Abu Zubair meriwayatkan dari Jabir bin Abdullah bahwa Nabi Muhammad SAW bersabda:

"Setiap penyakit ada obatnya. Jika obat yang tepat diberikan dengan izin Allah, penyakit itu akan sembuh".

(HR. Muslim, Ahmad dan Hakim).

Sabtu, 28 November 2009



Syncope is defined as a transient self-limited loss of consciousness, usually leading to a fall. It is a subset of a broader range of conditions causing transient loss of consciousness. Syncope is a common medical problem accounting for up to 1% of emergency department visits and is the sixth leading cause of hospitalization for people older than 65 years.

Syncope results from a self-terminating inadequacy of global cerebral nutrient perfusion. In some patients, brainstem hypoxia triggers a posturing reflex that can appear like a seizure. A number of cardiac and noncardiac conditions can cause syncope (see Causes).

The most common type of syncope, neurocardiogenic syncope, is characterized by a sudden failure of the autonomic nervous system to maintain blood pressure to maintain cerebral perfusion.

Although the exact mechanism is not clear, one proposed mechanism is that in patients who are predisposed to have increased peripheral venous pooling, a sudden drop in preload results in a hypercontractile state. The forceful contraction stimulates mechanoreceptors, located primarily on the floor of the left ventricle. This mechanical activation results in neural traffic (falsely), mimicking hypertension and leading to sympathetic withdrawal and parasympathetic activation. The result is bradycardia (cardioinhibitory), vasodilatation (vasodepressor), or both (mixed response). Similar mechanoreceptors are also present in other parts of the body such as the bladder, rectum, esophagus, and lungs. Thus, other situational triggers to reflex syncope include micturition, defecation, deglutition, and cough.

As highlighted in a recent review by Hainsworth, "the trigger for the switch in autonomic response remains one of the unresolved mysteries in cardiovascular physiology."

United States

Primary care physicians, cardiologists, and emergency department physicians frequently encounter patients with syncope. In the Framingham study, 822 (10.5%) of 7814 patients reported at least one syncopal event during the average follow up of 17 years. The incidence of new syncope was 6.2 per 1000 person-years. Assuming the constant incidence rate, a person living 70 years was estimated to have a 42% lifetime prevalence of syncope. The incidence rate is almost double in patients with cardiovascular disease compared with those without it.

The prognostic significance of syncope depends on its cause (cardiac syncope with worse prognosis), the nature and severity of underlying structural heart disease, and the treatment initiated. Mortality is likely highest in patients with left ventricular dysfunction due to coronary artery disease or nonischemic cardiomyopathy. In these patients, syncope is frequently due to ventricular tachyarrhythmias. This risk is reduced substantially in patients treated with implanted cardioverter-defibrillators (ICDs). Even in patients with a benign cause of syncope, spells can result in significant injury, particularly in elderly persons.

In a recent study, mortality was about 30% higher among all participants with syncope than in those without syncope.

No effect of race on the incidence of syncope is known.

Although earlier studies reported a slightly higher incidence of syncope in women compared with men, recent studies show similar incidence. A 72 per 1000 person-year incidence was noted in both men and women in a recent study based on the Framingham cohort.

The incidence of syncope increases with age. Syncope is not uncommon in younger patients; neurally mediated (ie, neurocardiogenic) syncope accounts for most cases in younger patients. Occasionally, syncope in young patients presages a potentially life-threatening problem such as congenital long QT syndrome, Wolff-Parkinson-White (WPW) syndrome, Brugada syndrome, or hypertrophic cardiomyopathy.

Patients with syncope may present with various complaints.

Patients may describe a syncopal episode in many ways, including blackout, dizzy spell, and seizure. Unexplained falls, particularly in elderly persons, also may be due to syncope.
Associated symptoms include palpitations, lightheadedness, diaphoresis, nausea and vomiting, warmth, chest pain, and shortness of breath.
Any history of focal neurologic symptoms or incontinence of bowel or bladder should also be sought.
Differentiating syncope from vertigo, in which a sensation of movement of either the patient or the surroundings transpires, is important. Vertigo usually reflects a neurologic or otolaryngologic problem.
Reports of eyewitnesses may be very helpful.
Triggers for the spells and a careful medication history, including over-the-counter and illicit drugs, should be sought.
The family history, particularly any family history of sudden death or syncope, should be reviewed, ie, the entire history is necessary.
The following clues suggest a higher risk of syncope and indicate that an expedient evaluation may be necessary:
Underlying structural heart disease, especially left ventricular dysfunction
Exertional syncope
Family history of sudden death
Significant traumatic injury due to loss of consciousness


A thorough physical examination should be performed on all patients who present with syncope.

Orthostatic vital signs at 1 and 3 minutes should be recorded.
The physician should look carefully for any cardiovascular or focal neurologic abnormalities.
Carotid sinus massage should be carefully performed during cardiac monitoring as long as carotid bruits or known carotid artery disease is not present.


Third-Degree Atrioventricular Block


In the heart, normal impulse initiation begins in the sinoatrial node. The excitation wave then travels through the atrium. During this time, surface ECG recordings show the P wave. Following intra-atrial conduction to the area of the lower intra-atrial septum, this wavefront reaches the inputs to the atrioventricular (AV) node. The AV node then conducts the impulse to the His bundle. The His bundle divides into the right and left bundles, which distribute this impulse to the ventricles. During atrial, AV node and His-Purkinje conduction, the PR segment is observed. Heart block occurs when slowing or complete block of this conduction occurs. Traditionally, heart block can be divided into first-, second-, and third-degree block.

First-degree AV block is a condition in which a one-to-one relationship exists between P waves and QRS complexes, but the PR interval is longer than 200 milliseconds (ms). Thus, first-degree AV block represents delay or slowing of conduction. Occasionally, first-degree AV block may be associated with other conduction disturbances, including bundle-branch block and fascicular blocks (bifascicular or trifascicular block).

First-degree block is generally not an indication for permanent pacing, but may become an indication for permanent pacing when patients develop symptoms attributable to the AV delay typically, when the PR interval is markedly prolonged (>300 ms) and the patient has documented left ventricular systolic dysfunction and symptoms of heart failure. In patients with muscular dystrophies and any degree of AV block, implantation of a pacemaker should be promptly considered. For more information, see eMedicine's article First-Degree Atrioventricular Block.

Second-degree AV block exists when more P waves than QRS complexes are seen on the ECG, but a relationship between P waves and QRS complexes still exists. In other words, not all P waves are followed by QRS complexes (conducted). Traditionally, this type of AV block is divided into subcategories as type I and type II.

Type I second-degree AV block is also known as Wenckebach block. In type I block, the PR interval is changing (prolonging) with each P wave to the point when the P wave is no longer conducted (followed by QRS complexes). In a typical Wenckebach block, the prolongation of PR interval from beat-to-beat is greatest in the first interval and progressively less with subsequent intervals. This is reflected in shortening of the R-R interval and the overall PR interval increases. Also, the R-R interval enveloping the pause is less than twice the duration of the first R-R interval following the pause.

Upon examination of the ECG tracing, type I second-degree block results in the characteristic appearance of grouping beats, and conversely, the presence of grouped beating should prompt a careful evaluation for Wenckebach conduction. Not all Wenckebach conduction is pathologic. For example, this type of AV block is often seen at rest in athletes or with sleep most likely resulting from increased vagal tone. It resolves spontaneously after physical deconditioning, and is less likely with advancing age.

Type II second-degree AV block is also known as Mobitz II block. In type II block, the PR interval is constant, but occasional P waves are not followed by the QRS complexes (nonconducted). Occasionally, the first PR interval following nonconducted P waves may be shorter by £ 20 ms. For more information, see eMedicine's article Second-Degree Atrioventricular Block.

To differentiate between type I block and type II block, at least 3 consecutive P waves must be present in the tracing. If only every other P wave is conducted (2:1), this block cannot be classified into either of these categories and is best described as 2:1 conduction, unless the mechanism can be inferred from surrounding patterns of atrial-to-ventricular conduction. Generally, Wenckebach block is related to a disease process within the proximal portion of the AV node, tends to respond to atropine, and may resolve. On the other hand, Mobitz II block usually results from the infrahisian block (process involving the His-Purkinje system), does not respond to atropine, and has more ominous clinical consequences.

Although the morphological criteria are somewhat helpful in ascertaining the location of the block in the conduction system, only an invasive electrophysiologic study is able to precisely determine the location of the block. All blocks resulting from prolongation of the HV interval on intracardiac tracing carry a poor prognosis and are an indication for permanent pacing.

An AV block resembling second-degree AV block has been reported with sudden surges of vagal tone associated with cough, hiccups, swallowing, carbonated beverages, pain, micturition, or airway manipulation in otherwise healthy subjects. The distinguishing feature is simultaneous slowing of the sinus rate. This condition is paroxysmal and benign but must be carefully differentiated from a true second-degree AV block because the prognosis is very different.

Third-degree AV block (also called complete heart block) exists when more P waves than the QRS complexes exist and no relationship exists between them (no conduction). The escape rhythm may arise within the AV node (narrow complex) or lower in the conduction system (wide complex). The ventricular rate, and thus the pulse, varies from 30-40 bpm. Characteristically in this block, the atrial rate is rapid, presumably in response to the hemodynamic consequences of block. In most cases of persistent third-degree AV block, permanent pacing is required.

Atrioventricular dissociation is present when atrial and ventricular activation are independent of each other. It can result from complete heart block or physiological refractoriness of conduction tissue. It can also occur in a situation when the atrial/sinus rate is slower than the ventricular rate, namely with accelerated junctional tachycardia and ventricular tachycardia. Occasionally, the atrial and ventricular rates are so close that the tracing would suggest normal AV conduction; only careful examination of the long rhythm strip may reveal a variation in PR interval. This form of AV dissociation is called isorhythmic AV dissociation. Maneuvers or medications resulting in acceleration of atrial/sinus rate will result in restoration of normal conduction.


Heart block results from various pathological states causing infiltration, fibrosis, or loss of connection in portions of the healthy conduction system. Acute myocardial infarction (MI) can cause complete AV block. Common causes of heart block are listed in Causes.
United States

The prevalence of third-degree AV block is 0.02%.

The prevalence of third-degree AV block is 0.04%.1

Third-degree AV block may be an underlying condition in patients who present with sudden cardiac death. The cause of death may often be tachyarrhythmias precipitated by the secondary changes in ventricular repolarization (QT prolongation) secondary to the abrupt changes in rate.

