Bundle Branches Block

What are the bundle branches?

Normally, your heart beats in a nice, regular fashion. The heartbeat starts in the upper chambers of the heart in an area called the SA node. The impulse then moves to the AV node. The AV node is an area of tissue that carries the impulse through the Bundle of His and then splits into two wire-like branches (the bundle branches). The branches carry the impulse to the Purkinje fibers, which are located in the muscular walls of the ventricles, and cause them to contract.

What is a bundle branch block?

A bundle branch block means the electrical impulses that control the heartbeat cannot move properly throughout the heart. A block in the branches causes the impulses to travel slower than normal.

Diagnosis of bundle branch block

A bundle branch block can be seen on an electrocardiogram (EKG).

How LBBB can affect other cardiovascular tests and conditions

Stress testing and heart attack

Left bundle branch block can make it more difficult to diagnose left ventricular hypertrophy (LVH) and ischemia (decreased blood supply to the heart) during exercise stress testing and during a heart attack.

If you have LBBB, make sure your doctor knows about the condition before you have a stress test. You may need additional testing or a different kind of stress test (done with medicine, not exercise).

You should also carry a copy of your EKG with you.

If you think you are having a heart attack, be sure to tell your doctor or nurse that you have LBBB and give them the copy of the EKG. This will help them see changes in your heart.

If you have signs of LVH, your doctor will use an echocardiogram to diagnose the condition.

Symptoms

In most people, bundle branch block doesn't cause any symptoms. Sometimes, people with the condition don't even know they have a bundle branch block.

For those people who do have signs and symptoms, they may include:

• Fainting (syncope)
• Feeling as if you're going to faint (presyncope)

Causes

Normally, electrical impulses within your heart's muscle signal it to beat (contract). These impulses travel along a pathway, including the right and the left bundles. If one or both of these branch bundles become damaged — due to a heart attack, for example — this change can block the electrical impulses and cause your heart to beat abnormally.

The underlying cause for bundle branch blocks may differ depending on whether the left or right bundle branch is affected. It's also possible that this condition can occur without any known underlying cause. Specific causes may include:

Left bundle branch block

• Heart disease
• Thickened, stiffened or weakened heart muscle (cardiomyopathy)
• A viral or bacterial infection of the heart muscle (myocarditis)
• High blood pressure (hypertension)

Right bundle branch block

• A heart abnormality that's present at birth (congenital) — such as atrial septal defect, a hole in the wall separating the upper chambers of the heart
• A heart attack (myocardial infarction)
• A viral or bacterial infection of the heart muscle (myocarditis)
• High blood pressure (hypertension)
• A blood clot in the lungs (pulmonary embolism)

Risk factors

Risk factors for bundle branch block include:

• Increasing age. Bundle branch block is more common in older adults than in people who are middle-aged.
• Underlying health problems. People who have high blood pressure or heart disease are more likely to have bundle branch block than people without those conditions.

Complications

The main complication of bundle branch block is a slow heart rate, which can sometimes cause fainting.
People who have a heart attack and develop a bundle branch block have a higher chance of complications, including sudden cardiac death, than do people who have heart attacks and don't develop a bundle branch block.
Because bundle branch block affects the electrical activity of your heart, it can sometimes complicate the accurate diagnosis of other heart conditions, especially heart attacks, and lead to delays in proper management of those problems

Diagnosis

Tests that may be used to diagnose a bundle branch block or the underlying problem causing it include:

• Electrocardiogram. An electrocardiogram records the electrical impulses in your heart through wires attached to the skin on your chest and other locations on your body. Abnormalities may indicate the presence of bundle branch block, as well as which side is being affected.
• Echocardiogram. An echocardiogram can be used to pinpoint an underlying condition that caused the bundle branch block. This test uses sound waves to produce images of the heart, allowing your doctor to see your heart in motion.
  
