Tachycardia-dependent bundle branch block

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Tachycardia-dependent bundle branch block
Other namesTDBBB

A tachycardia-dependent bundle branch block is a defect in the conduction system of the heart, and is distinct from typical bundle branch blocks due to its reliable, reproducible onset related to an increase in the rate of cardiac contraction. Tachycardia-dependent bundle branch block can prevent both ventricles from contracting efficiently and can limit the cardiac output of the heart.

Contents

Anatomy

The human heart is a four-chambered organ responsible for the distribution of blood throughout the body. While every physiological effort is made to ensure that such a vital organ can operate continuously without error, sometimes a pathological situation arises and the function of the heart is compromised. One such pathology arises when the electrical signal propagated throughout the heart (responsible for the heart's highly organized contractions) is hindered, resulting in a degradation of said conduction. This is referred to as a bundle branch block and is seen clinically as rate-dependent bundle branch block, right bundle branch block or left bundle branch block.[ citation needed ]

Normal functioning

In a healthy heart, specialized cells in the sinoatrial node are responsible for the generation of contractile stimuli that are directed throughout the heart. A direct neural-like pathway propagates this electrical signal from the SA node through the atrial tissue to a central nodal point in the center of the heart, the atrioventricular node. From here, the signal travels down a signal conducting channel (the bundle of His) where it will diverge into a left and right branch that will control the left and right ventricle, respectively.[ citation needed ]

Rate-dependent bundle branch block

The various components of a normal, healthy ECG tracing. SinusRhythmLabels.png
The various components of a normal, healthy ECG tracing.

As a result of underlying heart disease, this cardiac conductive tissue can become damaged from ischemia (a deprivation of oxygenated blood). This damage results in the inability of this neural-like tissue to conduct electrical signals and control the heart as efficiently as before, resulting in the cardiac abnormality known as a bundle branch block (BBB). This can affect either side of the heart, and is described as a right or left BBB. Some BBB are permanent and involve a complete bundle blockage while others are dependent on the underlying activity of the heart. [1] For example, certain situations of excessive or reduced heart rate (tachycardia or bradycardia, respectively) can cause a BBB known as a rate-dependent bundle branch block (RDBBB). This manifests in a similar fashion to a regular bundle branch block, but occurs only under conditions that affect contractile rate. Tachycardia-dependent bundle branch block (TDBBB) can affect either ventricle in the heart, and occurs when the heart's rate of contraction reaches an elevated level and becomes uncoupled from the heart's refractory period (the time it takes for a cardiac cell to "reset" for future contraction). Thus the cell is unable to contract by the time the next electrical stimuli is present, and a blocking of this signal occurs. [2] This prolongation of the refractory period is related to a decreased sodium channel response in damaged tissue that shows an inactivation of sodium channels responsible for repolarization. [3]

Diagnosis

TDBBB can be diagnosed with use of an electrocardiogram (ECG) which will "trace" the electrical activity of the heart, providing an overall view of the hearts electrical system. Typically, TDBBB will be evident on an ECG and manifest as a prolongation of the QRS complex (a QRS complex completion time that exceeds 120ms), notching or slurring of the R wave, or the absence of Q waves should the TDBBB affect the left ventricle. [4]

Treatment

If an affected individual begins to experience severe TDBBB, then medical intervention is often advised. Suggested therapy for the treatment of TDBBB can include the prescription of certain medications or the implantation of a pacemaker device. [5] Advised medications would possess anti-coagulant mechanisms to reduce the risk of blood clot formation ensuring that no further restriction of arteries would deprive the heart of oxygen and further damage the bundle branches. [5] The use of a pacemaker would ensure that the heart receives a constant rhythmic electrical input that never changes in frequency. While this would effectively eliminate the occurrence of TDBBB, the pacemaker would restrict the patient's heart to a permanent rhythm, eliminating the ability of patients to perform physical activity. [5] [6] Future pacemakers that adaptively respond to physiological requirements are being developed in order to negate the limitations observed with their current use. [6]

Related Research Articles

Bradycardia Heart rate that is below the normal range

Bradycardia is a condition typically defined wherein an individual has a resting heart rate of under 60 beats per minute (BPM) in adults, although some studies use a heart rate of less than 50 BPM. Bradycardia typically does not cause symptoms until the rate drops below 50 BPM. When symptomatic, it may cause fatigue, weakness, dizziness, sweating, and at very low rates, fainting.

