Concept and mechanism

When the heart rate is slow as a result of depressed sinus automaticity, sinoatrial block, or atrioventricular (AV) block, an AV junction pacemaker at a normal discharge rate (40–50 bpm) may pace the electrical activity of the heart by delivering one or more pacing stimuli (escape beat or complex and escape rhythm) (Figures 17.1–17.5). If the AV junction shows depressed automaticity, an idioventricular rhythm at a slower rate (<30 bpm) would command the heart’s activity. If the atrial rhythm is atrial fibrillation (AF), the escape rhythm is regular (Figure 17.2) and this is the demonstration of AV dissociation. This never occurs in the presence of atrial fibrillation with normal AV conduction. If the atrial rhythm is atrial flutter, a diagnosis of escape rhythm will be reached based on the slow and regular RR intervals observed, with a variable flutter wave–QRS complex interval (FR interval) (Figure 17.4).

ECG findings

In the ECG, the escape complex is recorded as a wide QRS complex not preceded by a P wave or the preceding P wave has a PR interval <0.12 sec (Figure 17.1A). The escape rhythm is identified as a sequence of dissociated escape QRS complexes (Figures 17.1–17.3), which may be interrupted by sinus captures (Figure 17.1B) that sometimes appear as bigeminal complexes. In this case, a differential diagnosis of bigeminy should be made (Figures 17.1B and 18.6I). The escape rhythm may show retrograde conduction to the atria that is usually slower than the anterograde to the ventricles (Figures 17.1C and 24.1). Sometimes, a progressively slower escape rhythm precedes asystole (Figure 17.5).

The QRS complex is narrow when the escape source is in the AV junction (Figure 17.1). Conversely, when the escape focus originates from the ventricle or from the AV junction but pre‐existent bundle branch block or phase 4 aberrancy exists, the resulting QRS complex is wide.

The occurrence of AV junctional escape rhythm or escape complexes at their usual discharge rates should not be necessarily considered pathologic, as this is usually observed in athletes or in subjects with increased vagal tone. In fact, it warrants protection against a slow rhythm. Frequently, if there is no depression of the AV junction automaticity, the implantation of pacemakers would be neither urgent nor most likely necessary. Obviously, pacemaker implantation is urgent if the slow heart rate is due to a depressed AV junctional or ventricular rhythm.

When the AV junction automaticity is very slow or an infrahisian AV block exists, the heart may be controlled by a slow ventricular pacemaker (Figure 17.3).

Concept and mechanism

In this situation, the sinus discharge rate is lower than 60 bpm. The following are the mechanisms explaining sinus automaticity depression (see Figures 14.7 and 14.8): (i) decrease of the slope of phase 4 partly due to the inactivation of the diastolic inward current (I_f); (ii) a threshold potential nearer to zero; and (iii) a more negative transmembrane diastolic potential (TDP).

Exercise, emotions, and adrenergic discharge induce a progressive acceleration of the sinus heart rate, which also shows a progressive deceleration when these physiologic stimuli disappear. The sinus node is considered to be pathologically altered when these physiologic changes do not take place.

Frequently, daytime sinus tachycardia alternates with occasional very slow bradycardia during the night, particularly in young athletes, (first‐degree or even second‐degree AV block may even occur during night) if right vagal (sinus node) and left vagal (AV node) overdrive exist (Figure 17.6) (see later).

ECG findings

Sinus automaticity depression is manifest by a slow sinus rhythm, which in young athletes or in patients with vagal predominance may even be less than 30 bpm (Bjeregaard 1983) (Figure 17.7). The sinus discharge rate is not fixed, particularly in children. All this is especially evident in the presence of sinus bradycardia. In adults, this variability from one cycle to another is usually less than 10–20%. Sinus arrhythmia may be diagnosed (Figure 17.7B,C) when RR interval variability from one cycle to another is greater than 20%. Sinus arrhythmia is considered to be mild when the change from one cycle to another is <50%, moderate when the change is between 50% and 100%, and severe if it is over 100%.

Sinus bradycardia is often observed with a normal PR interval (Figure 17.7). Sinus bradycardia and different degrees of AV block are present when a predominant vagal overdrive affects both the right vagus nerve (sinus node) and the left vagus nerve (AV node) (see above) (Figure 17.6).

Finally, it should always be taken into account that a slow sinus rhythm may rarely be explained by the presence of concealed atrial bigeminy (Figures 17.8 and 18.1). It is quite important to consider this possibility and try to identify the small P′ wave deflection at the T wave (Figure 17.8) or close to the end of the T wave, which may be confused with the U wave (Figure 18.1) (arrow), as in these cases the therapeutic approach is quite different to that of a slow rhythm due to a sinus bradycardia.