The incidence of AV conduction abnormalities increases with advancing age, resembling the age-related incidence of ischemic heart disease. An early peak in incidence occurs in infancy and early childhood due to congenital complete AV block, which is sometimes not recognized until childhood or even adolescence.
Symptoms attributable to complete AV block include syncope, near-syncope, lightheadedness, fatigue, dyspnea, and angina.
Some patients are asymptomatic.
Third-degree AV block may be an underlying condition in patients who present with sudden cardiac death.
History of cardiac interventions should be carefully investigated since aortic valve surgery, septal alcohol ablation, proximal anterior descending artery stenting (complicated by compromised flow in the first septal perforator branch), or ablation of slow or fast pathway of the AV node all may result in the complete heart block.
Initial triage of patients with complete heart block consists of determining symptoms, assessing vitals signs, and looking for evidence of compromised peripheral perfusion.
Careful examination of the neck veins can often show evidence of cannon a waves. A variable intensity S1 may be heard. In addition, the pulse rate may be slow.
If the slow rate or loss of atrial contraction prior to ventricular contraction has caused heart failure, then venous pressures will be elevated, including the jugular venous pressure.
Any new murmurs or gallops should be noted because strong associations exist between cardiomyopathies, mitral calcification, aortic calcification, or endocarditis and complete AV block.
If heart failure is present as evidenced by rales, an S3 gallop, peripheral edema, or hepatomegaly, then a more compelling need for immediate pacing exists.
Because endocarditis, rheumatic fever, and Lyme disease cause heart block, pay attention to any signs of infection or skin rashes during the general examination. This is particularly true in endemic areas for Lyme disease.
Neurologic examination may provide clues to the etiology of AV block because neuromuscular disease, especially myotonic dystrophy and Duchenne muscular dystrophy, can cause AV block.
A phenomenon known as ventriculophasic sinus arrhythmia (P-P intervals) refers to the P-P interval enveloping a QRS complex being slightly shorter than the other P-P intervals.
Lev disease (calcification of the conduction system and valves) has been found to have an inherited component.
The common causes of AV heart block are as follows:
Drugs - Calcium channel blockers, beta-blockers, quinidine, procainamide, lithium, digoxin, tricyclic antidepressant
Degenerative diseases – Lenègre disease (sclerodegenerative process involving only the conduction system) and Lev disease, noncompaction cardiomyopathy, nail-patella syndrome, mitochondrial myopathy2
Infectious causes - Lyme borreliosis (particularly in endemic areas), rheumatic fever, myocarditis, Chagas disease (Central America and South America), Aspergillus myocarditis, varicella zoster virus3 , valve ring abscess
Rheumatic diseases - Ankylosing spondylitis, Reiter syndrome, relapsing polychondritis, rheumatoid arthritis, scleroderma
Infiltrative processes - Amyloidosis, sarcoidosis, tumors, Hodgkin disease, multiple myeloma
Neuromuscular disorders - Becker muscular dystrophy, myotonic muscular dystrophy
Ischemic or infarctive causes - AV nodal block associated with interior wall myocardial infarction, His-Purkinje block associated with anterior wall myocardial infarction
Metabolic causes - Hypoxia, hyperkalemia, hypothyroidism
Toxins – "Mad" honey
Phase IV block (also known as bradycardia-related block)
Iatrogenic – Complicating aortic valve surgery, septal alcohol ablation, percutaneous coronary intervention to the left anterior descending artery, or ablation of slow or fast pathway of the AV node. Placement of catheters mechanically interfering with one fascicle when conduction is already impaired in the remaining conduction system (eg, bumping the right bundle with a PA catheter in a patient with existing left bundle branch block) almost always resolves spontaneously.
Special Circumstances

Heart block during myocardial infarction4,5

Contemporary AV block rarely complicates myocardial infarction. With early revascularization strategy, the incidence of AV block decreased from 5.3 to 3.7%. Occlusion of each of the coronary arteries can result in development of conduction disease despite redundant vascular supply to the AV node from all coronary arteries. Most commonly, the occlusion of the right coronary artery (RCA) is accompanied by AV block. In particular, the proximal RCA occlusion has high incidence of AV block (24%) since not only the AV nodal artery is involved but also right superior descending artery, which originates from the very proximal part of the RCA.

In most cases, AV block resolves promptly after revascularization but sometimes the course is prolonged. Overall the prognosis is favorable. AV block in a setting of occlusion of the left anterior descending artery (particularly proximal to the first septal perforator) has more ominous prognosis and usually requires pacemaker implantation. Second-degree AV block associated with bundle branch block and in particular with alternating bundle branch block is an indication for permanent pacing.

Heart block following cardiac surgery6

Heart block following cardiac surgery is seen in 1-5.7% of patients. Major risks factors identified for the need for permanent pacing are aortic valve surgery, preexisting conduction disease (either right or left bundle branch block), bicuspid aortic valve, annular calcification, and female gender. The time course for recovery varies widely with a significant portion of patients recovering during the 48 hours following surgery. Available evidence suggests that if no recovery in AV conduction is seen by the fourth or fifth day following surgery, a pacemaker should be implanted.


Second-Degree Atrioventricular Block


Second-degree atrioventricular (AV) block is characterized by disturbance, delay, or interruption of impulse conduction through the AV node. This excludes block due to premature atrial beats. The AV block can be permanent or transient, depending on the anatomical or functional impairment in the conduction system. Typically, it is classified into Mobitz type I block or Wenckebach block, Mobitz type II block, 2:1 block, and high-grade AV block.

The diagnosis of type I and II second-degree AV block is based on electrocardiographic patterns, not on the anatomic site of the block. Type I is characterized by a progressive lengthening of the conduction time until an impulse is not conducted; type II is characterized by occasional or repetitive sudden block of conduction of an impulse without prior measurable lengthening of the conduction time. Precise localization of the site of the block within the specialized conduction system is critical to the appropriate treatment of individuals with second-degree AV block.

By itself, a 2:1 AV block cannot be classified as type I or II because only 1 PR interval is available for analysis before the block. Both a 2:1 AV block and a block involving 2 or more consecutive sinus P waves are sometimes referred to as high-grade AV block. In high-grade AV block, some beats are conducted in contrast to third-degree AV block.


Type I atrioventricular (AV) block most often results from conduction disturbances in the AV node; however, in rare cases, it may be due to infranodal block. Type I block is rarely secondary to AV nodal structural abnormalities when the QRS complex is narrow in width and no underlying cardiac disease is present. In this setting, type I block can be vagally mediated and may be observed in conditions associated with relative activation of the parasympathetic nervous system such as in well-trained athletes, cardiac glycoside (ie, digoxin) excess, or neurally mediated syncope syndromes.

A vagally mediated AV block occurs in the AV node when vagal discharge is enhanced and often is associated with electrocardiographic evidence of sinus slowing. A vagally mediated AV block improves with exercise and may occur more commonly during sleep when parasympathetic tone dominates. If an increase in sympathetic tone (eg, exercise) initiates or exacerbates a type I block, infranodal block should be considered.

Cardioactive drugs are another important cause of AV block. They may exert negative (ie, dromotropic) effects on the AV node directly, indirectly via the autonomic nervous system, or both. Digoxin, beta-blockers, calcium channel blockers, and certain antiarrhythmic drugs have been implicated in second-degree AV block.

Various inflammatory, infiltrative, metabolic, endocrine, and collagen vascular disorders have been associated with AV nodal block. Less commonly, type I block can occur with a block localized to the His bundle or distal to the His bundle. In this situation, the QRS complex may be wide, and the baseline PR interval is usually shorter with smaller PR increments preceding the block. Type I block with infranodal block carries a worse prognosis compared with AV nodal block. The location of a type II block is most often infranodal. As such, this poses higher risk to the patient.
United States

Nearly 3% of patients with underlying structural heart disease develop some form of second-degree AV block.

The level of the block determines the prognosis. Atrioventricular (AV) nodal blocks, which are the vast majority of type I blocks, carry a favorable prognosis, whereas infranodal blocks, whether type I or type II, may progress to complete block with a worse prognosis. However, type I block may be significantly symptomatic.
Type I block (in the AV node) is often nonprogressive and benign from a mortality standpoint. The risk of progression to complete heart block is significant when the level of block is in the specialized His-Purkinje conduction system (infranodal).
Type II AV block often progresses to third-degree block and, as such, carries a more worrisome prognosis. Type II block may produce Stokes-Adams syncopal attacks.
Vagally mediated AV block is typically benign from a mortality standpoint but may lead to dizziness and syncope.
The male-to-female ratio of second-degree atrioventricular block is 1:1.

Symptoms related to type I block vary substantially, ranging from asymptomatic in well-trained athletes and those without structural heart disease, to recurrent syncope, presyncope, and bradycardia in patients with heart disease. AV block may provoke heart failure and angina.

Second-degree AV block may occur in the presence or absence of structural heart disease.
Enhanced vagal tone due to pain, carotid sinus massage, or hypersensitive carotid sinus syndrome can result in slowing of the sinus rate and/or the development of AV block. Therefore, vagally mediated AV block can be associated with electrocardiographic evidence of sinus slowing. High vagal tone can occur in young subjects or athletes at rest. Mobitz type I has been described in 2-10% of long distance runners.1
Cardioactive drugs are another important cause of AV block. They may exert negative effects on the AV node directly, indirectly via the autonomic nervous system, or both. Digoxin, beta-blockers, calcium channel blockers, and certain antiarrhythmic drugs have been implicated in second-degree AV block. Several antiarrhythmic medications may cause second-degree AV block, and among them, sodium channel blockers, such as procainamide, cause more distal block in the His-Purkinje system. Persistent second-degree AV block following adenosine infusion for nuclear stress testing has been reported.2 The AV block may not resolve in many of the patients who take cardioactive medications. This suggests an underlying conduction disturbance in addition to the medications as the etiology of the AV block. At toxic levels, other pharmacologic agents such as tricyclic antidepressants and lithium may be associated with AV block. Presynaptic alpha agonists (eg, clonidine) may also be associated with, or exacerbate, AVblock.
Various inflammatory, infiltrative, metabolic, endocrine, and collagen vascular disorders that have been associated with AV nodal block are as follows:
Inflammatory diseases
Lyme disease
Acute rheumatic fever
Infiltrative diseases
Sarcoidosis: AV conduction abnormalities can be the first sign of sarcoidosis.3
Infiltrative malignancies, such as Hodgkin lymphoma and other lymphomas, and multiple myeloma4
Metabolic and endocrine disorders
Addison disease
Thyrotoxic periodic paralysis5
Collagen vascular diseases
Ankylosing spondylitis
Rheumatoid arthritis
Lupus erythematosus
Reiter syndrome
Mixed connective tissue disease6
Other conditions associated with AV block:
Cardiac tumors
Trauma (including catheter-related, especially in the setting of preexisting left bundle branch block)
Myocardial bridging7
Ethanol septal reduction – Also called transcoronary ablation of septal hypertrophy for the treatment of obstructive hypertrophic cardiomyopathy
Transcatheter closure of atrial and ventricular septal defects8,9
Corrective congenital heart surgery, especially those near the septum
Progressive (age-related) idiopathic fibrosis of the cardiac skeleton
Valvular heart disease complications, especially aortic stenosis and aortic valve replacement surgery
Obstructive sleep apnea (OSA) is associated with a variety of cardiac arrhythmias including AV block.10
Muscular dystrophies: The conduction defects in patients with muscular dystrophy are progressive; therefore, these patients should undergo careful workup and follow-up, even if they present with a benign conduction defect such as first-degree atrioventricular block.11
Acute myocardial infarction (MI) may cause second-degree AV block.
In some patients, AV block may be an autosomal dominant trait and a familial disease. Several mutations in the SCN5A gene have been linked to familial AV block. Different mutations in the same gene have been reported in other dysrhythmias such as long QT syndrome and Brugada syndrome.


