Atrial Fibrillation

Intro to Atrial Fibrillation

Atrial flutter typically involves one stable reentrant circuit that leads to regular and predictable atrial behaviour. However, there is a very common rhythm known as atrial fibrillation (AF/A-Fib) characterized by erratic activation of the atria known as fibrillatory conduction. This type of conduction is typically referred to as being disorganized because there is no coordinated activation of any part of the atria, and therefore the myocardial contraction accompanying it is very erratic. In fact, the atria appear to "fibrillate" rather than having organized hemodynamically-sufficient contractions. Due to this, there is a tendency towards stasis of blood flow and formation of intra-atrial thrombi, increasing the risk of stroke. Atrial activation in this rhythm tends to occurs at a very high atrial rate (400-700 bpm). 

Pathobiology of Atrial Fibrillation

AF has many proposed mechanisms. In fact, AF might be a heterogeneous group of rhythms leading to fibrillatory conduction in the atria. In other words, the mechanism behind one patient's AF may not be the same as another's. 

There are different degrees of "disorganization" that can be found in the atria of patients with AF, as determined by experiments on pacing-induced AF. This depends on their underlying mechanism.  

Generally speaking, the mechanisms can be organized from least to most organized: 

There is a classification system in the literature (Type I AF, Type II AF, Type III AF) going from most organized to least organized. As you go from Type I to Type III, you can observe the following changes: 

Patients with coarse atrial fibrillation (see below) that resembles atrial flutter may have more of a "Type I" phenotype, whereas patients with fine atrial fibrillation (see below) may have more of a "Type III phenotype". 

Coarse atrial fibrillation 

Fine atrial fibrillation 

Clinically, identifying coarse AF may represent a patient who may have more success cardioverting to sinus rhythm, although the evidence is equivocal. 

There is some relation between underlying disease and coarseness of AF (i.e. cardiomyopathy tends to present with fine AF, whereas rheumatic heart disease may present with coarse AF) although there is great variability here as well with likely poor sensitivity and specificity. 

Some suggest that coarse AF may indicate left atrial enlargement (compared to fine AF). This is not entirely reliable, especially because AF may look "coarse" in one lead but not coarse in others. I wouldn't use the coarseness of someone's AF to predict their atrial size.

Overall, the most valuable reason for identifying coarse AF is so we can recognize it as an entity separate from atrial flutter, to avoid confusion between the two rhythms, as management may differ between the two (especially interventional strategies). 

Important factors in the pathogenesis of AF

A short atrial refractory period and slow atrial conduction velocity are important for the pathogenesis of AF. Decreasing refractoriness presumably increases the rate at which the atria can be activated. Both vagal and sympathetic impulses can reduce atrial refractoriness. Various metabolic states such as hyperthyroidism or cardiac ischemia may also decrease the atrial refractory period.  

Recall that the refractory period is closely related to action potential duration. 

The other problem is that the abovementioned stimuli may not cause uniform decreases in atrial refractoriness. This may create several islands of refractory tissue amidst areas of non-refractory tissue, which then creates a substrate for functional re-entry and fibrillatory conduction. 

The longer that a person stays in AF, the atria start to undergo electrical remodelling, whereby the intrinsic atrial refractory period is reduced, atrial conduction is slowed, and it becomes harder to revert to a more organized rhythm. Physical remodelling of the atria, i.e. via fibrotic remodelling, can also increase the risk of permanent atrial fibrillation. The scar tissue can form anatomic obstacles to conduction that facilitate re-entry and fibrillatory conduction. 

Atrial strain (such as chronic dilation due to heart failure with remodelling or acute strain due to MI or PE) may increase atrial excitability and trigger AF. 

A critical tissue mass may be necessary to engender AF. Some electrophysiological studies have shown that AF cannot be induced below a certain critical atrial tissue mass. Along the same lines, it may not be possible to maintain normal sinus rhythm once a high enough tissue mass is achieved. 

The pulmonary veins (PV) of the left atrium play an important role in the initiation and maintenance of AF. In many people, the PV may be the source of the AF as well. However, there have been many foci identified in people in AF, including those elsewhere in the LA or even in the RA. That being said, even in the people with foci other than the PV, the PV may play some role in maintaining the arrhythmia. 

Left atrial enlargement is a risk factor for AF, likely because the condition involves increased tissue mass and atrial strain of the cells near the pulmonary veins. 

