• Monitor the progress of treatment

In a metabolic acidosis the anion gap is usually either ‘Normal’ or ‘High’. In rare cases it can be ‘low’, usually due to hypoalbuminaemia.

Calculating the Anion Gap

An arterial blood gas (ABG) machine will often give a print out of the anion gap, but it can also be useful to know how it is calculated.

In blood, there are many cations (positively charged ions) and anions (negatively charged ions). However, the vast majority of the total number are potassium, sodium, chloride, or bicarbonate. The ‘anion’ gap is an artificial measure, which is calculated by subtracting the total number of anions (negatively charged ions – bicarbonate and chloride) from the total number of cations (sodium and potassium).

Thus, the formula is:
([Na⁺]+ [K⁺]) –([Cl^–]+ [HCO₃^–])
In reality, the concentration of potassium anions is negligible, and this often omitted, giving:

[Na⁺] – ([Cl^–]+ [HCO₃^–])

There are usually more measurable cations than anions, and thus a normal anion gap is value is positive.

A normal value is 3-16, but may vary slightly depending on the technique used by the local laboratory.

If the anion gap is <30, then there may not be ‘true’ high anion gap metabolic acidosis.

In a healthy individual, the main unmeasured anions are albumin  and phosphate. Almost all of the ‘gap’ can be attributed to albumin. This means that in patients with hypoalbuminaemia and metabolic acidosis, there may be a normal anion gap. Be wary in severely unwell patients because they often have a low albumin. You can adjust for this in your calculation. Corrected anion gap:

• [AG] + (0.25 x (40-albumin))

In an unwell patient with a high anion gap metabolic acidosis (HAGMA) the anion gap is increased due to:

• Accumulation of organic acids
• Inability to secrete H+ via the kidneys

High anion gap metabolic acidosis (HAGMA)

There are lots of mnemonics for remembering the causes. I’ve included three below, but my favourite is ‘KARMEL’ as it isn’t too long! CAT MUDPILES is the most extensive and quoted in the literature.

Causes – Simple – “LTKR”

• Lactate
• Toxins
• Ketones
• Renal Failure

Causes – Exhaustive list – “CAT MUDPILES”

• Cyanide , carbon monoxide
• Alcoholic ketoacidosis
• Toluline (methybenzine – used as an inhaled narcotic)
• Methanol, metformin
• Uraemia
• Diabetic Ketoacidosis
• Paracetamol
• Iron, isoniazid
• Lactate
• Ethanol, ethylene glycol
• Salicylate

Causes – “KARMEL”

• Ketones
• Aspirin (and paracetamol, and other toxins)
• Renal Failure
• Methanol
• Ehylene Glycol
• Lactate

Diabetic Ketoacidosis

In DKA, there is loss of bicarbonate from the kidney, due to altered kidney metabolism, secondary to the DKA. However, there is also extracellular fluid volume depletion. And thus, the HCO₃concentration may be only marginally reduced, whilst the actual base deficit is much larger.

In DKA, there is impaired metabolism of ketones which usually occurs by the brain and kidney, secondary to raised levels of insulin. This is contrary to the common belief that the main cause of raised ketones is due to overproduction as a results of altered metabolism, due to lack of glucose within cells.

Management

Severely ill patients (particularly those with DKA) may require intubation due to severely decreased conscious levels. However, intubation and ventilation should be done with caution, because it can worsen acidosis.

If we image the bicarbonate buffering system:

We can see that in severe acidosis, hyperventilation may occur as a response to managing high [H⁺]. As carbon dioxide is expelled via the lungs, the equilibrium shifts to the left, and the [H⁺] is lowered. However, this also reduces the [HCO₃^–].

Thus, in a newly intubated patient, care must be taken to match the ventilator settings to the patient’s prior ventilation to ensure that worsening acidosis does not occur.

There is also an argument for the use of therapeutic bicarbonate in these patients, to help improve their acidosis, but the evidence is poor. If you imagine adding more bicarbonate into the above equation, it will shift the equilibrium to the left again, but ONLY if there is capacity (of the lungs – vie hyperventilation) to reduce the CO2 concentration. Thus, in an already heavily hyperventilating patient, this is often not of benefit.

