Infra-Hisian Block
(Redirected from Infra-Hisian block)
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Infra-Hisian Block Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Sara Mohsin, M.D.[2]
Overview
Infra-Hisian block is defined as an impaired conduction in the electrical system of the heart that occurs below the atrioventricular node.
Historical Perspective
- In 1899, Dr. Wenckebach described the progressive delay between atrial and ventricular contraction and the eventual failure of a P wave to reach the ventricles.
- Dr. Mobitz then divided the second degree AV block into two subtypes.
- In 1905, Dr. John Hay discovered the second degree of AV block.[1]
- While Dr. Hay was examining a patient who complained of a slow pulse and had dyspnea on exertion for more than 2 years, he noticed the heart rate dropping from 80 beats to 40 beats per minute.
- Dr. Hay noted the a waves and the arterial pulse to remain stable in the beginning. However, recording the pulsation several times resulted in "a" waves that were not followed by c wave. The a-c jugular wave interval was used as a measurement of AV conduction.
- Dr. Hay figured out that the pause following a wave was due to failure of ventricular muscles to respond to a stimulus.
Classification
- Infra-hisian block describes the block of distal conduction system.
- Types of infra-hisian block are shown in the following table:
| Types of Infra-Hisian Block | Sub-type |
|---|---|
| Type 2 second degree heart block (Mobitz II) | _ |
| Left bundle branch block | Left anterior fascicular block |
| Left posterior fascicular block | |
| Right bundle branch block | _ |
- Out of all these types of infra-hisian block, Mobitz II heart block is considered as the most important because of the possible progression to a complete heart block.
Pathophysiology
Normal Cardiac Conduction
- The normal cardiac conduction proceeds in a way so as to allow time for the atrium to relax during atrial diastole.
- The electrical impulse generated in the SA node travels through the internodal pathways towards the AV node.
- The conduction through the AV node is slowed down as it travels through it. This decrease in velocity of conduction allows time for the atrium to contract ahead of the ventricle so that the blood from the atria can fill up the ventricles through the atrioventricular valves.
- As the impulse flows through the compact AV node, it rapidly conducts through the ventricular myocardial cells. Once the depolarization is complete, the ventricle relaxes during diastole in preparation for the next impulse.
Anatomy
- The conduction system of heart consists of specialized cells designed to conduct electrical impulse faster than the surrounding myocardial cells.
- Anatomically, the AV node is divided into three regions as follows:
- Transitional cell zone: This is the region where the internodal atrial pathways merge with the compact AV node.
- Compact AV node: This region is located at the apex of the triangle of Koch, which is formed by the ostium of coronary sinus, tricuspid annulus and the tendon of Todaro.
- Penetrating portion of the AV bundle: This region enters the tendon of Todaro and runs within the fibrous body of the membranous interventricular septum and eventually divides at the crest of the muscular interventricular septum into right and left branches.
- The left bundle branch penetrates the membranous portion of the interventricular septum and divides into several smaller branches. Parts of the left bundle branch include a pre-divisional segment, anterior fascicle/hemibundle and posterior fascicle/hemibundle. Rarely a median fascicle is present in some hearts.
- The anterior fascicle supplies the anterior papillary muscle and the Purkinje network of the antero-lateral surface of the left ventricle.
- The posterior fascicle supplies the posterior papillary muscle and the Purkinje network of the postero-inferior surface of the left ventricle.
- Left bundle branch receives its blood supply from left anterior descending artery.
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Pathophysiology of Mobitz type II second degree AV block
- Mobitz type II second degree AV block is characterized by a PR interval that remains unchanged with occasional dropped beats prior to a P wave that fails to conduct to the ventricles as compared to the gradually prolonging PR interval in Mobitz type I.
- ECG findings include intermittently non-conducted P waves not preceded by PR prolongation and not followed by PR shortening.
- It almost always results from a disease of the conduction system below the level of AV node, occurring in the bundle of His in approximately 20% of the cases and in the bundle branches in the remainder.
- Depending upon the location of the block, patients having bundle branch involvement also have axis shifts and QRS widening.
- At least two-thirds of the patients with Mobitz type II second degree AV block have bifascicular or even trifascicular disease.[2][3]
- In the presence of 2:1 AV block, Mobitz type I and Mobitz type II second degree AV block cannot be differentiated on the basis of electrocardiographic findings. In such cases, every other P wave is non-conducted without a chance to observe the constant PR interval that is characteristic of Mobitz type II second degree AV block.