First-Degree Atrioventricular Block


The PR interval of the surface electrocardiogram (ECG) is measured from the onset of atrial depolarization (P wave) to the beginning of ventricular depolarization (QRS complex). In the adult population, normal PR interval ranges from 0.12-0.20 seconds at normal heart rates. First-degree atrioventricular (AV) block is defined as a PR interval exceeding 0.20 seconds (see Image 1).

The PR interval represents the time needed for an electrical impulse from the sinoatrial (SA) node to conduct through the atria, AV node, bundle of His, bundle branches, and Purkinje fibers. Thus, as shown in electrophysiological studies, PR interval prolongation (ie, first-degree AV block) may be due to conduction delay within the right atrium, the AV node, the His-Purkinje system, or a combination of these. AV nodal dysfunction accounts for the majority of cases. First-degree AV block caused by conduction delay in the His-Purkinje system often is associated with bundle-branch block.

Structure and function of the AV node and His-Purkinje system

The AV node is the only normal electrical connection between atria and ventricles. It is an oval or elliptical structure, measuring 7-8 mm in its longest (anteroposterior) axis, 3 mm in its vertical axis, and 1 mm transversely. The AV node is located beneath the right atrial endocardium, dorsal to the septal leaflet of the tricuspid valve, and about 1 cm superior to the orifice of the coronary sinus. The bundle of His originates from the anteroinferior pole of the AV node and travels through the central fibrous body to reach the dorsal edge of the membranous septum. It then divides into right and left bundle branches. The right bundle continues first intramyocardially, then subendocardially, toward the right ventricular apex. The left bundle continues distally along the membranous septum and then divides into anterior and posterior fascicles.

Blood supply to the AV node is provided by the AV node artery, a branch of the right coronary artery in 90% of individuals and of the left circumflex coronary artery in the remaining 10%. The His bundle has a dual blood supply from branches of anterior and posterior descending coronary arteries. Likewise, the bundle branches are supplied by both left and right coronary arteries.

The AV node has a rich autonomic innervation and is supplied by both sympathetic and parasympathetic nerve fibers. This autonomic innervation has a major role in the time required for the impulse to pass through the AV node.
United States

First-degree AV block is rare in young healthy adults. It is reported in 0.65-1.1% of young adults older than 20 years. Higher prevalence is reported in trained athletes (8.7%). The prevalence also increases with age; first-degree AV block is reported in 5% of men older than 60 years. The overall prevalence is 1.13 cases per 1000 lives.

No mortality or morbidity is related to isolated first-degree AV block. However, in the setting of acute inferior myocardial infarction (MI), first-degree AV block may herald higher degrees of AV block. Markedly prolonged PR interval in patients with left ventricular systolic dysfunction may impair ventricular filling and thus reduce cardiac output.

Incidence of first-degree AV block increases with age.
Patients with first-degree AV block are generally asymptomatic at rest. Markedly prolonged PR interval may reduce exercise tolerance in some patients with left ventricular systolic dysfunction. Syncope may result from transient high-degree AV block, especially in those with infranodal block and wide QRS complex.
The intensity of the first heart sound (S1) is decreased in patients with first-degree AV block.
Patients with first-degree AV block may have a short, soft, blowing, diastolic murmur heard at the cardiac apex. This diastolic murmur is not caused by diastolic mitral regurgitation, because it reaches its peak before the onset of regurgitation. The diastolic murmur is thought to be related to antegrade flow through closing mitral valve leaflets that are stiffer than normal. Administration of atropine may reduce the duration of this murmur by shortening the PR interval.
Athletic training: Well-trained athletes can demonstrate first-degree (and occasionally higher degree) AV block owing to an increase in vagal tone.
Coronary artery disease
Acute MI: First-degree AV block occurs in fewer than 15% of patients with acute MI admitted to coronary care units.
His bundle electrocardiographic studies have shown that, in most of these patients, AV node is the site of conduction block.
AV block is more common in the setting of inferior MI.
In the Thrombolysis in Myocardial Infarction (TIMI) II study, high-degree (second- or third-degree) AV block occurred in 6.3% of patients at the time of presentation and in 5.7% in the first 24 hours after thrombolytic therapy. Patients with AV block at the time of presentation had a higher in-hospital mortality rate than patients without AV block; both groups, however, had similar mortality rates during the following year. Patients who developed AV block after thrombolytic therapy had higher mortality rates both in-hospital and in the following year than patients without AV block. Right coronary artery was more often the site of infarction in patients with heart block than in those without heart block. Patients with AV block are believed to have larger infarct size. However, the prevalence of multivessel disease is not higher in patients with AV block.
Angina pectoris
Prinzmetal angina
Idiopathic degenerative diseases of the conduction system
Lev disease: This is due to progressive degenerative fibrosis and calcification of the neighboring cardiac structures, "sclerosis of the left side of cardiac skeleton," including mitral annulus, central fibrous body, membranous septum, base of the aorta, and crest of the ventricular septum. Lev disease has an onset about the fourth decade and is believed to be secondary to wear and tear on these structures caused by the pull of the left ventricular musculature. It affects the proximal bundle branches and is manifested by bradycardia and varying degrees of AV block.
Lenègre disease: This is an idiopathic, fibrotic degenerative disease restricted to the His-Purkinje system. It is caused by fibrocalcareous changes in mitral annulus, membranous septum, aortic valve, and crest of the ventricular septum. These degenerative and sclerotic changes are not attributed to inflammatory or ischemic involvement of adjacent myocardium. Lenègre disease involves the middle and distal portions of both bundle branches and affects a younger population than Lev disease.
Drugs: Calcium channel blockers, beta-blockers, digoxin, and amiodarone all may cause first-degree AV block. Although first-degree AV block is not an absolute contraindication for administration of these drugs, extreme caution should be exercised in the use of these medications in patients with first-degree AV block, as they carry the risk of developing higher degree AV block on exposure to these drugs.
Mitral or aortic valve annulus calcification: The main penetrating bundle of His is located near the base of the anterior leaflet of the mitral valve and the noncoronary cusp of the aortic valve. Heavy calcium deposits in patients with aortic or mitral annular calcification is associated with increased risk of AV block.
Infectious disease: Infective endocarditis, diphtheria, rheumatic fever, Chagas disease, Lyme disease, and tuberculosis all may be associated with first-degree AV block.
Extension of the infection to the adjacent myocardium in native or prosthetic valve infective endocarditis (ie, ring abscess) can cause AV block.
Acute myocarditis caused by diphtheria, rheumatic fever, or Chagas disease can result in AV block.
Collagen vascular disease: Rheumatoid arthritis, systemic lupus erythematous, and scleroderma all may be associated with first-degree AV block.
Rheumatoid nodules may occur in the central fibrous body and result in AV block.
Fibrosis of the AV node or the adjacent myocardium in patients with systemic lupus erythematous or scleroderma can cause first-degree AV block.
Doppler echocardiographic signs of first-degree AV block have been demonstrated in about 33% of fetuses of pregnant women who are anti-SSA/Ro 52-kd positive. In most of these fetuses, the blocks resolved spontaneously. However, progression to a more severe degree of block was seen in 2 of the fetuses. Serial Doppler echocardiographic measurement of AV-time intervals can be used for surveillance of these high-risk pregnancies.
Infiltrative diseases such as amyloidosis or sarcoidosis
Myotonic dystrophy
First-degree AV block occurs in about 10% of patients who undergo adenosine stress testing and is usually hemodynamically insignificant. Patients with baseline first-degree AV block more often develop higher degrees of AV block during adenosine stress testing. These episodes, however, are generally well tolerated and do not require specific treatment or discontinuation of the adenosine infusion.
Marked first-degree AV block may occur following catheter ablation of the fast AV nodal pathway with resultant conduction of the impulse via the slow pathway. This may result in symptoms similar to the pacemaker syndrome.
First-degree AV block (reversible or permanent) has been reported in about 2% of patients who undergo closure of atrial septal defect using the Amplatzer septal occluder.
First-degree AV block can occur following cardiac surgery. Transient first-degree AV block may result from right heart catheterization.


Digitalis Toxicity


Native people in various parts of the world have used many plant extracts containing cardiac glycosides as arrow and ordeal poisons. The ancient Egyptians used squill as a medicine. The Romans employed it as a diuretic, heart tonic, emetic, and rat poison. Digitalis, or foxglove, was mentioned in AD 1250 in the writings of Welsh physicians. Fuchsius described it botanically 300 years later and gave it the name Digitalis purpurea.

William Withering published his classic account of foxglove and some of its medical uses in 1785, remarking upon his experience with digitalis. Indians in South America have used cardiac glycosides in their dart poisons. Digitalis toxicity was well known in previous centuries, and some have suggested that the toxic visual symptoms of digitalis may have played a role in Van Gogh's use of swirling greens and yellows.

During the early 20th century, as a result of the work of Cushny, Mackenzie, Lewis, and others, the drug was gradually recognized as specific for treatment of atrial fibrillation. Only subsequently was the value of digitalis for treatment of congestive heart failure (CHF) established. Cardiac glycosides enhances cardiac contractility and slows the conduction through the atrioventricular junction by increasing vagal tone.

In recent years, cardiac glycosides toxicity has been known to result from ingestion of some plants, including yellow oleander (Thevetia peruviana) and foxglove (D purpurea), and a similar toxidrome has been associated with the use of herbal dietary supplements.


