An Irregularly Irregular ECG – It must be Atrial Fibrillation… or is it?

You have taken your Patient’s pulse and have found it to be pretty irregular. In fact, there isn’t any pattern to the irregularity at all. It could be said that you have found their pulse to be irregularly irregular. You explain to your patient that you would like to carry out an ECG (at least a 3-Lead rhythm strip), to further investigate their potential arrhythmia – and you gain consent from the patient (let’s hope that we can get that far!). In your head you’re potentially thinking that the irregularity will be due to Atrial Fibrillation… On the ECG trace, you see that the R-R intervals confirm an irregularly irregular pattern (R-R Intervals; the time between each beat, each QRS complex – normally used to work out the heart rate).

It must be Atrial Fibrillation…..…….or is it?

Atrial Fibrillation (AF) is one of the most common forms of cardiac arrhythmia and can be a major cause of stroke (British Heart Foundation, 2016). There are over one million people with AF in the UK, and it is found much more commonly in the elderly. Approximately 70% of individuals with AF are between the ages of 65 and 85 years (Kannel, Abbott, Savage & McNamara, 2004). AF can increase your risk of stroke by approximately five times (Stroke Association, 2015), and currently the lifetime risk of developing AF over the age of 40 is ~25% (LITFL, 2016). It is paramount that if you have AF, that it is managed and treated correctly; oral anticoagulants (e.g Warfarin) or novel oral anticoagulants (e.g Apixaban, Dabigatran and Rivaroxaban) can reduce your risk of stroke by ~50-70% (Stroke Association, 2015).

There are two proposed physiological mechanisms of AF; Focal Activation and the Multiple Wavelet Mechanism. Focal Activation is where the fibrillatory waves originate from an area of focal activity (often the pulmonary veins) due to increased automaticity, and then maintained via micro re-entry circuits within the atria. The Multiple Wavelet Mechanism is where multiple wandering wavelets of impulses are formed, by a variety of cardiac pacemaker cells within the atria, then maintained via re-entry circuits (created by the wavelets themselves). Conditions such as a dilated Left Atrium (potentially as a result of high blood pressure, valvular heart disease or cardiomyopathies) amplify the effects and likelihood of developing AF, due to the larger surface area which has the ability to facilitate continuous waveform propagation (LITFL, 2016). It is a condition of disorganised atrial electrical activity, and disorganised atrial contraction.

Put Simply the atria are ‘wobbling’ or ‘shivering’ and they are not contracting effectively as they normally would do (with a normally ‘choreographed’ conduction cycle). As you can imagine, this erratic quivering is no longer as effective for delivering blood through to the ventricles, and causes blood to pool in the atria (Stop Afib, 2009).

The mechanisms underlying the creation of blood clots (thrombogenesis) in AF are more complex than we first thought; and still remain only partially understood. Abnormal changes in blood flow (stasis, pooling), vessel walls and blood constituents, fulfil Virchow’s Triad for a prothrombotic or hypercoagulable state promoting thrombogenesis. This clot formation directly relates to the increased risk of stroke; should this clot leave the atria and then enter the systemic circulation.


So let’s have a really good look at the ECG you have just taken. How can we confirm if this is Atrial Fibrillation? After all, there are four main considerations for an irregularly irregular rhythm……..’’are there!?’’ (—> we’ll look at these in a second! 😀 )

Atrial Fibrillation


 – An irregularly irregular rhythm.

 – No P waves – The best leads to scrutinise for P waves on the 12-Lead ECG (I find) are leads II and V1. Lead II generally looks closest to the ‘normal’ cardiac axis, therefore P waves are generally much more prominent and easier to see. After all, an upright P wave in lead II is one of the best pieces of evidence suggesting an impulse of normal sinus origin; make sure there aren’t any! Chest Lead V1 (Septal Precordial) generally presents with a biphasic P wave, meaning a P wave with an initially positive portion and a negative terminal portion. These deflections respectively show the depolarisation of the right atrium, followed by the left atrium. Sometimes this morphology can be easier to detect and scrutinise on the 12-Lead ECG; it can also easily give an indication for any right or left atrial enlargement! Right….sorry…back to what we were talking about…!

