A young athlete with bradycardia

Short answer

Second degree atrioventricular block.

Long answer

The ECG shows second degree atrioventricular block but this cannot be classified further into Mobitz type 1 (Wenckebach) or type 2 block.

Mobitz type 1 block usually occurs in the atrioventricular node and is most commonly caused by functional suppression of nodal conduction—for example, by drugs, ischaemia, or increased vagal tone. Under these circumstances, nodal cells exhibit progressive fatigue—seen on the ECG as a gradually increasing PR interval—which eventually culminates in failure of conduction and a “dropped” beat. Subsequent recovery of the nodal cells occurs during the ensuing pause, resulting in shortening of the next conducted PR interval. Although this is the typical “textbook” definition, atypical patterns are also seen, and in some instances (particularly when associated with a broad (≥120 msec) QRS complex) type 1 block can occur in the His-Purkinje system.1 Nodal type 1 block is usually reversible and benign.

In contrast, Mobitz type 2 atrioventricular block is an “all or nothing” phenomenon, resulting from disease in the His-Purkinje system. Cells suddenly fail to conduct an atrial impulse. Mobitz type 2 block usually reflects underlying structural damage to the conduction tissue distal to the atrioventricular node. Mobitz type 2 block is an indication for insertion of a permanent pacemaker, regardless of symptoms, because of the high incidence of progression to third degree atrioventricular block or asystole. The PR intervals before and after the blocked beat remain constant.

This young athlete’s ECG shows a regular rhythm with a narrow QRS complex at a rate of 40 beats/min, resulting from 2:1 atrioventricular block. The atrial rate remains regular at about 80 beats/min. When a 2:1 pattern is present, second degree atrioventricular block cannot be classified as Mobitz type 1 or 2 because this requires analysis of the PR interval in two consecutive conducted beats. In this situation, the rhythm is best described as “2:1 second degree atrioventricular block.”

Short answer

The atrioventricular conduction ratio is 2:1

Long answer

The ECG shows a fixed ratio of conducted to non-conducted atrial impulses, with one QRS complex for every two P waves (P1 and P2 on fig 2⇓). At first glance, the second P wave (P2; fig 2) may be misinterpreted as being a U wave after the preceding T wave; however U waves are of smaller deflection (<1 mm, usually 0.5 mm or <25% of the T wave voltage) and often best seen in V2 and V3.2 In this case, P2 has a relatively large amplitude and P1 and P2 have exactly the same morphology. The atrioventricular conduction ratio is therefore 2:1.

Fig 2 The young athlete’s 12 lead electrocardiogram showing the conducted (P1, black) and non-conducted (P2, red) P waves

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Short answer

Training related (exercise induced) second degree atrioventricular block.

Long answer

Second degree atrioventricular block is probably caused in this young athlete by a training related (exercise induced) increase in parasympathetic tone. Regular intensive physical activity results in several electrical, structural, and functional cardiac adaptations that together constitute the “athlete’s heart.” Cardiac output, the product of heart rate and stroke volume, can increase by as much as five to six times during intense exercise. Initially, heart rate is the main determinant of this rise and increases as a result of sympathetic activation and sustained parasympathetic withdrawal during physical activity.3 However, maximal heart rate is intrinsic to an individual, decreases with age,4 and does not increase with exercise training.5 This is in contrast to stroke volume, which increases with regular intensive physical activity from a combination of enhanced left ventricular filling, increase in left ventricular end diastolic volume, increased force of contraction (partly through left ventricular hypertrophy), and reduction in left ventricular end systolic volume. This increase in stroke volume, coupled with peripheral vascular changes and reduced peripheral vascular resistance, is the main mechanism that allows athletes to sustain an increased cardiac output for prolonged periods of time.6

At rest, partly because of the enhanced stroke volume stimulated by exercise, opposite autonomic effects occur, including parasympathetic activation (increased “vagal tone”) and a reduction in resting heart rate.7 However, the precise mechanisms that underlie training induced increases in resting cardiac vagal tone in humans are still unclear.8

As part of the constellation of athlete’s heart and increased parasympathetic tone at rest, conduction alterations on the ECG are common in trained athletes. Such alterations include sinus bradycardia, first degree atrioventricular block, and Mobitz type 1 second degree atrioventricular block. In almost all cases, these training related conduction changes are mediated by the increase in parasympathetic tone at the level of the atrioventricular node, are benign, and can be readily distinguished from pathological changes including Mobitz type 2 second degree and third degree block.9 10 Occasionally, however, the diagnosis may not be straightforward to the untrained eye.

Short answer

The easiest way to confirm the diagnosis and level of block would be to repeat the ECG after gentle exercise.

Long answer

It can be challenging to determine the site of atrioventricular block when a 2:1 conduction pattern is present because the location may be nodal or infranodal in either the bundle of His or Purkinje system.11 The distinction is clinically important, however, given the implications, management, and prognosis of atrioventricular block at these different sites. Several features can help solve the problem.12 13

Firstly, two consecutive conducted P waves should be identified on a long ECG rhythm strip. Generally, PR intervals that vary or are prolonged support the diagnosis of Mobitz type 1 block at the level of the atrioventricular node. If there is sudden intermittent block of a single P wave, but the PR intervals before and after the blocked impulse remain constant, then Mobitz type 2 block is present at the infranodal level. In the case of our athlete, a subsequent rhythm strip showed Mobitz type 1 block (fig 3⇓).

