Happy birthday, ECGBlog!

Happy birthday, folks!

It’s been a year since I created The ECG Blog, imagine that. I first started it because I needed a place where I could share my interest for ECG interpretation with others. I wanted to meet and discuss with people, to learn and be inspired. All of this and even more has come become true, so it´s been a great year. I could never have done this without you, my readers, so to all of you: I’m truly grateful to all of you for visiting and commenting! Thanks a lot!

A lot of things has happened during this first year in the blogosphere . It has been very rewarding, as it keeps me inspired in my own profession as an ER nurse (now specializing to become an ICU nurse, which in Norway requires 1.5 years at the university in addition to a nursing bachelor). I’ve also collected nearly 600 12 lead ECGs, bought 26 books about ECG interpretation and met a lot of inspiring people! One of those people is Tom Bouthillet over at the excellent Prehospital 12 Lead ECG blog. His knowledge on ECG interpretation, his tutorials and case presentations is simply amazing. Check him out! And while you’re at it, there is also The EKG Club, a Yahoo! discussion group open to everyone who likes discussing ECG. It’s a really friendly and great group, with more than 800 members and all kinds of health care professionals.

And then, in April I was contacted by the renowned Electrophysiology Lab Digest, who gave me the opportunity to present myself and The ECG Blog both online and in their printed magazine. And even more happened: Just a couple of months ago, I was lucky enough to be contacted by Billy Hurd at Pace Symposia. They are developing what is looking to be one of the possibly greatest ECG rhythm simulators on the market. I’ve been lucky enough to test it for them, and I wrote a short review of it here. Tom B. (above) wrote a better and more thorough review of it at his blog. The simulator can be downloaded as a free 24-hr trial version here.

Stats are always fun (I think), and I’d like to share with you the stats for this blog. After all, you created them!

Total stats in numbers

Visitors per month

Numbers months and days

Most popular posts

Last, but not least, I really would like your opinions on how to improve this blog. Any criticism or comments that are constructive are welcome! Anything you’re missing? What do you like and what not? Other ideas? Bring ‘em on! Help me make this site better and bigger!

Happy birthday!

-klaus

Adams-Stokes / Complete (Third Degree) Atrioventricular Block

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Patient: 75 y/o male. Medical history and anamnesis unknown. Experienced several Adams-Stokes episodes and his wife called EMS. This is a prehospital 12 lead from the LP12.

ECG description:

• No P-QRS relationship. Independent pacemakers.
• Atrial rate is 125 bpm. Ventricular rate is close to zero.
• No escape rhythm present
• P axis is normal at 60 degrees

Discussion:

This is ventricular standstill. The underlying rhythm is sinus tachycardia at 125 bpm, but there is complete failure of the impulses to reach the ventricles. The first QRS complex is of junctional origin, the second is from the ventricles, probably the right ventricle. Unfortunately, this 6 second recording does not tell whether this is an escape rhythm or just single beats.

Sinus Rhythm evolving into PEA and Asystole

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Patient: n/a

ECG discussion: The top strip starts with sinus rhythm at ca. 75 bpm. Note that this generates a mean arterial pressure (MAP) of only 18 mmHg. A marked horizontal ST depression is also seen, which correlates with the pleth signal showing SpO2 of 74%. After 8 beats, there is no visible sinus activity any longer. No junctional escape rhythm is initiated, which indicates that the atrioventricular junction is also poorly perfused and suffering. The following beats are wide and slow, at only 35 bpm. Even though they resemble a ventricular/Purkinje escape rhythm by their morphology and regularity, this electrical activity is not able to create myocardial contraction. In the second strip, MAP is 13 and flatlined. This is explained electrophysiologically as electromechanical dissociation (EMD), which is similar to the term pulseless electrical activity (PEA).

The final (bottom) strip shows how the electrical activity ceases. Although mechanical asystole probably has happened already (hard to say without echocardiography), electric asystole has now also occured. Note that at the end of the strip the pleth wave is also flat.

