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Dr A Röschl's picture

VENTRICULAR TACHYCARDIA, ATRIAL FIBRILLATION AND ABERRANT CONDUCTION

It is not uncommon for several different abnormal changes to occur simultaneously in an ECG, as in this Holter ECG strip. The explanation of the visible ECG changes can be found in the 2nd image

Dr A Röschl's picture

ATRIAL FIBRILLATION

Unfortunately, I can't remember who the author of this ECG is. Perhaps he/she will get in touch with me. However, the ECG is very nice (despite the less than optimal recording quality) and that's why I want to post it. I don't know the history.
In the first section of the ECG we see coarse fibrillation waves and QRS complexes with very different RR intervals, which is why this is atrial fibrillation. It is not atrial flutter because the fibrillation waves are of different size and polarity (depending on the lead) and the intervals between the atrial actions are irregular.

Dr A Röschl's picture

Atrial Fibrillation With Rate-related Left Bundle Branch Block

For a better overview, the leads aVL and V2-V4 are not shown in this ECG. The basic rhythm is atrial fibrillation (no P waves or flutter waves visible, but fibrillation waves). When the conduction rate drops, the QRS complexes are narrow. Faster conduction results in wide QRS complexes with LBBB morphology. This is an example of phase 3 (acceleration dependant) LBBB.

Dr A Röschl's picture

Atrial Flutter Degenerates Into Atrial Fibrillation

Atrial flutter and atrial fibrillation are two different cardiac arrhythmias, but occur frequently side by side in the same patient. Here is an example of how atrial flutter degenerataes into atrial fibrillation. The initially ordered atrial activity (left in the picture) with 2 flutter waves/1 QRS complex changes into irregular atrial activity (right in the picture) and the RR intervals become completely irregular.

Dr A Röschl's picture

SMART WATCH ECG

Many people are considerably unsettled by ECG recordings from smart watches. However, smartwatch ECGs can be helpful in the diagnosis of paroxysmal atrial fibrillation. Here. you can see an example. It is a 1-channel ECG that corresponds to lead I. Initially there is an irregular fast pulse without P waves, which corresponds to a tachyarrhythmia in atrial fibrillation. At the end of the first line, after a very short pause, there is sinus rhythm. In the third line you see a short SVT over 3 beats, then SR again. The QRS complex is widened to over 120 ms.

Dawn's picture

Atrial Fibrillation With Aberrant Conduction in Adolescent Patient

The Patient:  This ECG was taken from a 14-year-old girl with a complaint of palpitations.  Her medical history is not known.

The ECG:  The rate is about 160 bpm, with an irregularly-irregular rhythm.  There are no P waves.  This is atrial fibrillation.  There are several different morphologies noted in the QRS complexes.  First, a narrow QRS with normal axis, as demonstrated in beats #5 and #7.  There are distinctly wide QRS complexes with a right bundle branch block pattern.  See beats #2, #3, and #19.  This represents aberrant conduction.  Atrial fib often displays aberrant conduction, especially when a beat follows closely after a long R-R cycle followed by a short R-R cycle. The refractory period is set by the preceding cycle.  So a lont R-R causes a longer refractory period.  The short R-R that follows finds itself in a relative refractory period - not refractory enough to prevent conduction altogether, but in this case, the right bundle branch has not yet recovered, so the impulse continues down the left bundle, bypassing the right bundle branch.  The right ventricle depolarizes late, causing a widening of the QRS.

There is a sliight variation seen in the aberrant beats, notably in #1 and #2.  This may represent varying amounts of aberrancy, where the pathways change slightly from beat to beat.  Atrial fibrillation is rare in children and adolescents, but can be caused by many factors, including stress, caffeine, endocrine disorders, obesity, and heart infections.  

This ECG was published by me on Facebook nearly a decade ago, and received some excellent comments from Dave Richley and Dr. Ken Grauer (two of our favorite Gurus).  I will reproduce them here to spare them re-writing their comments.

Dawn's picture

Inferior Wall, Posterior Wall, and Right Ventricular M.I.