Relationship between atrial fibrillation and atrial flutter 

AF is closely related to atrial flutter (AFL). There's some evidence that wavelets from AF can generate re-entry about the tricuspid annulus in select scenarios, leading to AFL if fibrillatory conduction is halted. There's also evidence, on the other hand, that a rapid AFL circuit, with the appropriate atrial substrate, can lead to fibrillatory conduction and development of atrial fibrillation.  

AFL may play a role as an "intermediate rhythm" between sinus rhythm and AF, as people sometimes go transiently into AFL while they are converting from AF to sinus or vice-versa, as the AF gets "more organized". Some patients can even flip-flop between the two rhythms, as in the diagram below. 

Blue = sinus rhythm. Green = atrial flutter. Red = atrial fibrillation. (Source: Chou's)

Certain rhythms may have characteristics of both atrial fibrillation and atrial flutter, or it may appear to be flip-flopping between them. Such a rhythm is often referred to as atrial fibrillation-flutter ("fib-flutter") or atrial fibrillo-flutter, given the difficulty in differentiating the two. While these may just be more organized versions of atrial fibrillation (i.e. Type I atrial fibrillation), in some cases there might be a dual rhythm (a.k.a. a dissimilar atrial rhythm) where there is flutter/macro-reentry in one atrium and fibrillation in another. 

Source: http://dx.doi.org/10.1016/S1885-5857(07)60047-4 

Example of fibrillo-flutter, where it looks like AFL but there are slight variations in atrial wave morphology and irregularly irregular RR intervals suggestive of AF. 

Relationship between atrial fibrillation and sinus node dysfunction

AF is also related to other atrial electrical disorders such as sinus node dysfunction (SND) and inter/intra-atrial conduction blocks (IAB).

Source: https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.116.018011

These conditions (AF, SND, and IAB) often coexist in the same patients. While the exact mechanisms are unclear, there are a few possibilities: 

Clinically, an ECG finding resulting from the coexistence of SND and AF is tachycardia-bradycardia syndrome. This involves someone going sporadically from a bradycardic rhythm (associated with SND) to a tachycardic rhythm (associated with AF in this case, but can be other atrial arrhythmias as well, such as atrial tachycardia or atrial flutter), and vice-versa.  Again, we can see bradycardia preceding tachycardia (likely associated to lack of overdrive suppression of ectopic foci associated with AF) or tachycardia preceding bradycardia (likely associated with AF causing sinus node overdrive suppression, and potentially presenting with a post-conversion pause). 

Loss of coordinated atrial contraction with atrial fibrillation/flutter

This has two important clinically-relevant impacts: 

Loss of atrial kick: this can lead to reduced cardiac output. In some patients, the atrial kick can contribute up to 20% of cardiac output. Patients who are have preload-dependent left ventricles (for example, those with hypertrophic cardiomyopathy) may especially not tolerate atrial fibrillation well because of the loss of the atrial kick. The high heart rates typically seen in AF also reduce diastolic filling time and can further reduce cardiac output. In patients sensitive to the loss of atrial kick, we may need to consider a therapeutic approach of trying to revert to sinus rhythm and prevent recurrences of AF, rather than slowing the heart rate alone. 

Risk of mural thrombus: given their inability to effectively move blood, the quivering atria in AF tend to increase the risk of stasis of blood inside the atria. Blood stasis is especially pronounced in the auricles of the atria (a.k.a. the atrial appendages), where clots can form along the atrial walls (referred to as "mural thrombi"). These thrombi have a risk of breaking loose and causing systemic embolization, which can lead to several disastrous syndromes (such as stroke, acute limb ischemia, myocardial infarction, organ damage, and so on). The risk of embolization is higher with conversion of atrial fibrillation to sinus rhythm and restitution of atrial pumping function (since atrial contraction comes with a risk of dislodging the mural clots). This is why caution must be exercised when cardioverting patients with atrial fibrillation.   

The Cardinal ECG Features of Atrial Fibrillation 

There are 2 cardinal features of AF that can be helpful in identifying it on ECGs: 

Atrial activity in AF

ECG manifestation of atrial activity in AF involves fibrillatory waves (or "f waves" with a lower-case f). The appearance of these waves can vary from coarse to fine, based on how apparent the deflections are.  

Coarse fibrillatory waves - Notice that they somewhat resemble the sawtooth waves of atrial flutter, but aren't as uniform or regular.

Fine fibrillatory waves: Amplitude of waves <0.05 mV (0.5 mm). Can be easily mistaken as isoelectric baseline with no atrial activity. 

