Realise the power of global impression, of clinical gestalt (ie 'Something just isn't right), and the importance of having a solid foundation of knowing (and doing) the basics incredibly well.

The best clinicians that I have met and worked with have demonstrated exactly that; a sound knowledge and understanding of the basics of pre-hospital emergency care, that can work logically and methodically under dynamic pressures and challenging environments with compassion, that are aware of their own human factors and limitations (and those of others around them), working as a well-drilled team to collaboratively create well-informed clinical decisions, delivering excellent clinical care.

I am going to be putting a few bits together for you all on this website, to help and support your ability in making sound judgements in terms of 12-Lead ECG Interpretation and respective clinical decision making. This is not going to be designed as a thorough training course, nor will it support ECG interpretation from the 'beginning to the end'. However, I hope that these key learning points will help support you in your learning journey whilst developing as a Newly Qualified Paramedic (Temporary Registration... and beyond!!)

Wishing you all, the very best. It's been a pleasure working alongside you, albeit for a short spell of your education, and I'm looking forward to working with you as a team to make a positive difference during these challenging times.

Thank you for all of your hard work, your strive to make a difference, and your commitment to patient care - here's to the next chapter!

~Phil Poskitt

Paramedic - Yorkshire Ambulance Service

Specialist Visiting Lecturer (ECG) - Sheffield Hallam University

Clinical Educator - NAEMT, Polaris Academy, Resuscitation Council (UK) & the Society for Cardiological Science & Technology (SCST)

• 3-Lead ECG is for rhythm analysis and monitoring

• 12-Lead ECG is for diagnostics and rhythm analysis (ie, 'is my patient suffering from an Acute Coronary Syndrome?')

• I need to stress the point to have a low threshold for taking a 12-Lead ECG. For example, if your patient has any pain/discomfort between their nose and their navel, perform a 12-Lead ECG (where appropriate).

• If a Patient has chest pain, taking a 3-Lead ECG (and not a 12-Lead) is extremely poor practice; a 3-Lead ECG is not a diagnostic clinical test.

• Know the three main risk factors for the so-called 'Silent MI' (ie, patients may be pain free!); Female, Elderly & Diabetic. Be alert for symptoms such as acute shortness of breath (especially elevated respiratory rate with a clear chest on auscultation; could this be a cardiovascular presentation?), acute nausea, acute pallor, referred 'aches and discomforts' (for example, left arm discomfort, jaw discomfort), patients that are 'clammy', or your clinical gestalt kicks into gear and shouts up 'something isn't right' and other observations show no abnormalities.

• Know that treating hyperventilation/anxiety as a panic attack (Hyperventilation Syndrome; HVS) is a diagnosis of exclusion. Be sure to assess patient's for underlying potentially life-threatening illness prior to considering HVS. Many life-threatening medical conditions can cause hyperventilation - especially consider this in children where a medical cause is far more likely than anxiety.

• Electrocardiography is a supportive tool to be used in collaboration with a systematic patient assessment to better inform clinical decisions. Always correlate your patient's presentation, observations and assessments with 12-Lead ECG interpretation findings. A 12-Lead is not always diagnostic in isolation; however, clinically correlated, it can be a very powerful tool at your disposal!

• Adopt a stepwise approach to interpretation (see below!); this will continuously improve your knowledge, ability and confidence in making a 12-Lead ECG interpretation.

• Reflect and review on key aspects of ECG interpretation in bitesize chunks. ECG is a complicated subject; respect and appreciate that. For example, for one week, just have a read and look at various types of tachycardia. The following week, review a variety of STEMI presentations. The week after that, have a look at different types of Heart Block. Like most complicated subjects of both breadth and depth - repetition and practice, repetition, and practice... are often the best methods for learning, retaining, and for developing your own 'pattern recognition' for future ECG encounters.

• Know your limitations. Know what findings will/can influence your clinical decisions. Know your scope of practice. Appreciate that paramedics are not expected to, nor are they all able to, diagnose an Ostium Secundum Atrial Septal Defect (ASD) in a paediatric ECG looking for a narrow RBBB in the right precordium with right QRS Axis Deviation and respective fragmented QRS complexes. Having such specialist in-depth knowledge in one area of clinical practice may mean that another area of clinical practice may suffer! Know the basics of 12-Lead ECG really well, know (and practice) the changes of ECG that may influence your clinical decision making in emergency care (for example, STEMI/ACS presentations, VT, SVT and so forth!). You are learning how to use Windows on a computer; you are not learning how to design, create and understand the coding underneath the operating system.

