Month: July 2017

Thinking about a career in emergency medicine?

All your Q&As answered here! Study EM dishes the dirt on life as an ED doctor and making it:

What can I do as a student to get started in Emergency Medicine? 

1) Spend as much time as possible in A&E, even if you end up specialising in another area, the skills you learn in A&E will be invaluable as a Foundation Doctor. 

2) Do an elective in A&E – either at home or abroad 

3) Volunteer for life support courses eg. ATLS 

4) Attend a RCEM careers day 

5) Choose specialist study modules (SSC/SSM) in areas allied to emergency medicine, such as pre-hospital medicine and toxicology. 

 

What can I do as a Foundation Doctor to get involved in Emergency Medicine? 

1) Apply for a rotation that includes Emergency Medicine 

2) Select a taster week in A&E, CED or Pre-hospital medicine 

3) Chose an audit relevant to Emergency Medicine 

4) Try to get involved in some research or write a BestBET (http://www.bestbets.org) 

5) Ensure you attend at least an ALS course and maybe even an ATLS course 

6) Complete relevant elearning modules 

7) If you have some pennies left over then you could join the Royal College of Emergency Medicine. This gives you access to the Journal of Emergency Medicine and discounts on some courses and events.  

Thinking about a career in emergency medicine?

All your Q&As answered here! Study EM dishes the dirt on life as an ED doctor and making it:

So how do I become an Emergency Consultant? 

 You will be asked to apply for specialty training in the December of your F2 year with interviews being held from late January to late spring. Try to have evidence of your interest in emergency medicine before this point. It is worthwhile looking up the selection criteria 🙁http://specialtytraining.hee.nhs.uk/portals/1/Content/Person%20Specifications/Emergency%20Medicine/Emergency%20Medicine%20ACCS%20CT1.pdf) for the previous year and filling in any CV blanks sooner rather than later. If you do not feel you are ready to start specialty training then there is always the option of taking what is affectionately being referred to as an ‘F3’ year. Taking a year out gives you time to experience other areas of medicine either at home or abroad. You might even get the opportunity to try something different and exciting, which might not be an option later in life when children limit your options. It is no longer frowned upon to take time out as long as you can prove that you spent that year bettering yourself as a doctor (FYI, more experience = better doctor)  

Currently emergency medicine training consists of a 6 year run-through programme; 3 years of core training (Acute Care Common Stem [ACCS]) and 3 years of Higher Specialty Training (HST).  

CT1 – 6 months emergency medicine and 6 months acute medicine 

CT2 – 6/9 months anaesthetics and 3/6 months intensive care 

You are required to pass you FRCEM Primary exam (previously known as the MCEM Part A) before you can progress to CT3. 

CT3 – A&E with a focus on paediatrics and trauma – ideally this year will be split between a Children Emergency Department (CED) and an Emergency Department in a Major Trauma Centre/Trauma Unit. However, not all regions are able to provide this. As such you might spend some time in paediatrics and/or orthopaedics.  

You are required to pass your FRCEM Intermediate exam (previously known as the MCEM Parts B &C) prior to progressing to ST4.  

ST4-6 – More A&E and paediatric emergency medicine. You also need to become proficient in emergency ultrasound and get to grips with management and other qualities required to run an Emergency Department. It is during this time that you can take time out to dual qualify in specialties such as intensive care and paediatric emergency medicine. 

Before you are awarded the illustrious Certificate of Completion of Training (CCT) you need to pass the FRCEM Final exam. Once you have served your time, passed the required exams and convince someone to give you consultant job then you have finally done it and then the real hard work starts! 

Thinking about a career in Emergency Medicine?

All your Q&As answered here! Study EM dishes the dirt on life as an ED doctor.

What is it like to work in an Emergency Department? 

Emergency Departments are the ‘front door’ of the hospital. It is always open and usually busy! Emergency doctors diagnose patients presenting with a variety of problems, often with limited information. We rely heavily on our clinical skills, a wide range of investigations and of course the experience of our seniors. Emergency physicians work closely with a number of specialty doctors, nurses, physiotherapists, social workers and of course patients from every walk of life…if you do not like people, then A&E is unlikely to be the career for you!  

But isn’t A&E really hard work? It can be, but on the flip side, your day never drags and you never get bored.  