Concept and mechanism

If the sinus stimulus reaches the atria but with delay, a first‐degree sinoatrial block is observed, although the AV relation (P wave–QRS complex) is not altered. This is not the case in third‐degree sinoatrial block, where an AV junctional rhythm is the dominant pacemaker. Finally, the second‐degree sinoatrial block may be of Mobitz‐ or Wenckebach‐type, similar to the second‐degree blocks of the AV junction (see Figures 14.19 and 17.9).

ECG findings

First‐degree sinoatrial block

This cannot be detected by surface ECG and may require intracardiac recordings.

Concept and mechanism

Conduction block is observed in the AV junction. As in other types of heart block, we shall refer to first‐, second‐, and third‐degree blocks (see Chapter 14, Heart block). The etiology is due to a degenerative, infection, inflammatory or ischemic process of the AV junction. In rare cases, it may be congenital (see Chapter 24, Advanced AV block). The exact location of the block (suprahisian, hisian, or infrahisian block) is accurately determined only by intracardiac studies (see later; Figure 17.13). However, the presence of a narrow QRS complex escape rhythm and a second‐degree Wenckebach‐type AV block suggests that the block is located in the AV junction, whereas the presence of a wide QRS complex favors evidence of a block below the bundle of His.

ECG findings

We will discuss below the key diagnostic criteria of the different AV blocks that may be found in the surface ECG.

Second‐degree atrioventricular block

One or more P waves are not conducted to the ventricles despite being beyond the physiologic AV junctional refractory period (Figure 14.20B,C). Second‐degree AV block may be of a Wenckebach‐type (also known as Mobitz I) or of a Mobitz‐type block (Mobitz II). In the Wenckebach‐type AV block (Figure 17.12A), the progressive shortening of the RR interval is due to a progressive reduction of the AV block increment (180 ms–260 ms–300 ms) until a complete AV block is reached. The mechanism is explained as progressive and decremental prolongation of the PR interval until a P wave fails to conduct to the ventricles. The latter initiates a pause that is longer than any other RR interval. Therefore, a Wenckebach‐type AV block is characterized by: (i) a progressive lengthening of the PR interval, starting from the first PR interval after the pause; (ii) the most significant increase being observed in the second PR interval after the pause (Figures 14.20B and 17.12A); (iii) the pause being a longest RR interval; and (iv) the PR interval that initiates each sequence, it is always identical. However, for different reasons, these rules are not always present. Figure 14.21E shows two forms of atypical Wenckebach‐type AV block (see legend; Chacko et al. 2017).

In the second‐degree A Mobitz II‐type, the AV block and consequent pause occur abruptly without previous progressive lengthening of the PR interval. As a result, one or several P waves may be blocked (paroxysmal AV block) (Figures 14.20C and 17.12B). The second‐degree 2 : 1 AV block (one out of two P waves is blocked) may be explained by both Mobitz I or Mobitz II‐type blocks (Figure 17.12C).

On rare occasions, in the presence of a 2 : 1 block in the AV junction (higher portion), the Wenckebach phenomenon may arise from the conducted P waves themselves occurring in the lower part of the AV junction (alternating Wenckebach phenomenon) (Halpern et al. 1973; Amat y Leon et al. 1975; Baranchuk et al. 2009). Figure 14.20F shows an example of this odd electrophysiologic phenomenon.

The exact location of the block

This can only be determined by intracardiac recordings (see Chapter 25, Intracavitary ECGs and electrophysiologic studies). Figure 17.13 shows examples of first‐degree AV block after His level (prolonged HV interval) (A), second‐degree 2 × 1 block before His deflection (B), second‐degree AV block after His deflection (C), and second‐degree AV block at His level (see two H deflections—H–H′—and the block between the two His deflections H–H′) (D).

Cardiac arrest

A diagnosis of cardiac arrest is reached when the patient carotid pulse is not palpable and no cardiac sounds are heard by auscultation. In continuous ECG recording, it is observed how cardiac arrest may be preceded by a progressive bradyarrhythmia (Figure 17.5) or tachyarrhythmia, usually ventricular fibrillation (see Figures 16.30 and 16.32). Rarely, ventricular tachycardia may directly trigger the cardiac arrest (see Figure 16.8).

Patients in coronary intensive care unit usually are recovered with electrical cardioversion if the cardiac arrest is due to primary ventricular fibrillation (see Figures 16.31 and 16.32).

Hospitalized patients suffering from cardiac arrest should be treated as emergency patients (cardiac arrest protocol). The fight against out‐of‐hospital cardiac arrest

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