Fig 3 A rhythm strip from this young athlete showing features consistent with Mobitz type 1 block

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Several features of Mobitz type 1 block present in this strip are worth highlighting:

• Although successive PR intervals generally get longer, atypical patterns can occur in 50% of cases.12 For example in this rhythm strip, the third PR interval mid-sequence shortens. In other cases, the PR interval may stabilise mid-sequence. Hence it is PR inconsistency rather than progressive PR lengthening that is important to observe when making the diagnosis

• The greatest increase in the PR interval is usually (but not invariably) between the first and second conducted beats of a cycle (here 340−220 msec=120 msec)

• The blocked P wave may be partially buried in the T wave (as with the fifth P wave in the sequence shown)

• The longest PR interval is the one immediately before the dropped beat

• The PR interval of a conducted P wave immediately after the blocked beat always shortens.

Secondly, exercise causes sympathetic activation and hence improvement in conduction at the level of the atrioventricular node, which is innervated by the autonomic nervous system. Therefore, Mobitz type 1 block improves or disappears with exercise. After our young athlete jogged on the spot for five minutes, a repeat ECG showed sinus rhythm with first degree heart block (fig 4⇓).

Fig 4 The young athlete’s electrocardiogram after exercise

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In contrast, Mobitz type 2 block usually occurs in the His-Purkinje system, which is insensitive to the effects of sympathetic activation. Exercise increases the sinus rate and atrioventricular nodal conduction, allowing more impulses to reach the His-Purkinje tissue. However, this faster rate may now have a shorter cycle length than the intrinsic refractory period in the His-Purkinje tissues. This will therefore appear to “worsen” the block by increasing the number of blocked impulses and worsening the conduction ratio.

Thirdly, a narrow QRS complex suggests Mobitz type 1 block, whereas a broad QRS complex suggests Mobitz type 2 block.

The presence of several features stated above strongly suggests that the mechanism of 2:1 atrioventricular block in this young athlete is an exercise induced increase in vagal tone. One feature that is a little unusual, however, is the presence of a relatively high atrial rate of about 80 beats/min at rest (figs 1 and 2) and after exercise (fig 4). Given the rich innervation of the sinoatrial node by parasympathetic nervous system fibres, a lower atrial rate at rest would be expected, which subsequently increases with parasympathetic withdrawal and sympathetic activation during exercise.

Importantly, atrioventricular block with a 2:1 pattern can sometimes represent infranodal conduction disease in the His-Purkinje system and potentially warrant a permanent pacemaker.11 If the clinical diagnosis is unclear, certain features in the history should be elicited and the patient referred to a specialist for further investigations to rule out more sinister conduction defects. Such defects may be secondary to other medical disorders, including:

• Inflammatory diseases such as endocarditis, myocarditis, and Lyme disease. If these are suspected, investigations should include blood inflammatory markers, Lyme serology if there is a history of tick bites, and echocardiography

• Infiltrative diseases such as amyloidosis, haemochromatosis, and sarcoidosis. Investigations would include serum concentrations of ferritin and angiotensin converting enzyme, echocardiography, and cardiac magnetic resonance imaging

• Metabolic and endocrine disorders such as hypermagnesaemia, hyperkalaemia, Addison’s disease, hyperthyroidism, myxoedema. Investigations include measurement of serum electrolytes and glucose, thyroid function tests, and an adrenocorticotrophin stimulation test for Addison’s disease if clinically indicated

• Collagen vascular diseases such as rheumatoid arthritis, scleroderma, systemic lupus erythematosus, ankylosing spondylitis, Reiter’s syndrome, and mixed connective tissue disease. Investigations include rheumatoid factor and relevant autoantibodies

• Neuromuscular conditions such as myotonic dystrophy, Kearns-Sayre syndrome, Erb’s muscular dystrophy, and peroneal muscular atrophy. Investigations may include measurement of serum creatine kinase concentrations

• Infiltrative cancers such as lymphomas and multiple myeloma. Investigations include serum electrophoresis and measurement of urinary Bence-Jones proteins

Finally, invasive electrophysiological studies can help determine the level of block in patients with suspected but unconfirmed His-Purkinje (infranodal) disease. This can be achieved by measurement of the HV interval, which is the conduction time from the His bundle (located just below the atrioventricular node) to the first identifiable onset of ventricular activation.

Short answer

This young athlete should be managed conservatively. A permanent pacemaker is not warranted in this situation.

Long answer

Given our findings and the likely vagal, benign cause of the atrioventricular block, a permanent pacemaker is not warranted. The patient should be warned of sinister symptoms to look out for, including episodes of syncope, and simply monitored on a regular (annual or two yearly) basis.