As you progress you can develop other interests such as education, research, paediatric emergency medicine, sports medicine and pre-hospital medicine including trauma, refugee, wilderness and disaster medicine. Other interests help break up the pressure of working in A&E and keep us mentally healthy. 

But isn’t working so many antisocial hours difficult on your home life? It can be, but again there are many positives: 

1) You are off when other people are at work, so no queuing up with everyone else at the weekend.  

2) Most A&E rotas try to clump your time off so you can go on holiday without using up your annual leave.  

3) The late starts are great if, like me, you are not a morning person 

4) If you do have kids, then working when your partner is at home saves a fortune on childcare, plus part time work is more accessible in A&E due to its flexible nature.  

5) Antisocial hours come with a higher pay banding and since we don’t actually earn as much as the Daily Mail makes out, then every penny helps.  

ECG interpretation

First the basics:

Lead Placement:

Red – right arm

Yellow – left arm

Green – left leg

Black – right leg

Remember limb leads by: Ride Your Green Bike

 

Physical lead representation:

 

ECG cardiac representation:

 

  1. Checks
  • Check for any patient identifiers
  • Any previous ECGs for comparison
  • Often the presence of chest pain is documented on the ECG – this should be noted.
  • Check the calibration

A – standard (10mm/mV or 2 large squares)

B – half (5mm/mV or 1 large square)

C – double (20mm/mV or 4 large squares)

All should be 0.2secs (5 small squares) width

 

  1. Rate

Divide 300 by the number of large squares between 2 QRS complexes

or

Multiply the number of QRS complexes by 6 (ECG is 10 seconds long).

Useful for irregular rhythms.

This ECG has 10 QRS complexes

10 x 6 = 60

Therefore rate is 60 bpm

 

  1. Rhythm

Is it regular, irregular or irregularly irregular?

Is there is a P wave before every QRS complex?

If p waves are present, is the PR duration constant?

Commonly encountered rhythms:

Sinus rhythm:

  • P wave occurs before every QRS complex
  • PR duration 3-5 small square (0.12-0.2secs)
  • PR duration is constant

Normal sinus rhythm: HR 60 – 100bpm

Sinus tachycardia: HR >100bpm

Sinus bradycardia: HR < 60bpm (not considered clinically significant until <50bpm)

Supraventricular tachycardias:

Atrial Fibrillation:

  • RR duration is irregular
  • P waves are absent

Atrial Flutter:

  • Rate classically 75bpm or 150bpm (3:1 or 2:1 block respectively)
  • Saw tooth appearance

Paroxysmal SVT or AV nodal re-entry tachycardia:

  • Regular tachycardia (usually 140-280bpm)
  • Narrow QRS complexes (unless pre-existed bundle branch block)
  • P waves often not visible as buried in QRS complex, but if seen often are inverted in inferior leads
  • QRS alternans (alternating height of QRS complexes)

Ventricular tachycardias:

Ventricular tachycardia:

  • Wide QRS complexes
  • Usually monomorphic (QRS complexes are a similar shape)

Ventricular fibrillation:

  • Chaotic ECG with no identifiable P waves, QRS complexes or T waves#
  1. Axis

Normal axis is -30° to +90°

Axis is the overall direction of travel of electricity within the heart. In a healthy heart the electrical impulse starts in the SA node travels to the AV node, down the Bundle of His and through the Purkinje fibers, therefore normal axis is in this general direction (towards lead II).

Axis can be ascertained in a variety of ways:

  1. Look at the ECG print out! (unlikely to be present in an exam, so make sure you practice the other methods)

  1. Rule of thumbs: https://youtu.be/gy0gkh1foR4
  • Take you own thumbs and use them as a representation of lead I and lead II
  • QRS complex positive = thumb up
  • QRS complex negative = thumb down
  • If both lead I and lead II are positive:
    • 2 thumbs up = normal axis
  • If lead I is positive and lead II is negative:
    • thumbs are leaving each other = left axis deviation
  • If lead I is negative and lead II is positive:
    • thumbs are reaching towards at each other = right axis deviation
  1. Calculating axis:
  • Identify the most isoelectric limb lead (the lead in which the R wave and S wave are of equivalent heights). This identifies the angle perpendicular to the axis, therefore the axis will be 90° from this.
  • Using the diagram above (which you should commit to memory) move 90° clockwise and anticlockwise from your isoelectric lead and identify the closest lead.
  • The lead with the positive QRS complex is the axis.
    • For example:

aVL is the most isoelectric lead

aVL is at -30°

90° anticlockwise = -120° (aVR – negative QRS complex)