Mechanism of action

The positive inotropic effect of digitalis has 2 components.
Direct inhibition of membrane-bound sodium- and potassium-activated adenosine triphosphatase (Na+/K+ -ATPase), which leads to an increase in the intracellular concentration of calcium ([Ca2+]i)
Associated increase in a slow inward calcium current (iCa) during the action potential (AP) (This current is the result of movement of calcium into the cell, and it contributes to the plateau of the AP.)

Digitalis, in therapeutic concentrations, exerts no effect on the contractile proteins or on the interactions between them.

Digitalis glycosides bind specifically to Na+/K+ -ATPase, inhibit its enzymatic activity, and impair active transport of extruding sodium and transport of potassium into the fibers (3:2 ratio). As a result, intracellular sodium ([Na+]i) gradually increases, and a gradual, small decrease in intracellular potassium ([K+]i) occurs.

Cardiac fiber [Ca2+]i is exchanged for extracellular sodium (3:1 ratio) by a transport system that is driven by the concentration gradient for these ions and the transmembrane potential; increase in [Na+]i is related crucially to the positive inotropic effect of digitalis.

In addition, by a mechanism that is not defined clearly, the increase in [Ca2+]i increases the peak magnitude of iCa; this change parallels the positive inotropic action. The change in iCa is a consequence of the increase in [Ca2+]i and not of the increase in [Na+]i. Thus, more calcium is delivered during the plateau of each AP to activate each contraction.

A fall in intracellular pH accompanies the digoxin-induced increase in [Ca2+]i, which leads to activation of a sodium/hydrogen exchange pump. This results in extrusion of hydrogen, an increase in [Na+]i, and greater inotropy.

The mechanism described assumes that Na+/K+ -ATPase is the pharmacological receptor for digitalis and that, when digitalis binds to these enzymes, it induces a conformational change that decreases active transport of sodium. Many studies have provided evidence that digitalis binds to ATPase in a specific and saturable manner and that the binding results in a conformational change of the enzyme such that the binding site for digitalis probably is on the external surface of the membrane. Furthermore, the magnitude of the inotropic effect of digitalis is proportional to degree of inhibition of the enzyme.

Electrophysiological effects

The electrophysiological effects of cardiac glycosides include (1) decreased resting potential (RP) or maximal diastolic potential (MDP), which slows the rate of phase-0 depolarization and conduction velocity, (2) decrease in action potential duration (APD), which results in increased responsiveness of fibers to electrical stimuli, and (3) enhancement of automaticity, which results from an increase in the rate of phase-4 depolarization and from delayed after-depolarization.

In general, cardiac glycosides slow conduction and increase the refractory period in specialized cardiac conducting tissue by stimulating vagal tone. Digitalis has parasympathetic properties, which include hypersensitization of carotid sinus baroreceptors and stimulation of central vagal nuclei.

Digoxin also appears to have variable effects on sympathetic tone, depending on the specific cardiac tissue involved.

Vasomotor effects

Digoxin and other cardiac glycosides cause direct vasoconstriction in the arterial and venous system through inhibition of the Na+/K+ -ATPase pump in vascular smooth muscle.

Alterations in cardiac rate and rhythm occurring in digitalis toxicity may simulate almost every known type of dysrhythmia. Although no dysrhythmia is pathognomonic for digoxin toxicity, toxicity should be suspected when evidence of increased automaticity and depressed conduction is noted. Underlying these dysrhythmias is a complex influence of digitalis on the electrophysiologic properties of the heart as already discussed, as well as via the cumulative results of the direct, vagotonic, and antiadrenergic actions of digitalis. The effects of digoxin vary with the dose and differ depending on the type of cardiac tissue involved. The atria and ventricles exhibit increased automaticity and excitability, resulting in extrasystoles and tachydysrhythmias. Conduction velocity is reduced in both myocardial and nodal tissue, resulting in increased PR interval and atrioventricular (AV) block accompanied by decrease in QT interval.

In addition to these effects, the direct effect of digitalis on repolarization often is reflected in the ECG by ST segment and T-wave forces opposite in direction to the major QRS forces. The initial electrophysiologic manifestation of digitalis effects and toxicity usually is mediated by increased vagal tone. Early in acute intoxication, depression of sinoatrial (SA) or AV nodal function may be reversed by atropine. Subsequent manifestations are the result of direct and vagomimetic actions of the drug on the heart and are not reversed by atropine.

Ectopic rhythms—such as nonparoxysmal junctional tachycardia, extrasystole, premature ventricular contractions, ventricular flutter and fibrillation, atrial flutter and fibrillation, and bidirectional ventricular tachycardia—are due to enhanced automaticity, reentry, or both.

Bidirectional ventricular tachycardia is particularly characteristic of severe digitalis toxicity and results from alterations of intraventricular conduction, junctional tachycardia with aberrant intraventricular conduction or, on rare occasions, alternating ventricular pacemakers. Depression of the atrial pacemakers resulting in SA arrest also may be seen. Other features are SA block, AV block, and sinus exit block resulting from depression of normal conduction. Nonparoxysmal atrial tachycardia with block is associated with digitalis toxicity.

When conduction and the normal pacemaker are both depressed, ectopic pacemakers may take over, producing atrial tachycardia with AV block and nonparoxysmal automatic AV junctional tachycardia. Indeed, AV junctional block of varying degrees, alone or with increased ventricular automaticity, are the most common manifestations of digoxin toxicity, occurring in 30-40% of patients with recognized digoxin toxicity. AV dissociation may occur because of suppression of the dominant pacemaker with escape of a subsidiary pacemaker or inappropriate acceleration of a ventricular pacemaker.
United States

Approximately 0.4% of all hospital admissions are related to digitalis toxicity. Of people in nursing homes, 10-18% develop this toxicity. According to a large study published in 1990, definite digoxin toxicity occurred in 0.8% of patients with heart failure treated with digoxin.1

Approximately 2.1% of inpatients are taking digoxin. Of all admissions, 0.3% of patients develop toxicity.
Incidence of digitalis toxicity has declined in recent years because of a decrease in digitalis usage, improvement in digoxin formulation with more predictable drug bioavailability, better understanding of pharmacokinetics, improved laboratory radioimmunoassay, increasing awareness in drug-to-drug interactions, increased appreciation for factors that can increase the risk of toxicity, and availability of other drugs to treat heart failure and techniques like catheter ablation therapy for supraventricular tachycardias. The morbidity and mortality rates associated with digitalis toxicity have remained constant over the past 5 years.
According to the American Association of Poison Control Centers, of the patients reported in 1997 who developed cardiac glycoside toxicity, 34% demonstrated moderate or major morbidity, and 1% died.
The lethal dose of most glycosides is approximately 5-10 times the minimal effective dose and only about twice the dose that leads to minor toxic manifestations.

Older individuals with multiple comorbid conditions have lower tolerance of digitalis than younger individuals with few or no comorbid conditions, and they are prone to digitalis toxicity.
Withering recognized many of the signs of digitalis toxicity: "The foxglove, when given in very large and quickly repeated doses, occasions sickness, vomiting, purging, giddiness, confused vision, objects appearing green or yellow; increased secretion of urine, slow pulses, even as low as 35 in a minute, cold sweats, convulsions, syncope, death."
Extracardiac symptoms
Central nervous system: Drowsiness, lethargy, fatigue, neuralgia, headache, dizziness, and confusion may occur.
Ophthalmic: Visual aberration often is an early indication of digitalis toxicity. Yellow-green distortion is most common, but red, brown, blue, and white also occur. Drug intoxication also may cause snowy vision, photophobia, photopsia, and decreased visual acuity.
GI: In acute and chronic toxicity, anorexia, nausea, vomiting, abdominal pain, and diarrhea may occur. Mesenteric ischemia is a rare complication of rapid intravenous infusion.
Many extracardiac toxic manifestations of cardiac glycosides are mediated neurally by chemoreceptors in the area postrema of the medulla.
History of dementia, medication noncompliance
Cardiac symptoms
Shortness of breath
Swelling of lower extremities
Pharmacy - Recent addition of new drugs, such as verapamil, diltiazem, erythromycin or tetracycline, that can elevate digoxin level
General: Patient's mentation may change according to severity of digoxin toxicity, as well as associated comorbid conditions.
Vital signs: Pulse may be irregular depending on arrhythmias secondary to atrial fibrillation or arising from the digoxin toxicity itself. Hypotension may be observed if patient has CHF or dehydration secondary to decreased oral intake.
Neck: Findings include increased jugular venous pressure.
Cardiovascular: Findings may relate to severity of CHF. Associated cardiomegaly may be identified.
Respiratory: Sometimes, respiratory rate is increased. Basal crepitations are associated with CHF.
GI: Enlarged liver is secondary to CHF (ie, hepatic congestion). Hepatojugular reflux is present.
Neurological: Signs include changes in mental status.
Extremities: Pedal edema is noted if patient has renal failure or decompensated CHF.

The most common precipitating cause of digitalis intoxication is depletion of potassium stores, which occurs often in patients with heart failure as a result of diuretic therapy and secondary hyperaldosteronism.
Other causes include the following:
Advanced age
Myocardial infarction or ischemia
Renal insufficiency
Also consider drug interactions. Drugs that have been reported to potentiate digoxin toxicity include the following:
Verapamil, diltiazem, nifedipine
Anticholinergic drugs


Atrioventricular Block


Atrioventricular (AV) block occurs when the atrial depolarization fail to reach the ventricles or when atrial depolarization is conducted with a delay. Three degrees of AV block are recognized.

First-degree AV block consists of prolongation of the PR interval on the electrocardiogram (ECG) (>0.20 s in adults and >0.16 s in young children). The upper limit of the reference range for the PR interval is age-dependent in children. All atrial impulses reach the ventricles in first-degree AV block, however, conduction is delayed within the AV node

Second-degree AV block is characterized by atrial impulses (generally occurring at a regular rate) failing to conduct to the ventricles in one of the following 4 ways.

Mobitz I second-degree AV block (Wenckebach block) consists of progressive prolongation of the PR interval with the subsequent occurrence of a single nonconducted P wave that results in a pause. The pause is shorter than the sum of any 2 consecutive conducted beats (R-R interval). An episode of Mobitz I AV block usually consists of 3-5 beats, with a ratio of nonconducted to conducted beats of 4:3, 3:2, and so on (see Media file 2). The block is generally in the AV node but can occasionally occur in the His-Purkinje system and is termed infrahisian Wenckebach.

