Does p q possibly not mean p

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Atrioventricular blocks occur in patients of all ages who sometimes come to the doctor's office with unclear symptoms (tiredness, fatigue), which can delay diagnosis and treatment. The correlation between symptoms and ECG findings is essential for making a diagnosis. It can sometimes take a long time to produce this, and repeated EKGs or long-term EKGs may be required.


Atrioventricular blocks (AV blocks) are conduction disorders (delayed, temporarily or completely interrupted conduction of excitation) between atria and ventricles that arise as a result of an anatomical or functional obstacle. They can be transitory, intermittent or permanent, as well as symptomatic or asymptomatic. They can also occur in an apparently healthy heart, underlying heart disease, or other medical conditions. They can be triggered or worsened by taking certain medications. In their clinical work, general practitioners often deal with patients who suffer from AV conduction disorders. Although ECG diagnosis and treatment of these patients are generally unproblematic, certain difficulties may arise in some cases.

The AV blocks

A distinction is made between 1st, 2nd and 3rd degree AV blocks (or complete AV block), 2: 1 and high-grade AV blocks.

1st degree AV block

In a more precise sense, this is not a block, but a delayed transfer, since all sinus P waves are transferred to the ventricles. In the electrocardiogram (EKG) this can be recognized by a PQ interval of over 200 ms (normal value: 120–200 ms) (Fig. 1). While the PQ interval is rarely extended in young adults, the prevalence of 1st degree AV blocks (AVB) in> 70 year olds is over 5%. The PQ interval comprises the propagation of excitation via the conduction system through the atrium, the atrioventricular node, the trunk and the legs of the bundle of His and the Purkinje fibers. Contrary to popular belief, the PQ interval not only reflects the spread of excitation across the AV node, even if the latter makes up the bulk of the PQ interval. Although the delayed conduction of excitation in first degree AV block is mostly intranodal, it can also be localized in the atria or the His-Purkinje system. Physiologically, the PQ interval is shortened during exercise and lengthened during vagally stimulated activities (such as sleep, rest and in athletes).

1st degree AVB are usually asymptomatic. If the PQ interval is greatly prolonged, however, the atrial contraction occurs simultaneously with the ventricular contraction that was triggered by the previous QRS complex [1]. This change in the physiological contraction of the heart chambers can cause symptoms that resemble those of a pacemaker syndrome (malaise, dyspnoea, hypotension, etc.).

If the ECG shows a PQ interval of ≥300 ms, followed by a narrow QRS complex, the block is mostly located in the AV node [2]. If, on the other hand, the first degree AV block occurs together with a broad QRS complex, it may have arisen as a result of an infranodal conduction disorder (Table 1).

Table 1: Location of the block according to the ECG.
AV blockNarrow QRS complexBroad QRS complex
1st degreeMostly intranodalIntra- and / or infranodal
2nd degree type I (Wenckebach)Rarely infranodalMore often intra- than infranodal
2nd degree type II (Mobitz)Much more often infra- than intranodalRarely intranodal
≥2:1Intra- or infranodalRarely intranodal
3rd degreeMostly intranodalMostly infranodal

In the case of first-degree AVB, the prognosis differs depending on the study, as different patient groups were often included: In some studies, increased cardiovascular mortality or morbidity was found, while this was not the case in others. And finally, an increased risk of atrial fibrillation (AF) and the implantation of a permanent cardiac pacemaker have been reported with first-degree AVB [3, 4].

2nd degree AV block

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

A distinction is made between two types: the most common form, the AV block type I (Wenckebach) and the much rarer AV block type II (Mobitz).

In its typical form, the Wenckebach block is characterized by increasingly longer PQ intervals before a P wave is blocked. The PQ interval following the blocked P-wave is shorter than the previous one. The resulting pause corresponds to a little less than double the PP basic interval. This recurring sequence can be seen in the ECG in the form of so-called "occurring in groups" QRS complexes (Fig. 2). In the majority of cases, not all of the criteria mentioned apply. Then one speaks of an atypical Wenckebach block [2, 5]. Wenckebach's block occurs in 1–2% of young healthy patients, often during sleep.

