The primary evident abnormalities that took attention at the patient’s ECG were positive QRS complex; upright P and tall R wave in lead aVR. In such cases, incorrect lead placement, dextrocardia, acute coronary syndrome, and an often-overlooked detail, which is the ECG display format, should be considered. The first steps in ECG readingis to check the aVR lead before starting to evaluate the whole. The aVR stands for the augmented vector where the positive electrode is on the right shoulder. It is a unipolar lead facing the right upper side of the heart. It also gives reciprocal information on the left lateral side of the heart, which is already covered by leads aVL, I, II, V5, and V6. All waves (P, QRS, and T) are negative in aVR in normal sinus rhythm, as all the depolarization waves diverge away from lead aVR . Therefore, any difference in the QRS polarities suggests an abnormal situation as in our patient. We talk about possible reasons.
Incorrect limb lead placement is one of the most common reasons that should come to mind first. With LA and RA reversal, lead DI becomes inverted, lead aVR becomes positive and right axis deviation can be seen. With RA and LL reversal, leads I, II, III and aVF are all inverted and lead aVR becomes upright. AVR remains unchanged with LA and LL reversal .In contrast to dextrocardia, normal R-wave progression is present in the precordial leads.
Another reason that should primarily come to mind is dextrocardia. However, in dextrocardia, we should expect poor R wave progression in precordial leads with negative QRS complexes in lead I which were absent in our case .
One of the rare reasons other than those mentioned above is acute coronary syndrome. Especially in anterior myocardial infarction with ventricular aneurysm, we may see tall R waves in aVR, called Goldberger’s sign. However, it should be accompanied by persisted ST elevation in precordial leads .Butour patient had widespread ST depressions in the precordial leads.
Another reason that can be often overlooked is ECG display format. The classical system is widely use in United States, most of European countries, Asia and Africa. In the classical system, the limb leads are displayed within the frontal plane by dual sequences as 60° intervals between lead I, lead II and lead III and 120° intervals between lead aVR, lead aVL and lead aVF. The lead aVR exits at − 150 ͦ in the frontal plane. However, the Cabrera system presents six anatomically ordered frontal plane leads. It reverses the polarity of lead aVR and presents the ECG complexes in the order of aVL, I, -aVR, II, aVF, III, respectively (Fig. 4) . The lead -aVR exits at 30 ͦ in frontal plane. Thus, lead –aVR fills the gap between lead I and lead II in the coordinate system. While all depolarizations approach to lead -aVR, all waves (P, QRS, and T) are positive in aVR in normal sinus rhythm. Evaluation of leads aVL, I and -aVR together improves the diagnosis of acute lateral wall ischemia or infarction. In addition, using –aVR facilitates cardiac electrical axis determination. Cabrera system has been the routine display method in Sweden for many years. Routine use of the Cabrera sequence was recommended as an alternative by American Heart Association in their AHA/ACC/HRS scientific statements report . It was suggested that manufacturers should be encouraged to offer this display as a routine option in new electrocardiographs. At present, all modern ECG machines can be easily switched from the standard system (aVR) to the Cabrera system (-aVR).
We admit that we had never used the Cabrera system before. We did not pay attention to the minus sign in front of the aVR statement indicating -aVR in the ECG paper at first look. First, we excluded incorrect lead placement and dextrocardia. Then we realized the difference in the ECG display format and repeated ECG at standard display format using another machine.
Finally, it was decided that ECG changes mentioned above might be related to autonomic dysfunction due to acute cervical trauma. In the heart, sympathetic stimulation shortens action potential duration and reduces transmural dispersion of repolarization on both atrial and ventricular myocytes while parasympathetic stimulation prolongs action potential duration and effective refractory period in the ventricles, but reduces the atrial effective refractory period augments spatial electrophysiological heterogeneity and promotes early after depolarization toward the end of phase 3 in the action potential in the atria. Thus, autonomic dysfunction leads to varying changes action potential that affect to all ECG components including QRS complex, ST segment, QT duration.
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