Mobitz II second-degree AV block is characterized by a constant PR interval followed by sudden failure of a P wave to be conducted to the ventricles, such that either an occasional dropped P wave or a regular conduction pattern of 2:1 (2 conducted and 1 blocked), 3:1 (3 conducted and 1 blocked), and so on is observed

High-grade AV block consists of multiple P waves in a row that should conduct, but do not. The conduction ratio can be 3:1 or more and the PR interval of conducted beats is constant. It is a distinct form of complete AV block in that the P waves that conduct to the QRS complexes occur at fixed intervals. For complete AV block, no relationship exists between the P waves and QRS complexes.
2:1 AV block could be Mobitz I or Mobitz II, but distinguishing one form from the other is nearly impossible.

Third-degree AV block is diagnosed when no supraventricular impulses are conducted to the ventricles. P waves on the rhythm strip reflect a sinus node rhythm independent from QRS electrocardiographic wave complexes. The QRS complexes represent an escape rhythm, either junctional or ventricular. The escape rhythm originating from the junctional or high septal region is characterized by narrow QRS complexes at a rate of 40-50 beats per minute, whereas escape rhythm from low ventricular sites is characterized by broad QRS complexes at a rate of 30-40 beats per minute. No relationship exists between the rhythm of P waves and the rhythm of QRS complexes. The frequency of P waves (atrial rate) is higher than the frequency of QRS complexes (ventricular rate)

AV dissociation is a rhythm identified by atrial and ventricular activation occurring from different pacemakers. AV dissociation does not indicate the presence of AV block and is distinctly different. Ventricular activation may be from either junctional pacemakers or infranodal. AV dissociation can occur in the presence of intact AV conduction, especially when rates of the pacemaker, either junctional or ventricular, exceed the atrial rate. Third-degree AV block can occur with AV dissociation. However, in AV dissociation without AV block, the ventricular rate can exceed the atrial rate and conduction can occasionally occur dependent on the timing between the P wave and the QRS complex.

AV block may also occur in patients with atrial fibrillation. Regular R-R intervals are possible in the presence of AV block (generally at slow regular rates).

Read more on atrial fibrillation at Medscape's Atrial Fibrillation Resource Center.


The atrioventricular node (AVN) is part of the conduction system of the heart that allows electrical impulses to be transmitted from the sinus node via atrial tissue (intra-atrial fascicles) to the ventricles. The AV node consists of 3 parts—atrionodal (transitional zone), nodal (compact portion), and nodal-His (penetrating His bundle). The nodal part causes the slowest conduction. The AV node is supplied by the right coronary artery (90%) or by the circumflex artery (10%) and is innervated by both sympathetic and parasympathetic fibers. The AVN receives impulses anteriorly via the intra-atrial fibers in the septum and posteriorly via the crista terminalis. Impulses arriving at the AVN are transmitted to the ventricle 1:1. As faster impulses arrive, the conduction to the ventricles slows; this is called decremental conduction.

The His-Purkinje system is composed of 2 bundles of Purkinje fibers (the left and right bundle) that conduct electrical impulses to allow rapid ventricular activation. The His-Purkinje system is yet another location where AV block may occur.

First-degree heart block and second-degree Mobitz I AV block are usually caused by a delay at the AV node level, whereas second-degree Mobitz II AV block is generally caused by blockage in the His bundle or lower in the conduction system. Third-degree AV block is caused by conduction disturbances in the AV node or the His-Purkinje system. In most cases of complete AV block, an escape rhythm originates from the ventricles, with wide QRS complexes at a low regular rate of 30-40 beats per minute. A higher anatomic location of the block results in a higher location of the escape rhythm pacemaker, a faster escape rhythm (40-60 beats per min in the region of His bundle), and a narrower QRS duration.
United States

First-degree AV block can be found in healthy adults, and its incidence increases with age. At 20 years of age, the PR interval may exceed 0.20 seconds in 0.5-2% of healthy people. At age 60 years, more than 5% of healthy individuals have PR intervals exceeding 0.20 seconds.

Type II second-degree AV block (Mobitz II) is rare in healthy individuals, whereas type I second-degree AV block (Wenckebach) is observed in 1-2% of healthy young people, especially during sleep.

Congenital third-degree AV block is rare—1 case per 20,000 births. This form of heart block, in the absence of major structural abnormalities, is associated with maternal antibodies to Ro (SS-A) and La (SS-B) and secondary to maternal lupus. It is most commonly diagnosed between 18 and 24 weeks' gestation, and may be first, second, or third degree (complete). Mortality approaches approximately 20%; most surviving children require pacemakers.

AV blocks occur more frequently in people older than 70 years, especially in those who have structural heart disease. Approximately 5% of patients with heart disease have first-degree AV block, and about 2% have second-degree AV block. The incidence of third-degree AV block peaks after age 70 years (approximately 5-10%).


The international incidence is the same as incidence in the United States.

Progressive degrees of AV block carry increasing morbidity and mortality.

AV blocks generally are not associated with major morbidity. However, the low heart rate observed in third-degree or Mobitz II AV block may lead to syncopal episodes with major injuries (eg, head trauma, hip fracture), exacerbation of congestive heart failure, or exacerbation of ischemic heart disease symptoms due to low cardiac output.

Cheng et al found that first-degree AV block (ie, PR interval >200 milliseconds) is associated with an increased risk of atrial fibrillation, pacemaker implantation, and all-cause mortality. In a prospective, community-based cohort of 7,575 individuals from the Framingham Heart Study (mean age, 47 y; 54% women) who underwent routine 12-lead electrocardiography in 1968-1974, 124 individuals had PR intervals >200 msec on the baseline examination. On follow-up of the cohort through 2007, individuals with first-degree AV block had a 2-fold adjusted risk of atrial fibrillation (hazard ratio [HR], 2.06; 95% CI, 1.36-3.12; P < .001), a 3-fold adjusted risk of pacemaker implantation (HR, 2.89; 95% CI, 1.83-4.57; P < .001), and a 1.4-fold adjusted risk of all-cause mortality (HR, 1.44; 95% CI, 1.09-1.91; P = .01). For all 3 outcomes, each 20-msec increment in PR was associated with an increase in risk.1

No racial proclivity exists in AV blocks.
A 60% female preponderance exists in congenital third-degree AV block.
For acquired third-degree AV block, a 60% male preponderance exists.

The incidence of AV block increases with age. The incidence of third-degree AV block is highest in people older than 70 years (approximately 5-10% of patients with heart disease).
First-degree AV block is generally not associated with any symptoms and is usually an incidental finding on ECG. People with newly diagnosed first-degree AV block may be healthy individuals with high vagal tone (eg, well-conditioned athletes), or they may have a history of myocardial infarction or myocarditis. First-degree AV block also may represent the first sign of a degenerative process of the AV conduction system.
Second-degree AV block usually is asymptomatic. However, in some patients, sensed irregularities of the heartbeat, presyncope, or syncope may occur. The latter usually is observed in more advanced conduction disturbances such as Mobitz II AV block. A history of medications that affect AV node function (eg, digitalis, beta-blockers, calcium channel blockers) may be contributory and should be obtained.
Third-degree AV block frequently is symptomatic with fatigue, dizziness, lightheadedness, presyncope, and syncope being reported most commonly. Syncopal episodes due to slow heart rates are called Morgagni-Adams-Stokes (MAS) episodes in recognition of the pioneer work on syncope by these researchers in the 19th century. Patients with third-degree AV block may have associated symptoms of acute myocardial infarction either causing the block or related to reduced cardiac output from bradycardia in the setting of advanced atherosclerotic coronary artery disease.
Routine physical examination does not lead to the diagnosis of first-degree AV block.
Second-degree AV block may manifest on physical examination as bradycardia (especially Mobitz type II) and/or irregularity of heart rate (especially type I, Wenckebach).
Third-degree AV block is associated with profound bradycardia unless the site of the block is located in the proximal portion of the AV node. Exacerbation of ischemic heart disease or congestive heart failure caused by AV block related bradycardia and reduced cardiac output may lead to specific clinically recognizable symptoms (eg, chest pain, dyspnea, confusion, pulmonary edema). Cannon a waves may be observed intermittently in the jugular venous pulsation when the right atrium contracts against a closed tricuspid valve due to atrioventricular dissociation.

Delay or lack of conduction through the AV node has multiple causes.

First-degree and second-degree Mobitz I (Wenckebach) AV blocks may occur in healthy, well-conditioned people as a physiologic manifestation of high vagal tone. Mobitz I (Wenckebach) block also may occur physiologically at high heart rates (especially with pacing) due to increased refractoriness of the AV node, which protects against conducting a fast rhythm to the ventricles.
AV block may be caused by acute myocardial ischemia or infarction. Inferior myocardial infarction may lead to third-degree block, usually at the AV node level, and by other mechanisms via the Bezold-Jarisch reflex. Anterior myocardial infarction usually is associated with third-degree block due to ischemia or infarction of bundle branches.
Degenerative changes in the AV node or bundle branches (eg, fibrosis, calcification, infiltration) are the most common cause of nonischemic AV block. Lenegre-Lev syndrome is an acquired complete heart block due to idiopathic fibrosis and calcification of the electrical conduction system of the heart. It is most commonly seen in the elderly and is often described as senile degeneration of the conduction system and may lead to third-degree AV block. In 1999, degenerative changes in the AV conduction system were linked to mutations of the SCN5A sodium channel gene (mutations of the same gene may lead to congenital long QT syndrome type 3 and to Brugada syndrome).2
Infiltrative myocardial diseases resulting in AV block include sarcoidosis, myxedema, hemochromatosis, and progressive calcification related to mitral or aortic valve annular calcification.
Endocarditis and other infections of the myocardium, such as Lyme disease with active infiltration of the AV conduction system, may lead to varying degrees of AV block.
Systemic diseases, such as ankylosing spondylitis and Reiter syndrome, may affect the AV nodal conducting tissue.
Surgical (eg, aortic valve replacement, congenital defect repair) or other therapeutic procedures (eg, AV ablation in patients with supraventricular arrhythmias, alcohol septal ablation in patients with obstructive hypertrophic cardiomyopathy) may cause AV block. Patients with corrected transposition of the great vessels have anterior displacement of the AV node and are prone to develop complete heart block during right heart catheterization or surgical manipulation.
A variety of drugs may affect AV conduction. The most common drugs include digitalis glycosides, beta-blockers, calcium channel blockers, and other antiarrhythmic agents.


Atrial Tachycardia


Atrial tachycardia is a rhythm disturbance that arises in the atria. Atrial tachycardia is defined as a supraventricular tachycardia (SVT) that does not require the atrioventricular (AV) junction, accessory pathways, or ventricular tissue for initiation and maintenance of the tachycardia. In common with most of the SVTs, the ECG typically shows a narrow QRS complex tachycardia (unless bundle branch block aberration occurs). Heart rates during atrial tachycardia are highly variable, with a range of 100-250 beats per minute (bpm). The atrial rhythm is usually regular. The conducted ventricular rhythm is also usually regular but may become irregular, often at higher atrial rates because of variable conduction through the AV node, thus producing conduction patterns such as 2:1, 4:1, a combination of those, or Wenckebach AV block.