Second Degree AV Block Mobitz 1; Wenckebach with 4:3 conduction + Ventricular and Junctional Escape Beats

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Patient/anamnesis: n/a

ECG interpretation/discussion: This ECG is a printout from a telemetry station, derived from a 5 lead patient monitoring.  So, what have we here? The underlying rhythm is sinoatrial, but both PR and RR interval varies. Remember, Wenckebach is not the name of a certain type of block, but rather a type of conduction. This is often misunderstood, as Second Degree AV Block Type 1 or Mobitz 1 is also often labelled Wenckebach block. A more precise term would be Wenckebach periodity, phenomenon, conduction. Wenckebach conduction is usually considered benign and can be recognized by the following criteria:

1) PR interval is progressively prolonged until a P wave is blocked

2) The shortest PR interval is the one immediately following the dropped beat. The longest PR interval is the one immediately before the dropped beat. The incremental change in PR interval is in the beginning of the Wenckebach cycle, thus between the first and second PR interval in a sequence.

3) The RR intervals progressively shorten until a QRS is ‘dropped’ due to the non-conducted atrial/sinoatrial impulse.

Now, looking at this ECG, the two first beats are at the end of a Wenckebach cycle. After the second QRS a non-conducted P wave occurs. The following beat is wide and bizarre and is a ventricular escape beat that occurs due to the long preceding pause. After the escape beat, a new Wenckebach cycle starts. The PR interval lengthens until a P wave is blocked. After this pause, a narrow QRS is preceded by a P wave with a very, very short PR interval. This is a junctional escape beat. Then, the Wenckebach cycle restarts.

When counting P waves and QRS complexes in the cycles, we’ll see that for every three QRS complexes there are four P waves, since one of the QRS complexes gets dropped repeatedly. This gives a 4:3 atrioventricular (AV) ratio, which is also called 4:3 conduction.

What a beauty! Thanks to my colleague and fellow ECG-dork for bringing me this rare gem!

Pace Symposia’s ECG simulator – as close to real as it gets

Courtesy of Pace Symposia

Dear readers and fellow ECG enthusiasts.

The strict purpose of The ECG Blog is to discuss and educate ECG interpretation. I want to maintain a serious profile, so therefore every blog post has been a clear cut case presentation. Today however, I’ve decided to make an exception to be able to share some good news with you. The good news is that a US based company called Pace Symposia, has developed a fantastic ECG rhythm simulator. Rest assured, this is not an announcement that I’m paid to do. The only reason I want to advertise this product is because it’s an invaluable and powerful tool for learning arrhythmia recognition and interpretation. Additionally it is incredibly fun, as well as it looks and feels better than any other rhythm sim I’ve tried. And I’ve tried a few.

The cardiac rhythm simulator from Pace Symposia has a very clean, stylish and most importantly intuitive and simple user interface. It’s got a wide range of arrhythmias that can be inititated by a simple mouse click. The user can also add a variety of ectopic activity such as PVC’s and PAC’s, both unifocal and multifocal. Everything happens in real time with very realistic morphology. Just like when a real life patient is hooked up to your telemetry screen or ECG monitor, the arrhythmia shifts dynamically and seamlessly between different rates, conduction ratios and morphologic changes.

Pace Symposia has set up a website for the sim at ecgsimulator.net, where you can try an online flash based version and download a fully functional free trial version. The simulator is now 1.0, but they are working on a revised version and believe me – it’s going to be awesome.

This is really a milestone for cardiac rhythm simulators, which is why I want my readers to be aware of it. This is such excellent work from Pace Symposia that I felt the need to show my support and spread the word.

Post update 3. Oct: Tom Bouthillet over at the very excellent Prehospital 12 Lead ECG blog has posted a much more thorough review of this simulator. Check it out, and while you’re at it be sure to check his other posts, tutorials and case studies.

