ABCDE of Chest X-Ray - Use the RIPE Approach!

November 20, 2017 by James Thomas in Interpretation

In this podcast Dr. Harry Pick, Respiratory Registrar and Clinical Research Fellow at Nottingham University Hospitals NHS Trust came down to talk us through Chest X-ray Interpretation; a key skill in the Emergency Department!

Harry very kindly gave us a copy of the Powerpoint he uses when he teaches this topic; due to confidentiality reasons these slides don't have X-rays on them but great resources can be found at Radiology Masterclass. Click either side of the pictures to move through them.

Remember the step by step approach:

Right patient; day and time? - this is key for all investigations.

Is the film AP (anterior to posterior) or PA (posterior to anterior). This matters for two reasons. Firstly, an AP film tends to be an portable CXR and so tells you that the patient was sick when it was taken, this may be confirmed by the presence of chest leads, O2 tubes and central lines on the film. Secondly AP films exaggerate the size of the heart and so you cannot comment on cardiomegaly. You can on a PA film. In a healthy individual the heart should be no more than 50% of the thoracic width on a PA film. If the scapulae are not projected into the chest assume it is a PA film. It should always say if it is an AP film.

'RIPE' - Rotation (equal space between medial aspects of clavicles to spinous processes), Inspiration (>7 anterior and 9 posterior ribs, Picture (can you see everything you want to see?) and Exposure (can you see vertebral bodies behind the heart).

Then remember ABCDE - this varies - the Take Visually below follows Airway, Breathing, Circulation, Diaphragm and Everything else.

Harry's ABCDE covers the same things but in a different order - Apices, Behind the heart, Cardiophrenic and Costophrenic angles, Diaphragms - above and below and Everything else.

Don't forget to compare the chest x-ray with any previous ones (very easy on most programmes) - this is very useful to assess any acute changes. Older x-rays should also have been reported which will help your interpretation!

As you can see there's a subtle variation, make sure you find a method that works for you!

Here is the Take Visually for this podcast.

Geeky Medics have a great page on the subject as well.

Life's A (Blood) Gas

September 11, 2017 by James Thomas in Interpretation

Just as with ECGs arterial blood gases (ABGs) are an essential part of Medicine and unavoidable. They're a vital part of assessing the unwell patient.

Unfortunately students are often quite blood gas-phobic and this needs to be overcome and hopefully with a stepwise approach we can all learn to love the blood gas! Once again I'll be enlisting the help of Albert Einstein and his chalkboard - the meme generator can be found here.

It's worth saying that ABGs are not nice to receive and so think if you really need to do one or if you could get away with a venous blood gas (VBG). A VBG will give you a reliable pH, bicarbonate, electrolytes, glucose and lactate as well as carbon dioxide if it's normal. ABGs are really good for determining the oxygen partial pressure however. Life in the Fast Lane has a brilliant blog on the subject of VBG vs ABG. This blog will mostly focus on ABGs.

So as ever make sure the gas in your hand is from the right person at the right day and time and look at how much oxygen the patient is on. This is the amount of inspired oxygen or fraction of inspired oxygen (FiO2) the patient is receiving. The delivery device being used by the patient will tell us their FiO2.

Room air at sea level has a FiO2 of 21%.

Photo by Liuhsihsiang/iStock / Getty Images

The next oxygen delivery is nasal cannulae which are only good at delivering 1-4L/m of oxygen - beyond that the patient won't have any benefit and have very turbulent air up their nose! The FiO2 of oxygen delivered by nasal cannula is as follows:

1 L/m = 24%

2 L/m = 28%

3 L/m = 32%

4 L/m = 36%

The next oxygen delivery system to look at are Venturi masks; these deliver a guaranteed FiO2 of oxygen and are brilliant at titrating oxygen to patients especially patients with COPD.

Photo by porpeller/iStock / Getty Images

The Venturi come in different colours and will have the FiO2 written on their side as well as the l/min that are needed to provide that FiO2. Make sure they have the correct flow rate or they won't work. The range available will vary site to site but in the department I work at the Venturi available are 24%, 28% & 40%.

The next highest oxygen delivery system you'll commonly see are non-rebreather masks (NRM).

Photo by Image Source/Stockbyte / Getty Images

"15 litres through a non-breather mask" is a very common statement in an acute A-E station. It's less easy to predict the FiO2 here only that is is somewhere between 60-100%.

Make sure the FiO2 or oxygen delivery is documented on the gas.

pH: 7.35 – 7.45 (pH messages the amount of Hydrogen ions in a solution (in this case blood) the lower the pH the more acidic the blood, the higher it is the more alkalotic it is)

There are two main components contributing to the pH - the respiratory side (CO2) and metabolic (Bicarbonate). A problem with one can be compensated with the other - more of that later.