The P wave morphology as observed on the ECG may give clues to the site of origin and mechanism of the atrial tachycardia. In the case of a focal tachycardia, the P wave morphology and axis depend on the location in the atrium from which the tachycardia originates. In the case of macroreentrant circuits, the P wave morphology and axis depend on activation patterns. (For more in-depth discussion please see diagnosis section.)

Classification of atrial tachycardia

A number of methods are used to classify atrial tachycardia, including origin as based on endocardial activation mapping data, pathophysiologic mechanisms, and anatomy.

Based on endocardial activation, atrial tachycardia may be divided into 2 groups. The first is focal atrial tachycardia, which arises from a localized area in the atria such as the crista terminalis, pulmonary veins, ostium of the coronary sinus, or intra-atrial septum. Focal atrial tachycardia that originates from the pulmonary veins may trigger atrial fibrillation, and often forms a continuum of arrhythmias. The second group is the reentrant atrial tachycardias. These reentrant (usually macro-reentrant) atrial tachycardias most commonly occur in persons with structural heart disease, complex heart disease, and particularly after surgery involving incisions or scarring in the atria. Electrophysiologically, these atrial tachycardias are similar to atrial flutters, typical or atypical. Often, the distinction is semantic, typically based on arbitrary cutoffs of atrial rate.

Sinoatrial reentrant tachycardia (or sinus node reentry) is a subset of focal atrial tachycardia due to reentry arising within the sinus node situated at the superior aspect of the crista terminalis. The P wave morphology and atrial activation sequence are identical or very similar to those of sinus tachycardia. Another tachycardia that mimics atrial tachycardia is inappropriate sinus tachycardia. Inappropriate sinus tachycardia and postural orthostatic tachycardia syndrome (POTS) strictly are not atrial tachycardias because their origin is not abnormal. They are due to sinus tachycardia related to enhanced sinus automaticity or due to abnormal autonomic function (dysautonomia).

Atrial tachycardia may be classified according to the following pathophysiologic mechanisms: enhanced automaticity, triggered activity, or reentry.

Anatomical classification of atrial tachycardia is based on the location of the arrhythmicogenic focus. Atrial tachycardia can have either a right or a left atrial origin. Some atrial tachycardias actually originate outside the usual anatomic boundaries of the atria, in areas such as the superior vena cava, pulmonary veins, and vein of Marshall, where fingers of atrial myocardium extend into these locations. Rare locations like noncoronary aortic cusp1 and hepatic veins have been described as well. These may be focal or reentrant.

Arrhythmogenic atrial structures

A number of aspects of the atrial anatomy can contribute to the substrate for arrhythmia. The orifices of the vena cava, pulmonary veins, coronary sinus, atrial septum, and mitral and tricuspid annuli are potential anatomic boundaries for reentrant circuits. Anisotropic conduction in the atria due to complex fiber orientation may create the zone of slow conduction. Certain atrial tissues, such as the crista terminalis and pulmonary veins, are common sites for automaticity or triggered activity. Additionally, disease processes or age-related degeneration of the atria may give rise to the arrhythmogenic substrate.

Pathophysiologic mechanisms

Several pathophysiologic mechanisms have been ascribed to atrial tachycardia. These mechanisms can be differentiated based on the pattern of onset and termination and response to drugs and atrial pacing.

Enhanced automaticity

Automatic atrial tachycardia is observed both in patients with normal heart structure and in those with organic heart disease. The tachycardia typically exhibits a warm-up phenomenon, during which the atrial rate gradually accelerates after its initiation and slows prior to its termination. It is rarely initiated or terminated by single atrial stimulation or rapid atrial pacing, but it may be transiently suppressed by overdrive pacing. Carotid sinus massage and adenosine do not terminate the tachycardia even if they produce a transient AV nodal block. Electrical cardioversion is ineffective (being equivalent to attempting electrical cardioversion in a sinus tachycardia).

Triggered activity

Triggered activity is due to delayed after-depolarizations, which are low-amplitude oscillations occurring at the end of the action potential. These oscillations are triggered by the preceding action potential and are the result of calcium ion influxes into the myocardium. If these oscillations are of sufficient amplitude to reach the threshold potential, depolarization occurs again and a spontaneous action potential is generated. If single, this is recognized as an atrial ectopic beat (an extra or premature beat). If it recurs and spontaneous depolarization continues, a sustained tachycardia may result. These tachycardias can be also induced with rapid atrial pacing.

Most commonly, atrial tachycardia due to triggered activity occurs in patients with digitalis intoxication2 or conditions associated with excess catecholamines. Characteristically, the arrhythmia can be initiated, accelerated, and terminated by rapid atrial pacing. It may be sensitive to physiologic and pharmacologic maneuvers such as adenosine, verapamil, and beta-blockers, which all can terminate the tachycardia. Occasionally, this atrial tachycardia may arise from multiple sites in the atria, producing a multifocal or multiform atrial tachycardia. This may be recognized by varying P wave morphology and irregularity in the atrial rhythm.

Pulmonary vein tachycardias originate from the os of the pulmonary vein or even deeper localized atrial fibers. These strands of atrial tissue are generally believed to gain electrical independence since are they are partially isolated from the atrial myocardium. These tachycardias are typically very rapid (with heart rate >200-220 bpm), and although they frequently trigger episodes of atrial fibrillation, the associated atrial tachycardias may also be the clinically dominant or exclusive manifestation. The latter typically involves only a single pulmonary vein as opposed to multiple pulmonary vein involvement seen in atrial fibrillation.

Reentrant tachycardia

Intra-atrial reentry tachycardias may have either a macroreentrant or a microreentrant circuit.

Macroreentry is the usual mechanism in atrial flutter and in scar- and incision-related (postsurgical) atrial tachycardia. The more common and recognized form of atrial tachycardia seen with the advent of pulmonary vein isolation and linear ablation procedures is left atrial tachycardia, using gaps in the ablation lines that allow for slow conduction, providing the requisite anatomic substrate for reentry. These tachycardia may be self limiting, but if they persist, mapping and a repeat ablative procedure can be considered.

Microreentry can arise in a small focal area such as in sinus node reentrant tachycardia. Typically, reentrant atrial tachycardia arises suddenly, terminates suddenly, and is paroxysmal. Carotid sinus massage and adenosine are ineffective in terminating the tachycardia even if they produce a transient AV nodal block. During electrophysiologic study, it can be induced and terminated by programmed extrastimulation. As is typical in other reentry tachycardias, electrical cardioversion terminates this type of atrial tachycardia.
United States

Atrial tachycardia is relatively rare, constituting 5-15% of all SVTs. Because there is an association with congenital heart disease, it is more common in the pediatric population. Atrial tachycardia can be observed in persons with normal hearts and in those with structurally abnormal hearts, including those with congenital heart disease and particularly after surgery for repair or correction of congenital or valvular heart disease.

No national differences in the incidence of atrial tachycardia have been reported.

In patients with structurally normal hearts, this arrhythmia is associated with a low mortality rate. However, tachycardia-induced cardiomyopathies have been associated with atrial tachycardia in patients in whom the rhythm is persistent or frequently incessant. Patients with underlying structural heart disease, congenital heart disease, or lung disease are less likely to be able to tolerate atrial tachycardia. Other morbidity is associated with lifestyle changes and associated symptoms.

Atrial tachycardia has no known racial or ethnic predilection.

The condition has no known predilection for either sex. There may be some association with pregnancy.

Atrial tachycardia may occur at any age, although it is more common in children and adults with congenital heart disease.

Patients with focal atrial tachycardia usually present with episodic or paroxysmal atrial tachycardia.
Typically, atrial tachycardia manifests as a sudden onset of palpitations.
If atrial tachycardia is due to enhanced automaticity, it may be nonsustained but repetitive or continuous or sustained, as in reentrant forms of atrial tachycardia.
Patients may present with a tachycardia that gradually speeds up soon after its onset (warm-up phenomenon). The patient may be unaware of this. This finding during ECG monitoring, as with a Holter, is suggestive that the supraventricular tachycardia is atrial tachycardia.
If accompanied by palpitations, patients also may report dyspnea, dizziness, lightheadedness, fatigue, or chest pressure. One should recognize the early manifestations of tachycardia-induced cardiomyopathy, ie, a decline in effort tolerance and symptoms of heart failure, in patients with frequent or incessant tachycardias.
Lightheadedness may result from relative hypotension, depending on the heart rate and other factors such as the state of hydration and particularly the presence of structural heart disease. The faster the heart rate, the more likely a patient is to feel lightheaded. If the patient has a rapid rate and severe hypotension, syncope may occur.

The primary abnormality noted upon physical examination is a rapid pulse rate. In most atrial tachycardias this is regular. However, in rapid atrial tachycardias with variable AV conduction and in multifocal atrial tachycardia (MAT), the pulse may be irregular.
Blood pressure may be low in patients presenting with fatigue, lightheadedness, or presyncope.
The cardiovascular examination should be aimed at excluding underlying structural heart diseases such as valvular abnormalities and evidence of heart failure.
Abnormal thyroid function should also be in the differential diagnosis.
Atrial tachycardia can occur in individuals with structurally normal hearts or in patients with organic heart disease.
When it arises in patients with congenital heart disease who have undergone corrective or palliative cardiac surgery, such as a Fontan procedure, the occurrence of an atrial tachycardia can have potentially life-threatening consequences.
The atrial tachycardia that manifests during exercise, acute illness with excessive catecholamine release, alcohol ingestion, altered fluid states, hypoxia, metabolic disturbance, or with drug use (eg, caffeine, albuterol, theophylline, cocaine) is associated with automaticity or triggered activity.
Digitalis intoxication is one of the important causes of atrial tachycardia, with triggered activity as the underlying mechanism.
Reentrant atrial tachycardia tends to occur in patients with structural heart disease, including ischemic, congenital, postoperative, and valvular heart diseases.
Multifocal atrial tachycardia is a unique type of atrial tachycardia in which atrial activation originates from multiple atrial foci. See eMedicine article Multifocal Atrial Tachycardia.
Multifocal atrial tachycardia often occurs in patients experiencing an exacerbation of chronic obstructive pulmonary disease (COPD)3 , a pulmonary thromboembolism, an exacerbation of congestive heart failure, or severe illness especially under critical care with inotropic infusion.
It is often associated with hypoxia and sympathetic stimulation.
Digitalis toxicity also may be present in persons with multifocal atrial tachycardia, with triggered activity as the mechanism.
Unusual forms of atrial tachycardias can be seen in patients with an infiltrative process involving the pericardium and, by extension, the atrial wall.


