Filed under: IVCD (intraventricular conduction delay)
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
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Patient: Woman, 84 y/o with no known cardiac history. Lives in a nursing home and has reportedly been struggling with fatigue, dizzyness and general weakening the last two weeks. No syncopal episodes. She has recently been treated for a pneumonia. When presented in the ER, she is hemodynamically stable, but hypotensive with an initial BP of 80/40. Her SAT is 90 % with oxygen administered at two litres/min. She has a slow, palpable and irregular pulse in radialis, bilaterally. When palpated, the pulse is counted to around 35 bpm. Skin is normal and dry, but shows signs of dehydration. No cyanosis or diaphoresis. She is awake and conscious with a GCS of 15.
At first, a 12 lead ECG is obtained (above). This shows:
- Regular, narrow-complexed bradycardia of supraventricular origin
- Sinus bradycardia at 48 bpm
- Normal cardiac axis, at approx. 30°
- Minimal ST-depression laterally
- Prolonged QT interval, probably rate related. QTc is 470 ms
ECG comments: This ECG shows sinus bradycardia, but as the next strips will show, this is in fact a 2:1 SA Block. Persistent 2:1 SA Exit Block cannot be distinguished from marked sinus bradycardia, since the RR intervals are regular. The rhythm is so slow here, that this ECG only shows three cycles. A slow pulse at around 35 was palpated when she arrived, and considering her history of fatigue and dizzyness, a type of heart block should be suspected. In such cases, a longer rhythm strip must be obtained.
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These strips reveal the true problem: Long and frequent sinus pauses, resulting in a mean ventricular rate of approximately 35 bpm. This patient was hypotensive, which could be due to low cardiac output as a result of fewer ventricular contractions. Although, she was also clinically dehydrated. There are P waves preceding every QRS complex, with a normal and regular PR interval. The QRS complexes are sinus paced and does not represent any ectopy or escape. By using a caliper, a mathematical relationship between the normal cycles and the pauses is quickly established. Each long cycle is a multiple of the normal cycles. In fact, each pause is twice as long as the normal cycles. Every now and then, a P wave “falls out” without disturbing the underlying rhythm. Sinoatrial block may be due to failing SA Node automaticity or blocked conduction out of the node. These two mechanisms cannot be distinguished from a surface ECG.
Since the long cycles are twice as long as the normal cycles, we can establish the diagnosis of SA Block Type II. Same as with Second Degree AV Block, Type II, the giveaway here is the dropped complexes. Here, the P waves are dropped, not the QRS complexes as in an AV Block. In these strips, the block is intermittent, which is also why we can see it. If this 2:1 block was persistent, the rhythm would present as a marked sinus bradycardia and could not be seen on the ECG.
January 24, 2009
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ECG description:
- Sinus rhythm
- Multiple premature ventricular complexes (PVC) with varying morphology, appearing in bigeminy pattern (one PVC per normal sinus beat)
- Left Bundle Branch Block due to QRS width 130ms, slurred rS complex in V1, broad R wave in V6.
- Left Axis Deviation. The axis is at approximately -45°
- Normal PR interval: 180 ms
ECG comments:
This is a sinus paced rhythm. The P waves are easiest to spot in V1 and V2. What catches my eye at first, are those big wide beats following each normal sinus beat. These are of course Premature Ventricular Contractions, and are easily recognized (see PVCs explained below). Premature Ventricular Complexes are due to irritable, hypoxic foci in the ventricular tissue, and examining the morphology of these PVCs, they clearly arise from different foci, as they vary in shape and form. They are multiform and therefore multifocal. Look closely, and you can see that all although all the PVCs in this ECG have the same classic PVC configuration, they all look quite different.
PREMATURE VENTRICULAR CONTRACTIONS (PVCs) AND HOW TO SPOT THEM
- Premature (comes earlier than expected compared to the basic sinus cycle)
- Complexes with broad, large and bizarre configuration. Wider, taller and deeper than the normal QRS.
- Not preceded by a P wave. If there is a P wave before an early complex, the possibility is quite large that the focus is atrial.
- Often followed by T wave inversion (due to repolarization disorder)
- Usually a compensatory pause that is twice the regular PP interval
BUT THE 4TH BEAT IS PRECEDED BY A P WAVE! HOW CAN THAT BE A PVC?!
Usually, PVCs are recognized by the fact that they are not preceded by a P wave, which suggests that the electrical focus is ventricular. But there is one exeception to this rule, which is the case of an end-diastolic PVC that occur after the P wave. Remember, the diastole ends when the ventricles contract. The P wave shows atrial contraction and the QRS shows ventricular contraction. Sometimes a PVC can occur at the very end of the diastole, right before they were supposed to contract compared to the previous cycles. Such a PVC will therefore have a P wave preceding it. On the ECG, the P often falls very close to the premature QRS complex, and the PR interval is too short to have conducted this beat. Actually, this P wave is not too early, it is just the normal, regularly scheduled sinus beat coming on time. It just happens to fall right before a premature ventricular contraction.
The fourth beat in this ECG is a PVC preceded by a P wave, but is still a PVC. The preceding P wave is just the timely P wave from the sinus node that fires regularly.
POST-EXTRASYSTOLIC PAUSES: COMPENSATORY AND NON-COMPENSATORY
The cycle pause after a PVC is called a post-extrasystolic pauses. Such pauses are divided into two kinds: Compensatory Post-Extrasystolic Pauses and Non-Compensatory Post-Extrasystolic Pauses. These names are often too long to use, so the terms compensatory pause and non-compensatory pause are used instead.
Compensatory Post-Extrasystolic Pause
A PVC starts in the ventricles from an irritable, often hypoxic focus. Therefore, it only depolarizes the ventricles, not the SA Node. Therefore, the SA Node is not reset. So the SA Node fires as planned and on schedule. Often, if you use your caliper and measure PP intervals, you can spot that timely P within a PVC. The problem is though, that when the sinus node fires, the ventricles are still refractory, and the sinus impulse doesn´t get conducted. When this impulse reaches the ventricles, they´re not ready, and can´t depolarize. So there is a pause after the PVC as the ventricles finish repolarizing, making them receptive to the next sinus generated cycle. Remember that since the depolarization begins in the ventricular tissue, the SA Node will never know anything about this premature impulse. And if it doesn´t get depolarized by the impulse, it will not reset and will keep on pacing. And if the SA Node is not reset, the compensatory pause will be an exact multiple of the regular PP interval. So by measuring PP intervals, you can check if the pause is compensatory or not.
Non-Compensatory Post-Extrasystolic Pause
With non-compensatory pauses, the SA Node is reset and starts a new sinus cycle. The non-compensatory pause is not an exact multiple of the regular PP interval. The SA Node is usually reset by Premature Atrial Contractions (PACs) or Premature Junctional Contractions (PJCs). PVCs are sometimes followed by a non-compensatory pause, but only very rarely. Remember, for the SA Node to be depolarized by a PVC, there will have to be retrograde conduction through the AV Node. This is not very usual, but can happen. The take-home advice here, is that with non-compensatory pauses, you are usually dealing with a PAC or a PJC.
November 28, 2008