Tag: AV block
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: 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
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.
June 18, 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: Male, 84 y/o. No cardiac history. Acute onset of severe, pressing chest pain. No relief from large doses of intravenous morhpine.
ECG description:
- Broad complex bradycardia with third degree atrioventricular block (3AVB) and AV dissociation
- Ectopic pacemaker firing at 48 bpm.
- Atrial rate 52 bpm
- Axis at approx. 60°
- ST elevation > in leads II, III and aVF
- Reciprocal ST depression in leads I and aVL
ECG comments: This is 3AVB. If you march out the P waves here, you will see that there is regular and normofrequent atrial activity, but none of the atrial impulses gets propagated further down the conduction system. The atrias and ventricles are acting independently. This is called AV dissociation, and is a criteria for 3AVB, also referred to as complete heart block. Third degree heart block is caused by a conduction block most commonly in the bundle branch/Purkinje system. According to American Journal of Critical Care, the block most commonly occurs in the bundle branch/purkinje system (61%), at the level of the AV node(21%) or the His bundle (15%). When a block occurs, an automaticity focus below the block will assume pacemaking activity at its inherent rate. An escape rhythm above the His bundle normally would produce a heart rate at 40-60 bpm and narrow QRS complex. When the ectopic focus sits lower in the ventricles, the heart will be paced a slower rhythms at around 20-40 bpm, and the QRS will become broad.
In this ECG, the heart rate suggests that the ectopic pacemaker is junctional. But the QRS configuration is wide, so the block is probably below the AV junction after all. Yet, it is pacing faster than expected. This can be referred to as an accelerated idioventricular escape rhythm.
ECG interpretation: Acute Inferior STEMI with reciprocal change, Third Degree Atrioventricular Block and Accelerated Idioventricular Escape Rhythm.
Note: This patient was transferred to a cath lab, where he was revascularized. I will soon update the post with more info on the culprit vessel, a post pci ecg and more.
December 26, 2008
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Patient: Elderly woman, around 80 years. Unfortunately, I don´t have any clinical information on this patient. All i know is that she was rapidly admitted to a cath lab where the perfusionists did a successful revascularization. AV block is secondary to infarction, hence it is intermittent.
ECG description:
- ST elevation > 4 mm in leads I , II, aVF and > 1 mm in leads V5, V6
- Reciprocal ST segment depression in leads I, aVL
- Complete atrioventricular dissociation. No relation between P waves and QRS complexes. Regular PP interval, regular RR interval. PR interval is variable, hence there is no apparent relationship between P waves and QRS complexes.
- Junctional escape rhythm at 50 bpm.
ECG diagnosis: Inferior wall STEMI. Third degree atrioventricular block with complete AV dissociation that probably has appeared because of damage to the AV node during the infarction. Because of the complete AV dissociation, an accessory pacemaker has taken over the pacing. Based on the rate and the normally configured QRS complexes here, the escape rhythm is junctional/nodal.
The patient was then transferred to the cath lab, where the perfusionists did a successful revascularization. She was transferred to an ICU. This next ecg was recorded 25 hours later since the initial ecg showing the acute STEMI.
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ECG description:
- Normofrequent sinus rhythm at ca. 90 bpm
- PR interval is at 200 ms, so there is a borderline first degree AV block present.
- ST elevation ca. 2mm in II, III, aVF, and 1mm in V5 and V6
- Reciprocal changes still in I, aVL
ECG diagnosis: ST elevation and reciprocal ST depression due to inferior wall infarction. Third degree AV block has disappeared and the patient is in normal sinus rhythm. The AV block was transitory due to the infarction, and the AV node has recovered. The PR interval is 200 ms and signals a borderline first degree AV block which is may due to damage of the AV node.
Comments:
Now this is an interesting case, but also a classic display of heart block etiology. Coronary ischemia is the most common cause of third degree AV block. It is a known fact that acute inferior wall myocard infarction can sometimes cause damage to the AV node, causing third degree heart block. In such cases, the damage is often transitory and the AV node may be recovered if the perfusion is restored. This is the case here, where the patient was quickly admitted to a cath lab where revascularization was done successfully, and the AV node was then restored to a functioning state. The the heart block was terminated and reset into normal sinus rhythm. During the complete heart block, an accessory pacemaker takes over pacing control. The escape rhythm here probably originates in the AV junction, providing a narrow complex escape rhythm, aka a nodal or junctional escape rhythm.
Further reading on the web:
E-medicine: Third degree heart block
American Heart Association: Third degree heart block
The Merck Manuals: Atrioventricular blocks
E-medicine: Atrioventricular disassociation
Wikipedia: Third degree AV block
November 15, 2008