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Patient: Young female person with cardiac arrest. Initial ventricular fibrillation that was defibrillated x 3. Then asystole and long resuscitation ( 45 min) before ROSC was achieved.
ECG description:
- Regular junctional rhythm
- Ventricular rate 76 bpm
- No visible P waves preceding QRS
- Extreme right axis deviation – axis indeterminate
- Poor R wave progression
- Prolonged QT interval. QTc = 485 ms
ECG interpretation:
The ECG shows a regular, narrow-complex rhythm with no visible P waves. Sinoatrial pacing has failed, and an ectopic site in the AV junction has taken over pacing. Junctional automaticity normally provides heartrates in the range of 40 to 60 bpm, but here the rate is right below 80 bpm. When the rate of junctional impulse discharge is moderately increased like here, it is called an accelerated AV junctional rhythm (AJR). Chou (2008:389-391) states that AJR is seen predominantly in patients with heart disease. The QT interval is prolonged, with a QTc of 485 ms. Prolonged QT often occurs after CPR.
Calculating corrected QT-time (QTc) with Bazett’s Formula
QTc = QT / √ RR
QT is measured in milliseconds, while RR is measured in seconds. To calculate the RR interval in seconds, we use 60/heart rate. 60/80 is 0.75.
We enter this into Bazett’s formula and get:
QT = 420 / √ 0.75
QT = 420 / √ 0.866
QT = 484.988 ≈ 485 ms
May 23, 2009
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Patient: 55 y/o female with claudicatio intermittens. No cardiac history, but allegedly one similar episode 10 years ago when her heart “went crazy” for 20 minutes. When EMS arrives: Sudden onset of strong palpitations, dizziness, chest pain, paleness and mild diaphoresis. Blood pressure is 132/92 and the the patient has a rapid, regular pulse at around 180 mg. A 12 lead ECG is obtained.
ECG: The ECG shows a regular and fast narrow-complex tachycardia, probably of supraventricular origin. Inverted P waves are seen in V2 during the early phase of the T wave.
The patient arrives in the ER just a few minutes later and a new 12 lead is obtained
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ECG description:
- Regular, narrow-complex tachycardia.
- 150 bpm
- No visible P waves preceding QRS
- Retrograde P waves with an RP interval of 120ms. Inverted in inferior leads II, III, aVF and upright in aVR and right precordial leads V1 and V2. Also called pseudo S-waves (inferior leads) or pseudo R-waves (right precordial).
- Cardiac axis is normal at approx. 50°
Interpretation: A narrow-complex tachycardia is most likely to be supraventricular in origin, as this indicates normal His-Purkinje impulse propagation and simultaneous ventricular activation. However, there is no P wave preceding the QRS complex to indicate that a sinoatrial origin of the propagated impulse. The regularity rules out atrial fibrillation, and the fact that the P waves are not visible could of course just be due to the tachycardic rate. At a first glance we can only conclude that this is a supraventricular tachycardia. A natural next move would be to perform carotid pressure or other vagal manuevres to induce atrioventricular block in order to help us differentiate this rhythm. With the same intentions, and if carotid pressure doesn’t work, adenosine would be the drug of choice here.
A closer look
However, differentiation stop here, as the diagnosis lies right in front of us, clearly visible in both the ECGs. Although there is no sign of atrial activity preceding the QRS, take a look after the QRS complex. In all inferior leads, II, III and aVF, an inverted P wave with an RP interval of 120 ms followes each QRS complex. The same P wave with the same RP interval can be spotted in the right precordial leads V1 and V2, as well as in aVR. Logially, the P wave is upright in these leads. This means that the atrias are depolarized in a retrograde fashion, after ventricular systole.
Two tracts
The AV node normally has one conductive tract or approach leading the impulse to it. Some people however, have two. The two tracts are separated from each other and the rest of the myocardium by nonconductive tissues. When there are two tracts, these are named the anterosuperior or the fast “tract” and the posteroinferior or the “slow” tract. The two pathways, or tracts, are functionally different:
Anterosuperior / fast tract
- very rapid impulse conduction
- slow refractory time
Posterosuperior / slow tract
- rapid impulse conduction
- slow refractory time
Intranodal impulse conduction and establishment of the AV nodal reentry circuit
Consider a normal impulse coming from the sinoatrial node or the atria. When reaching the AV junction, it hits the two tracts simultaneously, and they will both start conducting the impulse at the same time. The fast tract however, will conduct the impulse faster. This way, the fast tract leads to AV node depolarization. The impulse travels further down His-Purkinje and causes ventricular contraction and a normal, narrow QRS. The electrical impulse will however spread in all directions, and some of it will also travel retrogradely and back up through the slow tract. Remember, this tract is much slower, and the impulse travelling retrogradely will meet the impulse still working its way down towards the AV node. The two impulses will collide and they essentially cancel each other out. Normally, this is what happens, and everything works out fine.
Now imagine that an ectopic site in the atria decides to fire prematurely. The premature impulse will reach the two tracts and and find the slow tract ready to accept it, because it has a shorter refractory period. The fast tract will be busy while it is still refractory from the previous impulse. The impulse is being conducted to the AV node through the slow tract, and when the AV node is depolarized, ventricular contraction and QRS occurs. It is the nature of electricity to spread in all directions possible, and the impulse will also this time try to spread retrogradely. Since it was conducted through the slow tract, the fast tract has had time to recover from its long refractory time and is now open for conduction again. The impulse spreads back up the fast tract. However, this time it will not be cancelled out by an impulse coming down simultaneously through the tract. When the retrograde impulse has been conducted back up again, it will now find the slow tract open for business again, because of the fast refractory time. And voilá, a reentry circuit is born. As you may understood, when the retrograde impulse reaches the atria again, atrial depolarization occurs. And as atrial activation happens after ventricular activation, the P wave follows the QRS complex. The P wave is inverted in leads II, III and aVF because it travels away from these leads.
Adenosine effect
This patient was given a 6mg rapid iv push of adenosine. Here is the electrocardiographic display of what happened. These complexes are extracted from the full rhythm strip presented further down.
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Here are the full 12 lead rhythm strips recorded during adenosine injection. They are recorded in 50mm/s to make it easier to distinguish P waves.
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May 11, 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