  An echocardiogram provides detailed images of the heart's structure and shows the thickness of your heart muscle and whether your heart valves are moving normally

Right bundle branch block (RBBB)

Right bundle branch block (RBBB) is very common, and the risk of developing the condition increases with age. Once your doctor sees RBBB on an EKG, the next step is to see if you have underlying heart disease.
If you do not have other heart disease, symptoms of heart disease, or other blocks in your electrical conduction system, no treatment is necessary.
If you have RBBB and another heart condition, such as heart attack or heart failure; dizziness or fainting; or other blocks in your electrical system, you will be treated for the heart disease. You may need a pacemaker if you have symptoms or another heart block.

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     In right bundle branch block, the right ventricle is activated via cell-to-cell transmission of the action potential.  This is illustrated in the following animation:

Notice the delay in the time of right ventricular depolarization.  This means that the right ventricle is activated after the left ventricle (which is depolarizing normally) and therefore contracts a "split second" after the left ventricle. Mechanically, this difference doesn't greatly influence the performance of the heart.  However, it does produce some characteristic changes in the ECG. 

Electrocardiographic changes in RBBB. As you might be able to guess from the animation, because the depolarization of the ventricle has been altered, the changes show up in the QRS complex and the T wave.  The following pictures illustrate right bundle branch block in different leads. 

Appearance of three different leads in RBBB:  From top to bottom:  Lead I, Lead V1 and Lead V6.  Due to the RBBB, the right ventricle is depolarizing after the left ventricle.  In all three leads, there is a prolongation of the QRS complex due to the blockade.  In leads I and V6 (which "see" the left ventricle best), the delayed depolarization of the right ventricle produces a late, negative going wave (S wave) that is very broad (there is no point to the wave) and prolonged.  In lead V1 (which has a good view of the right ventricle, the delay in depolarizing the right ventricle leads to the aptly-named "bunny ears"- the QRS complex is composed of an initial positive wave (the R wave), followed by a negative deflection (the S wave) produced when the left ventricle depolarizes, and then a second positive wave (called R' (spoken "R prime")) as the right ventricle finally depolarizes.  Because the normal conduction pathway was not followed for depolarization, the process of repolarization does not occur in the normal sequence leading to abnormalities in the T wave (seen best in V1).

Summary of electrocardiographic changes in RBBB:

• P wave of normal morphology (shape).
• rate and rhythm normal.
• QRS complex is prolonged (> 0.12 seconds).
• QRS complex is bizarrely shaped in leads with "good" views of the right ventricle, such as V1 and V2. 
  • The appearance of "bunny ears" is a hallmark of a bundle branch.
• The amplitude of the individual waves in the QRS complex is usually increased because the depolarization in the left and the right ventricles are no longer simultaneous (when they are simultaneous, they cancel each other out to some extent). 
• The T wave is abnormal in appearance because of alterations in the repolarization of the heart. 

Left bundle branch block (LBBB)

Left bundle branch block (LBBB) is less common than RBBB. As with RBBB, the risk of developing the condition increases with age. Once your doctor sees LBBB on an EKG, the next step is to see if you have underlying heart disease.

If you do not have other heart disease, symptoms of heart disease, or other blocks in your electrical conduction system, no treatment is necessary.

If you have another heart condition, such as hypertension, coronary artery disease or heart attack, myocarditis or heart failure; dizziness, fainting or chest pain; or another block in your electrical system, you will be treated for the heart disease. You may need a pacemaker if you have another type of heart block or have symptoms of heart block.

Left Bundle branch block (LBBB) is very similar to right bundle branch block, as the following animation illustrates. 

As with the RBBB, the major change is that the left ventricle is now depolarized due to the spread of the action potential via cell-to-cell conduction.  This results in the left ventricle depolarizes (and therefore contracting) a "split-second" after the right ventricle does.  As with RBBB, the mechanical effects of this on the heart are minimal. 