 – Absence of an Isoelectric Baseline – Have a look at the image above. There is no absolute baseline. It’s wobbling, it’s all over the place! Fibrillatory waves in the isoelectric baseline may either be coarse (> 0.5mm in amplitude) or fine (< 0.5mm in amplitude). Less than 0.5mm in height really is a small frequency…I mean…this easily could be seen as artefact. Note: Do not let artefact interfere with your interpretation. Maximise your efforts to reduce any artefact, and even then, scrutinise the artefact for a regular occurrence of potential P waves before QRS complexes. There really shouldn’t be any in Atrial Fibrillation!

 – Narrow QRS Complexes (less than 120ms, less than 3 small (0.04s) squares (0.12s)) *UNLESS* there is a pre-existing BBB/Accessory Pathway/Rate-Dependant Aberrancy.

(LITFL, 2016).

Note: Now this last criteria is an interesting one, especially the *unless* part. What if the ECG you have taken has wide complexes that are bizarre looking? Where do you start? Compare the R-R intervals as you would any other ECG. Is there a clear irregularity? You’ve already taken a pulse from the patient, let the ECG confirm your findings. Just because the QRS complexes are wide, does not mean that the ECG doesn’t show Atrial Fibrillation. If you think about it, in AF, the atria are quivering away with this disorganised electrical activity; eventually these impulses are going to ‘capture’ through to the ventricles via the AV node. If there is no BBB/Accessory Pathway/Rate-Dependant Aberrancy… then the QRS should look normal, and it should be narrow (< 120ms, < 3 small squares). Should there be a pre-existing BBB or any other conduction delay, the QRS will present with the respective morphology. If there is an accessory pathway (for example WPW, another pathway between the atria and the ventricles, that bypasses the AV node), then there could be a whole bunch of wide complexes at a very fast rate, as the fibrillatory waves are getting through to the ventricles (rather than being collected and controlled via the AV node, which itself has a natural delay of ~0.12s). A rate-dependant aberrancy is exactly what it says on the tin; a BBB that is rate-dependant…the morphologies may only present in changes of heart rate. Put Simply if you have a wide QRS complex ECG that is irregularly irregular throughout, it will either be Atrial Fibrillation as the underlying arrhythmia or one of the following arrhythmias that I will now discuss…..and let’s not go too deep into wide complex irregularities; it’s vitally important not to forget about life-threatening arrhythmias such as polymorphic ventricular tachycardia (VT) and especially let’s not forget Ventricular Fibrillation (VF)!!!! <—— These can be rather important to spot 😀😉

Treat the patient; ECG scrutinisation may take you a lot of time, which will have a direct impact on split second decisions often needed for the symptomatic patient in prehospital emergency care. I always hear the wise words of Tom Bouthillet of EMS-12-Lead in my conscience when looking at a difficult wide-complex ECG; ‘’A Wide Complex Tachycardia (WCT) is V-Tach until proven otherwise’’. Never forget that; it will save someone’s life.

Anyway bit off track there. The above isn’t such a bad ECG criteria for AF when you think about it, is it? You’ve found an irregularly irregular pulse (which electrocardiography then confirms!), you cannot see any P waves and there really isn’t any discernible isoelectric baseline.

There we go… Atrial Fibrillation!

…….but why do we sometimes get it wrong?

Let’s take a look at the other three possibilities for an irregularly irregular rhythm.

 – Multifocal Atrial Tachycardia

 – Atrial Flutter with Variable AV Conduction

 – Sinus Rhythm with Frequent Premature Atrial Complexes (PACs)

Multifocal Atrial Tachycardia (MAT)


What is it? – An irregularly irregular rhythm with inconsistent PP, PR and RR intervals due to having at least three distinct P wave morphologies in the same ECG lead. There is no dominant pacemaker in the atria (as opposed to a sinus rhythm with frequent PACs). There are three or more pacemaker sites competing against each other. Some impulses may be conducted through to the ventricles, others may not. Due to the different locations within the atria that are initiating an impulse, the PR interval will vary, and so will the P wave morphology (LITFL, 2016).

