The P wave is fundamental, and unlike other waves, the normal values do not change significantly at different ages. But T & R fly. In sinus rhythm , the P wave is the sequential activation of the right and left atrium. It can be monophasic, but it is not uncommon for it to be notched or biphasic. The right atrial vector points down and ahead, while the left atrial vector points to the rear, to the left and down (Fig. 3.1). The resulting axis is in the left lower quadrant (0–90°), and the lead that sees it best is lead II, in addition to V1. The P wave can be +/− biphasic in all three inferior leads, while in aVL, it can be biphasic −/+, positive or negative. It must not, however, be negative in lead I; in this case, ectopic rhythm, malposition of the electrodes or dextrocardia should be suspected.

For all age groups, the amplitude limit is 2.5 mm, apart from newborns/infants where it extends to 3 mm up to 6 months. Especially in the very young, left atrial hypertrophy can be missed when a time limit of 120 ms is employed, given the smaller size of the atria and the greater atrial conduction velocity.

The diagnosis of atrial enlargement is valid only with ECG in sinus rhythm, as atrial ectopic beats may create an infinite spectrum of amplitude and duration of P waves [1]. Atrial enlargements are a result of a pressure overload (outflow obstruction or ventricular hypertension) or volume (insufficiency of atrioventricular valves [AV] or shunt) of the atria.

In right atrial enlargement (Fig. 3.2), in sinus rhythm, and in situs solitus, there is an increase in voltage of the initial atrial vector, while the voltage of the left atrium is unaffected; since the P wave is the sum of the right and left components and the left follows the right, there is no appreciable prolongation of P wave duration in right atrial enlargement:

In left atrial enlargement (Fig. 3.3), you can see an increase of the voltage and the duration of the second component of atrial activation. Especially in smaller infants, the P wave distortion can be particularly evident in V1. The main criteria of left atrial enlargement are:

Chest deformities such as pectus excavatum can also alter the morphology of P waves, especially in the right precordial leads. This can sometimes be bizarre, as in pathological conditions marked by right atrial enlargement, for instance, Ebstein’s anomaly or pulmonary atresia with intact ventricular septum. Staying with V1, the negative component that is attributed to the left atrial overload has a low specificity and, if there are no clinical, pathological murmurs or other signs of left ventricular hypertrophy, is therefore not pathognomonic.

The polarity of the P wave can reveal the visceral-atrial situs: in situs solitus and levocardia , the axes of P and QRS are concordant in the lower left quadrant, while in situs inversus and dextrocardia , they point down and to the right (atrial situs usually follows the visceral situs) (Figs. 3.4, 3.5, and 3.6).

It is therefore a good sign that in levocardia, the right atrium is on the right and in dextrocardia it is on the left: in fact, the “squinting” between the P wave and the QRS axes shows a discrepancy between situs and heart position, such as dextrocardia in situs solitus (Table 3.2; Fig. 3.7). This can be an important clue as this pattern may be an indicator of complex heart defects not obvious in dextrocardia with situs inversus. When faced with abnormal P wave polarity within the framework of complex congenital heart disease, you should search for a heterotaxy condition, namely, ambiguous sites: the sinus node is a “right-hand” structure, so a right atrial isomerism can have two symmetrically located and competitive sinus nodes (Fig. 3.8). Conversely, with a left isomerism, the sinus node may be missing and replaced by ectopic and migrant pacemakers (Fig. 3.9). There may also be two AV nodes in the right isomerism, the so-called twin AV node, prone to the unusual node-to-node reentry, distinctive because of the possibility of finding two supraventricular tachycardias in the same patient, each with a different QRS morphology [2], since both AV nodes can be traveled alternately in an anterograde or retrograde direction (Fig. 3.10).

Sinus or phasic (respiratory) arrhythmia is common and normal; during inspiration, the heart rate increases. By definition, the morphology of the P wave should not change in the two phases; however, even in respiratory periodicity, it is possible to observe two distinct P wave morphologies. Due to the augmented vagal tone during expiration, the sinus node can be slightly inhibited with the escape of alternative atrial foci, located close to the sinus or more distally in the lower right atrium (the so-called coronary sinus rhythm); the P wave morphology therefore changes accordingly.

Note that the lower the heart rate, the more acceptable a physiological dualism of the atrial rhythm, while at high frequencies, the hypothesis of automatic atrial tachycardia should always be considered. A low rhythm of the coronary sinus is not rare, and in this case, the atrial vector follows a direction from bottom to top, and the inferior leads will record a negative P wave. The pathological significance therefore depends on the heart rate, and according to age and circadian persistence, you must rule out an automatic atrial tachycardia. The low atrial rhythm is more common in the presence of dilated coronary sinus, usually due to a persistent left superior vena cava (PLSVC) draining into it. This vascular anomaly can be found in various congenital heart diseases, from a simple bicuspid aortic valve to the more complex such as tetralogy of Fallot. Therefore, when faced with a low atrial rhythm, the patient’s medical history and objective examination must be more scrupulous than normal, and in the event of doubt, an echocardiogram is also warranted (Fig. 3.11).