Electrocardiographic changes in LBBB: 

The following pictures illustrate left bundle branch block as seen in three different leads: 

The appearance of LBBB in three different leads:  As with right bundle branch block, the major change is in the shape and duration of the QRS complex (since it is ventricular depolarization that has been altered).  All of the leads show a prolonged QRS complex due to the time it takes the left ventricle to depolarize.  Leads I and V6 record long R waves (lead I shows a small initial R wave (you might be mistaking it for a P wave) and a larger R' leading to a somewhat odd pair of "bunny ears") because the depolarization is heading "at" the lead for a prolonged period of time as the ventricle depolarizes.   Lead V1 (on the right side of the sternum sees an initial very small positive wave as the faster right ventricle depolarizes, followed by a prolonged S wave produced by the left ventricular depolarization (note that the S wave also has two peaks - an inverted pair of "bunny ears").

Summary of electrocardiographic changes in LBBB:

• P wave of normal morphology (Note:  like a lot of things in this world, the ECG tracing shown above for LBBB has more than one thing wrong with it - no P waves are visible because this person is in atrial fibrillation).
• Normal rate and rhythm. 
• Normal PR interval
• QRS complex is prolonged and bizarrely shaped.
  • Bunny ears
  • other leads may show QRS complexes that aren't "pointy", instead they are rounded at the top/bottom.
• The amplitude of the QRS complex peaks are often increased, due to the failure of the left and right ventricle to depolarize simultaneously. 
• The T wave is abnormal in morphology because repolarization cannot occur normally if depolarization did not. 

Treatment

Most people with bundle branch block are symptom-free and don't need treatment.

However, if you have an underlying heart condition causing bundle branch block, treatment of the underlying condition is recommended. Treatment of underlying conditions may involve using medications to reduce high blood pressure or lessen the effects of heart failure, or the use of a coronary angioplasty to open up the artery leading to your heart.

Additionally, depending on your symptoms and whether you have other heart problems, your doctor might also recommend:

• A pacemaker. For some people with bundle branch block and a history of fainting, doctors may recommend implanting a pacemaker. A pacemaker is a compact device implanted under the skin of your upper chest (internal pacemaker) with two wires that connect to the right side of your heart. The pacemaker provides electrical impulses when needed to keep your heart beating regularly.
• Cardiac resynchronization. Also known as biventricular pacing, this procedure is similar to having a pacemaker implanted. However, in cardiac resynchronization, there's a third wire that's connected to the left side of the heart so the device can keep both sides in proper rhythm.

Ventricular Tachycardia Overview

Ventricular tachycardia heartbeat

• In ventricular tachycardia, an abnormal electrical impulse originating in the lower chambers of the heart (ventricles) causes the heart to beat faster. The problem may involve either a small cluster of cells or a large area of scar tissue.

Ventricular tachycardia is a heart rhythm disorder (arrhythmia) caused by abnormal electrical signals in the lower chambers of the heart (ventricles).

Your heart rate is regulated by electrical signals sent across heart tissues. A healthy heart normally beats about 60 to 100 times a minute when at rest and is defined by signals that originate in the upper chambers of the heart (atria).

In ventricular tachycardia (V-tach or VT), abnormal electrical signals in the ventricles cause the heart to beat faster than normal, usually 100 or more beats a minute, out of sync with the upper chambers.

When that happens, your heart may not be able to pump enough blood to your body and lungs because the chambers are beating so fast or out of sync with each other that they don't have time to fill properly.

Ventricular tachycardia may be brief, lasting for only a few seconds, and perhaps not cause any symptoms. Or it can last for much longer and cause symptoms such as dizziness, lightheadedness, palpitations or even loss of consciousness.

In some cases, ventricular tachycardia can cause your heart to stop (sudden cardiac arrest), which is a life-threatening medical emergency. This condition usually occurs in people with other heart conditions, such as those who have had a previous heart attack or other structural heart disease (cardiomyopathy).