Some important facts about f waves: 

Ventricular activity in AF

In AF, the AV node is continuously being bombarded by the high rate of fibrillatory impulses from the atria. Since the AV node cannot physically accommodate atrioventricular conduction so frequently, a lot of fibrillatory waves are physiologically blocked and do not conduct into the ventricles. Only a small proportion of f waves actually end up causing QRS complexes. The proportion of waves that get through determine the ventricular rate (i.e. the heart rate).  

Because atrial activity is irregular and the AV node may be at a different stage of its refractoriness with each incoming impulse, conduction through the AV node can be irregular. Typically, AF causes irregularly irregular ventricular activation.  

A typical ECG of atrial fibrillation. Notice the coarse f waves in V1 going at about 500 bpm - they resemble flutter but there is a lot of variation in the frequency and morphology of these waves. Additionally, there are no sawtooth waves in the inferior leads, and the ventricular rate is irregularly irregular. 

This is an ECG with fine f waves of low amplitude, as well as an irregularly irregular heart rate. 

Fine and Coarse Atrial Fibrillation 

Fine Atrial Fibrillation

Fine AF presents with f waves of low amplitude (<0.05 mV, or 0.5 mm tall) that may mimic an isoelectric baseline. 

This is an example of fine AF. Looking at lead V1, we can see some small wave-like activity but it is quite inconspicuous. In some leads (such as lead V5) there is no observable atrial activity, and it appears as though the ECG reaches an isoelectric baseline in between QRS complexes. Other findings in this ECG: LBBB, and slow ventricular rate. 

While there is a differential diagnosis for rhythms without apparent p waves like this (i.e. sinus arrest, junctional rhythms, atypical flutter), there are not many that also present with irregularly irregular rates, such as in fine AF. 

Coarse Atrial Fibrillation

Coarse AF presents with f waves of large amplitude (>0.05 mV, or 0.5 mm tall) that may mimic the sawtooth waves of atrial flutter. 

This is an example of coarse AF. Notice that the f waves in V1 appear to be sawtooth-like, but there is great heterogeneity in the appearance of the waves. There's variation in the polarity, amplitude, width, and general contours of adjacent f waves throughout the strip. 

Additionally, the sawtooth-like appearance of the f waves is only really appreciable in lead V1. This is atypical of atrial flutter as well. 

Another example of coarse AF that closely resembles AFL. 

In this example, note that the f waves change polarity near the end of the strip in V1. Also note that the interval between the f waves is fluctuating between 3-4 mm (or 120-160 ms), which translates to atrial rates of between 375-500 bpm - way too fast for AFL! 

Differential Diagnosis of Coarse Atrial Fibrillation

Typical Atrial Fibrillation with variable block 

Compare the above ECGs to typical atrial flutter with variable block (below), where the F waves are much more uniform, and are apparent in several leads. 

If we compare the appearance of F waves in lead II along the entire strip: 

The slight variations in morphology that we do see are because of the superimposed effects of QRS complexes and T waves, which are causing distortions in the contours of the F waves. Accounting for this, there is no significant variation in the appearance of the F waves themselves. 

Atypical flutter with variable conduction

Atypical flutter with variable conduction may pose some diagnostic challenges. While we do see F waves, they might not be apparent in many leads, and they might not be as strictly uniform as typical flutter waves. It might not even be possible to fully differentiate these conditions on the basis of an ECG alone.  

See the example below. Looking at V1, there are clear negative atrial waves that occur at regular intervals at a rate of ~175 bpm (F-F interval is ~346 ms). While the F waves are fairly uniform in this example, there may be some more heterogeneity compared to typical flutter waves. There are also positive F waves in lead II, but are much harder to appreciate. Without close attention to lead V1, this may easily be mistaken for coarse AF.  

Other findings in the ECG above: anterolateral Q waves and ST elevations, left axis deviation.

So what is the difference between atypical AFL and AF if they can produce similar ECG findings?  

That being said, there may be more of a spectrum between atypical AFL and AF, rather than a concrete line in the sand. 

Fibrilloflutter

As mentioned above, fibrilloflutter is a condition that is almost a hybrid of AF and AFL.  

Some rhythms classified as fibrilloflutter may just be more organized versions of coarse AF. However, in some cases there might be a dual rhythm (a.k.a. a dissimilar atrial rhythm) where there is flutter/macro-reentry in one atrium and fibrillation in another. 