Atrial Flutter


Atrial flutter has many clinical aspects that are similar to atrial fibrillation (ie, underlying disease, predisposing factors, complications, medical management). However, the underlying mechanism of atrial flutter makes it amenable to cure this arrhythmia with percutaneous catheter-based techniques.

Some patients have both atrial flutter and atrial fibrillation. The elimination of atrial flutter has been noted to reduce or eliminate episodes of atrial fibrillation. Left untreated, persistent atrial flutter can degenerate into chronic atrial fibrillation. Uncommon forms of atrial flutter have been noted during long-term follow-up in as many as 26% of patients with surgical correction of congenital cardiac anomalies.


In most studies, approximately 30% of patients have no underlying cardiac disease, 30% have coronary artery heart disease, and 30% have hypertensive heart disease. Other conditions are also associated with atrial flutter, including cardiomyopathy, hypoxia, chronic obstructive pulmonary disease, thyrotoxicosis, pheochromocytoma, electrolyte imbalance, and alcohol consumption.

Animal models have been used to demonstrate that an anatomical block (surgically created) or a functional block of conduction between the superior vena cava and inferior vena cava, similar to the crista terminalis in the human right atrium, is key to initiating and maintaining the arrhythmia.

In humans, the most common form of atrial flutter (type I [classic]) involves a single reentrant circuit with circus activation in the right atrium around the tricuspid valve annulus (most often in a counterclockwise direction), with an area of slow conduction located between the tricuspid valve annulus and the coronary sinus ostium (subeustachian isthmus).

The crista terminalis acts as another anatomic conduction barrier, similar to the line of conduction block between the 2 venae cavae required in the animal model. The orifices of both venae cavae, the eustachian ridge, the coronary sinus orifice, and the tricuspid annulus complete the barrier for the reentry circuit. Atrial flutter is often referred to as isthmus-dependent flutter. Usually the rhythm is due to reentry, there is an excitable gap, and the rhythm can be entrained.

Classic counterclockwise atrial flutter has caudocranial activation (ie, counterclockwise around the tricuspid valve annulus when viewed in the left antero-oblique fluoroscopic view) of the atrial septum.

Classic atrial flutter can also have the opposite activation sequence (ie, clockwise activation around the tricuspid valve annulus). Clockwise atrial flutter is much less common. This arrhythmia is still considered type I, isthmus-dependent, clockwise flutter.

Type II (atypical) atrial flutters are less extensively studied and electroanatomically characterized. Atypical atrial flutters may originate from the right atrium (surgical scars [ie, incisional reentry]) or from the left atrium (pulmonary veins [ie, focal reentry] or mitral annulus).

Left atrial flutter is common after incomplete left atrial ablation procedures and may result in faster ventricular rates than seen during atrial fibrillation. Thus, tricuspid isthmus dependency is not a prerequisite for atrial flutter. Often, the atrial rate is faster (340-350 bpm) in atypical flutter and the arrhythmia can not be entrained.

United States

Atrial flutter is much less common than atrial fibrillation. From 1985-1990, of patients admitted to US hospitals with a diagnosis of supraventricular tachycardia, 77% had atrial fibrillation and 10% had atrial flutter. Based on a study of patients referred for tertiary care centers, the incidence of atrial flutter in the United States is estimated at 200,000 new cases per year.1


Prognosis depends on the patient's underlying medical condition. Any atrial arrhythmia can cause a tachycardia-induced cardiomyopathy. Intervening to control the ventricular response rate or to return the patient to sinus rhythm is important. Thrombus in the left atrium has been described in patients with atrial flutter (0-21%). Thromboembolic complications have also been described.

Due to conduction properties of the atrioventricular node, many people with atrial flutter will have a faster ventricular response (than those with atrial fibrillation). Heart rate is often more difficult to control with atrial flutter than with atrial fibrillation.


Atrial flutter is associated with a male predominance. In a study of 100 patients with atrial flutter, 75% were men. In another study performed at a tertiary care study, atrial flutter was 2.5 times more common in men.

Patients with atrial flutter, as with atrial fibrillation, tend to be older adults. In one study, the average age was 64 years (range 27-86 y).

The severity of symptoms and the patient's underlying cardiac condition dictate the initial management approach.

The most common symptom is palpitations. Other symptoms include fatigue, dyspnea, and chest pain.
Address symptoms of other noncardiac conditions (eg, hyperthyroidism, pulmonary disease) or cardiac conditions associated with atrial flutter that may be reversible.
The most common symptom is palpitations. Other symptoms include fatigue, dyspnea, and chest pain.
Assessing the onset of symptoms/palpitations is critical. Atrial flutter (of a duration >48 h) requires anticoagulation with warfarin or transesophageal echo to rule out thrombus in the left atrium prior to cardioversion to sinus rhythm. Thus, the duration of the episode and the onset of atrial fibrillation or flutter may affect the timing of cardioversion and the need to address anticoagulation.
Precipitating causes and modes of termination of the arrhythmia.
Previous response to pharmacologic therapy.
Often, atrial flutter is not as well tolerated as atrial fibrillation. This may be due to the rapid and difficult-to-control ventricular response, especially with minimal exertion.
Atrial flutter can cause hypotension, angina, congestive heart failure, and rarely syncope due to rapid ventricular response in the setting of compromised left ventricular function.
The general appearance and vital signs of the patient are important when determining the urgency with which to restore sinus rhythm. Thus, the initial cardiopulmonary evaluation and monitoring for signs of cardiac or pulmonary failure help guide initial management.
Evaluate the vitals with a close eye on heart rate, blood pressure, and oxygen saturation.
Palpate the neck/thyroid gland for goiter.
Evaluate the neck for jugular venous distention.
Auscultate the lungs for rales/crackles.
Auscultate/palpate the heart for extra heart sounds and murmurs, and palpate the point of maximum impulse.
Examine the extremities to access for lower extremity edema/perfusion.
Atrial flutter is most often associated with left ventricular dysfunction, rheumatic heart disease, congenital heart disease, and postcardiac surgery.
Thyroid disease, obesity, pericarditis, pulmonary disease, and pulmonary embolism have been associated with atrial fibrillation and atrial flutter. Rarely, mitral valve prolapse has been associated with atrial flutter.
Rarely, atrial flutter can be associated with an acute myocardial infarction.
Postcardiac surgery, atrial flutter may be reentrant as a result of natural barriers, atrial incisions, and scar.
Some patients develop atypical left atrial flutter after pulmonary vein isolation for atrial fibrillation.


Atrial Fibrillation


Atrial fibrillation (AF) is a supraventricular tachyarrhythmia characterized by disorganized atrial electrical activity and progressive deterioration of atrial electromechanical function. Electrocardiographic manifestations of atrial fibrillation include absence of P waves; rapid oscillations (or fibrillatory [f] waves) that vary in amplitude, frequency, and shape; and an irregular ventricular response.

Atrial fibrillation is the most common arrhythmia encountered in clinical practice (see Media file 1) and is a significant public health problem in the United States. Atrial fibrillation affects more than 2.2 million Americans and almost 5% of the population older than 69 years. The prevalence of atrial fibrillation increases dramatically with age. Atrial fibrillation is associated with known cardiovascular risk factors such as hypertension, coronary artery and valvular heart disease, heart failure (HF) and diabetes mellitus.1

Data from the Framingham heart study show that atrial fibrillation is associated with a 1.5- to 1.9-fold higher risk of death, which is in part due to the strong association between atrial fibrillation and thromboembolic events.2 While patients can be asymptomatic, many experience a wide variety of symptoms, including palpitations, dyspnea, fatigue, dizziness, angina, and decompensated heart failure. In addition, atrial fibrillation can be associated with hemodynamic dysfunction, tachycardia-induced cardiomyopathy, and systemic thromboembolism.

Overall, approximately 15-25% of all strokes in the United States (75,000/y) can be attributed to atrial fibrillation. Known risk factors for stroke in patients with atrial fibrillation include male sex, valvular heart disease (rheumatic valvular disease), heart failure, hypertension, and diabetes. Additional risk factors, such as advanced age and prior history of stroke, diabetes, and hypertension, place patients with preexisting atrial fibrillation at even higher risk for further comorbidities such as stroke(see Table 1)

Table 1. Risk Factors for Stroke in Patients with Nonvalvular Atrial Fibrillation
Risk Factors Relative Risk
Prior stroke or TIA 2.5
History of hypertension 1.6
Heart failure and/or reduced left ventricular function 1.4
Advanced age 1.4
Diabetes 1.7
Coronary artery disease 1.5

Patients with rheumatic heart disease and atrial fibrillation have an even higher risk for stroke (17-fold). At least 4 large clinical trials have clearly demonstrated that anticoagulation with warfarin decreases the risk of stroke by 50-80%.

Unlike most cardiovascular diseases, the prevalence of atrial fibrillation is increasing in the United States and worldwide. Atrial fibrillation is frequently encountered in both the inpatient and outpatient settings. Primary therapeutic goals include rate control, maintenance of sinus rhythm, and prevention of thromboembolism.


While the precise mechanisms that cause atrial fibrillation are incompletely understood, atrial fibrillation appears to require both an initiating event and a permissive atrial substrate. Significant discoveries in the last decade have highlighted the importance of focal pulmonary vein triggers, but alternative and nonmutually exclusive mechanisms have also been evaluated. These include multiple wavelets, mother waves, fixed or moving rotors, and macro-reentrant circuits. In a given patient, multiple mechanisms may be present at any given time. The automatic focus theory and the multiple wavelet hypothesis appear to have the best supportive data.

A focal origin of atrial fibrillation is supported by several experimental models showing that atrial fibrillation persists only in isolated regions of atrial myocardium. This theory has garnered considerable attention recently as studies have demonstrated that a focal source of atrial fibrillation can be identified in humans and that isolation of this source can eliminate atrial fibrillation.

The pulmonary veins appear to be the most frequent source of these automatic foci, but other foci have been demonstrated in several areas throughout the atria. Cardiac muscle in the pulmonary veins appears to have active electrical properties similar, but not identical, to those of atrial myocytes. Heterogeneity of electrical conduction around the pulmonary veins is theorized to promote reentry and sustained atrial fibrillation. Thus, pulmonary vein automatic triggers may provide the initiating event and heterogeneity of conduction may provide the sustaining event in many patients with atrial fibrillation.

