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ABG & VBG - Arterial and Venous Blood Gas - interpreting results
Normal Values
pH

PaCO2
PaO2

7.35-7.45
4.7-6.0 kPa / 35-45 mmHg
9.3-13.3 kPa / 80-100 mmHg
22-28 mmol/L

HCO3SaO2(Oxygen saturation)
92-98%
PA pressure in the alveoli
Pa pressure in the artery
To convert kPa to mmHg, multiply by 7.5

PaCO2 gives an indication ofventilation -how was is the patient breathing, how is their gas exchange
PaO2is a measure ofoxygenation

The oxygen dissociation curve

Note how:
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

The bicarbonate buffering system is the method by which the body controls pH and is crucial to understand arterial and venous blood gas results.

CO2 + H2O H2CO3 H+ +HCO3The equation demonstrates an equilibrium, between carbon dioxide, and hydrogen ions + bicarbonate. In normal physiology at a normal metabolic rate, this equilibrium
exists to keep the pH between 7.35 and 7.45

Remember the pH is a logarithmic scale and as such, increases exponentially. The concentration of hydrogen ions at pH 7.1 is double that at pH
7.4.
When a pathological abnormality occurs, this can cause various shifts in the equilibrium. We interpret these shifts to try to assess what the pathological abnormality is.

If the concentration of Hydrogen ions increases, the pH will decrease, causing an acidosis. This causes the equation to shift to the left, and more
CO2 is produced, of which some (or all) can be blown off by the lungs. This is the mechanism ofrespiratory compensation.
If CO2 is not able to blown off effectively, then the concentration of CO2 increases, as thus then so will the concentration of hydrogen ions, and
the pH will not be able to be resolved to normal. This ispartial respiratory compensation.
Most causes of acid-base disturbance are due to an acidosis. The causes of these are discussed in more detail below.

There can also bemetabolic compensationwhereby the concentration of HCO3 is altered to try to keep the equilibrium in cases of respiratory
dysfunction.
In arespiratory alkalosis, CO2 is blown off too quickly, thus the curve shifts to the left, to replace the CO2, and the concentration of hydrogen ions
is lowered
In a metabolic alkalosis there is a disturbance due a loss of H+ or an excess of HCO3, causing the curve to shift.

Basic interpretation Rules

Interpretation is best done as part of an overall case review of a patient. Chronic as well as acute factors in the history can influence the result, particularly:
Renal disease
Diabetes
Drugs; diuretics, aspirin(+are they on oxygen?)
The Rule of 19is a way of assessing whether or not the patient was on oxygen at the time of the sample. AddthePO2andPCO2 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 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 acompensatedacidosis 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 theHCO3-- is it normal or abnormal? Is the change in keeping with the pH?
1. Note the changes inbicarband base excess take at least a couple of days to occur after the initialcausatoryevent.
4. If the changes arent in keeping with the levels, then it is likely to be some sort of compensation!More on how to tell this later on.
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 aretention 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)
CO2 retention in COPD patients causing worsening drowsiness
Hypoventilation of any other cause

Signs of CO2 retention

Confusion as a result of peripheralvasodilation
Asterixis(renal failure, type 2respfailure, liver failure)
Warmextremeties
Bounding pulse
Morning headache CO2particularly high at these times.

Acute or Chronic?

Most well patients with COPD will have a high CO2, but normal pH, because they havemetabolically compensatedfor 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 tohyperventilation.
As PaCO2lowers, 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
This is used to help diagnose acid base disorders. It is usually used in suspected cases of metabolic acidosis. It can either be normal, or raised.
Low anion gap does not usually occur.
Anions are negatively charged ions.The two most common ones in the human body are chloride and bicarbonate.
Anions are hard to measure accurately. The anion gap is the difference between the number of measured anions, and the number of unmeasured
anions.
Negatively charged proteins make up most of the unmeasured anions in a normal individual, and the main one is albumin.
And thus in a normal individual, there is an anion gap of 4-16, made up mostly of albumin.
Some causes of metabolic acidosis, do not produce a large number of unmeasured anions, and the anion gap doesn't increase. This isnormal anion
gap metabolic acidosis - NAGMA
Some causes of metabolic acidosis produce a large number of both measured (e.g. HCO3- ) anions, and unmeasured anions. This isHigh anion gap
metabolic acidosis - HAGMA.
In HAGMA, the HCO3- will bind to H+ (which is also produced in excess) and be turned into CO2 which is blown off by the lungs. So although you
have produced more HCO3- , the amount of HCO3- is low on an ABG sample because of all the excess H+ binding to it. So the proportion of
unmeasurd anions compared to measured anions INCREASES and so in metabolic acidosis the anions gap increases.

To calculate the anion gap, you work out the difference between plasma cations and measureable plasma anions.
Anion gap = [Na+] - [Cl-] - [HCO3-]

Some calculations also include potassium, however this would results in a different reference range, and the above formula is generally the accepted
version.
Anion Gap = [Na+] + [K+] - [Cl-] - [HCO3-]

Sometimes it is also necessary to correct for a low albumin level in individuals with liver disease:
Corrected Anion Gap = [AG] + (0.25 x (40 - albumin))
The anion gap is discussed in more detail in a separate article.
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 CATMUDPILES

Cyanide , carbon monoxide
Alcoholicketoacidosis
Toluline(methybenzine used as an inhaled narcotic)
Methanol,metformin
Uraemia
DiabeticKetoacidosis
Paracetamol
Iron,isoniazid
Lactate
Ethanol, ethylene glycol
Salicylate

Causes KARMEL
Ketones
Aspirin (andparacetamol, and other toxins)
Renal Failure
Methanol
EhyleneGlycol
Lactate

Summary of Blood Gas Differentials

Examples
Example 1
Patient breathing room air
PaO2 6.6 very low
PaCO2 6.5 high
pH 7.14
HCO3 23
This is a primary respiratory acidosis without compensation because pH is low (acidosis) and CO2 is high (respiratory) and HCO3 is normal so
there is not metabolic compensation.

This is type 2 respiratory failure.

The acidosis is acute because it is not compensated - the bicarbonate is normal.

Example 2
PaO2 7.8 (low)
PaCO2 8.0 (high)
pH 7.35 (normal)
HCO3 31 (high)
High CO2 indicates a respiratory acidosis but the increased bicarbonate and the normal pH indicated t is fully compensated.
This is likely to be chronic respiratory failure

Example 3
FlO2 .21 (21% oxygen - room air)
PaO2 8.0 low
PaCO2 5.0 (normal)

pH 7.51 High
HCO3 30
pH is high. This is an alkalosis
CO2 is normal therefore not likely to be hyperventilation
This is ametabolic alkalosis with a possible other cause of the hypoxia.
In this particularly example the alkalosis was due to diuretics. The patient's actual presenting complaint was carbon monoxide inhalation, which
explains his hypoxia.

Example 4
Patient is on 3L oxygen
2L 24%
4L 28%

PaO2 9.5 (low)

PaCO2 2.8 (low)
pH 7.40 (normal)
HCO3 12-very low
O2 sats 95%
The pH is normal, but the PaCO2 is very low. This indicates a fully compensated metabolic acidosis, as indicated by the low bicarbonate.
We are not able to calculate the anion gap in this instance.

Copyright 2009 - 2013 - Dr Tom Leach

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