90° clockwise = +60° (lead II – positive QRS complex)

Axis = 60° (accurate to within 15°)

Causes of left axis deviation (LAD):

  • Left bundle branch block (LBBB)
  • Left anterior hemiblock
  • Pacemaker
  • Inferior MI
  • Left ventricular hypertrophy
  • Wolff-Parkinson-White

Causes of right axis deviation (RAD):

  • Normal in children and tall, thin adults
  • Right ventricular hypertrophy
  • Lateral MI
  • PE
  • Chronic lung disease
  • Left posterior hemiblock
  • Dextrocardia
  • Wolff-Parkinson-White

Extreme axis deviation:

  • Ventricular arrhythmias
  • Hyperkalaemia
  • Severe right ventricular hypertrophy
  1. P waves

Calculate PR duration – should be between 3 and 5 small squares

If the PR duration is prolonged or not constant with the QRS duration, then this is likely to represent a heart block.

1st degree heart block:

  • PR duration >5 small squares, but constant

2nd degree heart block:

Mobitz type 1/Wenkebach:

  • Progressive prolongation of the PR interval eventually resulting in a missing QRS complex

Mobitz type 2:

  • P waves occurring at a regular rate
  • Intermittently P waves are not conducted into a QRS complex
    • This can occur in a fixed relationship (ie. 3:1 or 2:1 block) or with no pattern

3rd degree/complete heart block:

  • No association between P waves and QRS complexes
  • Often associated with bradycardia
  • At risk of ventricular standstill

P wave morphology – best assessed in lead II or V1

  • Bifid P waves – left atrial enlargement (mitral disease)
  • Tall P waves (>2.5mm in lead II) – right atrial enlargement (pulmonary hypertension
  1. QRS

Duration 70-100ms (>100ms is abnormal, but >120ms is required to diagnose bundle branch block)

Causes of broad QRS complexes:

  • Bundle branch block
  • Hyperkalaemia
  • Sodium-channel blockade
  • Wolff-Parkinson-White
  • Pacemaker
  • Hypothermia

Left bundle branch block (LBBB)

  • QRS duration >120ms
  • Dominant S wave in V1
  • Broad R wave in V6
  • Left axis deviation

Right bundle branch block (RBBB)

  • Broad QRS >120ms
  • M-shaped QRS complex in V1
  • Wide slurred S wave in V6

Bundle branch blocks can be remembered through the mnemonic ‘William Marrow’

  • LBBB – has a W-shape in V1 and a M-shape in V6 (WiLLiaM)
  • RBBB – has a M-shape in V1 and a W-shape in V6 (MaRRoW)

Are Q waves present?

  • Q waves are considered pathological if they are present in at least 2 contiguous leads and are > 1 small square wide and/or >25% height of R wave. Q waves in V1-V3 are almost always pathological.

R wave progression

  • R waves should progressively increase in height from V1 to V6
  • If R wave height <3mm in V3, then they are considered to have poor R wave progression. This is a suggestion of:
    • prior anteroseptal MI
    • left ventricular hypertrophy
    • dilated cardiomyopathy
    • Inaccurate lead placement (lead I and V6 should look similar)

Left ventricular hypertrophy:

S wave in V1 + R wave in V5 or V6 > 35mm

Right ventricular hypertrophy:

Ratio between R wave and S wave in V1 >1

  1. ST segments

Is elevation or depression present?

ST segment elevation MI (STEMI) is diagnosed when:

  • There is ST elevation in at least 2 contiguous leads of:
    • >2mm in chest leads
    • >1mm in limb leads
  • Horizontal ST depression in V1-V3 (posterior MI)
  • New LBBB
  • ECG meets Sgarbossa criteria in patients with LBBB or ventricular pacing (knowledge of this is not required at undergraduate level)

Left main coronary artery (LMCA) incomplete occlusion is clinically important, but ECG findings can be subtle, they include:

  • Widespread ST depression
  • ST elevation in aVR >1mm
  • ST elevation in aVR >V1

Other causes of ST elevation include:

  • Pericarditis (saddle-shaped ST elevation)
  • Benign early repolarization
  • Brugada syndrome
  • Raised intracranial pressure

ST depression is generally is sign of coronary insufficiency or reciprocal changes during a STEMI.