Ventricular fibrillation

A dangerous condition related to ventricular tachycardia is ventricular fibrillation (V-fib). In V-fib, your lower heart chambers contract in a very rapid and uncoordinated manner.

Sometimes this rhythm may occur as a result of ventricular tachycardia degenerating into ventricular fibrillation, or it may originate from single ventricular beats. This abnormal rhythm happens most often in people with established heart disease or a prior heart attack. It may also occur due to electrolyte abnormalities (such as high or low potassium levels) or, rarely, in otherwise normal hearts.

Ventricular fibrillation may also cause sudden cardiac arrest and lead to death if not treated immediately.

Symptoms

Brief episodes of ventricular tachycardia may not cause any symptoms in some people. Others may experience:

• Dizziness
• Shortness of breath
• Lightheadedness
• Feeling as if your heart is racing (palpitations)
• Chest pain (angina)
• Seizures

Sustained or more serious episodes of ventricular tachycardia may cause:

• Loss of consciousness or fainting
• Cardiac arrest (sudden death)

When to see a doctor

A number of conditions can cause ventricular tachycardia. It's important to get a prompt, accurate diagnosis and appropriate care. See your doctor if you or your child experiences any V-tach symptoms.

If you faint, have difficulty breathing or have chest pain lasting more than a few minutes, get emergency care, or call 911 or your local emergency number. Seek emergency care for anyone experiencing these symptoms.

Causes

V-tach is caused by a disruption in the normal electrical impulses that control the rate of your ventricles' pumping action.
Many things can cause or contribute to problems with the heart's electrical system. These include:

• Lack of oxygen to the heart due to tissue damage from heart disease
• Abnormal electrical pathways in the heart present at birth (congenital heart conditions, including long QT syndrome)
• Structural heart disease (cardiomyopathy)
• Medication side effects
• An inflammatory disease affecting skin or other tissues (sarcoidosis)
• Abuse of recreational drugs, such as cocaine
• Imbalance of electrolytes, mineral-related substances necessary for conducting electrical impulses

In some cases, the exact cause of ventricular tachycardia can't be determined (idiopathic ventricular tachycardia).

The heart's electrical system

• Normal heartbeat

  In a normal heart rhythm, a cluster of cells at the sinus node sends out an electrical signal. The signal then travels through the atria to the atrioventricular (AV) node and then passes into the ventricles, causing them to contract and pump out blood.

To understand the causes of heart rate or rhythm problems such as ventricular tachycardia, it helps to understand how the heart's internal electrical system works.
Your heart is made up of four chambers — two upper chambers (atria) and two lower chambers (ventricles). The rhythm of your heart is normally controlled by a natural pacemaker called the sinus node, which is located in the right atrium. The sinus node produces electrical impulses that normally start each heartbeat.
From the sinus node, electrical impulses travel across the atria, causing the atria muscles to contract and pump blood into the ventricles.
The electrical impulses then arrive at a cluster of cells called the atrioventricular (AV) node — usually the only pathway for signals to travel from the atria to the ventricles.
The AV node slows down the electrical signal before sending it to the ventricles. This slight delay allows the ventricles to fill with blood. When electrical impulses reach the muscles of the ventricles, they contract, causing them to pump blood either to the lungs or to the rest of the body.
When anything disrupts this complex system, it can cause the heart to beat too fast (tachycardia), too slow (bradycardia) or with an irregular rhythm.

Risk factors

Any condition that puts a strain on the heart or damages heart tissue can increase your risk of ventricular tachycardia. Lifestyle changes or medical treatment may decrease the risk associated with the following factors:

• Heart disease (for example, prior heart attack, hypertrophic cardiomyopathy, inflammatory diseases of the heart or genetic conditions)
• Use of recreational drugs
• Severe electrolyte abnormalities
• Medication side effects

Other risk factors

If you have a family history of ventricular tachycardia or other heart rhythm disorders, you may have an increased risk of ventricular tachycardia.