• Use a variety of credible resources to support your learning with a variety of different learning styles (discussions with colleagues, reflection, online blogs, videos, websites (see list below) and text books).

• Adopt a stepwise approach (Rate, Rhythm, Axis, Intervals, Ischaemia) - I will elaborate on this shortly!

• Look through each and every lead throughout the 12-Lead ECG (except aVR - for now..). Focus your attention to each lead one-by-one, if you look at the whole trace in one go, you can quite easily experience 'information overload' and you will miss abnormalities.

• A Normal 12-Lead ECG of Normal Sinus Rhythm will have :-

  • 1) Upright P waves in Lead II

  • 2) A P wave before every QRS, a QRS after every P wave (evidence that the top of the heart is communicating normally with the bottom!)

  • 3) A rate of 60-100bpm (3-5 Large Squares between each QRS complex on 25mm/s paper)

  • 4) A regular rhythm (ie no variation in R-R intervals!)

  • 5) A normal PR Interval (3-5 small squares, 120-200ms, 0.12-0.20s)

  • 6) A narrow QRS complex (< 3 small squares, < 120ms, < 0.12s) - unless any pre-existing bundle branch block / conduction abnormalities

  • 7) A normal QTc (350-450ms) - (this is the QT of the ECG calculated should it be at 60bpm; the measurement from the beginning of the QRS to the end of the T wave - 'the total event' of depolarisation and repolarisation)

  • 8) Upright T waves in all of the leads (minus aVR, Lead III in isolation & Lead V1 in isolation - any variance of such - can be normal)

  • 9) No deviation of the ST segment (no elevation; no depression) - I will post some examples of how to find the J point and how to measure the ST segment shortly

  • 10) No pathological Q waves (initial negative deflections at the beginning of the QRS, that are >0.04s (or 1 small square) in width or >25% of the QRS amplitude)

  • 11) A normal R-wave progression (that is, an R wave (positive deflection of the QRS) that starts small/non-existent in V1, becomes increasingly taller until it becomes dominant in V6)

With the above information, it is clear already that a thorough description can be made of the 12-Lead ECG. Abnormalities can be identified. The clinician may not always have an answer as to the underlying electrophysiology, pathophysiology or reason as to why these abnormalities are visible - and that's ok; but the findings can be shared with the appropriate receiving clinician for further investigation - whether that be following transport, or as part of a clinician-to-clinician handover.

• A LBBB will change the ST segment; there WILL be ST-Elevation and ST-Depression throughout the ECG when there is a LBBB. This is normal for a LBBB. This is what we call a 'SECONDARY' ST-T change (repolarisation abnormalities SECONDARY to conduction abnormalities). Therefore, if you see a wide QRS, have a look at V1. If V1 has a wide QRS that is negative, this is likely a LBBB.

  • What isn't normal for a LBBB, is if the ST segment is changing over serial traces (ie, getting more elevated, or more depressed; taking into account that your patient is in the same position, with electrodes in the same anatomical positions - serial traces meaning a new 12-Lead ECG taken every 5-15 minutes). If the ST segment is evolving - this could be an MI. Also quite diagnostic in terms of sensitivity & specificity is the Sgarbossa Criteria (see for more: https://litfl.com/sgarbossa-criteria-ecg-library/) in the presence of LBBB - or a Paced Rhythm.

• A RBBB will never influence the ST segment in isolation. This means, if you find a wide QRS, look at V1, find a QRS that is positive of either qR or rSR' morphology, there is a RBBB (see examples below) - there should never be any ST elevation or depression. If you see ST-Elevation or Depression in an ECG with RBBB - this is pathological until proven otherwise. This could be an MI; clinically correlate your 12-Lead ECG with your patient. The reason that RBBB is not seen in the same light as LBBB in terms of being a conduction abnormality, is that the septum normally depolarises left-to-right as electrical activity travels towards the ventricles. Therefore, the Left Ventricle in a RBBB still conducts and depolarises as normal; the right bundle branches are blocked, the septum continues to depolarise left-to-right as normal. The Left Ventricle is the largest muscular mass of the cardiac tissue, the powerhouse of the heart, and the main aspect of the heart that all of our leads are 'viewing' on the 12-Lead ECG. As the Left Ventricle continues to 'conduct normally', then any repolarisation abnormalities in a RBBB are therefore presumed to be of a 'PRIMARY' cause (other than a couple of the leads that look more towards the right; we can sometimes see T-wave inversions in Lead III and V1/V2 in RBBB; this is quite normal). By PRIMARY changes, I mean repolarisation abnormalities (ST/T wave changes) in the presence of NORMAL conduction. This is in comparison to SECONDARY changes, which are expected repolarisation abnormalities in the presence of ABNORMAL conduction (LBBB, LVH etc.....).