MAT can often be mistaken for Atrial Fibrillation, as especially in a period of tachycardia, it can be difficult to scrutinise between differing P wave morphologies and coarse fibrillatory waves of the ‘isoelectric baseline’. MAT interpretation often needs a keen and thorough eye – and sometimes a rather long rhythm strip to scrutinise! If it helps, circle each of the differing P wave morphologies and see if they appear again throughout the trace.

What causes MAT? How is it treated? – This condition is a transient phenomenon and usually resolves following treatment of the underlying condition (e.g COPD, Respiratory Failure, Sepsis, Theophylline Toxicity, RAE, Hypercapnia, Electrolyte Abnormalities and Hypoxia). Treatment of the underlying problem takes therapeutic precedent (Tandon, Hemphill, Huott & Reddy, 2015)(LITFL, 2016).


– Irregularly Irregular rhythm with varying PP, PR and RR Intervals
– At least 3 distinct P-wave morphologies in the same lead
– An isoelectric baseline between P waves (i.e no fibrillatory or flutter waves)
– Absence of a unifocal dominating atrial pacemaker
– The heart rate is usually between 100 & 150bpm

Take a look at the following ECG, as an example for practice, provided by Jason E. Roediger (#FOAMed Wikipedia) of a Multifocal Atrial Tachycardia. Try and work through the criteria for both Atrial Fibrillation and MAT; try to locate the P waves. Luckily, there’re a few arrows at the bottom to help you out! And look at what Leads he was looking at for the rhythm strip portion (bottom) of the ECG….Lead II & V1! It’s quite easy to see, how on quick inspection, MAT may be overlooked and the trace regarded instantaneously as Atrial Fibrillation; which you now know it isn’t! 😀


Atrial Flutter with Variable Conduction


What is it? – Think back to the disorganised electrical and mechanical activity of the atria in Atrial Fibrillation. Atrial Flutter is another abnormal arrhythmia of the atria; yet it is more ‘controlled’, shall we say. The atria are quite literally ‘fluttering’; they are going at a pace much faster than the ventricles themselves; and as if by *MAGIC*, they tend to go at a pace of ~300bpm. The actual range of P wave rate is anything from 200-400 bpm (Heart Matters, 2016)(LITFL, 2016).

Now, when you look at an ECG trace to work out the rate, you tend to use the large squares right? (if not, take note of the following! It’s really handy!)

‘’300 divided by the *amount of large squares within the R-R interval* calculates an instant ~bpm’’

So if you think about it, 1 large square (300/1) should give you a rate of 300bpm. A nice little tip when looking for flutter waves, is to look for P wave peaks, or ‘sawtooth’ patterns, ~1 large ECG square apart! Similar to Atrial Fibrillation; there is a loss of the isoelectric baseline – but there is often a strong ‘sawtooth’ or ‘sharktooth’ pattern seen, which is more easily spotted in the inferior ECG leads (II, III and aVF) and the chest lead V1 (do these leads sound familiar again to you…!?).

Atrial flutter is the result of a much larger and consistent re-entry circuit in the atria; as opposed to the micro re-entry circuits made by tiny multiple wavelets in the ‘quivering’ Atrial Fibrillation. I tend to imagine a washing machine with Atrial Flutter; spinning round and around in the atria itself. This isn’t far wrong from the truth of how the re-entry circuit works to be honest! In 90% of patients with Atrial Flutter, this re-entry circuit will be in an anticlockwise rapid rotation within the right atrium; resulting in inverted flutter waves in the inferior leads (II, III and aVF); and positive flutter waves in V1 (V1 may also just resemble normal P waves at a rate of ~300bpm).

Atrial Flutter is often said to be of a certain ratio. The ratio depicts the amount of ‘P waves’ to ‘QRS Complexes’. For example, Atrial Flutter with 2:1 Conduction is quite simply, two P waves to every QRS. The Ventricular Rate in Atrial Flutter is determined by the degree of AV block (the AV conduction ratio e.g 2:1, 3:1, ‘variable’…!). It is said that the most common ratio of AV block is 2:1 – it is in this ratio that you would expect an atrial rate of ~300bpm, therefore a ventricular rate of ~150bpm. Higher degree AV blocks can be a result of vagal stimulation, medications and/or underlying heart disease (3:1, 4:1 +++).

