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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
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