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turquoise
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Anaemia revision :o( - 07-28-2007, 12:01 AM

Hi, was wondering if anyone had any tips as to how to go about revising/learning data interpretation for e.g. blood results/urinalysis/thyroid function tests? I don't know where to start, I know in the exams we'll be given normal values! Sorry if this sounds too vague Thanks!
 
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07-28-2007, 07:25 AM

raj has edited a few articles that may help you. Here is one on abg's

The others are in the medical school tutorial section

Arterial Blood Gases: a guide for medical students

Why are arterial blood gases (ABG’s) important? Well they can give a guide to how ill your patient is, why your patient is ill and also because it is easy and common for consultants to hand them to you on ward rounds and ask for your interpretations!
What follows is a useful guide to ABG interpretation for medical students but will also serve as a quick reminder for house officers, senior house officers and any respiratory health care provider.

Why do we do ABGs?

ABGs are performed to assess ventilation, oxygenation and the acid-base balance. Therefore common indications include:
1. diagnosis and assessment of respiratory disorders e.g. dyspnoea, COPD, asthma
2. assessment of oxygenation and guide oxygen therapy
3. assessment of metabolic disturbances e.g. diabetic ketoacidosis
4. cardiac arrest

How do you do ABGs?


Usually arterial blood is sampled from the radial artery near to the wrist. Other sites include the brachial artery in the antecubital fossa and the femoral artery in the groin. Ask a house officer to show you the technique and try to gain some experience with the procedure. Always remember to use an aseptic technique and apply firm pressure to the puncture area after samplings. ABG sampling hurts so try to be considerate!

What is included in an ABG?

This can vary but all ABG results contain the following:

Normal Values
pH 7.35-7.45
Partial Pressure of Oxygen (Pa02) >11 kPa
Partial Pressure of Carbon Dioxide (PaC02) 4.7-6.0 kPa
Bicarbonate (HCO3-) 21-28 mmol/L
Base Excess +/- 2
(kPa = kiloPascals)

Certain things you just need to know before you can approach ABGs!


1. pH is inversely proportional to the concentration of hydrogen ions in the blood
2. low pH = acidosis; high pH = alkalosis
3. any disturbance in acid-base balance can be caused by a respiratory cause, a
metabolic cause or a combined cause
4. to diagnose a respiratory cause look at the PaC02 levels
5. to diagnose a metabolic cause look at the HCO3- levels
6. to diagnose a combined respiratory-metabolic disorder is a bit more difficult

How to initially approach acid-base balance interpretation?

The first thing is to look at the pH. Remember that pH is inversely proportional to the concentration of hydrogen ions in the blood.

Now you should look at the PaC02 level. A raised PaC02 will cause an increase in hydrogen ions and so will result in an acidotic state. Alternatively, a low PaC02 will result in an alkalotic state.
If the change in pH is mirrored by the change in PaC02 level, then you can be fairly certain that the change is due to a respiratory cause.

↑PaC02 = ↑H+ = respiratory acidosis
↓PaC02 = ↓H+ = respiratory alkalosis

If the change is not mirrored then the cause is probably metabolic, so lets look at the HCO3- level.

HCO3- is a base and so a raised HCO3- level means more base and will cause a rise in the pH (alkalosis); a reduction in the HCO3- level will lead to a reduction in the pH (acidosis). Again, if the changes in pH are mirrored by the changes in the HCO3-level, then the cause of the acid-base imbalance is probably metabolic.

Just to a note about base excess. A base excess (positive value) indicates an excess of base in the body and so mirrors a raised HCO3- level (metabolic alkalosis). A base deficit (negative value) indicates a lack of base in the body and so mirrors a reduced HCO3- level (metabolic acidosis).

Hopefully you are now in a position to look at ABG results and make some kind of intelligent comment as to what is causing the acid-base imbalance. One further thing to look for is compensatory changes. This is to be expected because the body wants to bring the pH level back to normal and so needs to do something. Look at the table below to see the typical changes when the body compensates for the different acid-base disturbances. Just remember that respiratory compensation occurs quickly whereas metabolic compensation can take longer to occur.