Complications

Complications of ventricular tachycardia vary in severity depending on such factors as the rate, and duration of a rapid heart rate, the frequency with which it happens, and the existence of other heart conditions. Possible complications include:

• Inability of the heart to pump enough blood (heart failure)
• Frequent fainting spells or unconsciousness
• Sudden death caused by cardiac arrest

Prevention

The most effective way to prevent ventricular tachycardia is to reduce your risk of developing heart disease. If you already have heart disease, monitor it and follow your treatment plan to lower your ventricular tachycardia risk.
In some cases, ventricular tachycardia may occur in the absence of heart disease (idiopathic ventricular tachycardia).

Prevent heart disease

Treat or eliminate risk factors that may lead to heart disease. Take the following steps:

• Exercise and eat a healthy diet. Live a heart-healthy lifestyle by exercising regularly and eating a healthy, low-fat diet that's rich in fruits, vegetables and whole grains.
• Maintain a healthy weight. Being overweight increases your risk of developing heart disease.
• Keep blood pressure and cholesterol levels under control. Make lifestyle changes and take medications as prescribed to correct high blood pressure (hypertension) or high cholesterol.
• Stop smoking. If you smoke and can't quit on your own, talk to your doctor about strategies or programs to help you break a smoking habit.
• Drink in moderation. If you choose to drink alcohol, do so in moderation. For healthy adults, that means up to one drink a day for women of all ages and men older than age 65, and up to two drinks a day for men age 65 and younger. For some conditions it's recommended that you completely avoid alcohol.
  Ask your doctor for advice specific to your condition. If you can't control your alcohol consumption, talk to your doctor about a program to quit drinking and manage other behaviors related to alcohol abuse.
• Don't use recreational drugs. Don't use stimulants, such as cocaine. Talk to your doctor about an appropriate program for you if you need help ending recreational drug use.
• Use over-the-counter medications with caution. Some cold and cough medications contain stimulants that may trigger a rapid heartbeat. Ask your doctor which medications you need to avoid.
• Limit caffeine. If you drink caffeinated beverages, do so in moderation (no more than one to two beverages daily).
• Control stress. Avoid unnecessary stress and learn coping techniques to handle normal stress in a healthy way.
• Go to scheduled checkups. Have regular physical exams and report any signs or symptoms to your doctor.

Monitor and treat existing heart disease

If you already have heart disease, you can take steps to lower your risk of developing ventricular tachycardia or another arrhythmia:

• Follow the plan. Be sure you understand your treatment plan, and take all medications as prescribed.
• Report changes immediately. If your symptoms change or get worse or you develop new symptoms, tell your doctor immediately.

Atrial tachycardia

Atrial Tachycardia

Atrial tachycardia is the least common type of supraventricular tachycardia. It's generally seen in children with underlying heart disorders such as congenital heart disease, particularly those who've had heart surgery.

Atrial tachycardia may also be triggered by factors such as an infection or drug or alcohol use. For some people, atrial tachycardia increases during pregnancy or exercise.

Atrial tachycardia episodes typically begin slowly, gradually increasing to more than 100 beats per minute before returning to a normal heart rate of around 60 to 80 beats per minute. In some cases, these episodes occur more abruptly or occur continuously.

Atrial tachycardia is a form of supraventricular tachycardia that occurs when one focus in the atria begins to fire rapidly, overwhelming the sinoatrial node. This results in rapid conduction of action potentials through the atrioventricular node, causing elevated ventricular rates. The atrial rate during atrial tachycardia is usually between 100 and 200 beats per minute. A narrow complex tachycardia results with P wave morphologies that are different than normal sinus P waves. The QRS complex can be wide if aberrancy is present (ie, right or left bundle branch blocks).