Normal anion gap metabolic acidosis (NAGMA)

Causes of NAGMA tend to be more predictable and less obscure. NAGMA is typically due to a loss of bicarbonate, which is then subsequently replaced in plasma by chloride, and thus the overall anion concentration remains stable. Thus, most cases are a hyperchloraemic acidosis. 

Causes

• Diarrhoea (vast majority of cases)
• Renal tubular necrosis
• Chloride – e.g. in high volume IV normal saline (e.g. in patient requiring lots of volume resuscitation, e.g. in sepsis or DKA). Can be mitigated with use of more balanced fluids, such as Hartmann’s.

Causes – “ABCD”

• Addisons
• Bicarb loss (GI or Renal [RTA – renal tubular acidosis])
• Chloride
• Drugs (acetazolamide, acids)

The post The Anion Gap appeared first on almostadoctor.

Arterial Blood Gas interpretation can be a daunting and difficult skill for any medical student or junior doctor. Try to look at as many real life examples as you can, and don’t be afraid to get it wrong!

The use of Venous Blood Gasses is becoming more widespread, especially in the emergency department. Almost all of the same rules apply for VBG interpretation as for ABG interpretation with a couple of caveats:

• pO2 and pCO2 are unreliable in VBG interpretation. It may be possible to track a pCO2 trend, but take this with a pinch of salt.

Normal Values in ABG Interpretation

The oxygen dissociation curve

 

• The saturation declines rapidly at some points, and barely moves at other points. The curve starts its fast decline at about 90%, thus in the emergency situation, keeping oxygen saturations above 90% is important to avoid hypoxic injury (particularly hypoxic brain injury)
• Various factors, including pH and temperature can shift the curve to the right or the left

Bicarbonate Buffering System

Basic ABG interpretation

• Renal disease
• Diabetes
• Drugs; diuretics, aspirin(+are they on oxygen?)
  • The Rule of 19 is a way of assessing whether or not the patient was on oxygen at the time of the sample. Add the PO2 and PCO2 – if the sum of these is >19 then likely to be on inspired oxygen. If the level is lower than this, they are likely to be breathing room air.
• Symptoms and onset (lung disease?)

Basic ABG Interpretation Rules

1. Look at the pH – is it acidosis, alkalosis, or normal?
   1. If its acidotic, then the patient is acidotic
      1. If acidotic, calculate the anion gap to help differentiate the cause
   2. If its alkalotic, the patient is alkalotic
   3. ​If its it normal, there may be no acid-base dysfunction, or the patient could have a compensated acidosis or alkalosis. The CO2 and HCO3 values are required for further interpretation.
2. Look at the CO₂ – is it normal or abnormal?  Is this change in keeping with the pH? (See table below)
3. Look at the HCO3- – is it normal or abnormal? Is the change in keeping with the pH?
   1. Note the changes in bicarb and base excess take at least a couple of days to occur after the initial causatory event.
4. If the changes aren’t in keeping with the levels, then it is likely to be some sort of compensation! More on how to tell this later on.

Arterial Blood Gas Interpretation Table

CO2	pH	Normal Acid Base Status
CO2	↓ pH	Metabolic Acidosis
CO2	↑ pH	Metabolic Alkalosis
↑ CO2	pH	Respiratory Acidosis with full metabolic compensation
↑ CO2	↓ pH	Respiratory Acidosis
↑ CO2	↑ pH	Metabolic Alkalosis with partial respiratory compensation
↓ CO2	pH	Respiratory Alkalosis with full metabolic compensation
↓ CO2	↓ pH	Metabolic Acidosis with partial respiratory compensation
↓CO2	↑ pH	Metabolic Alkalosis with partial respiratory compensation

Respiratory acidosis

Respiratory acidosis is very straightforward. It is always due to a retention of CO₂, (Type II Respiratory failure) of which there are only a handful of causes:

• COPD
• Depressed respiratory drive (e.g. low GCS)
  • Brain Injury
  • Drug overdose (often opiates)
  • CO₂retention in COPD patients causing worsening drowsiness
• Hypoventilation of any other cause

Signs of CO₂ retention

• Confusion – as a result of peripheral vasodilation
• Asterixis (renal failure, type 2 resp failure, liver failure)
• Warm extremeties
• Bounding pulse
• Morning headache – CO₂ particularly high at these times.

Acute or Chronic?