In the example above, there are instances where the atrial waves organize and look more like classic sawtooth typical F waves, but other instances where the appearance changes and appears more like fibrillatory waves (even when accounting for the distorting effects of superimposed QRS complexes and T waves). This may be because the rhythm is bouncing between AFL and AF, or that both macro-reentry and fibrillatory conduction are coexisting simultaneously. 

Atrial Fibrillation with Rapid Ventricular Rate

 A very commonly-encountered clinical scenario is AF with rapid ventricular rate (i.e. ventricular rate > 100 bpm), also referred to as "rapid AF". Given that the atrial rate in AF is always fast (450-700 bpm), a high ventricular rate would mean faster conduction through the AV node (or conduction through an accessory tract, which is discussed below). Things that can enhance AV nodal conduction velocity include high sympathetic tone (i.e. sepsis, agitation, exercise) and active ischemia. AV nodal conduction is also faster with younger age.

The ECG below is an example of rapid AF with fine f waves and a ventricular rate of roughly 135 bpm. Calculating ventricular rate is best done by counting all the QRS complexes in the 10 second strip and multiplying by 6 to get beats per minute. Deducing the rate by using individual R-R intervals (i.e. in the so-called "300-150-100" rule) is not helpful as the R-R intervals fluctuate from beat-to-beat.

Below is another ECG of rapid AF captured on telemetry strip. There are 36 QRS complexes on this strip. The space between the black dots at the bottom of the strip is 5 big boxes (25 mm) at 25 mm/sec - in other words, the space between the black dots is 1 second. Each big box itself is 200 ms. The total length of the strip is 14.2 seconds. Therefore, the heart rate is 36 beats per 14.2 seconds = 2.535 beats per second. Multiplying by 60, you get an average heart rate of 152 beats per 60 seconds = 152 bpm. 

One of the tricky things with rapid AF is that the irregularity of the QRS complexes may be harder to visually distinguish, especially with faster ventricular rates. Notice how, visually, the QRS complexes look fairly regular in the strip below (except near the end). Careful measurement of R-R intervals will reveal beat-to-beat variations, however. 

The ECG below is another example of fine AF with rapid ventricular rate that looks visually quite regular but on closer inspection demonstrates the classic irregularity of AF. 

Differential Diagnosis of Rapid Atrial Fibrillation

There is a well-known set of conditions that can mimic rapid AF, in the sense that they cause irregularly irregular supraventricular tachycardia. 

Atrial flutter (or Focal Atrial Tachycardia) with Variable Block

AFL (or AT) with variable conduction ratios (and occurring at fast rates) can mimic AF. The key distinguishing factor is the presence of more organized atrial activity (i.e. p waves with atrial tachycardia, or F waves with atrial flutter) as opposed to the fibrillatory waves of AF. 

The ECG below demonstrates AFL with variable block and rapid rate (~102 bpm). Other findings include a bi-fascicular block (RBBB + LAFB) with secondary repolarization abnormalities.  

The regular flutter waves are harder to identify here given the fast heart rate and distorting effects of the QRS complexes and T waves, but this is where they are occurring: 

If required, you can get further diagnostic clarity by administering adenosine to induce a heart block (thereby temporarily eliminating QRS complexes and T waves, as well as their resultant distortions) to observe the underlying atrial activity for flutter waves or p waves. 

Multifocal Atrial Tachycardia (MAT)

MAT is a condition seen in some patients with hyperexcitable atria (classically in critically ill elderly patients with respiratory failure in the context of underlying pulmonary disease). In MAT, multiple foci in the atria can gain abnormal automaticity and compete with each other to pace the atria. There's a chaotic and unpredictable nature to atrial depolarization in this situation. That being said, atrial activation still occurs in an organized, 1:1 fashion with no fibrillatory conduction. Unlike AFL, MAT doesn't rely on a macroreentrant circuit either, so there is adequate opportunity for atrial recovery in between p waves. The combination of these factors means that MAT doesn't carry the same risk of intramural thrombus and systemic thromboembolization as AFL and AF. 

The ECG representation is as follows: 

Source: https://litfl.com/wp-content/uploads/2018/08/Multifocal-Atrial-Tachycardia-MAT-COPD-2-1024x518.jpg

Sinus Tachycardia with Premature Complexes 

Sometimes, even a sinus tachycardia might look irregular if there are multiple premature complexes (i.e. PACs or PJCs) scattered about adding irregularities. This is worsened by any underlying sinus arrhythmias. 