Causes of atrial tachycardia include chronic hypertension, congestive heart failure, valvular heart disease and, simply, aging of the heart. Brief atrial tachycardia is seen very commonly on ambulatory ECG monitoring in the elderly and is frequently asymptomatic.
Symptoms of atrial tachycardia depend on the ventricular rate and the duration of the tachycardia. The symptoms include palpitations from the rapid heart rate. If hypotension ensues, dizziness and weakness can occur. The shortened diastolic filling time during tachycardic states can lead to decreased cardiac output and symptoms of congestive heart failure.
Atrial tachycardia is best treated with AV blocking medications, such as beta-blockers or non-dihydropyridine calcium channel blockers. Adenosine can, at times, terminate the rhythm, but not always. Ablation of atrial tachycardia is also an option, especially when medical therapy fails.
Special Situations:
Atrial tachycardia with 2:1 block; when atrial tachycardia occurs with a 2:1 conduction block, digoxin toxicity should be considered.

Atrial Tachycardia with 2:1 conduction

Pathophysiology

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

Enhanced automaticity

Automatic atrial tachycardia arises due to enhanced tissue automaticity and is observed in patients with structurally normal hearts 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.

Automatic atrial tachycardia is rarely initiated or terminated by a single atrial stimulation or rapid atrial pacing, but it may be transiently suppressed by overdrive pacing. It almost always requires isoproterenol infusion to facilitate induction and is predictably terminated by propranolol. ^[10] 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.

Most commonly, atrial tachycardia due to triggered activity occurs in patients with digitalis intoxication         ^. 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 maneuvers and drugs such as adenosine, verapamil, and beta-blockers, all of which 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

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 they are partially isolated from the atrial myocardium. These tachycardias are typically very rapid (heart rate of 200-220 bpm or more)

Although pulmonary vein tachycardias frequently trigger episodes of atrial fibrillation, the associated atrial tachycardias may be the clinically dominant or exclusive manifestation. The latter typically involves only a single pulmonary vein as opposed to the 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 as a result of the advent of pulmonary vein isolation and linear ablation procedures, is left atrial tachycardia. In this situation, gaps in the ablation lines allow for slow conduction, providing the requisite anatomic substrate for reentry. These tachycardias may be self-limiting but if they persist, mapping and a repeat ablative procedure should be considered.

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

Classification of atrial tachycardia

Based on endocardial activation, atrial tachycardia may be divided into 2 groups: focal and reentrant. Focal atrial tachycardia arises from a localized area in the atria such as the crista terminalis, pulmonary veins, ostium of the coronary sinus, or intra-atrial septum. If it originates from the pulmonary veins, it may trigger atrial fibrillation and often forms a continuum of arrhythmias.

Reentrant (usually macroreentrant) atrial tachycardias most commonly occur in persons with structural heart disease or complex congenital heart disease, 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.

Some tachycardias cannot be easily classified. Reentrant sinoatrial 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.

Diagnostic Considerations

The differential diagnosis of atrial tachycardia is the differential diagnosis of supraventricular tachycardia (SVT) and includes the following:

• Sinus tachycardia
• Atrial flutter (see the image below)
• Atrial fibrillation
• Atrioventricular (AV) junction–dependent reentrant tachycardias (AV nodal reentrant tachycardia and AV reentrant tachycardia using an accessory pathway)

           

Differentiating among these diagnoses requires electrocardiographic (ECG) analysis of the tachycardia for P wave activity. In SVT, the ECG typically has narrow QRS complexes (unless aberrant conduction with typical left or right bundle-branch block occurs or a bystander preexcitation is seen).

Assessment of the relationship of the P waves to the QRS complex (R waves) can help to guide diagnosis. A short RP interval (P wave immediately following the QRS) suggests different causes of the tachycardia than does a long RP interval (interval wave preceding QRS).