Atrial Bigeminy and Premature Ventricular Contraction

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Patient: n/a

ECG description:

• Sinus tachycardia
• Supraventricular bigemeny
• One premature ventricular contraction

Discussion:

There is a baseline sinus tachycardia with a PR interval of 130ms, regularly interrupted by premature atrial contractions (PAC). Each PAC depolarizes the atria and resets the SA node, causing a change in automaticity and a noncompensatory extrasystolic pause. Judging by the PR interval as well as P axis and morphology of the premature beats, the ectopic pacemaker is atrial. The ectopic PR interval is 130ms, and it is plausible to think that the ectopic pacemaker is located near the SA node. The P wave axis is ca. 30 degrees, and the ectopic P wave axis is ca. 60 degrees, which means that the atria are depolarized anterogradely and in almost the same direction as from the SA node. QRS axis and morphology is slightly different in the QRS complex following the first premature beat and the second and third. Looking closely, we can see that P wave axis and morphology slightly differs from the first PAC to the next two. The PR interval however is the same. This could be due to multifocality, but since the PR interval is quite similar, the two foci must be very close to each other. After the third bigeminal beat, a broad QRS occurs. In spite of the aberrantly looking RBBB-like morphology, this is most likely a premature ventricular contraction (PVC). If this was aberrancy, it would be due a refractory right bundle branch that couldn’t cope with the rapid changes in automaticity caused by the PAC’s. However, the coupling interval before the broad complex is similar to the other coupling intervals, and this demonstrates that the RBB in fact handles the rapid changes in automaticity quite well. In the precordial leads, we can see a P wave following the PVC, suggesting that the atrias have been depolarized retrogradely from the PVC.

Sinus Arrest With Atrial Escape

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Patient: Woman, 55 y/o, using metoprolol. Diabetes Mellitus II, angina pectoris, adipositas. Admitted with general weakness and fatigue, dehydration and dyspnea. Blood pressure is 100/55. No signs of infection.

ECG description:

• Sinus rhythm with sinus arrest
• Axis within the normal quadrant, at ca. 0 degrees
• Poor R wave progression
• Low amplitude in limb leads
• Baseline artefact from patient movement
• T wave flat/inverted in I, aVL

Discussion: After two sinus beats, a two second atrioventricular asystole occurs, which is then terminated by atrial escape. By comparing the escape P wave with the P waves of the three sinus cycles (the two first and the very last on the ecg), we can see that both P wave morphology, axis and PR interval varies slightly. The PR interval in the sinus cycles is 170 ms, while the escape PR interval is 150 ms. This could indicate that the escape pacemaker is atrial ectopic, but is located in the near vicinity of the sinoatrial node. The sinus pause is longer than, but not a multiple of the normal interval, so this is most likely no SA block. There are also no signs of blocked atrial impulses or reciprocating impulses causing the pause. These observations are important to make, as sinus arrest is often confused with SA block and other mechanisms.

Dysrhythmia during hemodialysis

Arrhythmias frequently occur in patients undergoing hemodialysis. Shinichi, et al. (American Heart Journal, Vol. 131, Issue 6, 1996:1137-1144) reports that out of 221 patients receiving hemodialysis, a total of 65% (143 pts) had ECG abnormalities, excluding sinus tachycardia and sinus bradycardia. The study looks at ECG abnormalities, not only arrhythmias, and left ventricular hypertrophy has the highest prevalence in the sample group. This was followed by ventricular and supraventricular premature contractions, myocardial ischemia and nonspecific ST-T changes. Additionally, a wide range of other arrhythmias and electrocardiographic abnormalities were seen in the patients. The study discusses probable causes for the rather high prevalence of cardiac disorders and arrhythmias among these patients, but is not fully conclusive in it’s outcome. It points at although arrhythmias commonly appear during hemodialysis, the rather large (65%) prevalence is partly due to baseline cardiac conditions. The results indicate that a combination of changes in intra- and extracellular K levels, changes in other electrolyte levels such as Mg and Ca, rapid correction of metabolic acidosis and decreases of circulating blood volume, appear to trigger arrhythmias in patients with latent cardiac problems.

