Filed under: Atrial arrhythmias
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
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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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Hearts point at ectopic P' waves, displaying a 2:1 AV ratio
Patient: Male, 65 y/o. Reoccuring episodes of atrial tachycardia.
ECG description:
- Regular, narrow complex supraventricular tachycardia
- 2 P’ waves per QRS (2:1 ratio) complex, best seen in V2
- Atrial rate is ca. 260 bpm
- Ventricular rate is ca. 130 bpm
- P’ wave morphology suggests right atrial focus
- QRS axis normal, ca. 10°
- Poor R wave progression
ECG interpretation:
With ectopic atrial rhythms, V1 as well as V2 are often good leads to use to look for and differentiate P’ waves and/or flutterwaves in. Here however, ectopic P’ waves are marked by ♥’s in V2, as they were easier to spot here. In V2 there are small, sharp, inverted P’ waves with a regular rate of ca. 260 bpm. Each QRS complex is preceded by 2 P’ waves. The ventricular rate is regular at ca. 130 bpm. 260:2 is 130 and this correlates with our presumption of a 2:1 atrioventricular block. The P’ waves in V1 are negative, which strongly suggests a right atrial focus (Kistler, et al., JACC, Vol. 48, No. 5, 2006).
June 4, 2009
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Patient: Woman, 76 y/o. Admitted to the ER for palpitations. Medical history not available.
ECG description:
- Sinus rhythm
- Every fourth sinus beat is followed by a premature atrial contraction (PAC)
- PACs have fixed coupling interval, are preceded by an ectopic P wave and a short PR interval. P’ wave is upright in inferior leads.
- Normal, horizontal cardiac axis at ca. 10°
ECG interpretation:
Every fourth sinus beat is followed by a supraventricular extrasystole with a fixed coupling interval. This pattern is called quadrigeminy. The coupling interval is the interval between the sinus P wave and the ectopic P wave. While varying coupling intervals are often seen in parasystolia, a fixed coupling interval suggests the presence of an ectopic focus that due to increased automaticity decides to fire during normal sinus rhythm. The P wave preceding each premature beat is partially hidden in the preceding P wave, but the PR interval is clearly shorter than in the sinus cycles. This suggest that the PAC origins from a site nearby the sinus node, but closer to the AV junction. The PR interval exceeds 100ms, which suggests an atrial focus rather than a junctional, in which the PR interval would be expected to be shorter. In AV junctional extrasystolia, the atria is often depolarized in a retrograde fashion as the ectopic impulse starts around the AV junction and spreads upwards through the atrium. This normally produces inverted P waves in the inferior leads. Here however, the P wave is upright in the inferior leads, which also indicates an atrial focus.
May 25, 2009
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Patient: n/a
ECG description:
- Atrial fibrillation with varied ventricular response – ventricular rate 75-90 bpm
- Axis in the normal quadrant, at ca. 60°
- Early R-wave transition zone (V2)
- T wave inversion in leads inferior leads II, III, aVF and in precordial leads V4-V6
- Multiple and multiform/multifocal premature ventricular contractions (PVC)
- Multiform/multifocal PVC triplet
ECG description:
The three first beats of the ECG are PVCs in rapid succession. They are multiform and each have a different axis. Multiformity should not be considered as 100% specific to multifocality, as beats arising from the same ectopic focus can differ in morphology. However, it is common to both label and consider multiform extrasystoles as multifocal, as multifocality is a much more ominous sign of myocardial irritability. Three consecutive PVCs are per definition a short run of non-sustained ventricular tachycardia. However, the common term is a triplet or a salvo.
May 23, 2009
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Patient: Male, 91 y/o. Admitted to the hospital after he fell in his home and was found after 24 hours on the floor. No complaints over chest pain. He is put under observation for commotio cerebri. Cerebral CT scan is negative. Known angina pectoris and has had one AMI in 1983 (vessel unknown). He has a prerenal kidney failure. Troponine level on admittance is 0.04. 8 hours later it is 0.03.