- The conduction delay seen in Mobitz type II second degree block is almost always at the infra-nodal level involving the distal conduction system (His bundle (20%), bundle branches or/and fascicles).
- Although often both the terms, infranodal block or infrahisian block are applied to Mobitz type II second degree AV block, they are not synonymous with it.
- Infranodal block and infra-Hisian block are terms which refer to the anatomic location of the block, whereas
- Mobitz II refers to an electrocardiographic pattern associated with block at these levels.[4]
Pathophysiology of LBBB
- Unlike right bundle branch block (RBBB), left bundle branch block completely modifies the way of depolarization of the conduction system of the heart.
- In LBBB the activation of interventricular septum is from right to left due to uninterrupted conduction in the RBB.
- Then the electrical impulse propagates inferiorly to the left resulting in delayed depolarization and activation of the left ventricle especially the left lateral wall.[5]
- In LBBB, the right to left activation of the septum causes a small negative deflection (Q wave) in lead V1 and a positive deflection (R wave) in lead V6.
- The right ventricle depolarizes earlier than the left ventricle giving an R wave in lead V1 and an S wave in lead V6.
- Subsequent delayed depolarization of the left ventricle results in an S wave in lead V1 and another R wave in lead V6.
Pathophysiology of RBBB
- Right bundle branch block occurs when the electrical impulse is not conducted along the right bundle branch.
- As the conduction along the left bundle branch remains unaffected, the electrical impulse travels normally within the septum from left to right.
- However, the right ventricular contraction occurs comparatively slowly giving the characteristic 'M' pattern on the electrocardiogram.
Genetics
- Familial cases of right bundle branch block have been observed in 4 Lebanese families and the abnormality was mapped to chromosome 19.
- There is a subset of patients with Brugada syndrome who have mutations in SCN5A, the gene encoding for the voltage-gated cardiac sodium channel.
Associated Syndromes
- Duchenne muscular dystrophy
- Myotonic dystrophy: Other EKG findings include:
- Stokes-Adams attacks
- Kearns-Sayre Syndrome
- Brugada syndrome
Pseudo Right Bundle Branch Block
- Brugada syndrome is due to a channelopathy mediated by the SCN5A gene.
- The RBBB pattern seen in patients of Brugada syndrome is not actually RBBB but instead it is due to a repolarization abnormality. Therefore, the RBBB like pattern seen in Brugada syndrome is referred to as a 'pseudo right bundle branch block'.
- EKG findings include ST-segment elevation in leads V1-V3.
- Cocaine consumption and/or the use of the antiarrhythmic propafenone may unmask the EKG findings seen in Brugada syndrome.[6]
Causes
Mobitz type II second degree AV block causes
- Mobitz type II second degree AV block is rarely seen in the patients without any underlying heart disease.
- The most common causes of Mobitz type II second degree AV block include:
- Reversible causes (both pathologic and iatrogenic)
- Idiopathic causes similar to other degrees of AV block such as idiopathic progressive cardiac conduction disease with myocardial fibrosis and/or sclerosis affecting the conduction system.
- Details of all the possible etiologies are given in the table below:
| Physiologic and pathophysiologic | |
|---|---|
| Increased vagal tone |
|
| Ischemic heart disease |
|
| Progressive cardiac conduction system disease | Associated with:
|
| Infections | |
| Cardiomyopathy | Infiltrative processes such as:
Other non-ischemic cardiomyopathies include: |
| Congenital AV block |
|
| Other reversible causes | |
| Iatrogenic | |
| Drugs (altering conduction through AV node) | |
| Cardiac surgery |
|
| Catheter ablation of arrhythmias | |
| Alcohol septal ablation for hypertrophic cardiomyopathy | |
| Transcatheter closure of ventricular septal defect | |
| Post-transcatheter aortic valve implantation | |
Life Threatening Causes
Life-threatening conditions can result in death or permanent disability within 24 hours if left untreated.[7]
- Acute myocardial infarction[8][9]
- Acute rheumatic fever
- Bacterial endocarditis
- Myocarditis
- Severe hypothermia
Common Causes
- Acute rheumatic fever
- Bacterial endocarditis[10]
- Calcific aortic stenosis
- Digoxin
- Dilated cardiomyopathy
- Diltiazem
- Enhanced vagal tone
- HCM
- Hypertension
- Iatrogenic after surgical correction of VSD, tetralogy of Fallot, and endocardial cushion defect
- Inferior ST elevation MI
- Massive calcification of the mitral annulus
- Myocarditis
- Normal variants[3]
- Penetrating and non-penetrating trauma of the chest
- Sclerodegenerative disease of the electrical conduction system
- Verapamil
- β blockers
Causes by Organ System
Causes in Alphabetical Order
- For causes of Left bundle branch block, click here.