Regarding heart rate, the myth of the declining rate from fetus to old age (heart rate decreases from womb to tomb) should be debunked since the cardiac sympathetic nervous system can mature after the parasympathetic nervous system, justifying a certain bradycardia (Table 1.​2). So, during examination, a newborn can have a heart rate of around 80 bpm and a 6 year-old child a rate of up to 120 bpm. Consistently low heart rates and those unresponsive to stimuli or activities (a heart rate of 60–80 bpm of a baby while feeding or crying is unacceptable) should trigger a warning of long QT with 2:1 AVB (Fig. 3.12a), blocked bigeminal PAC (Fig. 3.12b), and congenital atrioventricular block (AVB)—associated or not with structural heart disease (Fig. 3.12c). Neonatal bradycardia may be due not only to primarily cardiac situations, such as neurological conditions (hypoxia, intracranial hypertension) or endocrine-metabolic conditions (hypothyroidism). Channelopathies such as Brugada syndrome or related to ion channels other than those of sodium may occur with undue sinus bradycardia. In general, fever increases the HR by about 10 beats per Celsius degree, and physiological sinus tachycardia is expected not to exceed 220 bpm. This concept only partially helps in the management of the newborn/infant that reaches the emergency room in a critical condition and tachycardia. In such cases, the differential diagnosis includes sepsis, heart failure, and paroxysmal tachycardia.

The PR interval depends on age and on the autonomic nervous system, and therefore a newborn usually but not necessarily has a shorter PR than a child’s PR. To make a diagnosis of pre-excitation, you should see a clear delta wave. Although pre-excitation is in the great majority of cases an isolated condition, it sometimes accompanies congenital heart disease and storage diseases, a concept which recommends an echocardiogram (Fig. 3.13). The accessory pathway can itself be defined as the smallest congenital heart disease: it is an anatomically distinct structure—although invisible to the naked eye—that can be ablated permanently with a transcatheter procedure. Before the advent of radio-frequency catheter ablation (RFCA), surgery was the only way to permanently remove an accessory pathway, like any congenital heart disease.

Pre-excitation syndromes include Mahaim fibers, meaning complex AV connections (atrio-fascicular, atrioventricular nodal, etc.), where the resting ECG may show a normal PR, a nuanced pre-excitation, and an rS pattern in lead III.

A short PR interval is also compatible with physiological and harmless low atrial rhythm (where the rhythm arises in a site close to the AV node) or severe storage disease and hypertrophic cardiomyopathy phenotype (Pompe, Danon, and Fabry disease, mitochondrial disease, PKRG2 etc.). In the newborn, the normal PR ranges from 80 to 150 ms, in children and adolescents from 120 to 200 ms. Ten percent of young people can have a PR at the upper limit for their age in the absence of heart disease; an intermittent second-degree AV block can be found in 5% of the young, especially in athletes, and is physiological during the night, while if it occurs in the waking state or during activity, it requires investigation.

At the normal rate for a child (100–150 bpm), the PR interval can range between 80 and 120 ms but occasionally can even reach 150 ms to 180 ms. During 24-h Holter monitoring, it is not uncommon to see values around 200 ms. An enhanced vagal tone may explain this phenomenon in the presence of concomitant bradycardia; conversely, in the case of sinus tachycardia or during exercise, the lengthening of the PR cannot be justified by the vagal tone (Table 2.​1).

A long PR associated with right bundle branch block (RBBB) is suggestive of ostium primum-type atrial septal defect (ASD) in the setting of endocardial cushion defects (atrioventricular canal) but can also be compatible with channelopathies such as Brugada syndrome. However, in causing first-degree AVB, benign causes are much more numerous than malignant ones, and medical history and context are important. First- and second-degree AVBs, up to complete block, can be explained by electrolyte imbalance and enhanced vagal tone but are nonetheless compatible with congenitally corrected transposition of the great vessels (CCTGA or L-TGA), atrioventricular canal (AVC), neuromuscular diseases, rheumatic and Kawasaki disease, borreliosis, and laminopathies. AVB 2:1 is typical of congenital long QT syndrome. In fact, prolonged repolarization can inhibit AV 1:1 conduction; the beta-blocker used in this setting resolves the block in a seemingly paradoxical way, reducing the sinus rate and allowing the 1:1 conduction, but without shortening the QT interval duration (Table 3.3). Even bradycardia due to bigeminal atrial extrasystole with “blocked” atrial impulses can surprisingly be treated with beta-blockers (Fig. 3.12b). In pregnant women with systemic lupus erythematosus, Sjögren’s syndrome, or other immunopathies, the fetal AV node can be damaged by the maternal antibodies, and when this happens, it usually results in complete AVB and very rarely in a lesser degree of AVB. Among the causes of acquired PR lengthening, we should not forget rheumatic disease, which represented a Jones minor criterion (now downgraded to a sign suggestive of recent streptococcal infection) [3]. A transient QT prolongation can also be very occasionally seen in the course of rheumatic disease.