• If the QRS is narrow (ie, <120ms, <0.12s, <3 small squares in width), then presume that any ST segment deviation is of a PRIMARY cause (ie, ischaemia/infarction!). Clinically correlate the ECG to the patient in front of you. Primary cause, meaning 'repolarisation abnormality' in the presence of normal conduction. If the heart is struggling to repolarise, struggling to 'reset/recharge its batteries', then it is telling us that blood flow has been restricted and therefore it is not receiving sufficient fuel needed to work, or any fuel at all. If this incredible specialised machinery has low batteries, or no battery left at all, it won't function the same, right? .. it might even stop working altogether..

My Wordpress Article: https://phildrummer64.wordpress.com/2017/09/25/my-stepwise-approach-to-ecg-interpretation/

RATE - RHYTHM - AXIS - INTERVALS - ISCHAEMIA/INFARCTION

Let's take the above ECG as an example!

'' An ECG of a 35 year old male with a 1 hour history of acute crushing central chest pain, radiating into his left arm, presenting pale, clammy, with no exacerbating/relieving factors, and a reported severity of 7/10. ''

Remember.... 'RATE - RHYTHM - AXIS - INTERVALS - ISCHAEMIA'

• RATE - There are approximately 5 large squares between each QRS complex. 300/5 = 60bpm.

• RHYTHM - The rhythm is regular. There is a P wave before every QRS and a QRS after every P wave. Remember: If struggling to find P waves, look at each and every lead throughout the trace. P waves are much more clear in the chest leads of this trace.

• AXIS - This is a more complicated trace to interpret QRS axis adequately as the QRS complexes are not as clear in terms of positivity/negativity. I would think to myself at this point, does this change my interpretation or management? In this case, entirely not. If you do not have a clear normal axis, a clear left axis or a clear right axis... move forwards with your interpretation. For more advanced users; There is a 'Borderline' Right QRS Axis. The QRS in Lead I is equiphasic (as positive as it is negative) therefore the QRS axis is at right angles to Lead I (0 degrees) in the direction of Lead aVF (90deg), though correctly calculated the axis is somewhere between +75 and +90 degrees; normal parameters!

• INTERVALS - The PR interval is normal (between 3&5 small squares), the QRS is narrow (< 3 small squares), we do not have a value for QTc on this trace. Intervals remain persistent (minimal variation) throughout the trace.

• ISCHAEMIA - Think 'ST segment, T waves, Q waves & R-Wave Progression'. We have 3.5 - 4 mm ST-Elevation in Lead II, 4 mm ST-Elevation in Lead III, 3.5 mm ST-Elevation in Lead aVF (All three of our INFERIOR leads - suggesting INFERIOR STEMI). Reciprocal to these changes we have 2 mm ST-Depression and T-wave inversion in Lead aVL, and 1 mm ST-Depression and T-wave inversion in Lead I. Already this trace, correlated with the given history, is unequivocally diagnostic of Inferior ST-Elevation Myocardial Infarction (Inferior STEMI). Looking further into this trace, we have down sloping ST-Depression and T-Wave Inversions V2, with slight ST-Depression V3 & V4 - likely reciprocal changes to the 'back' of the heart, the 'posterior' surface. This is therefore likely an Infero-posterior MI (a clot in the Right Coronary Artery in Right-Dominant Circulation!). The key information of this trace is to identify the ST segment and T wave abnormalities, to correlate this with the Patient history, and to then ensure that your patient receives the correct ACS treatment, with referral/transport direct to the nearest/most appropriate PCI centre. Considering the other aspects of Ischaemia, there are not (yet) any Q waves in this trace (initial negative deflections at the beginning of the QRS) and there remains to be a good R-wave progression in the chest leads (starting small in V1; progressively getting taller to V6). This ECG is therefore suggestive of ACUTE STEMI.

Using the above information, we have therefore created a descriptive interpretation of the ECG, followed by clinical correlation and an appropriate treatment plan.

RATE - RHYTHM - AXIS - INTERVALS - ISCHAEMIA/INFARCTION

Here's another example!