Below is an ECG of sinus tachycardia with several PACs (going at a rate of 162 bpm) causing an irregularly irregular rhythm confused for AF.   

Although this rhythm looks like a mess, we can recognize many p waves preceding the QRS complexes. 

The sinus p waves are delineated by the green arrows, and the ectopic p waves (PACs) are delineated by the red arrows. Note that there is a high density of PACs here, with multiple morphologies. Many of the ectopic p waves are difficult to identify given the fast heart rate and distortions introduced by the T waves. That being said, there is a dominant underlying sinus rhythm here too. 

Sometimes it is difficult to distinguish these rhythms from MAT. There are actually PACs of >3 morphologies, so the short run of 6 PACs near the beginning of the strip could technically count as a short run of MAT. However, given that there is a dominant sinus rhythm, it may be more appropriate to qualify this as sinus tachycardia with frequent multifocal PACs, rather than MAT (where we presume that there is a lack of a stable underlying sinus impulse). 

This ECG can be hard to distinguish from rapid AF, especially if those p waves weren't identified. In this case, the patient actually had a massive pulmonary embolism, and were inappropriately given IV calcium channel blockers due to misinterpretation of the rhythm as rapid AF. This led to hemodynamic decompensation with hypotension requiring shock management. This case underscores the importance of accurate rhythm diagnosis. 

Atrial Fibrillation with Slow Ventricular Rate

Another commonly encountered rhythm is AF with slow ventricular rate (<60 bpm), also referred to as "slow AF". Again, given that the atrial rate in AF is very fast, having a slow rate means essentially having slower conduction through the AV node. Slow AF can be thought of as AF with a second-degree AV block (although in the absence of PR intervals, it's difficult to differentiate from intranodal versus infranodal blocks - more on this later).

The ECG below demonstrates slow, coarse AF at a rate of ~40 bpm. There is also a non-specific intraventricular conduction delay with a left axis deviation. 

The ECG below demonstrates slow, coarse AF at a rate of ~60 bpm.  

Although the atrial activity does look like flutter waves in V1, there are a few factors that separate this from flutter: 

Regularized Atrial Fibrillation

Regularized AF is a subtype of AF characterized by regular R-R intervals, in contrast to the "irregularly irregular" QRS complexes normally seen with AF. This occurs in the context of AV dissociation, where the atrial waves are unable to conduct into the ventricles, and instead a regular rhythm from an ectopic focus takes over. This often occurs when complete AV blocks occurs alongside AF, with a regular rhythm from either a junctional or ventricular escape rhythm. This can also occur in the context of AF with a tachyarrhythmia from a lower focus (i.e. junctional tachycardia, JT, or ventricular tachycardia, VT, with AV dissociation). That being said, "regularized AF" typically refers to slow AF with a complete heart block, rather than AV dissociation with JT or VT.

The ECG below shows fine AF with complete heart block and a narrow, regular junctional escape rhythm at a rate of 42 bpm. 

The ECG below shows coarse AF with complete heart block and a wide complex escape rhythm at a rate of 48 bpm. While this could be a ventricular escape, it is rather fast for a ventricular escape rhythm.  

The differential diagnosis could include a junctional escape rhythm with aberrant conduction due to conduction blocks. Notice that the QRS complexes have a typical right bundle branch block (RBBB) morphology with a left axis deviation suggestive of left anterior fascicular block (LAFB). This combination is known as a bifascicular block. 

The same patient later devolved into a slower but similar escape rhythm at a rate of 30 bpm. We can see that the axis deviation is maintained and the QRS morphologies are fairly similar (except for the wider R wave in V6 in the ECG below, even after accounting for the significant amount of artefactual changes). This makes me believe that this is likely a ventricular escape rhythm. 

Differential diagnosis of regularized AF 

AF with Paced Rhythm

 Below is a rhythm strip of AF with complete heart block and a regular wide-complex rhythm due to an external pacemaker. There are subtle pacing spikes preceding each QRS complex, delineated by the green arrows in the picture below. 

In the same patient above, the external pacemaker was intentionally turned off temporarily to measure the patient's intrinsic rhythm. You can see a long pause corresponding to complete heart block with underlying AF (recognizable due to the fibrillatory waves) and insufficiency of the ventricular escape pacemakers. The pacemaker is eventually turned back on. As the amperage of the pacemaker is increased, the pacing spikes become more apparent. There is one intrinsic ventricular beat (a PVC labelled "V") amidst all the paced beats (labelled "P").  