The multiple wavelet hypothesis proposes that fractionation of wavefronts propagating through the atria results in self-perpetuating “daughter wavelets.” In this model, the number of wavelets is determined by the refractory period, conduction velocity, and mass of atrial tissue. In this model, increased atrial mass, shortened atrial refractory period, and delayed intra-atrial conduction increase the number of wavelets and promote sustained atrial fibrillation. This model is supported by data from patients with paroxysmal atrial fibrillation demonstrating that widespread distribution of abnormal atrial electrograms predicts progression to persistent atrial fibrillation.4 Intra-atrial conduction prolongation has also been shown to predict recurrence of atrial fibrillation.5 Together, these data highlight the importance of atrial structural and electrical remodeling in the maintenance of atrial fibrillation.

Atrial fibrillation shares strong epidemiologic associations with other cardiovascular diseases such as heart failure, coronary artery disease, valvular heart disease, diabetes mellitus and hypertension.1 These factors have been termed upstream risk factors, but the relationship between comorbid cardiovascular disease and atrial fibrillation is incompletely understood and more complex than this terminology implies. The exact mechanisms via which cardiovascular risk factors predispose to atrial fibrillation are not fully understood but are under intense investigation. Catecholamine excess, hemodynamic stress, atrial ischemia, atrial inflammation, metabolic stress, and neurohumoral cascade activation are all purported to promote atrial fibrillation.

United States

Atrial fibrillation affects more than 2.2 million Americans. One in 4 individuals 40 years of age and older will develop atrial fibrillation during their lifetime.6 Atrial fibrillation can occur in the absence of comorbidities, as it does in 10-15% of cases of atrial fibrillation (lone atrial fibrillation). However, atrial fibrillation is often associated with other cardiovascular diseases, including hypertension; heart failure; diabetes; ischemic heart disease; and valvular, dilated, hypertrophic, restrictive, and congenital cardiomyopathies.6

Atrial fibrillation can be triggered after cardiac surgery and is associated with pulmonary disease, thyrotoxicosis, acute ethanol intoxication, and electrolyte imbalance. Given the almost epidemic proportions of patients with atrial fibrillation, clinicians should be aware of the multiple mechanisms and triggers for atrial fibrillation. Correcting the underlying disorder is often necessary to successfully treat atrial fibrillation.


Atrial fibrillation is associated with increased morbidity and mortality, in part due to the risk of thromboembolic disease in atrial fibrillation and in part due to its associated risk factors. Disruption of normal atrial electromechanical function in atrial fibrillation leads to blood stasis. This, in turn, can lead to development of thrombus, most commonly in the left atrial appendage. Dislodgement of a clot can lead to embolic phenomena, including stroke.

One of the major management decisions in atrial fibrillation (and atrial flutter) is determining the risk of stroke and appropriate anticoagulation regimen for low-, intermediate-, and high-risk patients. For each anticoagulant, the benefit in terms of stroke reduction must be weighed against the risk of serious bleeding.

Most clinicians agree that the risk-benefit ratio of warfarin therapy in low-risk patients with atrial fibrillation is not advantageous. Warfarin therapy has, however, been shown to be beneficial in higher-risk patients with atrial fibrillation. A target international normalized ratio (INR) of 2-3 is traditionally used in this cohort as this limits the risk of hemorrhage while providing protection against thrombus formation.

The appropriate treatment regimen for patients with atrial fibrillation at intermediate risk is controversial. In this population, the clinician should assess risk factors for thromboembolic disease, patient preference, risk of bleeding, risk of falls or trauma, and likelihood of medication adherence. Warfarin is also superior to clopidogrel or a combination of clopidogrel and aspirin in the prevention of embolic events in higher-risk patients. A new class of oral direct thrombin inhibitors are in the late stages of clinical trial or pending approval and may be as effective and as safe as warfarin in higher-risk nonvalvular atrial fibrillation.

Several risk factor assessment algorithms have been developed to aid the clinician in decision-making regarding anticoagulation in atrial fibrillation. The CHADS2 index7 (Cardiac failure, Diabetes, Stroke [or S2 = TIA]) is the most widely used of these algorithms. The CHADS2 index uses a point system to determine yearly thromboembolic risk. Two points are assigned for a history of stroke or TIA, and one point is given for age over 75 or a history of hypertension, diabetes, or heart failure. The predictive value of this scoring system was evaluated in 1733 elderly patients with nonvalvular atrial fibrillation aged 65-95 who were not given warfarin at hospital discharge. Although high scores were associated with an increased rate of stroke, few patients had a score greater than 5 or a score of 0 (see Table 2).

Table 2. Adjusted Stroke Rate in Patients with Nonvalvular Atrial Fibrillation not Treated with Anticoagulation

Open table in new windowCHADS2 Score Adjusted Stroke Rate (%/y)
0 1.9
1 2.8
2 4.0
3 5.9
4 8.5
5 12.5
6 18.2

Recommendations for anticoagulation for patients with nonvalvular atrial fibrillation are based on 2006 ACC/AHA/ESC task force guidelines on the management of patients with atrial fibrillation8 (see Table 3).

Table 3. Recommendations for Antithrombotic Therapy in Patients with Nonvalvular Atrial Fibrillation

Open table in new windowRisk Category Recommended Therapy
No risk factors Aspirin 81-325 mg daily
One moderate-risk factor Aspirin 81-325 mg daily or warfarin (INR 2-3)
Any high-risk factor or more than 1 moderate-risk factor Warfarin (INR 2-3)

High-risk factors include prior stroke, TIA, and systemic thromboembolism.

Moderate-risk factors include age older than 75 years, hypertension, heart failure, left ventricular function <35%, and diabetes mellitus.

Risk factors of unknown significance include female gender, age 65-74 years, coronary artery disease, and thyrotoxicosis.

Atrial fibrillation is strongly age-dependent, affecting 4% of individuals older than 60 years and 8% of persons older than 80 years. The rate of ischemic stroke among elderly patients not treated with warfarin averages approximately 5% per year.


Initial evaluation of the patient with new-onset atrial fibrillation should focus on the patient's hemodynamic stability. An effort should also be made to evaluate for potential comorbid diseases that contribute to initiation or maintenance of atrial fibrillation. Immediate electrical cardioversion should be considered for patients with hemodynamic collapse or evidence of cardiac ischemia.

Initial history
Clinical type of atrial fibrillation should be documented (paroxysmal, persistent, or permanent)
Type, duration, and frequency of symptoms should be assessed
Precipitating factors should be assessed (ie, exertion, sleep, caffeine, alcohol use)
Modes of termination should be assessed (ie, vagal maneuvers)
Prior antiarrhythmics and rate-controlling agents used should be documented
Presence of underlying heart disease should be assessed
Any previous surgical or percutaneous atrial fibrillation ablation procedures should be documented


The physical examination is helpful in determining underlying causes and sequelae of atrial fibrillation. An initial examination of the patient with new-onset atrial fibrillation should attend particularly to their hemodynamic stability.

Vital signs: Heart rate, blood pressure, respiratory rate, and oxygen saturation are particularly important in evaluating hemodynamic stability and adequacy of rate control in atrial fibrillation.
Head and neck: May reveal exophthalmos, thyromegaly, elevated jugular venous pressures, or cyanosis. Carotid artery bruits suggest peripheral arterial disease and increase the likelihood of comorbid CAD.
Pulmonary: May reveal evidence of heart failure (ie, rales or pleural effusion). Wheezes or diminished breath sounds are suggestive of underlying pulmonary disease (ie, chronic obstructive pulmonary disease or asthma).
Cardiac: The cardiac examination is central to the physical examination of the patient with atrial fibrillation. A displaced point of maximal impulse or S3 suggest ventricular enlargement and elevated left ventricular pressure. A prominent P2 points to the presence of pulmonary hypertension. Thorough palpation and auscultation are necessary to evaluate for valvular heart disease or cardiomyopathy.
Abdomen: Ascites, hepatomegaly or hepatic capsular tenderness suggest right ventricular failure or intrinsic liver disease.
Lower extremities: Examination of the lower extremities may reveal cyanosis, clubbing or edema. Assessment of peripheral pulses may lead to the diagnosis of peripheral arterial disease or diminished cardiac output.
Neurologic: Evidence of prior stroke and increased reflexes is suggestive of hyperthyroidism.

Atrial fibrillation is strongly associated with established cardiovascular risk factors and advancing age. Hypertension, diabetes, and coronary artery disease promote atrial fibrillation. Structural heart disease, including valvular and congenital heart disease, is also associated with atrial fibrillation. Acute pulmonary processes, acute or chronic alcohol use (ie, holiday or Saturday night heart, also known as alcohol-related cardiomyopathy), illicit drug use (ie, stimulants, methamphetamines, cocaine) and hyperthyroidism also increase the risk of atrial fibrillation. Patients undergoing cardiothoracic or esophageal surgery are another population at risk for atrial fibrillation. In all, 20-40% of these patients experience postoperative atrial fibrillation. Certain poorly defined genetic factors may also contribute to an individual's propensity to develop atrial fibrillation.

Hemodynamic stress: Increased intra-atrial pressure results in atrial electrical and structural remodeling and predisposes to atrial fibrillation. Mitral or tricuspid valve disease and left ventricular dysfunction are the most common causes of increased atrial pressure. Systemic or pulmonary hypertension also commonly predispose to atrial pressure overload. Intracardiac tumors or thrombi are rare causes of increased atrial pressure.
Atrial ischemia: Coronary artery disease can infrequently lead directly to atrial ischemia and atrial fibrillation. More commonly, severe ventricular ischemia leads to increased intra-atrial pressure and atrial fibrillation.
Inflammation: Myocarditis and pericarditis may be idiopathic or may occur in association with the following:
Collagen vascular diseases
Viral or bacterial infections
Cardiac, esophageal, or thoracic surgery
Drug use: Stimulants, alcohol, and cocaine can trigger atrial fibrillation.
Endocrine disorders: Hyperthyroidism and pheochromocytoma have been associated with atrial fibrillation.
Neurologic: Intracranial processes such as subarachnoid hemorrhage or stroke can also precipitate atrial fibrillation.
Familial atrial fibrillation: History of parental atrial fibrillation appears to confer increased likelihood of atrial fibrillation (and occasional family pedigrees of atrial fibrillation are associated with defined ion channel abnormalities, especially sodium channels).9


Jual Rumah Kontrakan 2 Pintu

Jual Rumah Kontrakan 2 Pintu
Jl. Gang Biyuk, Bambu Kuning Raya. Akses Strategis = Jalan Raya Pramuka Narogong, Rawalumbu Bekasi, Bebas Banjir, Tanpa Perantara = Ibu Anni 021-95-08-20-42 *.(Klik Gambar untuk Keterangan Lanjut)




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