Arterial Blood Gas in MRCP(I)

Arterial Blood Gas in MRCP (I)

Recently I received an email from a MRCP Part 1 and 2 blog reader about ABG interpretation in MRCP. I share with him the same feeling that ABG interpretation is important in MRCP as well as your daily clinical practice.

Our blood PH is closely regulated in a tight range around 7.4±0.05 so that our body can function properly. As you might remember during your secondary school time, enzymes function in certain PH range and will be damaged by acidic or alkaline environments.

Although a lot of candidates ( and a lot of house officers) tend to make various mistakes in ABG interpretation. I would like to give a few simple rules to remember so that you will not make any more mistakes in future,

1) There are two important organs in our body which control our body PH- lung and kidney.
2) Carbon dioxide is an acidic gas, therefore, in acidic environment ( due to various insults), our body ( the lung) tends to compensate by exhaling out more CO2 ( therefore, patient tends to hyperventilate) and vice versa.
3) HCO3 is alkaline and its level is mainly regulated in our kidney.
4) PH=7.4 is normal, if PH less than 7.35 is acidic and more than 7.45 is alkaline.
5) Remember other normal values, normal HCO3=22-28 mmol, PaO2 more than 10.6 kpa ( 1kPa=7.6mmHg), PaCO2=4.7-6.0 kPa ( 35-45mmHg)

OK, for you to interpret ABG results correctly, follow these simple steps,

1) Read the PH first, if PH<7.35, it is acidosis, if it is more than 7.45, it is alkalosis.
2) Once you know whether it is acidosis or alkalosis, you must determine eithet it is respiratory or metabolic, I find two useful parameters to look at, HCO3 and PaCO2.

Let me show you a few examples,

1) Metabolic Acidosis

I still think this is the commonest and most important acid-base balance disorder you will find in your MRCP and daily clinical practice. Read the causes for metabolic acidosis in my previous post.

However, in daily practice, you commonly find metabolic acidosis in uraemia ( chronic kidney disease patient) , diabetic ketoacidosis, salicylates poisoning and lactic acidosis.

Therefore, in metabolic acidosis, you will find PH↓, HCO3↓ and PaCO2↓, it is easy to understand, in metabolic acidosis, our body cannot conserve HCO3, therefore the level of HCO3 is low, however, for our body to compensate ( try to push up PH level), we will hyperventilate to blow out more CO2 ( because CO2 is acidic), therefore, patient will hyperventilate in metabolic acidosis. (air hunger)

You must remember that there are two types of metabolic acidosis- reduced anion gap and normal anion gap ( normal anion gap=8-16 mmol) metabolic acidosis, I have covered this topic in my previous post.

MRCP Question

A 16-year old girl is admitted to your ward from A+E department due to vomiting and abdominal pain. She has no known medical problems and denies taking any illegal drugs.

On examination, you noticed she is dehydrated, blood pressure=90/50, pulse rate=120 and her abdomen is soft. Below are her blood results,

Full blood count
Total white 16,000 ( Normal 4000-11,000)
Hb=12.3
Plt= 235,000

K= 3.2
Creatinine= 110
Na= 131
Cl=100

ABG ( on room air)
PH=7.21
HCO3= 12
PaO2= 12.2 kPa
PaCO2=2.5 kPa

Q: What is the diagnosis?
For the above ABG result, you know that the patient has metabolic acidosis and she presents with history of vomiting and abdominal pain, the first provisional diagnosis you should think of as a SHO is diabetic ketoacidosis!

2) Respiratory Acidosis

This is the second commonest acid-base balance problem you will see in your daily practice. Patients develop this because he/she is unable to blow out CO2 in the lung leading to accumulation of CO2 and respiratory acidosis. Therefore, our body will try to compensate by keeping more HCO3 via the kidney to buffer the acidosis. However, you must remember that kidney works somehow slower than the lung, therefore in acute respiratory acidosis (acute CO2 retention), you may find the HCO3 level is normal but in chronic CO2 retention ( such as in CAPD/COAD or chronic lung disease patients), the HCO3 level tends to be high.

This remembers me when I was a medical student where my lecturer liked to ask me way to help clinicians to differentiate COAD/COPD from asthma by looking at ABG results.

If you are a SHO on call in chest ward, a patient comes in with acute breathlessness and you notice he/she has rhonci all over the lung, you will most probably find the following ABG if you put patient on oxygen supplement,

PH ↓, PaO2 ↑, PaCO2↑ ( Respiratory acidosis)

For COAD /COPD, since that patients may have chronic CO2 retention, you will notice the HCO3 level tends to be high but in asthmatic patients, since it is an acute asthmatic attack that leads patient to have acute CO2 retention, you may find the HCO3 level to be normal ( kidney needs sometime to conserve HCO3, therefore in acute CO2 retention, the HCO3 level may be normal)

However, I must warn you that this rule is only for your reference only, there is no 100% in clinical medicine but I find this rule rather useful in daily practice.