Below is another ECG of a different patient with underlying atrial fibrillation and a transvenous pacemaker. Notice the widely visible fibrillatory waves in this case. 

Sinus Arrest with Junctional or Ventricular Escape Rhythm

Since there are no perceivable p waves in sinus arrest as well, it's easy to confuse sinus arrest for fine atrial fibrillation. Combine this with a regular escape rhythm and it becomes hard to electrocardiographically differentiate from regularized AF without additional contextual clues (i.e. visible fibrillatory waves, other ECGs, or past medical history). 

Notice the ECG below, which looks very similar to regularized AF with a junctional escape rhythm. There even appear to be fibrillatory waves in V1. The only issue is that this particular patient never had a history of atrial fibrillation. 

So how do you tell the difference between sinus arrest with an escape rhythm or regularized AF? There were several clues in this case, which required closer analysis. 

Inspecting the ECG more closely, you can see that the 3rd QRS complex in this strip does not occur at a regular interval - in fact, it appears to arrive a little earlier than anticipated.  

Whenever there's any irregularity in a rhythm strip, it should raise suspicion of atrioventricular conduction (i.e. not necessarily a complete heart block), because escape rhythms should be regular.  

Examining closely, there appears to be a deflection prior to the early-arriving QRS complex that looks like a p wave, which is not apparent before any of the other QRS complexes. This may be either a sinus or non-sinus p wave (i.e. a PAC). 

Examining in the other leads, there appears to be a subtle negative deflection in leads aVF and aVR corresponding to this p wave. Since the p wave is negative in aVF, it is likely non-sinus, and moreso consistent with a PAC. 

So, if this is a sinus arrest with junctional escape rhythm, how would the atria be activated? Typically, with junctional rhythms, you would except to see retrograde atrial activation with associated retrograde p waves. On closer inspection again, we can see retrograde p waves closely following the QRS complexes of the presumed junctional escape beats.

The red arrows above point towards the retrograde p waves, which can be appreciated in several leads. The fact that these p waves are negative in II and aVF are suggestive of retrograde p waves. The only QRS complex not associated with a retrograde p wave is the one that appears to be activated via an anterograde fashion from the PAC. This makes sense as this is NOT one of the junctional escape beats. 

So, while the ECG appears to be regularized AF, it seems to be more consistent with sinus arrest with a junctional escape rhythm causing retrograde atrial activation + a single conducted PAC.  

This diagnosis is more apparent by examining the telemetry strip for the same patient, done at a later time: 

Labelling the relevant aspects: 

You can hopefully appreciate retrograde p waves preceding the QRS complexes. This time they occur before the QRS complexes, suggesting a high AV nodal escape rhythm (more on this later). The differential diagnosis is a low atrial ectopic rhythm. There is one conducted sinus beat near the end of the strip. The p waves rule out atrial fibrillation, which is further evidenced by the lack of fibrillatory waves when examining V1. 

The hardest part of this entire analysis is identifying the retrograde p waves, because they are very subtle in this case. On a single strip, analyzing the contours of the ECG right before the QRS is important. In the QRS complexes following a sinus p wave, this part is flat/isoelectric, whereas in the QRS complexes that appear to be junctional escape beats, there is an upgoing contour immediately preceding the QRS complex suggestive of a retrograde p wave. 

A: Junctional escape beat, with upgoing contour immediately preceding the QRS complex, suggestive of a negative retrograde p wave. 

B: The first beat is a junctional escape beat with a retrograde p wave before it. The second beat here is a sinus beat, with a flat isoelectric contour following the p wave but immediately before the QRS complex. 

The retrograde p waves are more apparent on some strips as opposed to others. This is why examining the telemetry closely is important in diagnosing complex rhythms such as this one. 

The patient had symptomatic fatigue and shortness of breath with this bradycardia. Whether or not this was regularized AF or sinus arrest with a junctional escape, the patient would have still required an implantable pacemaker. However, without a diagnosis of AF, there would not be a need for long-term anticoagulation, removing the need for an unnecessary medication and unnecessary bleeding risk. That being said, recall that patients with sinus node dysfunction may have an increased risk of AF, so this patient may at some point develop AF if he already hasn't. 

Atrial Fibrillation with Ashman's Phenomenon 

Ashman's phenomenon is a normal, physiologic situation whereby the QRS complex at the end of a long-short cycle is aberrantly conducted, usually with a RBBB morphology. 