The 2nd degree AV block type II (Mobitz), on the other hand, is characterized by the sudden absence of AV conduction: A P wave is blocked without prior extension of the PQ interval, which, in contrast to the Wenckebach block, occurs after each The transmitted P-wave remains regular (Fig. 3). The resulting pause, including the blocked P wave, corresponds to 2 basic PP intervals. The regular PQ interval can be normal or extended. If the latter is the case, a broad QRS complex often occurs [2, 5].

The second degree AV block type I is mostly intra-nodal in narrow QRS complexes and mostly infranodal in type II: in the case of a narrow QRS complex, it can occur intra-harsely and in the case of a broad QRS complex, it can occur infra-harsely (Table 1). An enlarged QRS complex, a bundle branch block or a deviating QRS axis (e.g. a hemiblock) are signs of an infranodal blockage of the conduction pathways. These ECG changes associated with the AV block must be taken into account, as they can help with its localization (Tab. 1).

An intra-hemisphere atrioventricular block is rare. It is generally characterized by a narrow QRS complex and a sudden change from 1: 1 conduction to 2: 1 block in sinus tachycardia. Sometimes it occurs in the stress test in the form of a ventricular heart rate that suddenly decreases by half. A 2nd degree type II AVB can develop into a complete AVB.

In order to better determine the AVB localization (intra- vs. infranodal), vagus maneuvers are also used: This slows down the intranodal conduction of excitation (increase in blocked P waves), but improves the conduction in the conduction pathways of the bundle of His, as the sinus rhythm drops (decrease in blocked P-waves). Conversely, stress and atropine improve the conduction of stimuli via the AV node, but the infranodal conduction disorders are intensified.

2nd degree AVB are often asymptomatic and the intensity of the symptoms can vary. Sometimes the patient can notice an irregular pulse. He can also complain of tiredness, dyspnoea, angina pectoris or syncope if the AVB suddenly progresses.

2: 1 AVB

The 2: 1 AVB is characterized by the ratio of one normal to two blocked sinus P waves (Fig. 4).

If there is a PQ interval of ≥300 ms in narrow QRS complexes, the block is most likely located in the AV node, but if the PQ interval is normal (especially ≤160 ms) the block is most likely below the AV node. If the QRS complexes (e.g. in the case of a bundle branch block) are wide, it is most likely that the block is located infranodal (Table 1). In order to be able to determine this more precisely, the ratio between P-waves and QRS complexes must be changed in such a way that at least two successive transferred P-waves arise. A spontaneous change in the excitation conduction may be observed in the long-term ECG. In some cases, in order to obtain at least two consecutive conditional P waves and convert the 2: 1 conduction into a 3: 2 or 4: 3 conduction, it is necessary to use the vagus maneuvers described in the 2nd degree AVB. If the PQ interval is prolonged, intranodal AV block is to be suspected, while if the PQ interval is regular, an infranodal block is likely [2, 5].

Atropine is contraindicated if the likelihood of infranodal blocks is increased (2: 1 AVB with broad QRS complex; 2: 1 AVB with constant period, 2nd degree AVB type I with broad QRS complex), since the block this can make it worse.

Highest AVB

In high-grade AVB (sometimes referred to as "advanced AVB II"), ≥2 consecutive sine P-waves are blocked, but the conduction is not completely interrupted as some P-waves are conveyed. For example, the P / QRS ratio can be 3: 1 or 4: 1.

From an anatomical point of view, the block can be localized intra- (in the case of generally narrow QRS complexes) or infranodal (in the case of generally broad QRS complexes) (Tab. 1) [2, 5]. In severe block, atropine injection is contraindicated as it can exacerbate the underlying conduction disorder. If the high-grade AVB is hemodynamically poorly tolerated, a dopamine (2-20 µg / kg / min) or isoprenaline infusion can be administered until transcutaneous electrical stimulation of the heart, implantation of a temporary or permanent pacemaker.