PaCO2: 4.7-6.0 kPa (Pa stands for Partial Pressure - the amount of pressure the gas in question contributes to the atmosphere measured in kilo Pascals. CO2 is acidic when dissolved in solution. Increasing respiration rate blows off CO2 while reducing respiration rate means we retain CO2. Normally PaCO2 is what drives our ventilation; this is not the case in chronic CO2 retention such as COPD where hypoxia then drives respiration)

PaO2: 11-13 kPa (if this is low then the patient is hypoxia - this is cause of cardiac arrest and so must be identified early)

HCO3-: 22-26 mEg/L (Bicarbonate is basic and so is used as a buffer against acid. Increasing the amount of bicarbonate however takes hours to days whereas it's almost instantaneous to alter respiration rate)

Base excess: -2 to +2 mmol/L (this is measure of the metabolic component of a problem with the pH. If the BE is below -2 then the patient has a base deficit and so has metabolic acidosis. If the BE is above +2 then the patient has a base excess and a metabolic alkalosis

Once you're happy with the ABG being for the right patient etc it's now time to first look at the pH - is it normal, high (alkalotic) or low (acidotic)?

Is the CO2 normal, high (hypercapnic) or low (hypocapnic)?

Is the O2 normal, high (hyperoxic) or low (hypoxic)?

At this point we need to remember the Alveolar-arterial (A-a) gradient. This is the gradient between the PaO2 of inspired air and that in the blood. In a healthy adult it should be about 5-10mmHg. That means the PaO2 on your ABG should be about ten less the FiO2, hence why in room air (FiO2 21%) the normal range of PaO2 is 11 - 13 kPa.

A-a gradient is accurate up until FiO2 of about 60% and over. Why is it important? Well, you could have a patient on a 28% Venturi with normal saturations but if their PaO2 is less than 18 kPa (say 12 kPa) then they have relative hypoxia and we should be more worried about them and make sure they are getting senior support.

If the patient is hypoxic check the PaCO2 again

If PaO2 is low and PaCO2 is low or normal then the patient has Type 1 Respiratory Failure - the lungs are failing in the function of taking O2 from the air to blood

If the PaO2 is low and PaCO2 is high then the patient has Type 2 Respiratory Failure - the lungs are failing in getting O2 from the air and removing CO2 from the blood. This may be acute, chronic or acute on chronic. The raised PaCO2 will lower pH acutely; the blood will respond by buffering this by increasing bicarbonate production in the kidneys. This process takes days to hours. Patients may walk around with a fully compensated Type 2 Respiratory Failure (such as COPD) but then decompensate and become acidotic again despite the raised bicarbonate - acute on chronic failure

Acute Type 2 Respiratory Failure (no compensation):

pH 7.2

PaCO2 10

Pa O2 7

Bicarbonate 24

Chronic Type 2 Respiratory Failure (fully compensated):

pH 7.39

PaCO2 10

PaO2 7

Bicarbonate 30

Decompensated Chronic Type 2 Respiratory Failure (Acute on Chronic):

pH 7.28

PaCO2 11

PaO2 6.8

Bicarbonate 30

Causes of Type 2 Respiratory Failure can be pulmonary (such as COPD); peripheral (such chest wall deformities or peripheral nervous diseases such as Motor Neuron Disease) or central (such as overdose of opiates or benzodiazepines causing respiratory depression)

So now we know the values for pH, PaCO2, PaO2 and Bicarbonate it's now time to put it together and identify whether it is a Respiratory or Metabolic cause for pH disturbance

I use the mnemonic 'ROME'

The problem is Respiratory when the PaCO2 is Opposite to pH

The problem is Metabolic when the bicarbonate (HCO3-) is Equal to pH

I find this is a very quick way of identifying the cause, being aware of course that you can have mixed acidosis (due to combined high PaCO2 and low bicarbonate) and mixed alkalosis (low PaCO2 and high bicarbonate)

If the problem is respiratory then there will be metabolic compensation (compensating high PaCO2 with high bicarbonate and vice versa) - this takes a long time remember

If the problem is metabolic then there be respiratory compensation which is much quicker

Compensation can be none, partial (there is an attempt but pH remains deranged) or full (pH back within normal limits)

Remember that there are other bits of information on an ABG

Sodium

Potassium - if deranged do not wait for serum U&Es before commencing treatment

Calcium

Chloride

Glucose - while BM machines will just say 'HI' once BM ~30 the ABG will measure up to about 50

Lactate - important measure of tissue perfusion

Haemoglobin - not entirely accurate but will give an idea of anaemia/bleeding

Carboxyhaemoglobin

It is important not to miss this information as well!

