Sorry for not posting much lately, folks! I guess I’ve just been too busy…! Anyway, hope you like this one. It was brought to me by a colleague who thought I might enjoy it. He was perfectly right about that!
The patient: Elderly male, admitted to the CCU for near syncopes and episodic dizziness. He had a known atrial flutter, and was using betablockers and flecainide. I’m afraid I do not have the full list here, nor the dosages. He was sleeping when this episode occured and didn’t notice anything. He also did not pass out.
EKG description: This is atrial flutter (type 1, counter-clockwise) at approx. 260 bpm, with a high and quite varied degree of atrioventricular block. The lowest F-wave/QRS ratio in the top strip, is 4:1, resulting in a ventricular rate of around 65 bpm. Medications might play a part here, but one would suspect the ratio to be lower at this atrial rate. The long blocked period shows ventricular standstill that lasts for almost 6 seconds. This is of course the reason for his episodic dizziness and near syncopes (I’m surprised he didn’t syncope completely). In the lower strip, the blocked periods get even longer, practically resulting in ventricular standstill. With such persisting absence of AV conduction, normally one would expect a ventricular ectopic focus to take over. This however, did not happen here.
Conclusively, this is atrial flutter with a high-degree atrioventricular block and intermittent episodes ventricular standstill. The patophysiology behind this could be AV-node tissue degeneration over time, leading to progressively increasing level of block.
December 16, 2009
Dear friends!
As you’ve probably discovered already, the ECG blog has been down for almost a week. And now it’s back up again, but looks weird…..! The address, ecgblog.com will be kept, by the way.
Well, it’s all my fault. I’ve moved the blog from the Wordpress servers to a private host, and it’s been a bit tricky. I had some trouble with the database files and blah blah blah..
Contentwise, everything should be transferred now, but I still have to do something about the layout and interface of the site. So, if the site acts or looks a bit weird during the next week or so, you know it’s because I want to make everything a bit better than it has been!
As always, comments are much appreciated! Please bring me your ideas on how to make the site better! Thanks a lot for your patience!
Klaus
October 27, 2009
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
October 12, 2009
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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.
October 3, 2009
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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.
September 8, 2009
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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!
September 6, 2009
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.
August 13, 2009
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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.
July 1, 2009
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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.
July 1, 2009
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.
June 21, 2009
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