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Type 2 Second Degree Heart Block | Management and treatment

Heart block or block: heart rhythm disorder secondary to an intracardiac electrical conduction defect, complete or incomplete. In this article, you’ll learn about Type 2 Second Degree Heart Block.

Atrioventricular blocks are seen in patients of all ages who sometimes present to the office with bastard symptoms (fatigue, lassitude), which can delay diagnosis and management. The correlation between symptoms and ECG is essential for making a diagnosis, but it can take a long time to establish and require repeated or long-term ECGs.

About Type 2 Second Degree Heart Block

Atrioventricular (AV) conduction disorders are conducive disorders (delay, momentary or complete interruption of conduction) between the atria and the ventricles following an anatomical or functional obstacle. 

They are transient, intermittent or permanent, symptomatic or not. They can be found in an apparently healthy heart, in underlying heart disease, or in other pathologies. Finally, they can be caused or worsened by taking certain medications. 

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The practitioner is frequently confronted in his clinical activity with patients suffering from AV conduction disorders; if the electrocardiographic diagnosis and therapeutic management are generally easy, they can nevertheless sometimes pose some difficulties.

AV blocks for Type 2 Second Degree Heart Block

One distinguishes the AV block 1 st , 2 e and 3 e  degree (or complete block), the blocks 2: 1, and the blocks of high degree.

1st degree AV block

Strictly speaking, it is not a block but a slowing down of conduction since all sinus P waves are conducted to the ventricles. It can be recognized on the electrocardiogram (ECG) at a PR interval greater than 200 ms (standard: 120 to 200 ms) (fig. 1). While the PR interval is rarely prolonged in young adults, the prevalence of 1st  degree AV block (AVB) is 5% beyond 70 years. The PR interval includes the passage of electrical conduction through the atria, the atrioventricular node, the trunk of the bundle of His and its branches, and the fibers of Purkinje. Contrary to popular belief, it is not just a reflection of conduction through the AV node which, it is true, represents the most important part of the PR interval. If in the AV block of 11st  degree, the conduction delay is most often intra-nodal, it can also sit in the atria or the His-Purkinje system. Physiologically, the PR interval shortens with effort and lengthens during vagal stimulation (sleep, rest, sports patient).

The AVB of 1 st degree is usually asymptomatic. However, when the PR interval massively lengthens, the atrial contraction occurs synchronously with the ventricular contraction initiated by the preceding QRS complex [1]. This alteration in the physiological sequence of the contraction of the cardiac chambers can cause symptoms similar to those of pacemaker syndrome (malaise, dyspnea, hypotension, etc.).

If the ECG shows a PR ≥ 300 ms followed by a fine QRS, the block is most often located in the AV node [2]. If the 1st-degree block is associated with a wide QRS, it may be secondary to an infra-nodal conduction disorder (tab. 1).

Table 1: Site of the block according to the ECG.
AV blockQRS endWide QRS
st  degreeMost often nodalNodal and / or infra-nodal
e  degree type I (Wenckebach)Rarely infra-nodalNodal more often than infra-nodal
e degree type II (Mobitz)Infra-nodal much more often than nodalRarely nodal
≥2: 1Nodal or infra-nodalRarely nodal
e  degreeMost often nodalMost often infra-nodal

As for the prognosis of 1st-degree AVB , it differs depending on the studies which have often included various groups: some of them show an increase in mortality or cardiovascular morbidity, others not. Finally, an increased risk of atrial fibrillation (AF) and permanent pacemaker implantation associated with 1st-degree AVB has also been reported [3, 4].

2nd degree AV block

nd degree AV block is characterized by the occasional block of a sinus P wave [2, 5].

There are 2 types: type I AV block (Wenckebach), the most common form, and type II block (Mobitz) much rarer.

In its typical form, the Wenckebach is characterized by the gradual lengthening of the PR intervals before a P wave is blocked; the PR interval following the blocked P wave is shorter than the one preceding it. The duration of the break thus caused is less than twice the basic PP interval. This repeating sequence gives the ECG a so-called “cluster beating” appearance of QRS (Fig. 2). In a large proportion of cases, the criteria described above are not actually all present; we then speak of atypical Wenckebach [2, 5]. Wenckebach is found in 1-2% of young, healthy patients, often during sleep.

The AV block 2 e  degree type II (Mobitz) meanwhile, is characterized by the sudden interruption of AV conduction: a P-wave is blocked without PR interval elongation which – unlike the Wenckebach – remains the same after each conducted P wave (fig. 3). The pause including the blocked P wave is equivalent to 2 basic PP intervals. The PR interval which is fixed can be normal or prolonged. If prolonged, the QRS complex is often enlarged [2, 5].