ECG description:
- Regulary irregular supraventricular rhythm
- Sinus rhythm
- Premature atrial contractions (PAC) in trigeminal pattern
- Normal cardiac axis
- Poor R wave progression
- Q wave in lead III
- 2mm horizontal ST-depression in leads V2-V4
ECG interpretation:
Sinus rhythm is interrupted by premature atrial contractions (PAC). Every second sinus beat is followed by a PAC, resulting in a trigeminal pattern. Each PAC resets the sinus node, and is therefore followed by a non-compensatory postextrasystolic pause, contributing to slowing the rhythm down. The ectopic P waves are best seen lead V1, where they are upright/positive. In the inferior leads (II, III, aVF), the same P waves are inverted. This indicates that the ectopic focus lies in or around the AV junction, depolarizing the atria in a retrograde fashion – away from the inferior leads, making the P wave negative. You will probably note that the first P wave in the ECG is negative in lead III. This could lead to confusion, as it would suggest that also this beat is ectopic. However, a diphasic or inverted sinus P wave in lead III is normal in small amounts of the population (Chou 2008:8). Also, note that the last P wave in the ECG has the same P wave axis and morphology as the rest of the ectopic P waves. Although it doesn’t seem to be much premature, it comes from the same ectopic pacemaker. It also breaks the trigeminal pattern.
Premature atrial contractions (PAC) and postextrasystolic pauses
Since we’re on the subject, let’s do a quick recap of the essentials regarding PACs and their pauses.
- A PAC originates from an ectopic site in the atria, and therefore produces a P wave morphology that differs from that of the sinus P wave. It will also produce a normal QRS, as the premature atrial impulse will conduct through His-Purkinje normally. Unless of course, some kind of intraventricular conduction delay is present or if aberrant conduction of the impulse occurs. A PAC produces a pause in the heart rhythm, which can be seen on the ECG. A PAC will usually depolarize the whole atrium (logically, since there is nothing there to stop the impulse from spreading all over the place). When the impulse therefore reaches the sinus node, the node will be “reset” and start a “new” sinus rhythm. This will be manifested on the ECG as a pause, which will be longer than the sinus cycle.
- Such a pause is either labeled a compensatory or a non-compensatory postextrasystolic pause. To differentiate these pauses, we need to look at the three intervals: the normal interval, the coupling interval and the postextrasystolic pause. The normal interval is the basic cycle in the ECG, in this ECG it is the sinus cycle, the cycle starting with the third P wave and ending with the fourth P wave in this ECG. The coupling interval is the interval between the sinus P wave and the premature P wave. The postextrasystolic pause is the pause after the premature beat, consisting of the interval between the premature P wave and the sinus P wave following the pause.
- Now, if the coupling interval + postextrasystolic pause is less than twice of the normal interval, the pause is non-compensatory. If the two added intervals equals twice or more than twice the length of the normal interval, the pause is compensatory. With PACs, non-compensatory pauses are the common finding. Only very rarely, a premature beat originating near or in the AV junction can spread only in the anterograde direction and avoid resetting the sinus node and thereby produce a compensatory pause.
- Now, let’s take a look at lead III from this ECG. By using a ruler or a caliper we will find that the coupling interval + the postextrasystolic pause is less than twice the length of the normal interval. Which is what we expected to find. This is a premature atrial contraction producing a non-compensatory pause.
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May 20, 2009
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Patient: Woman, 51 y/o. Mitral valve replacement 21 years ago. Known paroxysmal atrial fibrillation. Presents in the ER with nausea, pale skin, mild diaphoresis, palpitations and diffuse chest pain.
Prehospital ECG:
- Supraventricular tachycardia
- Ventricular rate is ca. 120 bpm
- Normal axis at ca. 10°
- Atrial activity best visible in lead V1, showing P waves with a slightly varying and prolonged PR interval.