 

  1. T waves

T waves represent ventricular repolarization

T wave inversion is normal in aVR and V1 and can be a normal variant in lead III.

Also normal in children in V1-V3

Assess morphology:

  • T wave inversion
    • Infarction
    • Ischaemia
    • Bundle branch block
    • PE
    • HOCM
  • Biphasic T waves
    • Post-MI
    • Hypokalamia
    • Wellens syndrome ***can link to MOTM***
  • Peaked T waves
    • Hyperkalaemia
  • Flattened T waves
    • Ischaemia
    • Hypokalemia and other electrolyte disturbance
  1. U waves

U waves occur immediately after the T wave

They are best seen in V2 and V3

Occur in the same direction as the T wave

Prominent U waves occur with:

  • Bradycardia
  • Hypothermia
  • Severe hypokalaemia
  • Digoxin

  1. QT duration

Measured from the beginning of the QRS complex to the end of the T wave.

The QT interval shortens as the heart rate increases, therefore it should be corrected for heart rate.

This can be done via a number of formulas, the most well known being Bazett’s:

QTc = QT / √RR

However, these formulae are not very accurate at extremes of HR and therefore a QTc normogram is recommended.

In the absence of a normogram, QT can be crudely estimated as normal if the T wave finished before the midpoint of the RR interval.

Prolonged QTc puts the patient at risk of VT.

Causes of prolonged QTc:

  • Congenital long QT syndromes
  • Drugs ie. antipsychotics, TCAs, antihistamines, antiarrhythmics
  • Hypothermia
  • Hypokalaemia and other electrolyte disturbances

 

 

ABG interpretation

ABG INTERPRETATION by StudyEM

STEP 1

Check ABG is for correct patient

 

STEP 2

Assess oxygenation

  • pO2 <10.5 kPa = hypoxic

 

Was the patient on oxygen when the ABG was performed?

  • In general the pO2 should be approximately: FiO2(%) -10
    • For example:
      • On 40% O2: pO2 should be 30 kPa

 

Is there a significant alveolar-arterial gradient?

A-a gradient = PAO2 – PaO2

  • Alveolar (A)
  • Arterial (a)
  • Partial pressure of oxygen in the airways (PAO2)
  • Partial pressure of oxygen in the artery (PaO2)
  • PAO2 = FiO2 (Patm –PH20) – PaCO2/kQ
    • Patm-PH2O = 713 at sea level
    • kQ = 0.8 (constant)
  • Therefore:
    • PAO2 = (FiO2 x 713) – (PaCO2/0.8)
  • A-a gradient helps identify where the source of the hypoxia is coming from.  A high A-a gradient suggests a V/Q mismatch or right-to-left shunt.
  • Normal A-a gradient is dependent on age as for every decade of life the A-a gradient increases by 1 mmHg.
  • Age-adjusted normal A-a gradient = (age/4) + 4
    • Therefore a 40yo should have an A-a gradient less than 14.

 

Identify type of respiratory failure

  • Type 1 – normal/low pCO2
  • Type 2 – high pCO2

 

STEP 3

Determine the pH status

<7.35 – acidosis

>7.45 – alkalosis

 

Find the primary source of the pH disturbance

  • Acidosis:
  • pCO2 > 6.0 kPa – respiratory
  • HCO3– <22 mmol/l – metabolic

 

  • Alkalosis
    • pCO2 < 4.7 kPa – respiratory
    • HCO3– >26 mmol/l – metabolic

 

Is there a mixed picture?

  • Respiratory and metabolic acidosis

or

  • Respiratory and metabolic alkalosis

 

STEP 4

Is there compensation?

  • Compensation present if:
  • Respiratory acidosis: High HCO3– (commonly seen in COPD patients)
  • Respiratory alkalosis: Low HCO3– (rare)
  • Metabolic acidosis: Low pCO2 (limited to pCO23 kPa)
  • Metabolic alkalosis: High pCO2 (only able to hypoventilate slightly)
    • Metabolic compensation take 3 days
    • Respiratory compensation occurs quickly
    • Over compensation CANNOT occur

 

Is there full or partial compensation?