- For causes of Right bundle branch block, click here.
Epidemiology and Demographics
Prevalence
- In United States, the prevalence of second-degree AV block is believed to be 3 in 100,000 individuals.[12]
- Nearly 3% of the patients with underlying structural heart disease develop some form of second-degree AV block.
- The male-to-female ratio of second-degree AV block is 1:1.
Gender
- Men and women are affected equally by second degree AV block.
Risk Factors
- Common risk factors associated with second degree AV block include the following:[13][14][15][16]
- Intrinsic atrioventricular node disease
- Myocarditis
- Acute myocardial infarction
- Prior cardiac surgery
- Older age
- Heart attack or coronary artery disease
- Cardiomyopathy
- Sarcoidosis
- Lyme disease
- High potassium levels
- Severe hypothyroidism
- Certain inherited neuromuscular diseases
- Medicines that slow the heart rate
- After open heart surgery
Natural History, Complications and Prognosis
Natural History
- Mobitz II second degree AV block is due to the block inferior to the AV node (infra-Hisian structures) and it rapidly progresses to a complete heart block in which no escape rhythm may emerge.[17]
Complications
Prognosis
- Mobitz II, as it involves the infra-nodal structures, carries the risk of progression to complete heart block and carries an unfavorable prognosis.[13]
Diagnosis
Diagnostic Study of Choice
- Electrocardiography (ECG) is employed to determine the type of second-degree atrioventricular (AV) block present[7][19][9].
- Follow-up ECGs and cardiac monitoring are appropriate.[20]
- Routine imaging studies are not required. However, if myocarditis is a concern, echocardiography may be indicated.[4][21]
- If myocardial ischemia is a concern, a chest radiograph may be indicated.[22]
History and Symptoms
- History from patients with second degree AV block should involve asking about the following:[23][22]
- Congenital heart disease
- Current heart condition
- Recent or previous cardiac procedures
- History of medications
- Most people with Wenckebach (Type I Mobitz) do not show symptoms.[13][7]
- If the sinus rate is slow and only few beats are conducted (higher grade blocks) there may be a significantly reduced cardiac output.
- Usual symptoms in such patients include:[18][3]
Physical Examination
- Patients with Mobitz II can appear asymptomatic as well. However, in more cases they may be in distress or progress to the more severe third degree AV block.
- Patients may appear pale in cases of bradycardia with decreased cardiac output.[24]
- Bradycardia with an irregular pulse[25]
- Lightheadedness
- Hypotension[26]
- Syncope or presyncope
- Jugular venous distension
- Bibasilar crackles in patients with exacerbated heart failure
- Peripheral edema
Laboratory Findings
Patients with second degree AV block should be checked for the following laboratory tests:[27]
- Serum electrolytes
- Calcium
- Magnesium
- Myocardial enzymes in patients with myocardial infarction
- Myocarditis related laboratory tests as the following:[28]
Electrocardiogram
- There are intermittent blocked P waves.
- In the conducted beats, the PR intervals remain constant.
- The PR is fairly constant except that slight shortening may occur in the first beat after the blocked cycle. This is the result of improved conduction following the block.
- Most patients with type II second-degree AV block have associated bundle branch block.
- In these instances, the block is usually located distal to the His bundle. However, in approximately 27% to 35% of the patients, the lesion is located in the His bundle itself, and a narrow complex may be inscribed.
- 2:1 AV Block:
- Impossible to determine whether the second-degree AV block is type I or type II.
- A long rhythm strip is helpful to document any change in the behavior of the conduction ratio.