- Several P waves superimposed and partially hidden in T waves
- Pseudo R waves in lead V1
Interpretation: This faxed ECG shows a supraventricular tachycardia, but right precordial lead V1 shows clear atrial activity. The small, peaked P waves with a slightly changing and prolonged PR interval suggests atrial ectopy. Ectopic Atrial Tachycardia rarely occurs with 1:1 ratio, as the AV node usually blocks half or more of the impulses. A common AV block ratio is 2:1. With a ventricular rate of 120 bpm, a 2:1 AV block would indicate an atrial rate of 240 bpm. This would be a typical atrial rate for ectopic atrial tachycardia. Using a ruler or a caliper and measuring from one of the visible P waves here, we will see exactly that: P waves appear at a rate of 240 bpm. The most visible P waves are right after or superimposed on T waves, and the others are hidden in or appearing right after each QRS, creating what looks like a small S wave, a pseudo S wave.
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To confirm the diagnosis, carotid pressure is applied while a rhythm strip is recorded. Paper speed is set to 50 mm/s in order to discern P waves more easily. When pressure is applied, a larger AV block is induced and 3:1 periods occur intermittently. During these blocks, clearly discernable P waves are seen in the right precordial leads. The P waves show atrial ectopic activity at a rate of 240 bpm, just as we suspected from the previous ECG. By marching out the P waves with a caliper, we’ll see that every other P wave gets completely or partially hidden in the QRS complexes when the ratio changes back to 2:1.
May 17, 2009
Patient: Male, 55 y/o. Near-drowning accident due to suicide attempt by jumping into the cold sea at a city harbor. The patient was intoxicated with benzodiazepines and alcohol. He arrives in the ER after being helped out of the water by passers-by who also called EMS. The patient was never unconscious. On arrival, rectally measured body temperature is 32.0 degrees celcius. At this point, rewarming treatment has already been started by EMS on the way to the hospital, which indicates that the temperature probably has been somewhat lower. The patient has no previous cardiac history.
ECG at 32.0 degrees:
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Atrial fibrillation with rapid ventricular response. Ventricular rate is approx. 125 bpm
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Normal cardiac axis
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Baseline artifact due to patient shivering
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2mm upward terminal deflection in inferior leads and V4-V5 (at the end of QRS/early portion of the ST segment). This is not present in the next ECG.
ECG at 34.8 degrees:
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Sinus rhythm at approx. 80 bpm
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Normal cardiac axis
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Baseline noise due to patient shivering
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Terminal deflections in inferior leads are normalized, but are still present in V4-V5.
As the patient has no cardiac history, atrial fibrillation is most probably induced by the hypothermia. Rapidly induced hypothermia can cause atrial fibrillation at temperatures ranging from 32.0 degrees to 22.5 degrees (Chou, 2008). Atrial fibrillation is spontaneously converted to normal sinus rhythm in this patient when he is rewarmed and has reached normal body temperature.
Hypothermia is also often associated with so called J-waves, also called Osborne-waves. They are seen as a slow, upward deflection at the terminal portion of the QRS and the early portion of the ST segment. They increase in amplitude as the body temperature falls, and gradually decrease in amplitude as the body temperature is gradually normalized.
Whether the terminal deflections in leads II, III, aVF and V4-V5 are small Osborne waves, is uncertain. However, the fact that they have disappeared in inferior leads when body temperature is normalized, could indicate this.
April 13, 2009
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Patient: Woman, 70 y/o. Congestive Heart Failure. Using digitalis.
ECG description:
- Narrow complex tachycardia of supraventricular origin.
- Variable ventricular rate. Rate varies from 73-105 bpm.
- Right Axis Deviation. Cardiac axis is at approx. 150°
- Multiple P’ waves. Atrial rate is 210 bpm.
- Varying AV Block. P:QRS ratio ranging from 1:1 to 3:1.
- Ectopic P’ waves, inverted in inferior leads II, III, aVF. P waves superimposed on QRS complexes.
- Prominent Q waves in inferior leads, II, III aVF.