In short RP interval SVT, the differential diagnosis includes the following:

• Typical AV nodal reentrant tachycardia
• AV reentrant tachycardia using accessory pathways
• Atrial tachycardia with long first-degree AV block
• Atrial tachycardia originating from the os of the coronary sinus or junctional tachycardia

To determine the diagnosis requires additional maneuvers, such as vagal stimulation (eg, carotid sinus massage, Valsalva maneuver), or adenosine.

In long RP interval SVT, the differential diagnosis includes the following:

• Atypical (fast-slow) AV nodal reentrant tachycardia
• Permanent junctional reciprocating tachycardia (PJRT) due to a slowly conducting retrograde accessory pathway
• Atrial tachycardia
• Sinus tachycardia
• Sinus node reentry
• Atrial flutter
• AV reentrant tachycardia

Diagnosis requires assessment of the patient condition, vagal maneuvers, adenosine, and cardioversion—namely, procedures that may not only be diagnostic but also therapeutic.

For multifocal atrial tachycardia (MAT), the differential diagnosis includes atrial fibrillation because both can manifest with an irregular pulse. MAT with aberration or preexisting bundle branch block may be misinterpreted as ventricular tachycardia (VT).

This 12-lead electrocardiogram demonstrates an atrial tachycardia at a rate of approximately 150 beats per minute. Note that the negative P waves in leads III and aVF (upright arrows) are different from the sinus beats (downward arrows). The RP interval exceeds the PR interval during the tachycardia. Note also that the tachycardia persists despite the atrioventricular block.

Anterior-posterior projection is shown. An example of activation mapping using contact technique and EnSite system. The atrial anatomy is partially reconstructed. Early activation points are marked with white/red color. The activation waveform spreads from the inferior/lateral aspect of the atrium through the entire chamber. White points indicate successful ablation sites that terminated the tachycardia. CS = shadow of the catheter inserted in the coronary sinus; TV = tricuspid valve.

Diagnosis

Tests and procedures used to diagnose atrial tachycardia may include:

• Blood tests to check thyroid function, heart disease or other conditions that may trigger atrial tachycardia
• Electrocardiogram (ECG) to measure the electrical activity of your heart and measure the timing and duration of each heartbeat
• Holter monitor, which is a portable ECG device designed to record your heart's activity as you go about your routine
• Echocardiogram, which uses sound waves to produce images of your heart's size, structure and motion

Your doctor might also try to trigger an episode with other tests, which may include:

• Stress test, which is typically done on a treadmill or stationary bicycle while your heart activity is monitored
• Electrophysiological testing and mapping, which allows your doctor to see the precise location of the arrhythmia

Treatment

Treatment of atrial tachycardia depends on the severity of the condition and the factors that trigger it. In addition to managing any underlying conditions that could trigger your atrial tachycardia, your doctor may recommend or try:

• Vagal maneuvers. You may be able to temporarily slow your heart rate by using particular maneuvers that include holding your breath and straining, dunking your face in ice water, or coughing.
• Medications. Your doctor may suggest intravenous or oral medication to control your heart rate or restore a normal heart rhythm.
• Cardioversion. If your arrhythmia (irregular heart beat) does not respond to vagal maneuvers or medication — and if there's no identifiable, treatable condition triggering it to occur — your doctor may use electrical cardioversion. In the procedure, a shock is delivered to your heart through paddles or patches on your chest. The current affects the electrical impulses in your heart and can restore a normal rhythm.
• Catheter ablation. In some cases, your doctor may recommend catheter ablation. For this procedure, your doctor threads one or more catheters through your blood vessels to your heart. Electrodes at the catheter tips can use heat, extreme cold or radiofrequency energy to damage (ablate) a small spot of heart tissue and create an electrical block along the pathway that's causing your arrhythmia.
• Pacemaker. If you experience frequent episodes of atrial tachycardia and all other treatment options are unsuccessful, your doctor may suggest implanting a small device called a pacemaker to emit electrical impulses that stimulate your heart to beat at a normal rate. For people with atrial tachycardia, this procedure is typically followed by an ablation of the AV node.