- When the atrial rate is increased by exercise or by atropine, the AV block in type I tends to decrease and that in type II tends to increase.
Shown below is an electrocardiogram of a 12 lead EKG with a 2:1 AV block.
Copyleft image obtained, courtesy of ECGpedia, http://en.ecgpedia.org/wiki/Main_Page
Shown below is an electrocardiogram of a type II second degree AV block (Mobitz type II).
Copyleft image obtained, courtesy of ECGpedia, http://en.ecgpedia.org/wiki/Main_Page
Treatment
Medical therapy for Mobitz II
- Correction of reversible causes of the block such as ischemia, medications, and vagotonic conditions should be considered.[4]
- Treatment may also include medicines to control blood pressure and atrial fibrillation, as well as lifestyle and dietary changes to reduce the risk factors associated with heart attack and stroke.[29]
- Treatment in emergency situations are atropine and an external pacer.[9][3]
Contraindicated medications
Second degree AV block(except in patients with a functioning artificial pacemaker)[30][31] is considered an absolute contraindication to the use of the following medications:
- Adenosine
- Atenolol
- Betaxolol
- Bisoprolol
- Brimonidine tartrate and Timolol maleate
- Carteolol
- Diltiazem
- Disopyramide
- Dronedarone
- Flecainide
- Metoprolol
- Mexiletine
- Nadolol
- Nebivolol
- Penbutolol
- Pindolol
- Propranolol
- Sotalol
- Timolol
- Labetalol[32]
Surgery for Mobitz II
Definitive treatment-Pacemaker insertion
- Type II Mobitz (symptomatic or asymptomatic) is by itself an indication for insertion of a pacemaker (definitive treatment). Other indications include:[21][33][34][35]:
- Myotonic dystrophy
- Kearns-Sayre syndrome
- Erb's dystrophy
- Peroneal muscular atrophy. These neuromuscular disorders have a high potential for unpredictable rapid progression to complete heart block.
- Implantation of permanent pacemakers in both asymptomatic and symptomatic patients is usually done. Asymptomatic Mobitz II are prone to be converted to symptomatic or third degree heart block. Thus, they should be considered for a pacemaker even if asymptomatic.
- A dual chamber DDD pacemaker is preferred over a single chambered VVI pacemakers as it maintains physiologic AV synchrony.
- A dual-chamber artificial pacemaker is a type of device that typically listens for a pulse from the SA node and sends a pulse to the AV node at an appropriate interval, essentially completing the connection between the two nodes. Pacemakers in this role are usually programmed to enforce a minimum heart rate and to record instances of atrial flutter and atrial fibrillation.
Prevention
Primary Prevention
- Effective treatment of hypertension and maintenance of normal blood glucose levels may be useful strategies in preventing the AV block.
Differentiating Infra-Hisian Block from other Diseases
References
- ↑ Upshaw CB, Silverman ME (2000). "John Hay: discoverer of type II atrioventricular block". Clin Cardiol. 23 (11): 869–71. doi:10.1002/clc.4960231118. PMC 6655013 Check
|pmc=value (help). PMID 11097138. - ↑ Puech P, Wainwright RJ (1983). "Clinical electrophysiology of atrioventricular block". Cardiol Clin. 1 (2): 209–24. PMID 6544636.
- ↑ 3.0 3.1 3.2 3.3 Wogan JM, Lowenstein SR, Gordon GS (1993). "Second-degree atrioventricular block: Mobitz type II". J Emerg Med. 11 (1): 47–54. doi:10.1016/0736-4679(93)90009-v. PMID 8445186.
- ↑ 4.0 4.1 4.2 Li X, Xue Y, Wu H (2018). "A Case of Atrioventricular Block Potentially Associated with Right Coronary Artery Lesion and Ticagrelor Therapy Mediated by the Increasing Adenosine Plasma Concentration". Case Rep Vasc Med. 2018: 9385017. doi:10.1155/2018/9385017. PMC 5933017. PMID 29850368.
- ↑ Francia P, Balla C, Paneni F, Volpe M (2007). "Left bundle-branch block--pathophysiology, prognosis, and clinical management". Clinical Cardiology. 30 (3): 110–5. doi:10.1002/clc.20034. PMID 17385703. Unknown parameter
|month=ignored (help) - ↑ Yildiz BS, Gungor H, Gul I, Bilgin M, Zoghi M, Akilli A (2013). "Is a drug-challenge test with propafenone adequate to exclude Brugada syndrome?". Cardiovascular Journal of Africa. 24 (2): e4–6. doi:10.5830/CVJA-2012-068. PMID 23613002.