'' An ECG of a 28 year old female student that has had an episode of collapse whilst watching a surgical procedure in theatre. ''

Remember.... 'RATE - RHYTHM - AXIS - INTERVALS - ISCHAEMIA'

• RATE - There is approximately 3-4 large squares between each QRS complex. 300/4 = 75bpm, 300/3 = 100bpm. The rate is between 75 and 100bpm. For more advanced users, there are 17 small squares between each QRS complex. 1500/17 = 88bpm.

• RHYTHM - The rhythm is regular throughout. There are no irregularities. There is a P wave before every QRS, there is a QRS after every P wave. There is therefore evidence of normal conduction and communication; there are no signs of heart block or conduction abnormalities.

• AXIS - The cardiac axis is normal. Electrical activity is mostly going towards lead II, towards the majority of the left ventricular mass. QRS complexes are positive in Lead I & II.

• INTERVALS - The PR interval is normal (3-5 small squares), the QRS is narrow (< 3 small squares), the QTc is not recorded.

• ISCHAEMIA - There are no ST segment abnormalities, the T wave is inverted in aVR and V1 (however this is in isolation, and we know that is a normal finding), there are no pathological Q waves, and there is a normal r-wave progression across the chest leads. Nil acute.

This is an entirely normal resting 12-Lead ECG with no abnormalities identified. Further assessment is needed for this Patient who has suffered a transient loss of consciousness. Given the circumstances, we could consider exploring situational syncope given the graphical procedure that occurred.

Using the above information, we have therefore created a descriptive interpretation of the ECG, followed by clinical correlation and an appropriate treatment plan.

RATE - RHYTHM - AXIS - INTERVALS - ISCHAEMIA/INFARCTION

...and another!

'' An ECG of a 64 year old female who presents with gradually worsening shortness of breath and palpitations, over the last 8 hours ''

Remember.... 'RATE - RHYTHM - AXIS - INTERVALS - ISCHAEMIA'

• RATE - There are 28 complexes over this 10 second Lifepack [15] 12-Lead ECG trace. 28x6 gives us 168bpm... Tachycardia!

• RHYTHM - We can see that this rhythm is irregularly irregular - there are no patterns of irregularity. We cannot see any P waves, and any atrial activity we do see seems to be fibrillatory/chaotic/uncoordinated. It is therefore presumed to be Atrial Fibrillation until proven otherwise. Therefore, we already now know we have Atrial Fibrillation with a Rapid Ventricular Response (AF-RVR or... Fast AF!) due to the given rate of 168bpm. Remember, Atrial Fibrillation does not have a set rate, it normally has a range. It is quite useful to give a range that has been viewed over time, for example, an Atrial Fibrillation with a rate of 120-180bpm - obviously this will have been monitored throughout assessment/transport.

• AXIS - Leads I and III are 'LEAVING' the page, suggestive of a LEFT axis deviation. This is opposite to when we might see Lead I and III 'REACHING' for each other; which would suggest a RIGHT axis deviation. The above ECG has a LEFT axis deviation.

• INTERVALS - There are no P waves therefore it is impossible to measure the PR segment. The QRS is notably wide, I look at V1 and see a negative QRS complex representative of LBBB morphology. We therefore have a LBBB. There is no place for measuring the QTc in the presence of Atrial Fibrillation and/or Bundle Branch Block (as the QT will always change with AF, and the QRS is naturally wider in BBB!).

• ISCHAEMIA - There are ST/T wave abnormalities throughout this trace, however we have identified that there is already a LBBB, therefore these are expected SECONDARY ST/T abnormalities to the conduction abnormality that is LBBB. We have appropriate 'discordance', meaning that where a QRS is mostly negative, there is ST-Elevation and a positive T-wave; where the QRS is mostly positive, there is ST-Depression and T-wave inversion - 'opposite vectors'.

This 12-Lead ECG could therefore be described as Atrial Fibrillation with a Rapid Ventricular Response (or Fast AF) of ~168bpm with LBBB. This Patient is showing signs of decompensation (shortness of breath) and therefore requires emergency intervention (appropriate to the guidelines of your service/organisation).

NOTE: This CANNOT be Ventricular Tachycardia... the rhythm is irregular!

Using the above information, we have therefore created a descriptive interpretation of the ECG, followed by clinical correlation and an appropriate treatment plan.

RATE - RHYTHM - AXIS - INTERVALS - ISCHAEMIA/INFARCTION

...last one!

'' An ECG of a 38 year old male presenting as anxious, with some gradually worsening chest pain (4/10 severity) whilst sitting at home. ''

Remember.... 'RATE - RHYTHM - AXIS - INTERVALS - ISCHAEMIA'

• RATE - There are approximately 2 large squares between each QRS complex. 300/2 = 150bpm... Tachycardia!