3rd degree AVB or total AV block

The total AV block is characterized by a complete failure of the conduction between atria and ventricles. No P waves are transferred and the atria and ventricles beat independently of each other. The P waves and QRS complexes have their own, independent rhythm and the ventricular heart rate (= equivalent rhythm) is slower than the sinus rhythm (Fig. 5). It can be an intra- (substitute rhythm mostly with narrow QRS complexes) or infranodal block (substitute rhythm mostly with broad QRS complexes) (Tab. 1) [2]. In the case of atrial fibrillation with a regular ventricular heart rate, an underlying complete AVB can be assumed.

Patients with complete AVB usually have symptoms such as fatigue, dyspnoea, angina pectoris, and syncope.

A complete AVB often has negative hemodynamic effects. In general, dopamine or isoprenaline infusions can be used to restore stability until a temporary or permanent pacemaker is implanted.

And finally there is the congenital AV block, which has a prevalence of 1 / 10,000-15,000 births. This is associated with maternal antibodies after lupus erythematosus or Sjogren's syndrome and is usually located in the AV node.

The etiology of AV blocks

1st and 2nd degree AV blocks type I occur due to vagal hypertension in competitive athletes during sleep or due to severe pain. They are physiological and reversible. The most common so-called idiopathic cause of AV conduction disorders is fibrosis or sclerosis of the conduction tissue. Heart diseases that cause AV conduction disorders include: ischemic heart disease, myocarditis (sarcoid, Lyme disease, lupus erythematosus, etc.), dilated cardiomyopathies, infiltrative cardiomyopathies (amyloidosis), endocarditis and congenital heart disease. There are also familial forms of autosomal dominant inherited AV blocks. Other known causes are hyperkalemia, thyroid disease, hereditary degenerative neuromuscular diseases (Duchenne, Emery-Dreyfuss, Becker muscular dystrophy, etc.) and dermatomyositides.

In addition, an active search for drugs such as beta blockers, calcium channel blockers (not belonging to the dihydropyridine class), digoxin, sotalol and amiodarone, all of which affect AV conduction.

Even with invasive cardiological therapies, such as heart valve operations, percutaneous aortic valve replacement, catheter ablation, arrhythmogenic substrate in the vicinity of the conduction pathways of the AV node or the bundle of His (nodal tachycardia, accessory bundle, atrial tachycardia) and septal alcohol ablation can be complications in hypertrophic cases or adverse effect AV conduction disorders occur. The last treatment option for atrial tachyarrhythmia with a ventricular heart rate that cannot be adjusted by medication is to ablate the AV connection, followed by implantation of a definitive pacemaker.

Electrophysiological examination

If an ECG is not sufficient, an electrophysiological examination may be indicated if it is suspected that the AVB is the cause of syncope or its anatomical location is to be determined.


The prognosis is directly related to the degree of AVB and the underlying disease. Patients with advanced AVB who do not have a definitive pacemaker implanted are at increased risk of syncope and sudden cardiac death, all the more so if they have underlying heart disease [1].

Care and treatment

Immediate treatment is required due to the negative hemodynamic effects (hypotension, confusion, malaise, syncope). The initial treatment consists of IV administration of 0.5–1 mg atropine. However, atropine is not indicated if an infra-strict AV block is suspected. In this case, an infusion of dopamine (for hypotension) or isoprenaline (for heart failure) is given as the first treatment. However, caution should be exercised with these drugs in patients with acute ischemia or unstable coronary artery disease, as they can exacerbate the underlying ischemia or cause potentially malignant ventricular arrhythmias. And finally, until an endocavitary ventricular probe is implanted as quickly as possible, transcutaneous stimulation can be carried out using self-adhesive patches.