- ↑ 7.0 7.1 7.2 7.3 Mangi MA, Jones WM, Napier L. PMID 29493981. Missing or empty
|title=(help) - ↑ Misumida N, Ogunbayo GO, Kim SM, Abdel-Latif A, Ziada KM, Elayi CS (November 2018). "Frequency and Significance of High-Degree Atrioventricular Block and Sinoatrial Node Dysfunction in Patients With Non-ST-Elevation Myocardial Infarction". Am. J. Cardiol. 122 (10): 1598–1603. doi:10.1016/j.amjcard.2018.08.001. PMID 30227965.
- ↑ 9.0 9.1 9.2 Barold SS, Herweg B (December 2012). "Second-degree atrioventricular block revisited". Herzschrittmacherther Elektrophysiol. 23 (4): 296–304. doi:10.1007/s00399-012-0240-8. PMID 23224264.
- ↑ Kamatani T, Akizuki A, Kondo S, Shirota T (Fall 2016). "Second-Degree Atrioventricular Block Occurring After Tooth Extraction". Anesth Prog. 63 (3): 156–9. doi:10.2344/15-00042.1. PMC 5011958. PMID 27585419.
- ↑ Menicagli F, Lanza A, Sbrocca F, Baldi A, Spugnini EP (2016). "A case of advanced second-degree atrioventricular block in a ferret secondary to lymphoma". Open Vet J. 6 (1): 68–70. doi:10.4314/ovj.v6i1.10. PMC 4833871. PMID 27200273.
- ↑ 12.0 12.1 Zehender M, Meinertz T, Keul J, Just H (1990). "ECG variants and cardiac arrhythmias in athletes: clinical relevance and prognostic importance". Am Heart J. 119 (6): 1378–91. doi:10.1016/s0002-8703(05)80189-9. PMID 2191578.
- ↑ 13.0 13.1 13.2 Meimoun P, Zeghdi R, D'Attelis N, Berrebi A, Braunberger E, Deloche A; et al. (2002). "Frequency, predictors, and consequences of atrioventricular block after mitral valve repair". Am J Cardiol. 89 (9): 1062–6. doi:10.1016/s0002-9149(02)02276-2. PMID 11988196.
- ↑ Meimoun P, Zeghdi R, D'Attelis N, Berrebi A, Braunberger E, Deloche A; et al. (2002). "Frequency, predictors, and consequences of atrioventricular block after mitral valve repair". Am J Cardiol. 89 (9): 1062–6. doi:10.1016/s0002-9149(02)02276-2. PMID 11988196.
- ↑ Kerola T, Eranti A, Aro AL, Haukilahti MA, Holkeri A, Junttila MJ, Kenttä TV, Rissanen H, Vittinghoff E, Knekt P, Heliövaara M, Huikuri HV, Marcus GM (May 2019). "Risk Factors Associated With Atrioventricular Block". JAMA Netw Open. 2 (5): e194176. doi:10.1001/jamanetworkopen.2019.4176. PMC 6632153 Check
|pmc=value (help). PMID 31125096. - ↑ Schoeller R, Andresen D, Büttner P, Oezcelik K, Vey G, Schröder R (March 1993). "First- or second-degree atrioventricular block as a risk factor in idiopathic dilated cardiomyopathy". Am. J. Cardiol. 71 (8): 720–6. doi:10.1016/0002-9149(93)91017-c. PMID 8447272.
- ↑ Rodstein M, Wolloch L, Iuster Z (1979). "The natural history intraventricular conduction disturbances in the aged: an analysis of the developing second and third degree heart block with clinical pathological correlations". Am. J. Med. Sci. 277 (2): 179–88. doi:10.1097/00000441-197903000-00006. PMID 463945.
- ↑ 18.0 18.1 Bexton RS, Camm AJ (March 1984). "Second degree atrioventricular block". Eur. Heart J. 5 Suppl A: 111–4. doi:10.1093/eurheartj/5.suppl_a.111. PMID 6373268.