• RHYTHM - The rhythm is regular throughout, there are no irregularities/variations. We cannot see any clear P waves throughout the trace, but be mindful that a tachycardia at 150bpm could be an Atrial Flutter with 2:1 conduction. Remember; flutter waves tend to go at approximately 300bpm (1 large square apart), therefore if we have a rate of 150bpm, then this could be x2 flutter waves for every x1 QRS complex (2:1 conduction).

• AXIS - There is a normal QRS axis, the QRS complexes are positive in leads I and II.

• INTERVALS - We cannot measure the PR interval as it is impossible to identify P waves throughout this trace; however, being mindful that this rhythm is regular throughout. The QRS is narrow (< 3 small squares). We do not have a documented QTc.

• ISCHAEMIA - There is widespread ST-Depression, more visible in the chest leads (see V3-V6), correlated with the rate of this trace (150bpm) this could be a rate related demand ischaemia. However, considering a likely differential of an ECG of 150bpm to be Atrial Flutter with 2:1 conduction, the ST changes could be 'false' in that they are actually the result of superimposed flutter waves throughout. R waves appear smaller in V1 & V2, however progression continues through the chest leads and R waves remain dominant in V6.

Exploring and ruling out initial differentials such as haemorrhage and alternative forms of shock, we are likely faced with a form of Supraventricular Tachycardia (SVT). Given the rate and presentation, this is likely to be an Atrial Flutter with 2:1 conduction. Vagal manoeuvres should be attempted (which may either convert the rhythm, or increase the R-R interval which may present you with flutter waves to narrow your differential diagnosis). This Patient is starting to show signs of decompensation (chest discomfort) which requires emergency intervention (following the appropriate guidelines of your service/organisation).

Using the above information, we have therefore created a descriptive interpretation of the ECG, followed by clinical correlation and an appropriate treatment plan.

RATE - RHYTHM - AXIS - INTERVALS - ISCHAEMIA/INFARCTION

LBBB further information (LITFL) --> https://litfl.com/left-bundle-branch-block-lbbb-ecg-library/

RBBB further information (LITFL) --> https://litfl.com/right-bundle-branch-block-rbbb-ecg-library/

Life in the Fast Lane https://litfl.com/ecg-library/diagnosis/ - an invaluable reference website covering a wide variety of ECG abnormalities. Great for rapid reference, easy to access and a credible resource.

12-Lead ECG 'I've Got the Rhythm' Facebook Group - https://www.facebook.com/groups/ivegotthethythm/

EMS 12-Lead http://ems12lead.com/#gref

Ken Grauer ECG Blog http://ecg-interpretation.blogspot.com/

Dr. Stephen Smith ECG Blog http://hqmeded-ecg.blogspot.com/ <-- Advanced Users

ECG Resources from the LITFL website https://litfl.com/ecg-library/ecg-references/

The ECG in Acute MI (free online book - advanced users) http://bezak.umms.med.umich.edu/CIRHT/Content/Emergency%20Medicine%20-%20Open%20Textbooks/ECG_in_Acute_MI-OutOfPrint-FreeAllRightsReserved.pdf

Ken Grauer Pocket Brain (ECG) https://www.amazon.co.uk/Pocket-Brain-2014-Expanded-Version/dp/1930553250 - available on amazon

The ECG Made Easy https://www.amazon.co.uk/ECG-Made-Easy-Book-ebook/dp/B07NQJ8TW7/ref=sr_1_1?dchild=1&keywords=ecg+made+easy+john+hampton&qid=1586187731&s=books&sr=1-1 - available on amazon

Recommended Courses

Foundation of ECG Interpretation (Essential Electrocardiography) - Society for Cardiological Science and Technology - http://www.scst.org.uk/pages/page_box_contents.asp?pageid=779

Pre-Hospital Electrocardiography (Foundation) & Pre-Hospital Electrocardiography (Advanced) - Pre-Hospital Care Consultancy - http://prehospitalcareconsultancy.co.uk/ --> in development; watch this space, a certain virus has delayed me slightly!

Just to add that twitter is a fantastic platform (when used appropriately) for clinical discussions, learning, and development. It is especially useful for staying current with updated guidelines, new research and for sharing information. However, like most social media platforms, evidence and resources should still be approached with caution and should always be critically appraised before allowing anything shared on Twitter to influence your practice.