As you can imagine, an Atrial Flutter of 1:1 Conduction is going to be ineffective and life threatening; how long can someone possibly sustain a pulse of ~300bpm with a terrible cardiac ejection fraction (the heart doesn’t really have any time to ‘fill’ itself with blood before doing it’s thing!). Atrial Flutter 1:1 will present with a severely haemodynamically compromised patient; and a rapid progression to Ventricular Fibrillation (VF). Now that’s ‘shocking’ news isn’t it….no….man at the back…. is this thing on!?. Mr Atrial Flutter with 1:1 needs more than just some TLC – or you’ll be jumping on his chest in no time!

An Atrial Flutter with Variable Conduction (Variable AV Block) is exactly what it states. The ratio is not constant; it is varying throughout i.e 2:1, 3:1, 2:1, 4:1, 1:1, 2:1…..and so on! It produces an irregularly irregular rhythm.

What causes Atrial Flutter? How is it treated? – Atrial Flutter is less common than Atrial Fibrillation; but the arrhythmia often presents with similar symptoms (Tiredness, Shortness of Breath, Dizziness, Palpitations or Feeling Faint). Some patients will present with mild symptoms; others, asymptomatic. Interestingly enough, up to a third of patients with atrial flutter will also have atrial fibrillation! Both conditions carry their risks of an increased risk of stroke (Heart Matters, 2016).

Cather Ablation is often the preferred first-line of treatment for Atrial Flutter (obviously, patients are treated on a case-by-case basis). Ablation involves the passing of a long extremely-thin catheter into an artery or vein, which is then threaded through to the appropriate site of the heart; to the area which is ‘allowing’ or ‘potentiating’ the re-entry circuit in Atrial Flutter. Radiofrequency energy is then used, quite literally, to destroy the particular cells within the heart tissue that are causing and/or allowing the abnormal cardiac rhythm. Should the AV node be affected during this process, this is the time where a pacemaker may also be fitted (often referred to as ‘ablate and pace’)(Heart Matters, 2016).

Similar to Atrial Fibrillation, oral anticoagulants (e.g Warfarin) or novel oral anticoagulants (e.g Apixaban, Dabigatran and Rivaroxaban) can reduce the risk of stroke by ~50-70% (Stroke Association, 2015).

There are a few medical conditions that can increase the risk of developing Atrial Flutter, which include: Heart Failure, Previous MI, Valve Abnormalities, Congenital Defects, High Blood Pressure, Recent Surgery, Thyroid Dysfunction, Alcoholism (*Binge Drinking), Chronic Lung Disease, Acute Illness and Diabetes. Left untreated, Atrial Flutter can lead to a rapid pulse rate for a prolonged period. Over time, the heart muscle will weaken (cardiomyopathy); potentially leading to heart failure and long-term disability (Heart Rhythm Society, 2016). Treatment is paramount!

ECG Criteria

– Regular Atrial Activity at ~300bpm
– Flutter waves (Sawtooth/Sharktooth) seen in the inferior leads (II,III,aVF) and/or V1
– Flutter waves in V1 may resemble P waves
– Loss of the Isoelectric Baseline
– Ventricular Rate is a Fraction of the Atrial Rate (e.g 2:1=150bpm, 3:1=100bpm)
– The R-R Intervals are therefore mathematical multiples of the P-P interval
(LITFL, 2016).

Take a look at the following ECG, as an example for practice, provided by James Heilman, MD (#FOAMed Wikipedia) of an Atrial Flutter with Variable AV Conduction. Apply the above ECG criteria to this trace and see how it differs from Atrial Fibrillation. Check out the inferior leads (II, III and aVF) and V1; see how much more prominent the flutter waves are – and hence why these leads are utilised!


Frequent Premature Atrial Complexes (PACs)


What are PACs? – Premature Atrial Complexes are ectopic beats from an atrial focus; the pathophysiology is extremely similar to that of a PVC, but it is just that the impulse originates from within the atria themselves. If there is no underlying BBB/Accessory Pathway/Rate-Dependant-Aberrancy, then the QRS complexes normally appear narrow (< 120ms, < 3 small (0.04s) squares) as the impulses may, or may not be, conducted to the ventricles via the AV node. Similarly to PVCs, PACs will have an appropriate ‘Compensatory Pause’; Put Simply, the R-R interval will be double the preceding R-R interval, should a QRS complex be missed.