There is a brilliant RCEM module on ABGs here.

Check out the brilliant Geeky Medics page on ABG interpretation here.

How I Learned to Stop Worrying and Love the ECG

July 28, 2017 by James Thomas in Interpretation

ECGs are an essential part of Medicine and unavoidable as a student and junior doctor. I remember being bleeped as an F2 on call by an Orthopaedic surgeon to read the ECG of one of his patients as he had forgotten...ECGs are definitely a case of improving confidence and knowledge through repeated practice and exposure.

Once again I cannot recommend Life in the Fast Lane enough for incredible resources when it comes to ECG.

Here is our video on how to take an ECG:

In the latest Take Aurally podcast I discuss an approach to ECG interpretation and in this blog I've enlisted the help of Albert Einstein to help me through. You can find the tool for making this meme here.

Remember, it doesn't matter how the patient describes their chest pain as an ''ache'', ''twinge'', 'indigestion''...whatever chest pain is chest pain and needs an ECG.

This step is vital, is the ECG in your hands from the right patient, right day and time? Also, get an idea about the presentation behind the ECG, do they have pain, shortness of breath, collapse or palpitations?

Only in certain BBC television dramas (cough, Casualty, cough) does a flat line on an ECG mean death. In real life it means that the ECG lead in question is not connected properly and needs reattaching. Make sure you can see electrical activity in all 12 leads.

Most ECGs will tell you this anyway but it is important to be able to work this out for yourself. In a regular rhythm (equal distance between all R waves) you can count the number of large squares between each R wave and divide 300 by this number. Alternatively you can count the number of beats on the rhythm strip and times this by 6.

There's about 3.5 big squares between each R wave here.  Using 300/3.5 gives a heart rate of 86.Alternatively, there are 15 beats on the rhythm strip,  15 x 6 = 90. — There's about 3.5 big squares between each R wave here. Using 300/3.5 gives a heart rate of 86.
Alternatively, there are 15 beats on the rhythm strip, 15 x 6 = 90.

This is all about looking at the R-R distance for successive beats. This can be marked on a separate piece of paper and moved along to confirm.

If the rhythm is irregular you can then also see if it's regularly irregular or irregularly irregular

By looking at successive R-R distances we can see that this ECG shows a regular rhythm.

The QRS complex should be 3 small squares wide. This is important for two reasons. In tachycardia the duration of QRS points to the diagnosis and management as shown in the Resus Council flowchart below. In normal rates it also points to a bundle branch block.

My method for working out LBBB or RBBB...without a William or Marrow in sight

P waves indicate sinus rhythm. PR interval should be 3-5 small squares.

First degree heart block: PR interval is prolonged and remains the same (occurs between SA and AV node)

Second degree heart block: Mobitz 1 - the PR interval gets longer and longer until there is a dropped QRS and the cycle starts again. (Occurs in the AV node) Mobtiz 2 - the PR interval is long, stays the same length but there is a dropped QRS in a ratio: 3-1, 4-1 etc (occurs after AV node in bundle of His/Purkinje fibres)

Third (complete) heart block: No relationship between P waves and QRS (occurs anywhere from AV node down)

PR interval could also be shortened as seen in WPW.

Axis is all about the general spread of electrical activity across the heart.

Here I look at leads I and II. Usually the R waves should both be positive as here:

In left axis deviation the R wave in II is now negative so they pointing away from each other or 'leaving'.

Leaving = Left Axis Deviation

This is a sign of ischaemia

Here the R wave is I is negative so they reaching for each other.

Reaching = Right axis deviation

RAD is a sign of RVH

This is important to notice ST elevation - STEMI (2mm or more in 2 or more chest leads or 1mm or more in 2 or more limb leads) or ST depression or T wave inversion - can be seen in NSTEMI

Be wary if you see regional ST depression - this could be reciprocal depression so make sure you look for ST elevation in other leads

Remember to look at the J point - the point where the S wave joins the ST segment - this can be raised in young, thin patients giving the appearance of ST elevation. This is caused benign early repolarisation or 'high take off'

T waves can also point to other conditions - the tall T waves in hyperkalaemia; biphasic T waves in hypokalaemia or ischaemia; or flattened in ischaemia or electrolyte imbalance.

U waves, small deflections after the T wave can be seen in a number of conditions; hypokalaemia, hypothermia or antiarrhythmic therapy like digoxin

My colleague James Pratt has made an excellent e-Learning package on ECG interpretation which can be found here

Geeky Medics have a great page on ECG interpretation here

ECGs courtesy of the amazing Life in the Fast Lane

You can hear our ECG Interpretation podcast here: