Third degree AV block overview: Difference between revisions
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==Overview== | ==Overview== | ||
[[Complete heart block]] is a [[disease]] of the [[cardiac]] [[electrical conduction system]] where there is complete dissociation of the [[atrial]] and [[ventricular]] activity because of the absence of conduction through the [[atrioventricular node]] ([[AVN]]) or [[His-Purkinje system]]. 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 the impairment of AV conduction and blockage.[[Complete heart block]] may be transient due to increased [[parasympathetic]] tone defining [[vagally]] mediated [[atrioventricular block]] or due to [[infranodal block]] whether there is evidence of conduction block distal to the [[atrioventricular node]]. 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. The most common cause of a [[complete heart block]] is [[coronary ischemia]], but there are many other etiologies. The progressive [[degeneration]] of the [[electrical conduction system]] of the [[heart]] due to aging can cause a [[third-degree heart block]]. [[Complete heart block]] can be preceded by first degree [[AV block]], second degree [[AV block]], or [[bifascicular block]]. [[Acute myocardial infarction]] may present as a third-degree heart block. [[Lupus]] in a [[pregnant]] mother can cause [[congenital heart block]] in [[newborns]]. [[Maternal]] [[antibodies]] can cross the [[placenta]] and lead to a [[complete heart block]] during [[gestation]]. Sometimes no cause can be identified. [[Third degree AV block|Third-degree heart]] block should not be confused with high-grade [[Atrioventricular block|AV block]] which is a second-degree block with a very slow [[ventricular]] rate with occasional [[AV conduction]], or [[AV Dissociation]] defining to indicate the occurrence of independent [[atrial]] and [[ventricular]] contractions caused by entities other than [[third-degree heart block]].[[Atrioventricular block|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. Common risk factors associated [[atioventricular block]] include older [[age]], [[male sex]], history of [[myocardial infarction]], history of [[congestive heart disease]], [[high]] [[systolic blood pressure]], increased [[fasting]] blood [[glucose]] level. | [[Complete heart block]] is a [[disease]] of the [[cardiac]] [[electrical conduction system]] where there is complete dissociation of the [[atrial]] and [[ventricular]] activity because of the absence of conduction through the [[atrioventricular node]] ([[AVN]]) or [[His-Purkinje system]]. 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 the impairment of AV conduction and blockage.[[Complete heart block]] may be transient due to increased [[parasympathetic]] tone defining [[vagally]] mediated [[atrioventricular block]] or due to [[infranodal block]] whether there is evidence of conduction block distal to the [[atrioventricular node]]. 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. The most common cause of a [[complete heart block]] is [[coronary ischemia]], but there are many other etiologies. The progressive [[degeneration]] of the [[electrical conduction system]] of the [[heart]] due to aging can cause a [[third-degree heart block]]. [[Complete heart block]] can be preceded by first degree [[AV block]], second degree [[AV block]], or [[bifascicular block]]. [[Acute myocardial infarction]] may present as a third-degree heart block. [[Lupus]] in a [[pregnant]] mother can cause [[congenital heart block]] in [[newborns]]. [[Maternal]] [[antibodies]] can cross the [[placenta]] and lead to a [[complete heart block]] during [[gestation]]. Sometimes no cause can be identified. [[Third degree AV block|Third-degree heart]] block should not be confused with high-grade [[Atrioventricular block|AV block]] which is a second-degree block with a very slow [[ventricular]] rate with occasional [[AV conduction]], or [[AV Dissociation]] defining to indicate the occurrence of independent [[atrial]] and [[ventricular]] contractions caused by entities other than [[third-degree heart block]].[[Atrioventricular block|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. Common risk factors associated [[atioventricular block]] include older [[age]], [[male sex]], history of [[myocardial infarction]], history of [[congestive heart disease]], [[high]] [[systolic blood pressure]], increased [[fasting]] blood [[glucose]] level.[[Transthoracic echocardiography]] may be helpful in the diagnosis of the underlying diseases that tend to third-degree [[AV block]]. [[Echocardiography]] might show shreds of evidence in favor of [[Cardiomyopathy|cardiomyopathies]] or [[Valvular heart disease|valvular heart diseases]]. In particular case scenarios, [[Transesophageal echocardiogram|transesophageal echocardiography]] is warranted and may help to diagnose etiologies such as [[valvular]] ring [[abscess]]. Furthermore, the [[left ventricular]] function can be determined using an echo and provide pieces of evidence in favor of the placement of a [[pacemaker]] or [[defibrillator]]. . Common indications for [[echocardiography]] in suspicion of [[cardiac origin]] of [[bradycardia]] or [[conduction disorder]] may include [[syncope]], [[lightheadedness]]/[[presyncope]], [[symptoms]] related to [[aortic stenosis]], [[hypertrophic cardiomyopathy]], [[heart failure]].There are no x-ray findings associated with [[third-degree AV block]]. However, a [[chest x-ray]] may be helpful in the diagnosis of complications of [[third degree AV block]] such as [[pulmonary edema]]. Additionally, a [[chest x-ray]] may be helpful in the diagnosis of the underlying [[disease]] tend to [[third degree AV block]], or in the diagnosis of the other complications of that [[disorder]] which may include [[cardiomegaly]] and [[hilar adenopathy]]. [[CT scan]] may be helpful in the diagnosis of [[cardiac ]] and [[chest]] abnormalities related to the underlying organic [[disease]] in those with [[third-degree AV block]]. [[Cardiac MRI]] may be helpful in selected [[patients]] to identify the underlying [[structural heart disease]] associated [[conduction disturbance]] such as [[sarcoidosis]], [[hemochromatosis]], and [[amyloidosis]]. [[Nuclear imaging]] techniques might rarely be used and may be helpful in the diagnosis of complications of [[third-degree AV block ]] or provide shreds of evidence in favor of the underlying disease in those with [[complete heart block]]. [[Ambulatory monitoring]] is warranted in cases of possible [[transient heart block]], or some other [[bradyarrhythmias]] that might be mistaken with [[third-degree AV block]]. Worsening [[atrioventricular block]] with [[isoproterenol]] and [[atropine]] may be suggestive of [[infranodal block]]. Improvement of [[atrioventricular conduction]] with [[carotid sinus massage]] may be observed in [[patients]] with [[infranodal]] [[atrioventric-ular block]]. The management of third-degree [[AV block]] depends on the severity of signs, [[symptoms]], and the underlying cause. In symptomatic [[patients]] and with [[hemodynamic]] distress, [[pharmacological]] therapy should be initiated immediately to increase [[heart rate]] and [[cardiac output]]. Most of the [[patients]] who do not respond to [[pharmacologic]] therapy require a [[temporary pacemaker]]. After stabilizing the [[patients]], assessment and treatment of potentially [[reversible ]] causes should be done. Some [[patients]] without reversible cause or unidentified [[etiology]] require a [[permanent pacemaker]. [[Cardiac]] [[Pacemaker|pacemakers]] are effective treatments for a variety of [[cardiac]] conduction abnormalities and can reestablish adequate [[circulation]] by generating appropriate [[heart rate]] and [[cardiac]] response. Two main factors guide the majority of decisions regarding [[permanent pacemaker]] insertion. First is the association of [[symptoms]] with [[Cardiac arrhythmia|arrhythmia]], and second is the potential for progression of the [[rhythm]] disturbance. [[Symptoms]] related to [[atrioventricular block]] are determining factor of placing [[permanent pacemaker]], regardless of the level of [[atrioventricular block]]. [[Permanent pacemaker]] is warranted if the site of [[atrioventricular]] block is Infranodal, regardless of the presence or absence of [[symptoms]]. [[Temporary transvenous pacing]] is used to provide [[hemodynamic]] support or back-up pacing to prevent [[asystole]]. If [[atrioventricular]] block seems to be irreversible, it is better to proceed directly with [[permanent pacemaker]] implantation. | ||
[[Patients]] with [[renal insufficiency]], [[potassium]] electrolyte disturbances, and [[dehydration]] are predisposed to develop [[digoxin toxicity]]. Careful monitoring of electrolytes, drug levels, and renal function is essential in patients on chronic [[digoxin]] therapy. Patients on multiple nodal agents are susceptible to the development of [[third-degree AV block]]. These [[patients]] should be carefully monitored for [[heart blocks]]. There is no [[secondary prevention]]. | |||
==Historical Perspective== | ==Historical Perspective== | ||
In 1894, Dr. Engelman was the first to describe | In 1894, Dr. Engelman was the first to describe the phenomenon of [[AV]] interval lengthening in detail. In 1899, Karel Frederik published a paper on irregular [[pulses]] describing AV conduction and blockage impairment. 1906 Einthiven was the first to present a presentation of normal and abnormal electrocardiograms recorded with a string galvanometer. Dr. Ashmar in 1925 studied and described in detail these blocked impulses and their impact on the conduction in the muscle of the [[heart]]. In 1952 Dr. Paul Zoll developed the first [[temporary transcutaneous pacing]]. | ||
==Classification== | ==Classification== | ||
[[Complete heart block]] may be transient due to increased [[parasympathetic]] tone defining [[vagally]] mediated [[atrioventricular block]] or due to [[infranodal block]] whether there is evidence of conduction block distal to the [[atrioventricular node]]. | [[Complete heart block]] may be transient due to increased [[parasympathetic]] tone defining [[vagally]] mediated [[atrioventricular block]] or due to [[infranodal block]] whether there is evidence of conduction block distal to the [[atrioventricular node]]. | ||
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===History and Symptoms=== | ===History and Symptoms=== | ||
Patients with third degree | Patients with [[third-degree AV block]] typically experience a low [[blood pressure]], decreased heart rate, and poor [[circulation]]. Some [[patients]] with [[complete heart block]] may experience difficulties in doing [[exercise]], as the [[heart]] cannot react quickly to [[sudden]] changes in demand or sustain the higher [[heart rates]] required for sustained [[physical activity]]. [[Complete heart block]] associated with a slower [[pacemaker]] can result in [[dizziness]], [[presyncope]] and[[syncope]]. | ||
=== Physical Examination === | === Physical Examination === | ||
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=== Other Imaging Findings === | === Other Imaging Findings === | ||
[[Nuclear imaging]] techniques might rarely used and may be helpful in the diagnosis of complications of [[third-degree AV block ]] or provide shreds of evidence in favor of the underlying disease in those with [[complete heart block]]. | [[Nuclear imaging]] techniques might rarely be used and may be helpful in the diagnosis of complications of [[third-degree AV block ]] or provide shreds of evidence in favor of the underlying disease in those with [[complete heart block]]. | ||
=== Other Diagnostic Studies === | === Other Diagnostic Studies === | ||
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=== Primary Prevention === | === Primary Prevention === | ||
Patients with [[renal insufficiency]], [[potassium]] electrolyte disturbances, and dehydration are predisposed to develop [[digoxin toxicity]]. Careful monitoring of electrolytes, drug levels, and renal function is essential in patients on chronic [[digoxin]] therapy. Patients on multiple nodal agents | Patients with [[renal insufficiency]], [[potassium]] electrolyte disturbances, and dehydration are predisposed to develop [[digoxin toxicity]]. Careful monitoring of electrolytes, drug levels, and renal function is essential in patients on chronic [[digoxin]] therapy. Patients on multiple nodal agents are susceptible for the development of third-degree atrioventricular (AV) block ([[Third degree AV block|complete heart block]]). These patients should be carefully monitored for heart blocks. | ||
=== Secondary Prevention === | === Secondary Prevention === | ||
Revision as of 06:56, 1 July 2021
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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 disease of the cardiac electrical conduction system where there is complete dissociation of the atrial and ventricular activity because of the absence of conduction through the atrioventricular node (AVN) or His-Purkinje system. 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 the impairment of AV conduction and blockage.Complete heart block may be transient due to increased parasympathetic tone defining vagally mediated atrioventricular block or due to infranodal block whether there is evidence of conduction block distal to the atrioventricular node. 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. The most common cause of a complete heart block is coronary ischemia, but there are many other etiologies. The progressive degeneration of the electrical conduction system of the heart due to aging can cause a third-degree heart block. Complete heart block can be preceded by first degree AV block, second degree AV block, or bifascicular block. Acute myocardial infarction may present as a third-degree heart block. Lupus in a pregnant mother can cause congenital heart block in newborns. Maternal antibodies can cross the placenta and lead to a complete heart block during gestation. Sometimes no cause can be identified. Third-degree heart block should not be confused with high-grade AV block which is a second-degree block with a very slow ventricular rate with occasional AV conduction, or AV Dissociation defining to indicate the occurrence of independent atrial and ventricular contractions caused by entities other than third-degree heart block.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. Common risk factors associated atioventricular block include older age, male sex, history of myocardial infarction, history of congestive heart disease, high systolic blood pressure, increased fasting blood glucose level.Transthoracic echocardiography may be helpful in the diagnosis of the underlying diseases that tend to third-degree AV block. Echocardiography might show shreds of evidence in favor of cardiomyopathies or valvular heart diseases. In particular case scenarios, transesophageal echocardiography is warranted and may help to diagnose etiologies such as valvular ring abscess. Furthermore, the left ventricular function can be determined using an echo and provide pieces of evidence in favor of the placement of a pacemaker or defibrillator. . Common indications for echocardiography in suspicion of cardiac origin of bradycardia or conduction disorder may include syncope, lightheadedness/presyncope, symptoms related to aortic stenosis, hypertrophic cardiomyopathy, heart failure.There are no x-ray findings associated with third-degree AV block. However, a chest x-ray may be helpful in the diagnosis of complications of third degree AV block such as pulmonary edema. Additionally, a chest x-ray may be helpful in the diagnosis of the underlying disease tend to third degree AV block, or in the diagnosis of the other complications of that disorder which may include cardiomegaly and hilar adenopathy. CT scan may be helpful in the diagnosis of cardiac and chest abnormalities related to the underlying organic disease in those with third-degree AV block. Cardiac MRI may be helpful in selected patients to identify the underlying structural heart disease associated conduction disturbance such as sarcoidosis, hemochromatosis, and amyloidosis. Nuclear imaging techniques might rarely be used and may be helpful in the diagnosis of complications of third-degree AV block or provide shreds of evidence in favor of the underlying disease in those with complete heart block. Ambulatory monitoring is warranted in cases of possible transient heart block, or some other bradyarrhythmias that might be mistaken with third-degree AV block. Worsening atrioventricular block with isoproterenol and atropine may be suggestive of infranodal block. Improvement of atrioventricular conduction with carotid sinus massage may be observed in patients with infranodal atrioventric-ular block. The management of third-degree AV block depends on the severity of signs, symptoms, and the underlying cause. In symptomatic patients and with hemodynamic distress, pharmacological therapy should be initiated immediately to increase heart rate and cardiac output. Most of the patients who do not respond to pharmacologic therapy require a temporary pacemaker. After stabilizing the patients, assessment and treatment of potentially reversible causes should be done. Some patients without reversible cause or unidentified etiology require a [[permanent pacemaker]. Cardiac pacemakers are effective treatments for a variety of cardiac conduction abnormalities and can reestablish adequate circulation by generating appropriate heart rate and cardiac response. Two main factors guide the majority of decisions regarding permanent pacemaker insertion. First is the association of symptoms with arrhythmia, and second is the potential for progression of the rhythm disturbance. Symptoms related to atrioventricular block are determining factor of placing permanent pacemaker, regardless of the level of atrioventricular block. Permanent pacemaker is warranted if the site of atrioventricular block is Infranodal, regardless of the presence or absence of symptoms. Temporary transvenous pacing is used to provide hemodynamic support or back-up pacing to prevent asystole. If atrioventricular block seems to be irreversible, it is better to proceed directly with permanent pacemaker implantation. Patients with renal insufficiency, potassium electrolyte disturbances, and dehydration are predisposed to develop digoxin toxicity. Careful monitoring of electrolytes, drug levels, and renal function is essential in patients on chronic digoxin therapy. Patients on multiple nodal agents are susceptible to the development of third-degree AV block. These patients should be carefully monitored for heart blocks. There is no secondary prevention.
Historical Perspective
In 1894, Dr. Engelman was the first to describe the phenomenon of AV interval lengthening in detail. In 1899, Karel Frederik published a paper on irregular pulses describing AV conduction and blockage impairment. 1906 Einthiven was the first to present a presentation of normal and abnormal electrocardiograms recorded with a string galvanometer. Dr. Ashmar in 1925 studied and described in detail these blocked impulses and their impact on the conduction in the muscle of the heart. In 1952 Dr. Paul Zoll developed the first temporary transcutaneous pacing.
Classification
Complete heart block may be transient due to increased parasympathetic tone defining vagally mediated atrioventricular block or due to infranodal block whether there is evidence of conduction block distal to the atrioventricular node.
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
The most common cause of a complete heart block is coronary ischemia, but there are many other etiologies. The progressive degeneration of the electrical conduction system of the heart due to aging can cause a third-degree heart block. Complete heart block can be preceded by first degree AV block, second degree AV block, or bifascicular block. Acute myocardial infarction may present as a third-degree heart block. Lupus in a pregnant mother can cause congenital heart block in newborns. Maternal antibodies can cross the placenta and lead to a complete heart block during gestation. Sometimes no cause can be identified.
Differentiating Third degree AV block from other Diseases
Third-degree heart block should not be confused with high-grade AV block which is a second-degree block with a very slow ventricular rate with occasional AV conduction, or AV Dissociation defining to indicate the occurrence of independent atrial and ventricular contractions caused by entities other than third-degree heart block.
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.
Risk Factors
Common risk factors associated atioventricular block include older age, male sex, history of myocardial infarction, history of congestive heart disease, high systolic blood pressure, increased fasting blood glucose level.
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 syncope, musculoskeletal injuries due to falling, and sudden cardiac death. 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 good prognosis.
Diagnosis
Diagnostic Study of Choice
A 12-lead Electrocardiography (ECG) is the gold standard test for the diagnosis of third degree AV block.
History and Symptoms
Patients with third-degree AV block typically experience a low blood pressure, decreased heart rate, and poor circulation. Some patients with complete heart block may experience difficulties in doing exercise, as the heart cannot react quickly to sudden changes in demand or sustain the higher heart rates required for sustained physical activity. Complete heart block associated with a slower pacemaker can result in dizziness, presyncope andsyncope.
Physical Examination
Initial triage of patients with complete heart block consists of determining symptoms, taking vital signs, and looking for evidence of hemodynamic instability. Patients with complete heart block may have serve bradycardia, S3 gallop, new murmurs, peripheral edema, and hepatomegaly. Patients may have signs of hypoperfusion, such as altered mental status, lethargy, and hypotension.
Laboratory Findings
There is not any recommendation about routine laboratory tests in patients presented with bradycardia or conduction disorder. However, in suspicion of the underlying causes of bradycardia including sepsis, rheumatologic disorder, or thyroid disease specific tests are warranted.
Echocardiography
Transthoracic echocardiography may be helpful in the diagnosis of the underlying diseases that tend to third-degree AV block. Echocardiography might show shreds of evidence in favor of cardiomyopathies or valvular heart diseases. In particular case scenarios, transesophageal echocardiography is warranted and may help to diagnose etiologies such as valvular ring abscess. Furthermore, the left ventricular function can be determined using an echo and provide pieces of evidence in favor of the placement of a pacemaker or defibrillator. . Common indications for echocardiography in suspicion of cardiac origin of bradycardia or conduction disorder may include syncope, lightheadedness/presyncope, symptoms related to aortic stenosis, hypertrophic cardiomyopathy, heart failure.
X-Ray
There are no x-ray findings associated with third-degree AV block. However, a chest x-ray may be helpful in the diagnosis of complications of third degree AV block such as pulmonary edema. Additionally, a chest x-ray may be helpful in the diagnosis of the underlying disease tend to third degree AV block, or in the diagnosis of the other complications of that disorder which may include cardiomegaly and hilar adenopathy.
CT scan
CT scan may be helpful in the diagnosis of cardiac and chest abnormalities related to the underlying organic disease in those with third-degree AV block.
MRI
Cardiac MRI may be helpful in selected patients to identify the underlying structural heart disease associated conduction disturbance such as sarcoidosis, hemochromatosis, and amyloidosis.
Other Imaging Findings
Nuclear imaging techniques might rarely be used and may be helpful in the diagnosis of complications of third-degree AV block or provide shreds of evidence in favor of the underlying disease in those with complete heart block.
Other Diagnostic Studies
Ambulatory monitoring is warranted in cases of possible transient heart block, or some other bradyarrhythmias that might be mistaken with third-degree AV block. Worsening atrioventricular block with isoproterenol and atropine may be suggestive of infranodal block. Improvement of atrioventricular conduction with carotid sinus massage may be observed in patients with infranodal atrioventric-ular block.
Treatment
Medical Therapy
The management of third-degree AV block depends on the severity of signs, symptoms, and the underlying cause. In symptomatic patients and with hemodynamic distress, pharmacological therapy should be initiated immediately to increase heart rate and cardiac output. Most of the patients who do not respond to pharmacologic therapy require a temporary pacemaker. After stabilizing the patients, assessment and treatment of potentially reversible causes should be done. Some patients without reversible cause or unidentified etiology require a permanent pacemaker.
Surgery
Cardiac pacemakers are effective treatments for a variety of cardiac conduction abnormalities and can reestablish adequate circulation by generating appropriate heart rate and cardiac response. Two main factors guide the majority of decisions regarding permanent pacemaker insertion. First is the association of symptoms with arrhythmia, and second is the potential for progression of the rhythm disturbance. Symptoms related to atrioventricular block are determining factor of placing permanent pacemaker, regardless of the level of atrioventricular block. Permanent pacemaker is warranted if the site of atrioventricular block is Infranodal, regardless of the presence or absence of symptoms. Temporary transvenous pacing is used to provide hemodynamic support or back-up pacing to prevent asystole. If atrioventricular block seems to be irreversible, it is better to proceed directly with permanent pacemaker implantation.
Primary Prevention
Patients with renal insufficiency, potassium electrolyte disturbances, and dehydration are predisposed to develop digoxin toxicity. Careful monitoring of electrolytes, drug levels, and renal function is essential in patients on chronic digoxin therapy. Patients on multiple nodal agents are susceptible for the development of third-degree atrioventricular (AV) block (complete heart block). These patients should be carefully monitored for heart blocks.
Secondary Prevention
There is no secondary prevention.