- ↑ Thiruganasambandamoorthy V, Hess EP, Turko E, Tran ML, Wells GA, Stiell IG (July 2012). "Defining abnormal electrocardiography in adult emergency department syncope patients: the Ottawa Electrocardiographic Criteria". CJEM. 14 (4): 248–58. PMID 22813399.
- ↑ Barold SS, Van Heuverswyn FE, Timmers L, Stroobandt RX (August 2014). "Mobitz type II second-degree atrioventricular block during dobutamine stress echocardiography. True or false?". Echocardiography. 31 (7): 799–801. doi:10.1111/echo.12577. PMID 25080840.
- ↑ 21.0 21.1 Fu Md J, Bhatta L (2018). "Lyme carditis: Early occurrence and prolonged recovery". J Electrocardiol. 51 (3): 516–518. doi:10.1016/j.jelectrocard.2017.12.035. PMID 29275956.
- ↑ 22.0 22.1 Kashou AH, Goyal A, Nguyen T, Chhabra L. PMID 29083636. Missing or empty
|title=(help) - ↑ Zeppilli P, Fenici R, Sassara M, Pirrami MM, Caselli G (September 1980). "Wenckebach second-degree A-V block in top-ranking athletes: an old problem revisited". Am. Heart J. 100 (3): 281–94. doi:10.1016/0002-8703(80)90140-4. PMID 7405798.
- ↑ Rosen KM, Dhingra RC, Loeb HS, Rahimtoola SH (1973). "Chronic heart block in adults. Clinical and electrophysiological observations". Arch Intern Med. 131 (5): 663–72. PMID 4701376.
- ↑ Schneider MD, Roller DH, Morganroth J, Josephson ME (July 1978). "The syndromes of familial atrioventricular block with sinus bradycardia: prognostic indices, electrophysiologic and histopathologic correlates". Eur J Cardiol. 7 (5–6): 337–51. PMID 699934.
- ↑ Trappe HJ (September 2016). "[Consciousness disorders from cardiological view]". Dtsch. Med. Wochenschr. (in German). 141 (19): 1361–9. doi:10.1055/s-0042-103177. PMID 27642736.
- ↑ Gupta PK, Lichstein E, Chadda KD (1976). "Chronic His bundle block. Clinical, electrocardiographic, electrophysiological, and follow-up studies on 16 patients". Br Heart J. 38 (12): 1343–9. doi:10.1136/hrt.38.12.1343. PMC 483178. PMID 1008977.
- ↑ Steere AC, McHugh G, Damle N, Sikand VK (2008). "Prospective study of serologic tests for lyme disease". Clin Infect Dis. 47 (2): 188–95. doi:10.1086/589242. PMC 5538270. PMID 18532885.
- ↑ Schernthaner C, Kraus J, Danmayr F, Hammerer M, Schneider J, Hoppe UC, Strohmer B (March 2016). "Short-term pacemaker dependency after transcatheter aortic valve implantation". Wien. Klin. Wochenschr. 128 (5–6): 198–203. doi:10.1007/s00508-015-0906-4. PMID 26745972.
- ↑ Brignole M, Deharo JC, Guieu R (August 2015). "Syncope and Idiopathic (Paroxysmal) AV Block". Cardiol Clin. 33 (3): 441–7. doi:10.1016/j.ccl.2015.04.012. PMID 26115830.
- ↑ Kelkar PN (August 1998). "Atenolol induced high grade AV block". J Assoc Physicians India. 46 (8): 748, 751. PMID 11229299.
- ↑ Zeltser D, Justo D, Halkin A, Rosso R, Ish-Shalom M, Hochenberg M, Viskin S (July 2004). "Drug-induced atrioventricular block: prognosis after discontinuation of the culprit drug". J. Am. Coll. Cardiol. 44 (1): 105–8. doi:10.1016/j.jacc.2004.03.057. PMID 15234417.
- ↑ Tuohy S, Saliba W, Pai M, Tchou P (January 2018). "Catheter ablation as a treatment of atrioventricular block". Heart Rhythm. 15 (1): 90–96. doi:10.1016/j.hrthm.2017.08.015. PMID 28823599.