Given that AF is an irregularly irregular rhythm, there are many potential instances where such long-short cycles can occur and give rise to an aberrant beat. 

There is a principle known as action potential restitution, whereby the duration of the action potential for any given heart beat is dependent on the diastolic interval of the preceding heart beat.  

A few concepts to understand before the Ashman's phenomenon makes sense: 

Aside from action potential restitution, it's important to know that all parts of the ventricles don't repolarize at the same rate. In fact, the bundle branches tend to recover slowly and the right bundle branch, in particular, recovers slowest in most people. 

Even after the end of the T wave, which signifies the end of repolarization for the ventricular myocardium, the RBBB may still be refractory. 

If another QRS complex were to try to be conducted at the point where the ventricular muscle itself has recovered but the RBBB is still refractory, you end up with an aberrant beat that has a RBBB morphology. Similarly, in patients in whom the left bundle branch recovers slowest, they might see aberrant conduction with a LBBB morphology. 

Therefore, in Ashman's phenomenon, the following typically happens: 

Above is an ECG of AF with the 12th beat being aberrantly conducted with a RBBB due to Ashman's phenomenon. 

Differential Diagnosis of Atrial Fibrillation with Ashman's Phenomenon 

Atrial Fibrillation with a PVC

The main differential diagnosis for Ashman's phenomenon in AF is a wide QRS complex due to a premature ventricular complex (PVC). 

Note that the 6th beat in the ECG above is a ventricular beat (PVC). This differs from Ashman's phenomenon in several ways: 

Below is an ECG that actually demonstrates both the Ashman's phenomenon and a PVC on the same ECG: 

This is an ECG of someone with slow, coarse AF with non-specific intraventricular conduction delay. The 6th QRS complex follows a long-short cycle and has a typical appearance of RBBB (delayed positive terminal deflection in V1 and slurred S wave in V5) with a likely preserved QRS axis (notice that the QRS is still negative in lead II). The last QRS complex is a PVC. Although it also follows a long-short cycle, and while there is a delayed positive terminal deflection in V1, there is also a change in QRS axis (now positive in lead II), with a positive R wave in V6 without an S wave. In fact, although we only see the QRS complex in the precordial leads V1, V4, V5, and V6, this may actually be an example of positive precordial concordance, which is a feature of ventricular rhythms. 

Clinically-speaking, differentiating between Ashman's phenomenon and PVC is not usually of importance. It's mostly for academic interest. 

Atrial Fibrillation with Bundle Branch Block

Bundle branch blocks can cause wide QRS complexes with AF. Unlike other supraventricular tachycardias conducted aberrantly, however, the irregularity of AF helps distinguish it from monomorphic VT, which tends to be fairly regular. 

Below is an ECG is rapid, fine AF with LBBB. There is also a left axis deviation. 

Below is an ECG of rapid, coarse AF with RBBB.

Differential Diagnosis of Atrial Fibrillation with Bundle Branch Blocks 

Other irregularly irregular supraventricular tachyarrhythmias with conduction aberrancy 

The main differential diagnosis for AF with bundle branch blocks is one of the other irregularly irregular supraventricular tachyarrhythmias (i.e., AFL with variable block, AT with variable block, MAT, etc.) with bundle branch blocks. 

AF with Wolff-Parkinson-White syndrome 

More on this below, but AF with Wolff-Parkinson-White syndrome (a.k.a. "pre-excited AF") can also cause AF with wide QRS. Importantly, however, the QRS complexes don't typically fit a typical bundle branch block morphology. 

Ventricular tachycardia 

Wide complex tachycardias should always raise concern for VT. In most cases, an irregular wide-complex rhythm with monomorphic QRS complexes (i.e. all the QRS complexes look identical) would rule out VT and be more indicative of AF conducted with some sort of abnormality (i.e. toxin/electrolyte issue causing QRS-widening, bundle branch blocks, accessory pathways, etc.). However, in some cases, VT can present with a small degree of irregularity which can be confused for AF. 

The ECG above is slightly irregular, and does somewhat resemble a RBBB morphology with a mostly positive QRS complex in lead V1 and a slurred S wave in V6.  

However, there are a few factors that can help differentiate this from AF, which are shown below: 

As you can see above, there are several factors that help distinguish this rhythm from AF: 

A-Fibrillation & Wolff-Parkinson-White syndrome

AF with WPWS, also known as "pre-excited AF", is an uncommon manifestation of AF.  

