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
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
This is a case of an 84 y/o man who just had his VVI pacemaker replaced. The first night after changing the pacemaker, he woke up in the middle of the night with breathing problems. Paramedics reported on the way in to the emergency room that he was bradycardic and hypotensive with a low, but stable BP of 80/40. He is also reported to be respiratory stable. As they are not far away from the hospital and he seems stable in spite of his hypotension, he is not paced externally by the paramedics. He has a congestive heart failure and an EF (ejection fraction) of 45%. He also has a persistent/chronic atrial fibrillation. He was given his first VVI pacemaker 20 years ago because of a high-grade AV block.
He presents in the ER with a slow, but palpable radial pulse bilaterally. He is awake with GCS 15, no chest pain, dry and pale skin. No cyanosis. Initial blood pressure is 140/80, probably due to prehospital fluid resuscitation. He says he can feel that there is something wrong with his pacemaker.
First, a 12 lead ECG is obtained:
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ECG description:
- Narrow complex bradycardia with irregular rate from 30-50 bpm
- Axis approx. 0°
- No visible P waves
- Regular pacemaker spikes, best seen in precordial leads. All pacemaker spikes dissociated from QRS complexes.
- QRS is
- T-inversion in leads II, III, aVF and all precordial leads
- ST-depression 1-2 mm in leads V2-V5
With a VVI pacemaker, one would expect a wide QRS configuration and a regular ventricular rate. The narrow QRS complexes and the irregular rate shown here suggests that the pacemaker is not functioning properly. This is confirmed by the pacemaker spikes, which are best seen in the precordial leads. The spikes are regular, but in no relation to the QRS. When marching out the pacemaker spikes, the pacemaker lead seems to be dissociated from the ventricles. Either the sensor or the pacing lead is misplaced or has moved out of position. When comparing the rates, the pacemaker is emitting charges at at a rate of 59 bpm, while the ventricular rate here is much lower.
With these irregular and narrow-complexed QRS complexes, one can exclude a junctional escape rhythm. If this was junctional escape, the RR intervals would be regular. I would assume that these QRS-complexes are paced from the atria. Remember, this patient has atrial fibrillation, but since he also has a sick AV Node, only a small amount of impulses are conducted through to the ventricles. This patient has a high grade (also called ‘advanced’) AV Block, which explains why only an uneven and small amount of atrial impulses are conducted through the AV Node.
In this 12 lead tracing it seems that none of the pacemaker discharges succeed in depolarizing the ventricles, but still this is a potentially dangerous condition for the patient. If the pacemaker lead discharges to the ventricles while they are refractory, this could induce life-threatening tachyarrhythmias. As we can see from the rhythm strips below, which were recorded immediately after the 12 lead tracing, the pacemaker occasionally succeeds in depolarizing the ventricles. This also means that pacemaker discharge could be conducted to the ventricles during the refractory period.
The paced complex is at the end of the second strip below. Atrial fibrillatory waves are also seen here. They are best seen in leads I, II and aVR.
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January 26, 2009