• Most well patients with COPD will have a high CO₂, but normal pH, because they have metabolically compensated for their high CO₂.
• Patients with an acute cause, will likely have a acidotic pH, because the metabolic system has not had time to compensate
• COPD patients with an acute exacerbation, or another acute illness an also have an acute CO2 retention on top of their chronic retention.
• Compensation starts at about 6 hours and is complete (i.e. at the limits of physiology) by 4 days.
• Assessing the HCO3 in conjunction with the CO2 can help differentiate if the CO2 retention is acute or chronic. This is known as the  1 for 10 rule.

1 for 10 rule

• ACUTE: For every rise of 10 of the PaCO2 above 40 mmHg, the bicarbonate will rise by 1
• CHRONIC: For every rise of 10 of the PaCO2 above 40mmHg, the bicarbonate will rise by 4

Respiratory alkalosis

This is due to hyperventilation. 

• As PaCO2 lowers, so pH rises
• Any cause of hyperventilation:
  • Anxiety
  • Pain
  • Fever
  • Sepsis
  • Hypoxia (due to acute illness (sepsis / pneumonia) or altitude)

Metabolic Alkalosis

Is caused by:

• Loss of hydrogen ions
  • Diarrhoea (sometimes vomiting too)
  • Burns
• Excess Bicarbonate
  • Diuretics
  • Ingestion of alkaline substances

Hydrogen Ion loss

Most commonly cause by diarrhoea. In diarrhoea, there is a loss of K+ into the GI tract. This causes K+ to leave cells, and enter the bloodstream in an attempt to keep K+ levels normal. In order to maintain the electrical charge of the cell, H+ is then taken up by the cell.

May also be caused by burns

Excess Bicarbonate

Normal kidneys are very effective at excreting bicarbonate. Diuretics prevent the re-absorption of sodium from the renal tubule, and thus they promote sodium loss. The normal mechanism for recovering this sodium, involves an exchange with bicarbonate, and thus the ability of the renal tubule to excret bicarbonate is reduced.

May also be cause by too much bicarbonate (sometimes iatrogenic) or ingestion of other alkaline substances.

Metabolic Acidosis

Metabolic acidosis is the most common and the most complex of the acid base disturbances. There are a wide variety of causes, which can be differentiated with the help of the anion gap.

The Anion Gap

Normal Anion Gap Metabolic Acidosis (NAGMA)

This is also sometimes called Hyperchloraemic metabolic acidosis, as the cause is sometimes an increase in chloride ions.
The causes can be remembered with the mnemonic ABCD:

• A – Addison’s Disease
• B – Bicarbonate loss
  • ​Diarrhoea
  • Renal Failure
• C – Chloride Excess – e.g. from lots of normal saline
• D – Drugs (acetazolamide)

High Anion Gap Metabolic Acidosis (HAGMA)

HAGMA is due to an increase in unmeasured ions (but not albumin). There are several mnemonics to remember the causes, and I have included three below; LTKR, KARMEL and CAT MUDPILES. Pick your favourite!

Causes – Simple – “LTKR”

• Lactate
• Toxins
• Ketones
• Renal Failure

Causes – Exhaustive list – “CAT MUDPILES”

• Cyanide , carbon monoxide
• Alcoholic ketoacidosis
• Toluline (methybenzine – used as an inhaled narcotic)
• Methanol, metformin
• Uraemia
• Diabetic Ketoacidosis
• Paracetamol
• Iron, isoniazid
• Lactate
• Ethanol, ethylene glycol
• Salicylate

Causes – “KARMEL”

• Ketones
• Aspirin (and paracetamol, and other toxins)
• Renal Failure
• Methanol
• Ehylene Glycol
• Lactate

Summary of Blood Gas Differentials

Examples

Example 1

• PaO2     6.6 – very low
• PaCO2   6.5 – high
• pH 7.14
• HCO3     23

Example 2

• PaO2                     7.8 (low)
• PaCO2                  8.0 (high)
• pH                          7.35 (normal)
• HCO3                    31 (high)

Example 3

• FlO2                  .21 (21% oxygen – room air)
• PaO2                8.0 low
• PaCO2             5.0 (normal)
• pH                     7.51 High
• HCO3               30

Example 4

• PaO2                9.5 (low)
• PaCO2             2.8 (low)
• pH                     7.40 (normal)
• HCO3               12 -very low
• O2 sats            95%

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