Filed under: LAFB (Left Anterior Fasicle Block) or Hemiblock
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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
This case displays the a relatively young, male patient with a recent myocardial infarction who developes junctional tachycardia. Three 12 lead ECGs are presented: One that is 9 days prior to this admittance, one that is obtained on scene by EMS and finally the ECG obtained in on arrival in the ER. The three ECGs are compared to obtain the correct diagnosis.
Patient: Male, 45 y/o. Non-smoker, non-drinker. Diabetes Mellitus type I with early stage retinopathy. Previous anterior infarction (two months prior to this admittance), followed by PCI to the LAD. Now presented in the ER with minor pressing chest pain. The pain occured when he was bicycling home from work. Having had a previous MI he immediately called EMS, who arrived quickly and recorded a 12 lead ECG. EMS adminstered 0.4 mg Nitro sl and 2.5 mg Morphine iv, which relieved the patient of his pain. He was transported to the hospital for blood tests and a check-up. On arrival in the ER he was pain free, with no dyspnea, normal aand dry skin. Vital stats on initial assessment were BP 135/85, regular pulse, RF 16/min, SpO2 97% with O2 2 ltr/min.
This is the 12 lead ECG (LP12) that was obtained by EMS:
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The ECG is at 50 mm/s and shows:
- a regular, narrow complex bradycardia at 46 bpm
- no P waves
- left axis deviation (LAD)
- Left Anterior Fascicle Block
- poor R wave progression (PRWP); late precordial transition zone: lead V6.
- normal ST-T segments
- minor baseline noise
Intepretation:
RHYTHM: This narrow, complex bradycardia has no visible P waves. The rhythm is regular and in the bradycardic range. What is the rhythm here? Narrow QRS complexes tell us that the rhythm is supraventricular, and added up with the regularity of the RR intervals, one should immediately suspect a junctional rhythm. The ventricles are paced at 46 bpm, which is slow enough to call this a bradycardia. Every myocardial cell has the ability to pace the heart, and each type of cell has its own intrisic rate that is slower than the type of cell preceding it. The fastest pacer is the SA node. Junctional and AV nodal cells pace in the range of ca. 45-50 bpm. Which means that this rate of 46 bpm also supports the theory of this being a junctional rhythm. As with all supraventricular impulses, the atria is usually depolarized. With junctional automaticity, the atria is normally depolarized in a retrograde fashion. With junctional rhythms, the P wave is therefore often found right after the QRS complex or in the following T wave, unless retrograde conduction is delayed, creating a prolonged RP interval. If visible, the P wave occuring from the retrograde atrial activation should be inverted in the inferior leads II, III and aVF.
R WAVE PROGRESSION: This patient’s previous anterior MI can be seen from the poor R wave progression in the precordial leads. To determine the R wave progression, one needs to identify the transition zone. This is the lead with equal R and S wave voltage (R/S=1). Normal R wave progression has an increasing R wave amplitude across the precordial leads, and a transition zone in V2, V3 or V4, where the voltage decreases again towards V6. Poor R wave progression is defined when the transition is late and doesn’t occur until V5 or V6. In this ECG the transition occurs in lead V6, indicating loss of myocardial tissue. Note that abnormal R waves and R wave progression can occur due to several other reasons, as for instance misplaced leads. However in this case, the PRWP correlates with the patient’s previous anterior MI.
Cherchez le P!
Again, those famous words by Dr. Marriott become useful. In this ECG the sinus node seems to be completely silent. There are no obvious P waves preceding any of the QRS complexes. By closely examining the QRS morphology in the right precordial leads V1 and V2, we find a small terminal R wave. These are actually pseudo R waves, and are called so because they are not really R waves, but instead retrograde P waves that occur right after the QRS complex.
Let’s compare to a previous ECG, taken 9 days prior to the first one:
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- Sinus rhythm at 76 bpm
- Left Axis Deviation (LAD)
- Left Anterior Fascicle Block
- First Degree Atrioventricular Block (1AVB); the PR interval is 220 ms
- One non-conducted premature atrial contraction (PAC); best seen in lead V2 as a small bump on the initial part of the T wave after the third QRS complex from the left)
- Poor R Wave Progression (PRWP); late transition zone – the transition occurs in V6.
First of all, the most striking observation here, is that this ECG shows a normal sinus rhythm. This tells us that this patient’s heart was had a working sinoatrial node just 9 days ago. However, there is a 1AVB present, which could be a sign of AV nodal disease.
This next ECG is taken on arrival in the ER, only 50 minutes later than the prehospital ECG:
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As we can see, the rate has increased. The rhythm is still junctional, but now pacing at a rate faster than the normal intrinsic rate of AV nodal and junctional pacemaker cells. The rate is 100bpm, making this an accelerated junctional rhythm (AJR). The retrograde atrial activation is still seen as pseudo R waves in lead V1.
March 26, 2009
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Patient: n/a
ECG description:
- Sinus rhythm with varied rate: 75-130 bpm
- Premature Atrial Contractions (PAC) presenting in couplets
- Left Axis Deviation (LAD). Cardiac Axis is deviated leftwards and superiorly at approx. 90°
- Left Anterior Fascicular Block (LAFB) due to LAD, deep S in III, no sign of LVH or MI
- Low Voltage in Limb Leads
- Poor R Wave Progression (PRWP)
Atrial Couplets, PACs and P waves
After one sinus cycle, the rhythm is interrupted by a PAC (complex no. 3 from the left). The change in P wave axis and morhpology of this complex suggests ectopy. The P’ wave is inverted in leads II, III and aVF, suggesting that the ectopic impulse originates in the left atria, spreading in a retrograde fashion. Determining by the PR interval, which is 100 ms, the ectopic pacemaker is atrial and not junctional, and sits closer to the AV Node than the SA Node.