A PAC can only occur if the ectopic focus occurs outside of the absolute refractory period; either in the terminal T wave portion (relative refractory period where the cardiomyocytes have almost reached full repolarisation) or within the TP segment (resting period).

Due to the originating impulse within the atria being somewhere away from the sinoatrial node, the P wave morphology will be different. It may be wider, it may be superimposed on the previous T wave (a slight notching to the terminal portion), it may be inverted (if close to the AV node) and the PR segment may be much shorter than normal (< 0.12s, < 3 small (0.04s) ECG squares). As previously mentioned, the P wave may or may not be conducted through to the ventricles; there won’t always be a QRS complex following a PAC.

Please see my previous article on PVCs for more information; again, the pathophysiology and causes are extremely similar for any ectopic focus:

What causes PACs? – The causes are extremely similar for any ectopic focus within the heart. Please see my previous article on PVCs for more information; there is an image at the end of the article with a variety of causes (and also a section on Lown’s Grading).

Looking at the image above demonstrating PACs, the rhythm is irregularly irregular; there is no definite pattern. What you can notice is that the rhythm is regular other than when there are PACs, which cause appropriate compensatory pauses before the sinus rhythm returns. You can also see why this may be confused with Atrial Fibrillation or potentially a sinus arrhythmia; but make sure you fully understand what a PAC is, how they present on an ECG and the different P wave morphologies. As with any premature complex, they can be of unifocal origin, multifocal origins and can be in patterns (every other beat can be said to be ‘bigeminy’  for example).

I hope this blog post has been of some interest; please do leave a comment with some honest feedback, and don’t hesitate to get in touch with any queries!

All the best,


Further Reading

 – PVCs: What are they? What causes them? —> Have a read of my previous article to help you further understand PACs… the underlying pathophysiology isn’t much different other than a different ectopic focus! —>

 – Follow @PreHospECG on Twitter —> Get involved with CPD discussions, online quizzes and be a part of case study discussions to move forwards with your ECG Interpretation ability. A friendly and approachable team who are more than happy to help with any questions that you may have. There are no silly questions here! Follow us and make yourself known! 🙂 —>

 – ‘A Wide Complex Tachycardia (WCT) is V-Tach until Proven Otherwise—> Head over to EMS-12-Lead for this great ECG blog series; and to find many other interesting articles that will immediately increase your ECG Interpretation skills from the get go! —>

 – Head over to the ECG Library: Life in the Fast Lane —> A complete bible of knowledge in the ECG world, and a fantastic resource to continuously use as a reference throughout your learning —>

 – Meet Ken Grauer and read through his incredibly descriptive blog posts on ECG-Interpretation —> Some truly fantastic case studies and in-depth descriptions. An invaluable resource for all students, written in a clear and concise way —>


British Heart Foundation. (2016). Atrial Fibrillation. Retrieved from
Heart Rhythm Society. (2016). What is Atrial Flutter. Retrieved from
Heart Matters. (2016). What’s the difference between atrial flutter and atrial fibrillation. Retrieved from
Kannel, W. B., Abbott, R. D., Savage, D. D., & McNamara, P. M. (2004). Electrophysiologic and electroanatomic changes in the human atrium associated with age. J AmColl Cardiology, 44, 109-116.
LITFL. (2016). Atrial Fibrillation. Retrieved from
LITFL. (2016). Atrial Flutter. Retrieved from
LITFL. (2016). Multifocal Atrial Tachycardia. Retrieved from
Selner, M., & Sullivan, D. (2015). Atrial Premature Complexes. Retrieved from
Stroke Association. (2015). Atrial Fibrillation. Retrieved from
Stop Afib. (2009). What is Atrial Fibrillation?. Retrieved from
Tandon, N., Hemphill, R. R., Huott, M. A., & Reddy, P. C. (2015). Multifocal Atrial Tachycardia Overview of Multifocal Atrial Tachycardia. Retrieved from
Watson, T., Shantsila, E., & Lip, G. Y. H. (2009). Mechanisms of thombogenesis in atrial fibrillation: Virchow’s triad revisited. The Lancet, 373(9658), 155-166.

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