WPWS is a condition associated with the presence of an anatomic accessory tract that can provide an alternate route of signal conduction from the atria to the ventricles, and vice-versa, separate from the AV node. Because of this additional pathway for atrioventricular conduction, patients with WPWS tend to be prone to several tachyarrhythmias (such as orthodromic and antidromic AVRT, and pre-excited atrial tachyarrhythmias). More on this in the [WPWS section].  

The accessory tract does not have the same protective property as the AV node [link to physiology section]. The long refractory period of the AV node can cause a "physiologic block" that prevents a large majority of the atrial waves in AF from conducting to the ventricles. Moreover, the "decremental conduction" property of the AV node makes it worse at conducting impulses the more frequently it is stimulated. This effectively adds another layer of protection to prevent rapid atrial tachyarrhythmias from being conducted in a 1:1 fashion to the ventricles, protecting the ventricles from some of those impulses. 

[Image needs to be re-done] 

The accessory tract provides another pathway for atrial waves to reach the ventricles, and usually conducts faster than the AV node. This allows a small degree of ventricular activation via "leakage" through the accessory tract before the AV node has a chance to rapidly activate the ventricles via the His-Purkinje system. This phenomenon is known as pre-excitation, and it causes a slurred initial portion of the QRS complex known as the delta wave. 

The problem with the accessory tract is, since it does not express decremental conduction to the same degree as the AV node, it can effectively conduct a higher proportion of atrial waves in AF to the ventricles, causing a dramatically fast heart rate and unstable tachycardia. This is made worse if the AV node is further blocked (i.e. using beta blockers, adenosine, or calcium channel blockers), since this means all atrial impulses are forced to funnel through the accessory tract, which can lead to further increases in the rate of atrioventricular conduction (i.e. >300 bpm). The rapid activation of the ventricles can give rise to fibrillatory conduction in the ventricles, which would cause ventricular fibrillation (similar to how rapid firing in the atria can cause AF). This is why AV nodal blocking agents should be avoided in patients with pre-excited AF. 

On the ECG, pre-excited AF has a few properties: 

The amount of ventricular mass that gets pre-excited depends on how quickly or slowly the accessory tract conducts. A rapidly-conducting accessory tract will lead to earlier pre-excitation and a wider delta wave, whereas a slowly-conducting accessory tract leads to later pre-excitation and a narrower delta wave. For accessory tracts with sufficiently long action potential durations, as they get stimulated more rapidly, they tend to be more refractory and conduct slower.  

On an ECG, as the R-R intervals get narrower (more rapid stimulation of the accessory tracts), so does the delta wave (slower accessory tract conduction and less pre-excitation). This phenomenon is known as the concertina effect. The concertina is a type of accordion, wherein the pleats get wider as the bellows get pulled apart and the space between the pleats increase. Conversely, as the bellows are pushed together and the space between the pleats decreases, the pleats themselves get narrower. 

The ECG below is an example of pre-excited AF in a patient with WPWS. Notice that very rapid heart rate (282 bpm) occurring in an irregularly irregular manner with wide QRS complexes.  

Below is another ECG of AF with WPWS at 192 bpm.  

Notice the Concertina effect and variable QRS width/delta wave presence, easily visible in leads V1-V3: 

Notice that the delta waves are narrower following shorter R-R intervals, and wider following longer R-R intervals. 

Differential Diagnosis of Pre-Excited Atrial Fibrillation

Polymorphic Ventricular Tachycardia (PMVT)/Torsades de Pointes (TdP)

The rapid, irregular, and wide complex nature of pre-excited AF (along with the concertina effect and changing QRS morphologies) can make it difficult to differentiate from PMVT and TdP.  

Take, for example, the ECG of pre-excited AF below: 

Source: https://litfl.com/atrial-fibrillation-in-pre-excitation/

Note the similarity to the ECG below, of a patient going into a short run of TdP: 

Source: https://litfl.com/polymorphic-vt-and-torsades-de-pointes-tdp/ 

The main difference between the two rhythms is that PMVT and TdP are typically associated with changing QRS axes (which, in individual leads, looks like constantly changing QRS amplitudes and morphologies). While the width of QRS complexes may change from beat-to-beat in pre-excited AF (due to the concertina effect), the amplitudes should generally stay preserved.  

Below you will see pre-excited AF where the QRS amplitudes and axis preserved.

Below you see Torsades de pointes with gradually shifting QRS axis and changing QRS amplitudes as a result.