This case is from a 70 y/o man, initially operated for a perforated ulcus ventriculi. In the postoperative phase, severe sepsis and DIC (Disseminated Intravascular Coagulation) occured, and this participated in a following multiple organ failure including tubuar necrosis and total anuria. His medical history revealed no known cardiac disorders. These ECGs were obtained during a 6 hour session of hemodialysis which involved total fluid removal of 1000 ml.

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The baseline rhythm here is atrial fibrillation with rapid ventricular response. The QRS axis is at 30 degrees. The first beat is a premature ventricular contraction (PVC), which is then followed by two supraventricular beats being aberrantly conducted. The right bundle is still refractory after the PVC, and the following two supraventricular impulses are blocked in the RBB, and are being conducted aberrantly, thus causing a QRS with RBBB morphology.

Tachy-brady syndrome: A cascade of arrhythmias and various high degrees of AV block

The patient is an 80 y/o woman with known sick sinus syndrome, aortic sclerosis, aortic valve insufficiency, mitral valve insufficiency, tricuspidal valve insufficiency and left ventricular hypertrophy.

About the sick sinus syndrome and the tachy-brady syndrome

There are two types of Sick Sinus Syndrome (SSS): one with and one without associated tachyarrhythmias. SSS is due to many mechanisms related to SA-nodal failure, and in many patients with the syndrome more than one of the mechanisms are present. The most common mechanisms for SSS are severe, persistent sinus bradycardia, sinus arrest, both brief and sustained, with or without initiation of escape pacemakers, sometimes resulting in sustained asystole. Both Stokes-Adams attacks and sudden death is seen with SSS. When SSS is associated with tachyarrhytmhias, this is called the tachy-brady syndrome. Tachy-brady syndrome occurs in more than half of the patients with SSS.¹  The tachy-brady syndrome itself is not a specific condition, but more of a mixture of combinations of arrhythmias. I find it confusing that even the most profilic authors on this subject, as both Marriott² and Chou¹, tend to disagree on whether SSS should be considered part of the tachy-brady syndrome or vice versa. However, there seems to be consistency upon the fact that SSS can occur in two forms, with our without the associated tachycardias. Furthermore the tachy-brady syndrome is usually described as the condition where a tachycardia mechanism is directly associated with the mechanism of a bradycardia or the other way around. One author³ also differentiates between a tachy-brady syndrome and a brady-tachy syndrome, depending on what mechanism that initiates the next.

This series of telemetry strips from the patient described above, show the tachy-brady syndrome in action, manifested by a large and complex cascade of arrhythmic events. Note that there is a baseline first degree AV block at approximately 260 ms.

Note that each strip is not an exact continuation of the strip before it, meaning that i.e. strip number 2 can repeat some of the events in strip 1.

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Top strip: After 4 cycles of sinus bradycardia (43 bpm), atrial flutter occurs. The atrial rate is approximately 260 bpm, and 2:1 AV conduction occurs, resulting in a ventricular rate of 130 bpm. There are F waves (flutter waves) superimposed on each T wave.

Middle strip: Note that this strip is not an exact continuation of strip 1. The first 12 beats are the same. It shows however the atrial flutter persisting with the same AV ratio for several seconds.

Bottom strip: After a while, 4:1 conduction occurs for one cycle. The next cycle is interrupted by a PVC triplet, or a short run of ventricular tachycardia (VT). After the ventricular triplet, the AV node alternates with 2:1 and 3:1 conduction.

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Top strip: Atrial flutter still persists, while 2:1, 3:1 and 4:1 AV conduction occurs successively, before a four beat salvo of premature ventricular contractions occur. Such a salvo would also be considered non-sustained ventricular tachycardia. Following the salvo, AV ratio continues to vary and also with higher degrees of block. 2:1, 3:1 4:1 and 5:1 AV block occurs successively towards the end of the strip.