The PAC is immediately followed by a new PAC, creating an atrial couplet. This second PAC seems to originate from another focus, as there is a change in P’ wave axis and configuration. The PR interval of this PAC is 110ms, and the P’ waves are upright in the inferior leads, suggesting that it spreads inferiorly and towards the left. The second PAC is followed by two sinus cycles, which is then followed by another PAC couplet. The PACs in this couplet seem to originate from the same ectopic foci as in the first couplet, although there is a variation in coupling interval length.
Atrial couplets can be benign, but are less common in healthy hearts, and should increase suspicion towards onset of atrial fibrillation. Ultimately, one would prefer to print a longer rhythm strip at this point, to see the phenomenon over a longer time interval. Unfortunately this is not available for this particular case.
The Postextrasystolic Pause
With supraventricular premature impulses, the dominant automaticity focus (normally the SA Node, as in this case) is usually reset by the premature impulse. The supraventricular impulse usually activates the whole atria and thereby also the SA Node. The early activation of the SA Node interrupts the pacing function of the node, and causes a delay in impulse generation. The next impulse will then be slightly delayed, causing the following RR interval to be prolonged. This is called a noncompensatory pause. If the SA Node is not reset, then its pacing function will not be disturbed, and the following RR interval will be an exact multiple of the normal interval, resulting in a compensatory pause.
PACs usually present with non-compensatory pauses, as ectopic atrial impulses will usually activate the whole atria, including the SA Node, and thereby interrupting the sinus pacing activity. In this EKG, the pause after the first PAC is interrupted early by another ectopic impulse, so this pause cannot be determined. The second PAC however (complex no. 4 from the left) is followed by a postextrasystolic pause that is prolonged, but still not an exact multiple of the normal sinus cycle length. This is a non-compensatory pause, which tells us that the SA Node has been reset. This helps to establish and diagnose an atrial origin for the ectopic beats.
January 30, 2009
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Patient: Woman, ca. 60 y/o, sudden onset of palpitations and dyspnea. Prehospital EKG showed rapid atrial fibrillation, but she converted spontaneously during transport. When presented in the ER, she still feels palpitations, although not as rapid and intense as they were.
ECG description:
- Sinus rhythm with varying rate, ca. 55-70 npm
- Multiple premature atrial complexes
- Left Axis Deviation (LAD). Axis at approx. – 40°.
- Left Anterior Fasicle Block (LAD, QRS<120ms, no sign of LVH)
- Deep Q waves in V1-V2
- Poor R wave Progression (PRWP)
ECG interpretation: Sinus rhythm with Left Anterior Fasicle Block and Multiple Premature Contractions
ECG comments: The postextrasystolic pause can be compensatory or non-compensatory, depending on whether the premature depolarization of the atria has reset the SA Node or not. When the premature atrial depolarization resets the SA Node, the node will use a variable time period to restart, causing a pause. This pause is longer than the normal PP interval, but not twice as long. If the SA Node is not reset, the pause will be an exact multiple or twice as long as the normal PP interval.
This is measured by adding the PP interval of the coupling interval with the PP interval of the pause. If the sum of these is equal to the normal PP interval, the pause is compensatory. If it is shorter than the normal PP interval, the pause is non-compensatory. See this previous post, where distinguishing between compensatory and non-compensatory pauses is explained.
Why are these PACs and not PJCs?
It is not very usual for PACs to present with compensatory pauses as in this ECG. PACs usually present with non-compensatory pauses, as an atrial depolarization usually resets the SA node. Still, I’d like to think that the ectopic beats here are atrial. If they were junctional, the P waves would fall close to or right after the QRS. With a PJC the PR interval is usually 10 ms or less when the P wave precedes the QRS complex. With PJC, P waves are also inverted in the inferior leads. Another suggestion that this ECG shows PACs, is that the configuration of the premature P wave differs from that of the sinus P waves, which is because the premature impulse originates in a different part of the atria and depolarizes them in a different way.
From measuring the normal intervals, coupling intervals and postextrasystolic pauses, you can see that all the pauses in this ECG are compensatory, except one: The second PAC in the first strip is followed by a pause that is less the sum of the normal PP interval and the coupling PP interval.
Lastly, this ECG shows a Left Anterior Fasicle Block, based on Left Axis Deviation, narrow QRS (>120ms) and no sign of Left Ventricle Hypertrophy measuring by the Sokolow-Lyon index).
December 30, 2008
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Patient: Woman, 90 y/o. Presents in ER with abdominal pain. Diabetes Mellitus type II. Initial BT 80/30. Pulse 35 bpm. No pain, but very fatigued. Glasgow Coma Scale 15.
ECG description:
- Sinusbradycardia, 35 bpm.
- Constant PR interval at 110ms
- Left axis deviation. The cardial axis is ca. -40 degrees.
- Left Anterior Fascicular Block
- Q-wave in V1-V2.
- Poor R-wave Progression in precordial leads.
- ST-elevation >2mm in V1-V2.
- Baseline electrical noise
ECG interpretation: Sinusbradycardia with LAFB
October 14, 2008