Partial: pH remains abnormal

Full: pH has normalized

 

Is compensation adequate?

Not required at undergraduate level. For more information see http://lifeinthefastlane.com/investigations/acid-base/

 

STEP 5

Is there an anion gap?

Anion gap = Na+ – (Cl– + HCO3–)

Normal = 12 ± 4

  • Potassium is generally excluded as it is relatively stable
  • Should be corrected in patients with albumin <40 g/L (add 2.5 per 10 g/L decrease)
  • Sodium should be corrected in hyperglycaemia (cNa+ = Na+ + (glucose -5) ÷ 3)
  • Anion gap is calulcating the difference in measured cations and anions. Since cations and anions will be balanced, a high anion gap is eluding to unmeasured substances ie. Ethanol
  • Click here for causes of high anion gap metabolic acidosis (HAGMA) and non-anion gap metabolic acidosis (NAGMA) – see “ABG Mneumonics” on the data interpretation page.

 

Consider calculating other metabolic acid-base disorders eg

  • Delta Gap = (anion gap – 12) ÷ (24 – HCO3–)
  • Osmolality = (2 x Na+) + urea + glucose + ethanol
  • Osmolar gap = measured osmolality – calculated osmolality

 

STEP 6

Check the other values especially:

  • Hb
  • Glucose
  • Lactate

 

Remember to treat the patient and not the numbers. ABGs are a guide to management, but should be used in the wider clinical context (and don’t forget the possibility that the ABG machine may have given an incorrect result!)

ABG Mnemonics

Differential diagnosis of acid base disorders

1. High Anion Gap Metabolic Acidosis

C Carbon Monoxide, Cyanide
A Alcohol, Alcoholic Ketoacidosis
T Toluene
M Metformin, Methanol
U Uraemia
D Diabetic Ketoacidosis
P Paraldehyde, Phenformin, Paracetamol, Propylene glycol
I Iron, Isoniazid
L Lactic acidosis (any cause)
E Ethylene glycol
S Salicylates

2. Causes of Lactic Acidosis

Type A: Imbalanced oxygen supply and demand Type B: Metabolic derangement

Carbon monoxide

Shock

Severe anaemia

Severe hypoxia

Excessive oxygen demand:

Fever, seizure, exercise, shivering

 

B2 agonists

Cancer

Cyanide

Ethanol

Hepatic failure

Ketoacidosis

Metformin / Phenformin

Sepsis

Thiamine deficiency

Inborn errors of metabolism

3. Non-anion Gap Metabolic Acidosis

U Ureteroenterostomy
S Small bowel fistula
E Extra chloride, Normal saline hydration
D Diarrhoea
C Carbonic anhydrase inhibitors (acetozolamide, topiramate etc)
A Adrenal insufficiency
R Renal tubular acidosis
P Pancreatic fistula

4. Causes of a low anion gap

Increased cations Calcium, magnesium, lithium, multiple myeloma
Decreased anions Dilution, hypoalbuminaemia
Artefactual Bromism, Iodism, Propylene glycol, Triglycerides

5. Metabolic Alkalosis

C Contraction (volume contraction)
L Licorice, diuretics
E Endocrine (Hyperaldosteronism, Bartter’s, Cushing’s, Conn’s)
V Vomiting, NG suction (chloride loss)
E Excess alkali (antacids, dialysis, milk-alkali syndrome)
R Refeeding alkalosis
R Renal bicarbonate retention (Hypochloraemia, Hypokalaemia, Chronic hypercapnia)

6. Respiratory acidosis

Acute Chronic

Airway obstruction

Aspiration

Bronchospasm

CNS depression

Muscle weakness

Pulmonary disease

Chronic lung disease

Neuromuscular disorders

Obesity

7. Respiratory alkalosis

C CNS disease (Raised ICP)
H Hypoxia (Altitude, anaemia, VQ mismatch)
A Anxiety
M Mechanical hyperventilation
P Progesterone, pregnancy
S Sepsis, Salicylates and other toxins (nicotine, xanthines)