There is one thing that neonatologists and one of the greatest Italian poets, Giacomo Leopardi, agree on: the first 48 h of man are the most dangerous—man is born with labor, and the risk of death is birth [1, 2]. Even the easiest childbirth involves dramatic adaptations. Dystocia, asphyxia, diaphragmatic hernia, and infectious, toxic, metabolic, or respiratory agents affect the pulmonary circulation, opposing the physiological decline in arterial resistance. The right ventricle is the first to pay the hypoxic-ischemic bill, but in severe cases the left is not much better off. We are talking in these cases of persistent pulmonary hypertension or neonatal transient ischemia. There are mild forms with slight cyanosis and tricuspid regurgitation and lethal forms with severe global dysfunction. The ECG reveals, in order, right overload beyond the norm or diffuse ischemia. Likewise, therapy ranges from just a whiff of oxygen to extracorporeal membrane oxygenation (ECMO) ; the latter drastic resolution is nowadays often obviated by sildenafil and nitric oxide [3].

Does anyone remember the controversy about neonatal long QT screening that inflamed the 1990s? Only the members of the lined-up troops remain, skeptics versus incurable optimists [4, 5]. Now each country behaves in its own way, with a trend to a historical opposition between “Americans” and “Italians.”

The first would never do an ECG; the second do it to everyone. According to the Italians, the ECG is a valuable tool because it sees not only diseased ion channels but also canal diseases (partial, intermediate, and complete atrioventricular canal defect).

Complete neonatal AVB affects one newborn in 20,000 and is always pathological. In a third of cases, it is associated with structural heart disease (CCTGA, CAVC, Ebstein’s anomaly); in others it is idiopathic or autoimmune as in children of mothers with SLE. Complete AVB is usually recognized during ultrasound fetal examination.

There are serious heart diseases that can escape a fetal ultrasound and can manifest dramatically in the first month of life, due to the closure of the ductus arteriosus. Aortic coarctation stands out in this group, and an ECG could contribute to the diagnosis, when palpation of femoral pulses is not enough.

In summary, if for some reason you come across a neonatal ECG, you should assess three main aspects: P waves and HR, QRS axis, and repolarization. The parameters of normality of all these points have already been described. Even a quick glance should never miss a left axis deviation: if associated with long PR and RBBB, you have to consider AVC (partial or complete defect); if associated with normal PR and too “adult” precordial leads, without the expected right ventricular prevalence typical of infants, then tricuspid atresia must be considered. As far as repolarization is concerned, not only is the quantity (in the neonate the QT is normal up to 490 ms) important but also the quality. You must take into account that especially in the precordial leads, finding slightly elevated ST traits and small negative T waves can be normal in the first week of life, much more than finding a depressed ST and negative, large, and symmetrical T waves (Figs. 5.1 and 5.2).