In the AV block 2 e  degree type I, if the QRS complexes are fine, the block headquarters is mostly intra-nodal. In type II, the block is most often infra-nodal: it can be intra-Hisian if the QRS complex is fine or infra-Hisian if the QRS is large (tab. 1). The presence of a widening of the QRS complex, a bundle branch block, or an abnormality of the QRS axis (eg presence of a hemiblock) is a sign of infra-nodal impairment of the conduction pathways; these associated electrocardiographic changes should be taken into account because they are useful in determining the site of the AV block (tab. 1).

Intra-Hisian AV block is rare; it is usually signaled by a fine QRS and a sudden transition from a 1: 1 conduction to a 2: 1 block in sinus tachycardia. It is sometimes encountered during a stress test characterized by a ventricular cadence suddenly dropping by half. 2 nd  degree type II AVB can progress to full AVB.

To better locate the level of AVB (nodal vs infra-nodal), we will also use vagal maneuvers: they will slow down intranodal conduction (increase in blocked P waves) but improve conduction in the hisic tract because the sinus frequency will be slowed down. (decrease in blocked P waves). Conversely, exercise and atropine will improve conduction through the AV node but worsen infra-nodal conduction disorders.

The AVB 2 th  degree is often not symptomatic and the importance of symptoms can vary. Sometimes the patient may notice an irregular heartbeat. He may complain of fatigue, dyspnea, angina, or even syncope if the AVB suddenly progresses.

BAV 2: 1 Type 2 Second Degree Heart Block

It is defined by a blocked sinus P wave of 2 (fig. 4).

BAV 2: 1 Type 2 Second Degree Heart Block

In the presence of fine QRS complexes, if the PR interval is ≥ 300 msec the site of the block is most likely nodal but if the PR is normal (especially ≤160 ms) the block is most likely infra-nodal. If the QRS complexes are large (in the presence of bundle branch block, for example), the site of the block is most likely infra-nodal (tab. 1). To be more precise, it is necessary to modify the relation between the P waves and the QRS complexes to obtain at least 2 successive conducted P waves. A long-term ECG may show a spontaneous change in conduction. But sometimes for obtaining at least two successive P waves and transform conduction pipes 2: 1 3: 2 4: 3, we will vagal maneuvers for the BAV 2 e degree; prolongation of the PR interval suggests a block located in the NAV while a fixed PR suggests an infra-nodal block [2, 5].

Atropine is contraindicated when the probability of an infra-nodal block is high (2: 1 AVB with wide QRS; 2: 1 AVB of prolonged duration, 2 nd  degree AV block type I with broad QRS) because it risks to worsen the block.

High degree AVB

In high degree AVB (sometimes called “  advanced 2 nd degree”) ≥2 successive sinus P waves are blocked but conduction is not completely interrupted because some P waves are conducted. The relation P: QRS can be for example 3: 1, 4: 1.

The anatomical level of the block can be nodal (QRS complexes are generally thin) or infra-nodal (QRS complexes are generally wide) (tab. 1) [2, 5]. In high degree block, atropine injection is contraindicated because it may worsen the underlying conduction disorder; if the high degree block is poorly tolerated hemodynamically, an infusion of dopamine (2–20 µg / kg/min) or isoprenaline should be used while waiting for the establishment of transcutaneous cardiac stimulation, a temporary stimulation probe or implantation of a permanent pacemaker.

3rd degree or full BAV Type 2 Second Degree Heart Block

It is defined by the total interruption of conduction between the atria and the ventricles. No P wave is conducted and there is the dissociation between the sinus and ventricular activities. P waves and QRS have their own – unrelated frequency – and the ventricular rate (= escape rate) is lower than the sinus rate (Fig. 5). The block can be intranodal (the escape rate is most often at fine QRS) or infra-nodal (the escape rate is most often at wide QRS) (tab. 1) [2]. Fixed ventricular rate atrial fibrillation should raise the suspicion of an underlying complete AVB.

3rd degree or full BAV Type 2 Second Degree Heart Block

The patient on complete AVB is generally symptomatic: fatigue, dyspnea, angina, syncope.

Complete AVB is often poorly tolerated hemodynamically; an infusion of dopamine or isoprenaline generally makes it possible to restore the situation before the implantation of a temporary stimulation lead or that of a permanent pacemaker.

Finally, congenital AV block is present in 1 / 10,000–15,000 births; it is linked to the presence of maternal antibodies resulting from lupus or Sjögren’s disease and most often located in the NAV.

Etiology of AV blocks 

Hypertonicity vagal as encountered in major sports, during sleep or when severe pain is responsible for AV block 1 st  degree and 2 e physiological and reversible type I degree. Fibrosis/sclerosis of the conduction tissue is the most common so-called idiopathic cause of AV conduction disorders. Among the heart attacks responsible for AV conduction disorders include: ischemic heart disease, myocarditis (sarcoidosis, Lyme disease, lupus, etc.), dilated, infiltrative cardiomyopathies (amyloidosis), endocarditis, and congenital heart disease. Familial forms of AV blocks transmitted in an autosomal dominant fashion are also encountered. Other known causes are hyperkalemia, dysthyroidism, heredodegenerative neuromuscular diseases (Duchenne, Emery-Dreyfuss, Becker’s disease, etc.), and dermatomyositis.