- T wave inversion in inferior leads, II, III, aVF
ECG comments: This EKG shows an Ectopic Atrial Tachycardia (EAT) with variable degree of AV Conduction, and was in the clinical setting mistaken for atrial flutter when the patient was presented in the ER. A common mistake to make, as atrial flutter is probably the arrhythmia that resembles EAT the most electrocardiographically. Atrial flutter is a common differential diagnosis with EAT, but making the wrong diagnosis here can however, be dangerous for the patient. The pitfall is that paradoxically, atrial flutter is treated with digitalis, which again induces EAT. Which means that if EAT is being mistakenly treated with digitalis, the arrhythmia will be sustained, as well as the degree of AV block could be increased. This will be like adding fuel to a fire. Untreated EAT with block can at some point compromise the patient’s cardiac output and result in hemodynamic unstability. The treatment for EAT is, of course to remove the digitalis intoxication.
Differentiating Ectopic Atrial Tachycardia and Atrial Flutter
The reason that EAT is often mistaken for atrial flutter, is because of the multiple P waves. Depending on their axis and morphology, they can for the untrained eye easily resemble flutter waves (F waves). Also, if one suspects an atypical flutter pattern, one might think that the P waves are due to flutter activity. However, the key is to understand the electrophysiology behind the two mechanisms and how they will appear on a surface EKG. If you understand the underlying electrophysiologic mechanisms of atrial flutter, differentiating it on a surface EKG is much easier. Also, by examining both the P waves and the baseline of the different leads, the correct diagnosis will be easily within reach in most cases.
Atrial Flutter
- Is characterized by a rapid and regular atrial rhythm at rates from 250 to 400 bpm.
- Due to the macroreentry mechanism of atrial flutter, where an ectopic impulse travels counterclockwisely in a circular fashion usually within the right atria, flutter waves are created on the EKG. When the impulse has travelled a full circle, it reactivates the same focus again, creating a reentry loop mechanism. Thus, where one F-wave ends, the next one arises immediately. Several F waves together makes out the hallmark saw tooth baseline.
- Flutter waves (F waves) and the saw tooth pattern are best seen in the inferior leads, II, III and aVF. Sometimes, F waves are more clearly visible in lead V1.
- Seldom coexist with ectopic atrial tachycardia in the same patient
Ectopic Atrial Tachycardia with block
- Is characterized by a rapid and regular atrial rhythm at rates from 150 to 250 bpm
- Has abnormal P (or P’) waves whose morphology is different from that of the sinus P waves. P waves are often inverted in inferior leads (II, III, aVF) if the ectopic focus sits distally in the atria.
- Has isoelectric intervals between P waves in all leads.
- When atrial rates become fast, the AV Node usually blocks signals. EAT never occurs with First Degree AV Block. Always presents with Second Degree or Third Degree AV Blocks. Wenckebach conduction can also occur.
- P waves are often difficult to spot as they are often small and dysmorph, and often get buried in or superimposed on the QRS complex. Lead II is often difficult to use, while lead V1 is often a good lead for discerning P waves.
- Often occurs due to digitalis intoxication
Cherchez le P!
The above are the famous words by EKG master Henry J. L. Marriott, and is french for “Look for the P!”. What Marriott meant, was that finding and evaluating the P waves is the key to understanding and diagnosing arrhythmias. Marriott especially pointed out that one must look for P waves buried in T waves. In both premature contractions, like for instance a PAC, and in other conditions, P waves can get buried in both the preceding T wave, in the QRS and practically anywhere. And as we will see with this EKG, spotting P waves is what pinpoints the diagnosis.