- ↑ Kusumoto FM, Schoenfeld MH, Barrett C, Edgerton JR, Ellenbogen KA, Gold MR, Goldschlager NF, Hamilton RM, Joglar JA, Kim RJ, Lee R, Marine JE, McLeod CJ, Oken KR, Patton KK, Pellegrini CN, Selzman KA, Thompson A, Varosy PD (August 2019). "2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society". J. Am. Coll. Cardiol. 74 (7): e51–e156. doi:10.1016/j.jacc.2018.10.044. PMID 30412709.
- ↑ Strasberg B, Amat-Y-Leon F, Dhingra RC, Palileo E, Swiryn S, Bauernfeind R, Wyndham C, Rosen KM (May 1981). "Natural history of chronic second-degree atrioventricular nodal block". Circulation. 63 (5): 1043–9. doi:10.1161/01.cir.63.5.1043. PMID 7471363.
- ↑ Kerola T, Eranti A, Aro AL, Haukilahti MA, Holkeri A, Junttila MJ; et al. (2019). "Risk Factors Associated With Atrioventricular Block". JAMA Netw Open. 2 (5): e194176. doi:10.1001/jamanetworkopen.2019.4176. PMC 6632153 Check
|pmc=value (help). PMID 31125096. - ↑ Barold SS (1996). "Indications for permanent cardiac pacing in first-degree AV block: class I, II, or III?". Pacing Clin Electrophysiol. 19 (5): 747–51. doi:10.1111/j.1540-8159.1996.tb03355.x. PMID 8734740.
- ↑ Upshaw CB (2004). "Comparison of the prevalence of first-degree atrioventricular block in African-American and in Caucasian patients: an electrocardiographic study III". J Natl Med Assoc. 96 (6): 756–60. PMC 2568382. PMID 15233485.
- ↑ Friedman HS, Gomes JA, Haft JI (1975). "An analysis of Wenckebach periodicity". J Electrocardiol. 8 (4): 307–15. doi:10.1016/s0022-0736(75)80003-3. PMID 1176840.
- ↑ OSTRANDER LD, BRANDT RL, KJELSBERG MO, EPSTEIN FH (June 1965). "ELECTROCARDIOGRAPHIC FINDINGS AMONG THE ADULT POPULATION OF A TOTAL NATURAL COMMUNITY, TECUMSEH, MICHIGAN". Circulation. 31: 888–98. doi:10.1161/01.cir.31.6.888. PMID 14297523.
- ↑ Movahed MR, Hashemzadeh M, Jamal MM (October 2005). "Increased prevalence of third-degree atrioventricular block in patients with type II diabetes mellitus". Chest. 128 (4): 2611–4. doi:10.1378/chest.128.4.2611. PMID 16236932.
- ↑ Lankveld TA, Zeemering S, Crijns HJ, Schotten U (July 2014). "The ECG as a tool to determine atrial fibrillation complexity". Heart. 100 (14): 1077–84. doi:10.1136/heartjnl-2013-305149. PMID 24837984.
- ↑ Harris K, Edwards D, Mant J (2012). "How can we best detect atrial fibrillation?". J R Coll Physicians Edinb. 42 Suppl 18: 5–22. doi:10.4997/JRCPE.2012.S02. PMID 22518390.
- ↑ Cosío FG (June 2017). "Atrial Flutter, Typical and Atypical: A Review". Arrhythm Electrophysiol Rev. 6 (2): 55–62. doi:10.15420/aer.2017.5.2. PMC 5522718. PMID 28835836.
- ↑ Katritsis DG, Josephson ME (August 2016). "Classification, Electrophysiological Features and Therapy of Atrioventricular Nodal Reentrant Tachycardia". Arrhythm Electrophysiol Rev. 5 (2): 130–5. doi:10.15420/AER.2016.18.2. PMC 5013176. PMID 27617092.
- ↑ Letsas KP, Weber R, Siklody CH, Mihas CC, Stockinger J, Blum T, Kalusche D, Arentz T (April 2010). "Electrocardiographic differentiation of common type atrioventricular nodal reentrant tachycardia from atrioventricular reciprocating tachycardia via a concealed accessory pathway". Acta Cardiol. 65 (2): 171–6. doi:10.2143/AC.65.2.2047050. PMID 20458824.
- ↑ "Atrioventricular Nodal Reentry Tachycardia (AVNRT) - StatPearls - NCBI Bookshelf".
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