Finally, the taking of drugs that alter AV conduction should be actively sought: beta-blockers, non-hydropyridine calcium-free agents, digoxin, sotalol, amiodarone.

Invasive cardiological therapies can have complications or undesirable consequences of AV conduction disorders: valve surgery, percutaneous valve replacement, ablation of arrhythmogenic substrate close to the nodo-hisian conduction pathways (nodal tachycardia, accessory bundle, atrial tachycardia, etc.), alcoholism septal for hypertrophic cardiomyopathy. Finally, the ablation of the AV junction followed by the implantation of a permanent pacemaker is the treatment of last resort in the event of atrial tachyarrhythmia with a ventricular rate not controlled by drugs.

Electrophysiological exploration of Type 2 Second Degree Heart Block

When the ECG is insufficient, electrophysiological exploration may be indicated when the AVB is suspected to be the cause of syncope or to determine the anatomical site of the AVB.

Prognosis

The prognosis of AVB is directly related to its degree and the underlying pathology. Patients with advanced AVB who are not treated with a permanent pacemaker are at risk of syncope and sudden death, especially if there is underlying heart disease.

Management and treatment of Type 2 Second Degree Heart Block

Poor hemodynamic tolerance (hypotension, confusional state, malaise, syncope) requires urgent management. Atropine 0.5 mg – 1 mg iv is the first treatment; it is not indicated in the event of a suspected infra-Hisian block. In these cases, an infusion of dopamine (in case of hypotension), dobutamine (in case of heart failure), or isoprenaline will be started. 

However, these drugs should be handled with caution in patients with acute ischemia or unstable coronary artery disease as they may worsen the underlying ischemia or cause potentially malignant ventricular arrhythmias. 

Finally, transcutaneous stimulation patches are applied and ready to be used until the establishment, as soon as possible, of an effective endocavitary ventricular stimulation.

Since AVB may be the expression of an underlying cardiac or non-cardiac pathology, the additional assessment will be guided by the history and cardiovascular status. 

Inflammatory, infectious, or metabolic pathologies will be looked for by laboratory examinations (e.g. Lyme disease, sarcoidosis, hypothyroidism, etc.) and the patient will be referred to the specialist for a search for heart disease. 

We must think of a genetic cause in cases of unexplained BAV in young patients (<40 years) keeping in mind that the AVB 1 st degree AV block and 2 e degree of type I are physiological in sportsmen; in these cases, the conduction disorders are asymptomatic and reversible and do not justify an additional assessment in the absence of symptoms and status anomaly. 

In older patients, 1st-degree AVB can be a marker of cardiovascular morbidity and mortality and AF. For 1st  degree AVB, no treatment is required unless the interval is very prolonged causing the equivalent of pacemaker syndrome.

The important step is to establish the correlation between the symptoms and the presence of AV block on the ECG. If this is not achieved by a simple ECG, a stress test, a Holter recording – which sometimes has to be repeated – or even the implantation of a subcutaneous event recorder may be necessary to prove that the symptoms are indeed the consequence of the AVB.

In all cases, it is necessary to exclude by a complete and precise anamnesis, a reversible cause (for example a drug effect, ischemia) at the origin of the AVB. We will therefore wait for the disappearance of the effect of conduction-inhibiting drugs or the correction of ischemia before considering the implantation of a permanent pacemaker, the indications of which are summarized in Table 2.

Table 2: Indications for implantation of a permanent pacemaker.
Atrioventricular block (AVB)Class
BAV 3 e  degree and 2 e  degree type II (Mobitz) is not symptomaticI
BAV 2 e  degree type I (Wenckebach), symptomatic or location infra-nodal electrophysiological explorationthere
AVB 1 st  degree with pacemaker syndrome (PR> 300 ms).there
No indication in the presence of a reversible AVBIII

The Essentials For Practice for Type 2 Second Degree Heart Block

• Atrioventricular blocks (AVB) can be asymptomatic, express themselves insidiously (fatigue, adynamia) but also lead to syncope.

• EKG diagnosis is usually easy but can sometimes be problematic. It is essential to establish the correlation between the AVB and the patient’s complaints, therefore to obtain a recording of the heartbeat at the time of the symptoms. This may require long recordings, provocation maneuvers or even additional investigations to obtain the diagnosis, specify the type of block and its location.

• AVB can be a simple marker of cardiovascular morbidity and mortality or the expression of an underlying pathology – cardiac or not – which should be systematically sought, especially if the patient is young.

• Treatment of the underlying pathology may allow regression or even disappearance of AVB (Lyme disease, for example).

• The implantation of a pacemaker is reserved for non-reversible, symptomatic or advanced AVBs.

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