The patient:    79-year-old man complaining of severe “burning” chest pain, radiating to his neck. Walking exacerbates his discomfort.  He has had nausea and vomiting for 24 hours. Past medical Hx includes high cholesterol and atrial fibrillation. Medications not known.

 

The ECGs:  These ECGs could be called “classic”.  There is a 100% occlusion of the right coronary artery (RCA), which was successfully repaired in the cath lab.  About 80% of inferior wall M.I.s are due to occlusion of the right coronary artery.  Depending on how proximal the occlusion is, we can expect a pattern on the ECG representing injury to all areas supplied by the RCA.  This “package deal” can include:

·         Inferior wall ST elevation.

·         Posterior wall extension.

Dawn's picture

Atrial fibrillation and Type 2 M.I.

The Patient:     This excellent teaching case was donated to the ECG Guru by our friend, Sebastian Garay (who is an ECG Guru himself).  It was taken from a 33-year-old man who was complaining of chest pain and palpitations. He reported a similar episode about six months prior, but failed to follow up with cardiology. Was told by his medical care provider that he had atrial fib.

The ECG:      We are able in this case to provide a 12-lead ECG with each lead recorded for the entire width of the paper. This has the advantage of producing twelve ten-second rhythm strips.  Page one contains the limb leads, and page two shows us the precordial leads.

The rhythm is atrial fibrillation, with a heart rate of 133 bpm and an irregularly irregular rhythm. The QRS axis is extreme left at about -75 degrees.  This has caused Leads II, III, and aVF to be negatively deflected, and aVR and aVL to be positive. Lead I is biphasic, low voltage, and mostly positive, indicating that the axis travels almost perpendicular to Lead I, but slightly toward it.

The machine mistakenly gives us a reading for PR interval and P wave axis, even though there are no P waves.  The QRS is on the wide side without being abnormal at .10 seconds (100 ms). The QTc is within normal limits, although it might be considered “borderline”, with 431-450 usually considered borderline.

Dawn's picture

Inferior Wall M.I. With Atrial Fibrillation

The Patient   This ECG was obtained from a 74-year-old man who had a history of COPD. He was complaining of severe chest pain at the time of the ECG.

The ECG     The rhythm is atrial fib or flutter (the R to R intervals are irregular, but seem to repeat about 4 interals).  Flutter waves are seen during some of the longer intervals. The rate is approximately 90 beats per minute.  The ST segments are very noticeably elevated in Leads II, III, and aVF.  There is reciprocal ST depression in Leads I and aVL, and also in all the precordial leads. 

Dawn's picture

ECG Basics: Onset of Atrial Fibrillation

This strip shows the onset of atrial fibrillation.  A fib can be "paroxysmal," meaning that it has a sudden onset, but then stops spontaneously, usually within 24 hours to a week.  A fib can also be classified as "persistent", meaninging that the a fib lasts more than a week.  It can stop spontaneously, or be halted with medical treatment.  "Permanent" a fib is a fib that is resistent to treatment.  

The first three beats in this strip represent sinus rhythm at 75 beats per minute.  At the onset of atrial fibrillation with beat number four, the rhythm becomes irregularly irregular, and the rate is around 140-150 bpm. We can expect new-onset a fib to have a fast ventricular rate, as the atria are sending hundreds of impulses to the AV node every minute. The AV node will conduct as many of those impulses as it can to the ventricles.  Most AV nodes can easily transmit 130-160 bpm.  In a fib, the atria are quivering, not contracting. Because of this fibrillation of the atrial muscle, a fib has no P waves, and therefore, no "atrial kick".  The contribution of the atria to cardiac output (25-30%) is lost. An extremely fast rate can also lower output and overwork the heart, so one treatment goal for a fib is to lower the rate.  This can be done independently of attempts to convert the rhythm.

During a fib, blood clots can form in parts of the atria, especially the left atrial appendage.  If sinus rhythm is restored after these thrombi form, they can embolize and travel to the brain, causing stroke.  Before electively converting atrial fib to a sinus rhythm, the patient may need to be anticoagulated.

 

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