Acid-Base Disturbance Primary Disturbance Compensation
Metabolic Acidosis ↓ HCO3- ↓ PaC02
Metabolic Alkalosis ↑ HCO3- ↑ PaC02
Respiratory Acidosis ↑ PaC02 ↑ HCO3-
Respiratory Alkalosis ↓ PaC02 ↓ HCO3-







Respiratory Acidosis


This is caused by alveolar hypoventilation.

Causes:
1. Chronic obstructive pulmonary disease
2. Neuromuscular diseases - e.g. Guillain-Barre syndrome, Myasthenia Gravis,
 Muscular Dystrophy
3. CNS depression - e.g. drugs (opiates, barbiturates), neurological disorders (trauma, brainstem disorders)

Respiratory Alkalosis

This is caused by alveolar hyperventilation

Causes:
1. Shock
2. Lung causes (pneumonia, pneumothorax, oedema, pulmonary embolism)
3. Central nervous system causes (meningitis, intracerebral haemorrhage)
4. Metabolic causes (fever, hyperthyroidism)
5. Psychogenic causes (pain, anxiety)

Metabolic Acidosis


This disorder can be caused by a variety of conditions and the treatment is directed according to the cause. The causes can be separated by evaluating the “anion gap”.
The anion gap can be calculated by using the following formula:

Anion gap = cations - anions
= (sodium + potassium) - (chloride + bicarbonate)
= 10-16 mmol/L

The result is positive as there are certain anions in the body that we are unable to measure; these are mainly proteins but also include sulphates, phosphates, lactate and ketones.
Therefore a metabolic acidosis with a raised anion gap means that there are more unmeasured anions in the body than normal; caused of a raised anion gap include:

1. Ingestion of exogenous acid: salicylate, tricylcics, methanol or ethylene glycol
2. Increased body production of acid: lactic acidosis, ketoacidosis
3. Inability to excrete acid: renal failure

Causes of a metabolic acidosis with a normal anion gap includes any loss of bicarbonate. This is usually from the GIT (diarrhoea, ileostomy) or the kidneys ( renal tubular acidosis).



Metabolic Alkalosis

This can result from the loss of acid or the addition of alkali.

Causes:

1. Loss of stomach acid
2. Oral administration of acids (e.g. antacids)
3. volume depletion (e.g. on diuretics)
4. Hypokalaemia



Assessment of Oxygenation


Respiratory Failure

This is defined as a failure to fully oxygenate the blood passing through through the lungs, giving rise to hypoxia (PaO2 less than 8 kPa) and/or hypercapnia (PaCO2 greater than 6 kPa).

Type 1 Respiratory Failure is characterized by hypoxia with a normal or low PaCO2. Causes include anything that impairs gas exchange:

1. Atelectasis
2. Pulmonary oedema
3. Pneumonia
4. Pleural effusion
5. Haemo/pneumothorax

Type 2 Respiratory Failure is characterized by hypoxia with hypercapnia and is caused by alveolar hypoventilation. Therefore the causes are the same as those for respiratory acidosis.

Summary

This is an introduction guide to ABG interpretation for medical students. For the more keen amongst you will want to look at acid-base balance in a physiology book to understand compensatory mechanisms in more detail (included the Henderson-Hasselbach Equation).

Further Reading

1. Student BMJ. Acute care: Arterial blood gases by Nicola Cooper
(http://www.studentbmj.com/issues/04/...cation/105.php)
This article provides an overview of ABG analysis and also some practice
questions with answers.



2. Resuscitation council. Acid–Base Balance: Interpreting Arterial Blood Gases.
(www.resus.org.uk/pages/alsmBGap.pdf)
This article has a useful definitions page.

3. Virtual Hospital website.
(http://web.archive.org/web/200410130...g/ABGHome.html)
This article uses cases to explain ABG analysis.
 
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Thanks! - 07-28-2007, 06:57 PM

Wow thanks so much for that- and for replying so quickly, it was really helpful- appreciate it!
 
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