Third degree AV block overview: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
Normally [[Sinoatrial node|SA node]] generates impulses that travel to the [[Atrioventricular node|AV node]] and gets delayed there to assure that the [[contraction]] cycle in [[atria]] is complete before a contraction begins in the [[ventricles]]. From the [[AV node]], the impulses pass through the [[Bundle of His|His-Purkinje]] system to cause ventricular contraction. Pathological delay in the [[AV node]] is visualized on an [[electrocardiogram]] as a change in the [[PR interval|P-R interva]]<nowiki/>l. These delays are known as an [[AV block]]. No impulses from the [[SA node]] get conducted to the ventricles, and this leads to a complete [[atrioventricular dissociation]]. The SA node continues to activate at a set rate, but the ventricles will activate through an escape rhythm that can be mediated by either the AV node, one of the fascicles, or by ventricular myocytes themselves. The heart rate will mostly be less than 45 to 50 beats/min, and most patients will be hemodynamically unstable. | |||
==Causes== | ==Causes== | ||
Revision as of 19:30, 14 July 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Soroush Seifirad, M.D.[2] Cafer Zorkun, M.D., Ph.D. [3]Qasim Khurshid, M.B.B.S.
Overview
Complete heart block is a disorder of the cardiac conduction system where there is complete dissociation of the atrial and ventricular activity due to the absence of conduction through the atrioventricular node (AVN) or His-Purkinje system.
Historical Perspective
In 1894, Dr. Engelman was the first to describe in detail the phenomenon of AV interval lengthening. In 1899, Karel Frederik published a paper on irregular pulses describing impairment of AV conduction and blockage. 1906 Einthiven was the first to present a presentation of normal and abnormal electrocardiograms recorded with string galvanometer. Dr. Ashmar in 1925 studied and described in detail this blocked impulses and their impact on the conduction in the muscle of the heart. In 1952 Dr. Paul Zoll developed first temporary trans-cutaneous pacing.[1]
Classification
There is no established system for the classification of third degree AV block. But AV dissociation can be further classified into two subtypes as AV dissociation by default and AV dissociation by usurpation.
Pathophysiology
Normally SA node generates impulses that travel to the AV node and gets delayed there to assure that the contraction cycle in atria is complete before a contraction begins in the ventricles. From the AV node, the impulses pass through the His-Purkinje system to cause ventricular contraction. Pathological delay in the AV node is visualized on an electrocardiogram as a change in the P-R interval. These delays are known as an AV block. No impulses from the SA node get conducted to the ventricles, and this leads to a complete atrioventricular dissociation. The SA node continues to activate at a set rate, but the ventricles will activate through an escape rhythm that can be mediated by either the AV node, one of the fascicles, or by ventricular myocytes themselves. The heart rate will mostly be less than 45 to 50 beats/min, and most patients will be hemodynamically unstable.
Causes
Many conditions can cause third degree heart block, but the most common cause is coronary ischemia. Progressive degeneration of the electrical conduction system of the heart can lead to third degree heart block. This may be preceded by first degree AV block, second degree AV block, bundle branch block, or bifascicular block. In addition, acute myocardial infarction may present with third degree AV block. Third degree heart block may also be congenital and has been linked to the presence of lupus in the mother. It is thought that maternal antibodies may cross the placenta and attack the heart tissue during gestation. The cause of congenital third degree heart block in many patients is unknown.
Differentiating Third degree AV block from other Diseases
Epidemiology and Demographics
AV blocks are fairly common however, third-degree AV block is relatively rare. The incidence in the general population appears to be low, approximately 20 to 40 in 100,000 individuals in the United States. Given the etiology of the disease, the incidence among the apparently healthy and presumptively asymptomatic is even lower at approximately 1 in 100,000.[2][3][4]
Risk Factors
Risk factors for complete heart blocks can be congenital or acquired.
Screening
There is insufficient evidence to recommend routine screening for third degree AV block. However, screening for congenital AV block is recommended
Natural History, Complications and Prognosis
Spontaneous recovery from third-degree heart block is not common. Untreated third-degree heart block is associated with high mortality, which appears to occur as a consequence of the complications of decreased perfusion as a consequence of bradycardia and decreased cardiac output. Common complications of third-degree AV block include sudden cardiac death due to asystole, syncope, and musculoskeletal injuries secondary to fall after syncope. The prognosis of the third-degree heart block is most likely dependent on the patient's underlying disease burden and severity of the clinical presentation on arrival. Patients treated with permanent pacemaker have an excellent prognosis.
Diagnosis
History and Symptoms
Patients with third degree AV block typically experience a lower overall measured heart rate (as low as 28 beats per minute during sleep), low blood pressure, and poor circulation. In some cases, exercising may be difficult, as the heart cannot react quickly enough to sudden changes in demand or sustain the higher heart rates required for sustained activity. Complete heart block associated with a slower pacemaker can result in dizziness, presyncope andsyncope.
Imaging
Echocardiography
Transthoracic echocardiography is used to diagnose cardiomyopathies and valvular heart diseases as causes of third degree heart block. Transesophageal echocardiogram aids in the diagnosis of valvular abnormalities like valve abscesses. Left ventricular function can be determined using an echo, before placement of a pacemaker or defibrillator.
Treatment
Medical Therapy
Correction of reversible causes of the block such as ischemia, medications, and vagotonic conditions should be considered. Treatment may also include medicines to control blood pressure and atrial fibrillation, as well as lifestyle and dietary changes to reduce risk factors associated with heart attack and stroke. Treatment in emergency situations are atropine and an external pacer.
References
- ↑ LANGENDORF R. Concealed A-V conduction; the effect of blocked impulses on the formation and conduction of subsequent impulses. Am Heart J. 1948;35(4):542-552. doi:10.1016/0002-8703(48)90641-3
- ↑ OSTRANDER LD Jr, BRANDT RL, KJELSBERG MO, EPSTEIN FH. ELECTROCARDIOGRAPHIC FINDINGS AMONG THE ADULT POPULATION OF A TOTAL NATURAL COMMUNITY, TECUMSEH, MICHIGAN. Circulation. 1965;31:888-898. doi:10.1161/01.cir.31.6.888
- ↑ Benjamin EJ, Blaha MJ, Chiuve SE, et al. Heart Disease and Stroke Statistics-2017 Update: A Report From the American Heart Association [published correction appears in Circulation. 2017 Mar 7;135(10 ):e646] [published correction appears in Circulation. 2017 Sep 5;136(10 ):e196]. Circulation. 2017;135(10):e146-e603. doi:10.1161/CIR.0000000000000485
- ↑ Movahed MR, Hashemzadeh M, Jamal MM. Increased prevalence of third-degree atrioventricular block in patients with type II diabetes mellitus. Chest. 2005;128(4):2611-2614. doi:10.1378/chest.128.4.2611