Since an AVB can be due to a heart or other disease, further examinations must be carried out according to the medical history and the cardiovascular examination. Laboratory tests are used to search for inflammatory, infectious or metabolic diseases (such as Lyme disease, sarcoid, thyroid disease, etc.) and the patient is to be referred to a specialist for clarification of heart disease. In the case of inexplicable AVB in young patients (<40 years), a genetic cause should also be considered, whereby it should be noted that AVB 1st and 2nd degree type I are physiological in athletes. In these cases, the conduction disorders are asymptomatic and reversible and do not require further investigation unless symptoms and abnormalities are evident on the cardiovascular examination. In elderly patients, Grade 1 AVB can be a marker of cardiovascular morbidity and mortality as well as AF. No treatment is required for Grade 1 AVB unless the PQ interval is greatly prolonged, causing symptoms similar to those of pacemaker syndrome [1].

The most important measure is to establish the correlation between symptoms and AV block by means of an EKG. If a simple ECG is not sufficient, it may be necessary to carry out multiple stress tests and Holter ECG or to implant a subcutaneous event recorder in order to prove that the symptoms are actually caused by an AVB.

In any case, a reversible cause of the AVB (e.g. drug side effects or ischemia) must be ruled out by means of a complete and thorough medical history. If there is, wait until the drug that blocked the conduction or the ischemia has subsided before considering implanting a definitive pacemaker. The corresponding indications are listed in Table 2 [1].

Table 2: Indications for the implantation of a definitive pacemaker.
Atrioventricular Block (AVB)class
3rd degree AVB and symptomatic or asymptomatic 2nd degree AVB type II (Mobitz)I.
Symptomatic or infranodal localized AV block on the electrophysiological examination, 2nd degree type I (Wenckebach)lla
1st degree AVB with pacemaker syndrome (PQ> 300 ms).lIa
Not indicated for reversible AVBIII

The most important thing for practice

• Atrioventricular blocks (AVB) can be asymptomatic, express themselves in the form of unclear symptoms (fatigue, adynamia), but they can also lead to syncope.

• The diagnosis by means of an ECG is usually unproblematic, but in certain cases it can be associated with difficulties. Establishing the correlation between the AVB and the patient's complaints is essential. To do this, it is necessary to record the heart rhythm while the symptoms are occurring. For this purpose, a long-term ECG, provocation maneuvers or additional examinations may be required in order to be able to make the appropriate diagnosis and determine the type and location of the AV blocks.

• AVB can be a simple marker of cardiovascular morbidity and mortality, or the consequence of an underlying heart or other disease. This must be systematically clarified, the more the younger the patient is.

• Treatment of the underlying disease (e.g. Lyme borreliosis) can cause the AVB to regress or completely subside.

• The implantation of a pacemaker should only be carried out in the case of irreversible, symptomatic or severe AVB.

Disclosure statement
The authors have declared no financial or personal connections in connection with this post.

PD Dr. med. Juerg Schläpfer
Service de cardiologie, Center Hospitalier
Universitaire Vaudois
Rue du Bugnon 46
CH-1005 Lausanne
jurg.schlaepfer [at]

1 Brignole M, Auricchio A, Baron-Esquivias G, et al. 2013 ESC Guidelines on cardiac pacing and cardiac resynchronization therapy: the Task Force on cardiac pacing and resynchronization therapy of the European Society of Cardiology (ESC). Developed in collaboration with the European Heart Rhythm Association (EHRA). Eur Heart J. 2013; 34: 2281-329.
2 Issa ZF, Miller JM, Zpes DP. Clinical Arrhythmology and Electrophysiology. 2nd ed. 2012. Philadelphia (USA): Elsevier Saunders; Chapter 9, Atrioventricular conduction abnormalities; p. 175-93.
3 Kwok CS, Rashid M, Beynon R, Barker D, Patwala A, Morley-Davies A, et al. Prolonged PR interval, first-degree heart block and adverse cardiovascular outcomes: a systematic review and meta-analysis. Heart. 2016; 102: 672-80.
4 Aro AL. First degree atrioventricular block: risk marker or innocent finding? Heart. 2016; 102: 655-6.
5 Barold SL, Hayes DL. Second-Degree atrioventricular block: A reappraisal. Mayo Clin Proc. 2001; 76: 44-57.

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