I will talk about metabolic and respiratory alkalosis in my next post!

Happy Chinese New Year!

Happy Chinese New Year!





For all MRCP Part 1 and 2 blog readers, Happy Chinese New Year! May your wish comes true this year!

Addison's Disease in MRCP

Addison’s disease in MRCP

OK, today I am going to talk about one condition which is important in two ways, Addison’s disease is an important endocrine condition because,

1) It is a popular condition in your MRCP examination,
2) It is important clinically because the mortality is high if you do not pick it up fast in clinical practice especially if patients present with acute Addison's crisis!

Adrenal insufficiency can be due to dysfunction of the adrenal gland itself ( primary- Addison’s Disease) or due to disordered pituitary or hypothalamus function ( secondary)

I think we will cover Addison’s disease today and you can forget about secondary Adrenal insufficiency because it is rather rare.

Addison’s disease refers to primary failure of the adrenal gland leading to loss of production of glucocorticoids and mineralcorticoids.

Causes of Addison’s disease

1) Always remember that it is mainly due to autoimmune adrenalitis and it is associated with Polyglandular autoimmune syndrome. ( Never get yourself confused this with Multiple Endocrine Neoplasia, MEN)
Remember as well that you may find antibodies against the 21-hydroxylase enzyme in 90% of autoimmune cases.

2) Tuberculosis

3) Distant metastasis

Signs and symptoms

As I remember as a medical student, there are 3 main medical causes( non-surgical causes) of abdominal pain, of course Addison’s disease is one of them. The other two are Diabetic ketoacidosis and intermittent Porphyria. ( Always remember this and later you will realize that it is very common for your friends in A+E missing diabetic ketoacidosis simply because patients present with abdominal pain)

Other symptoms include lethargy, nausea and vomiting, dizziness.

Important signs to look for are
1) hyperpigmentation ( it is a popular case in MRCP PACES as well) and I hope you know the reason behind this.
2) postural hypotension
3) loss of body hair ( due to reduced production of androgen)

Investigations
Remember the important clues to look for are
1) Low Sugar
2) Low Sodium
3) High Potassium
------- SSP. Patient may present with fever as well.

Diagnosis

Synacthen test. I think you do not need to know the details and the values. Just know the principles, in normal people, cortisol level will increase significantly after synacthen ( ACTH) stimulation but for Addison’s disease, since there is primary failure of adrenal gland, it will not be stimulated to produce more cortisol after synacthen.

Management

Remember that acute Addsison’s crisis is a medical emergency and it is usually due to prolonged adrenal suppression secondary to exogenous drugs such as steroids.

For chronic Addison’s disease, supplement patients with glucocorticoid ( hydrocortisone) and mineralcorticoid ( fludrocortisone)

Tips for MRCP

You may give a case in your MRCP Part 2 where you are given some electrolytes imbalances in a patient who presents to A+E due to abdominal pain.

ECG in MRCP(2)

ECG in MRCP(2)

In sinus rhythm, we know that every P wave is followed by QRS, you must learn hard the following conditions that do not give you sinus rhythm,

1) Atrial fibrillation

This is the commonest condition being asked in MRCP, I have covered this in my previous post.

2) Atrial flutter

Always described as “ Saw-Tooth” ECG in medical textbook. The atrial activity is usually between 250-350 beats /min and there is sually 2:1 or 3:1 block. Causes for atrial flutter are similar to atrial fibrillation as well as the management.

3) Ventricular tachycardia

Defined as three or more successive ventricular extrasystoles at a rate more than 120/min. Remember than VT has a wide QRS complex. Causes of VT include
a) Ischaemia to the heart
b) Hypo-or hyperkl\alaemia
c) Long QT interval ( a very popular question in MRCP, I will cover this in depth in my future post)
d) Cardiomyopathies

4) Torsades des pointes

Actually it is a type of ventricular tachycardia with a varying axis. It often happens after heart attack but can be due to drugs and other causes of prolonged QT interval.

5) Ventricular fibrillation

This rhythm needs immediate cardioversion. Usually happens after a hear attack

Important Tips for MRCP,

It is often difficult to differentiate an SVT with abberant ventricular conduction from VT ( both also have wide QRS complexes), however always remember in clinical practice, always assume VT if you are in doubt and treat accordingly because VT is commoner and life threatening. However, following features suggest SVT with abberant blocks,

1) No fusion or capture beats
2) Presence of P waves associated with ORS
3) Classical RBBB and LBBB ORS morphology
4) ORS <0.14s

5) Same QRS morphology as in sinus rhythm

6) Normal axis