The rhythm is obviously supraventricular, as QRS complexes are within the normal range (<120 ms). There are multiple, small P waves before many of the QRS complexes. The P:QRS ratio varies from 3:1 in the longest cycles to what seems like 1:1 in the shortest cycles. However, the latter is actually 2:1. When examining the QRS complexes, there are P waves buried in the QRS complex. The buried P waves appear at the end of the QRS, and are best seen in leads V2-V5, as they create a pseudo S wave at the end of each QRS. By marching out the P waves with a caliper, the buried P waves are easy to spot. With this in mind, and knowing that First Degree AV Block doesn’t occur with EAT, we will conclude that where AV block ratio seemed to be 1:1, the block is really 2:1. This means that in those cycles, there are actually two P waves for each QRS, but the second P wave is buried in the QRS itself. These are however, not sinus P waves. They are deflections from an ectopic atrial focus, and should therefore be referred to as P’ waves, which is the correct labelling for ectopic P waves.
By measuring the P’P’ interval, the atrial rate is constant and regular at 210 bpm. In the 2:1 block cycles, the ventricular rate is 105 bpm. The ventricular rate is half the atrial rate, which correlates with a 2:1 block. Now, remembering what Dr. Marriott preached, when examining the T waves, there are clearly P waves buried in their humps. This is best seen in lead V3, where T wave morphology changes throughout the lead. The extra peaks and bumps on the T waves are actually buried P’ waves. If these were not observed, this rhythm could be mistaken for an AV Nodal Reentry Tachycardia, as there would be no P waves preceding the QRS, with seemingly retrograd P waves shortly after ventricular depolarization. Also, you will note that:
- The baseline is perfectly isoelectric between each P’ wave, ruling out the macro reentry impulse rotation mechanism of atrial flutter.
- In inferior leads II, III and aVF, the P’ waves are inverted as the P wave axis is shifted superiorly. This indicates a low atrial focus and is a common sign of atrial ectopy. This again rules out atrial flutter, which would produce F-waves in the same leads.
- Unlike MAT (Multifocal Atrial Tachycardia), there are not multiple ectopic foci here. The P wave configuration is constant and unimorph throughout the leads.
February 3, 2009
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Patient: n/a
ECG description:
- Sinus arrhythmia / sinus rhythm with varied rate. V-rate varies from 45-110 bpm.
- Left Axis Deviation (LAD). Cardiac axis approx. – 40°
- Left Anterior Fascicle Block
- Premature Atrial Contractions (PAC) in bigeminal pattern
- Widespread T wave abnormalities. T flat/negative in leads II, III, aVF, V5, V6
- Deep Q-wave in lead V1
Detection of Atrial Bigeminy
The 12 lead ECG displays multiple supraventricular extrasystoles. Each sinus beat is followed by a supraventricular extrasystole with a fixed coupling interval throughout the recording. Since the coupling interval is fixed and the P’ waves are morphologially similar, the term unimorph is used. Unimorph complexes signal that all the premature beats arise from the same automaticity focus, insinuating ectopic unifocality. Though, there is always a possibility that unimorph complexes can originate in different foci. Therefore, the term unimorph is used instead of unifocal.
Determining from the P wave axis and morphology, the ectopic focus is not sinoatrial. The narrow QRS suggests that the ectopic impulse is being conducted normally through the His-Purkinje fibers, ruling out a ventricular ectopy. The PR interval measures 120 ms, which lets us conclude that the irritable focus is atrial, not junctional. The inverted P waves suggests that the ectopic impulse is spreading retrogradely and inferiorly from its focus.
Each premature complex is followed by a postextrasystolic pause, slowing down the rhythm. By measuring the pause, the coupling interval and the normal sinus interval, the pause can be labeled compensatory or noncompensatory, with the latter being the normal finding with premature atrial contractions. As premature atrial impulses normally depolarize the whole atrium and thereby resets the SA Node, sinus pacing is usually interrupted, causing a pause after the extrasystole. This pause is a result of the sinoatrial slowing and is longer than, but not a multiple of the normal interval. With noncompensatory pauses, the coupling interval + the postextrasystolic pause is less than twice the normal interval. With compensatory pauses, the sum of the coupling interval and the postextrasystolic pause is exactly twice the normal interval length. Because of the bigeminal pattern here, there is no “normal” sinus cycle, making it difficult to establish whether the pauses are compensatory or non-compensatory.
January 31, 2009
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