Filed under: Bundle Branch Blocks
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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: Male, 60 y/o. Medical history unknown.
ECG description:
- Sinusbradycardia at 46 bpm
- Normal cardiac axis. Approx. 30°
- AV Junctional Escape Complex
- Left Bundle Branch Block. Q
- T inversion in lead III and biphasic T wave in lead aVF.
ECG comments:
Supraventricular escape complexes are usually precipitated by long pauses, such as sinus arrest, intermittent SA block or long postextrasystolic pauses. Slow phases in sinus bradycardia however is also a common cause of such escape beats. The last QRS complex in this ECG is preceded by an inverted P wave in the inferior leads. The PR interval is also shorter. These morphologic clues tell us that the atria is depolarized retrogradely. The depolarization wave spreads away from leads II, III and aVF, making the P wave inverted. The shortened PR interval indicates an ectopic focus located closer to the AV node.
January 29, 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
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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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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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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
Patient: n/a
ECG description:
- Sinus rhythm at 85 bpm
- Ventricular extra systoles in trigeminy pattern. Every third beat is a Premature Ventricular Complex (PVC).
- Marked First Degree AV Block. PR interval is 310 ms.
- Incomplete Left Bundle Branch Block (LBBB). QRS width 100ms.
- Axis normal at approx. 60°
ECG diagnosis: Ventricular trigeminy with marked (severe) 1° AV Block and incomplete LBBB.
ECG Comments:
PVC TRIGEMINY: When every third beat is a PVC, the term trigeminy is used. The PVCs here are unimorph and therefore unifocal, which means they all have the same morhpology and therefore arise from the same ectopic focus. Premature beats originates in irritable autmaticity foci that fires spontaneously. Such beats come earlier than expected in the rhythm. It is also important to understand that although PVCs in many ways are considered to be benign, they are early signs of hypoxia. 6 PVCs per minute is considered pathological. Remember that a continuous run of bigeminy or trigeminy will quickly exceed that criteria, and will then usually indicate that a very irritable focus is hypoxic and needs attention.
1° AV BLOCK: The PR interval in this ECG is 310ms. This is a so called marked First Degree AV Block. This term indicates that the PR interval is markedly prolonged. This is noted because sometimes the AV conduction delay becomes so severe that pacemaker insertion may be needed. I am not completely sure about the exact criteria here, but from what I have read permanent pacing is indicated when the patient is symptomatic and when the PR interval exceeds 300ms. This article from Emergency Medicine News discusses the matter, and says that those with a PR interval >300ms are at risk of developing complete heart block.
INCOMPLETE LBBB: The morphology here resembles LBBB, but the QRS is only 100ms. To diagnose BBB, the QRS complex must be at least 120 ms. Therefore, this LBBB must be considered incomplete.
November 19, 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