Middle strip: This strip is almost a repetition of the top strip, and can be ignored.

Bottom strip: Here we can see that even higher degree of AV block occurs, with AV ratio as high as 6:1 before progressively decreasing again.

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Top strip: This strip is recorded at 50mm/s, and shows the baseline atrial flutter being conducted with high degrees of AV block, and interrupted by a 5-beat run of ventricular tachycardia at 140 bpm.

Middle strip: Various degrees of AV block are seen throughout the strip. The deep, negative deflection towards the end is due to a loose electrode.

Bottom strip: AV block continues to vary, here mostly between a 2:1 and 3:1 ratio.

¹ Surawicz, Borys,  Chou’s electrocardiography in clinical practice. Philadelphia: Saunders Elsevier, 2006:336-343, 6th edition.

² Wagner, Galen S., Marriott’s Practical Electrocardiography. Philadelphia: Lippincott Williams & Wilkins, 396-404, 10th edition

³ Sandøe, Erik and Bjarne Sigurd, Klinisk Elektrokardiografi. Bingen: Publishing Partners Verlag GmbH, 326-331, 1st edition.

Digitalis Intoxication: Slow Atrial Fibrillation with Ventricular Escape

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Patient: Woman, 82 y/o with permanent atrial fibrillation. Accidental digitalis intoxication. Serum digoxin level when arriving in the ER is 6.6 ng/ml. General fatigue, but no recent history of syncopal episodes.

ECG description:

• Irregular, narrow QRS bradycardia at approx. 35 bpm
• Atrial fibrillation with slow ventricular response
• Normal axis at ca. 60 degrees
• Prominent U waves, best seen in leads V2 -V3
• Cohn effect: ST segment depression and  flattened T wave in leads V4-V6
• Poor R wave progression
• Low amplitude in limb leads
• Baseline noise artefact

Discussion: This 12 lead ECG displays atrial fibrillation with slow ventricular response. There is a high degree of AV block, resulting in a bradycardic rate at ca 35 bpm (50 mm/s).  The axis is in the normal quadrant and at ca. 60 degrees. Limb leads show T wave flattening, and there is perhaps a slight ST segment depression visible in leads II and AVF. There is a quite prominent U wave. Normally, the U wave is best appreciated in the lateral precordial leads (V5-V6). Here however, it is seen in leads V2 and V3. The classic ST segment morphology induced by digitalis both at therapeutic and toxic serum levels, is the “coved” or “scooped”, or sometimes referred to as “bowl shaped” ST segment depression. It is sometimes described as if the ST segment has been dragged downwards from a point at the middle of the segment. Digitalis intoxications may however, manifest with or without the classic morphology even at high serum levels. The classic digitalis effect on the ST segment is sometimes called the Cohn Effect, named after Alfred E. Cohn, the American cardiologist, for his early 1900-century studies on the effect of digitalis on T wave morphology. It is generally recognized by ST segment depression together with T wave flattening in the same lead. Although this ECG lacks the coving ST segment, the Cohn effect is present in leads V4-V6.

Overall, digitalis has a positiv inotropic effect and a negative chronotropic effect. The negative chronotropy is due to both decreased automaticity of the SA node as well as prolongation of  the refractory period of the AV nodal tissue, thus inducing higher degrees of AV block. It also increases AV nodal automaticity which often results in for instance accelerated junctional rhytm and junctional extrasystolia.

This ECG is in the low bradycardic range at around 35 bpm, which is due to the high serum levels of digoxin. Different AV ratios can occur, but 2:1 is rare. With second degree AV blocks, Wenckebach conduction is common. In this ECG it’s impossible to determine the AV ratio, due to atrial fibrillation, and one can only conclude that it is varying. Following is a continous rhythm strip (25 mm/s) of the patient that was obtained 10 minutes later, showing the development of higher degrees of AV block, resulting in long bradycardic cycles.

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Note the long, asystolic pauses. The first and third cycles are so long (>2 seconds) that ventricular escape occurs.