Electrocardiography Method to record the electrical activity of the heart through passive electrodes placed over the skin.

Electrocardiography is the process of producing an electrocardiogram. It is a graph of voltage versus time of the electrical activity of the heart using electrodes placed on the skin. These electrodes detect the small electrical changes that are a consequence of cardiac muscle depolarization followed by repolarization during each cardiac cycle (heartbeat). Changes in the normal ECG pattern occur in numerous cardiac abnormalities, including cardiac rhythm disturbances, inadequate coronary artery blood flow, and electrolyte disturbances.

Cardiac pacemaker Network of cells that facilitate rhythmic heart contraction

The contraction of cardiac muscle in all animals is initiated by electrical impulses known as action potentials. The rate at which these impulses fire, controls the rate of cardiac contraction, that is, the heart rate. The cells that create these rhythmic impulses, setting the pace for blood pumping, are called pacemaker cells, and they directly control the heart rate. They make up the cardiac pacemaker, that is, the natural pacemaker of the heart. In most humans, the concentration of pacemaker cells in the sinoatrial (SA) node is the natural pacemaker, and the resultant rhythm is a sinus rhythm.

Third-degree atrioventricular block

Third-degree atrioventricular block is a medical condition in which the nerve impulse generated in the sinoatrial node in the atrium of the heart can not propagate to the ventricles.

Electrical conduction system of the heart Transmits signals generated usually by the sinoatrial node to cause contraction of the heart muscle

The electrical conduction system of the heart transmits signals generated usually by the sinoatrial node to cause contraction of the heart muscle. The pacemaking signal generated in the sinoatrial node travels through the right atrium to the atrioventricular node, along the Bundle of His and through bundle branches to cause contraction of the heart muscle. This signal stimulates contraction first of the right and left atrium, and then the right and left ventricles. This process allows blood to be pumped throughout the body.

Supraventricular tachycardia Abnormally fast heart rhythm arising from improper electrical activity in the upper part of the heart

Supraventricular tachycardia (SVT) is an abnormally fast heart rhythm arising from improper electrical activity in the upper part of the heart. There are four main types: atrial fibrillation, paroxysmal supraventricular tachycardia (PSVT), atrial flutter, and Wolff–Parkinson–White syndrome. Symptoms may include palpitations, feeling faint, sweating, shortness of breath, or chest pain.

AV nodal reentrant tachycardia

AV-nodal reentrant tachycardia (AVNRT) is a type of abnormal fast heart rhythm. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men. The main symptom is palpitations. Treatment may be with specific physical maneuvers, medications, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.

Bundle branch block

A bundle branch block is a defect of the bundle branches or fascicles in the electrical conduction system of the heart.

Atrioventricular block is a type of heart block that occurs when the electrical signal traveling from the atria, or the upper chambers of the heart, to ventricles, or the lower chambers of the heart, is impaired. Normally, the sinoatrial node produces an electrical signal to control the heart rate. The signal travels from the SA node to the ventricles through the atrioventricular node. In an AV block, this electrical signal is either delayed or completely blocked. When the signal is completely blocked, the ventricles produce their own electrical signal to control the heart rate. The heart rate produced by the ventricles is much slower than that produced by the SA node.

Ventricular escape beat

In cardiology, a ventricular escape beat is a self-generated electrical discharge initiated by, and causing contraction of, the ventricles of the heart; normally the heart rhythm is begun in the atria of the heart and is subsequently transmitted to the ventricles. The ventricular escape beat follows a long pause in ventricular rhythm and acts to prevent cardiac arrest. It indicates a failure of the electrical conduction system of the heart to stimulate the ventricles.

Lorcainide

Lorcainide is a Class 1c antiarrhythmic agent that is used to help restore normal heart rhythm and conduction in patients with premature ventricular contractions, ventricular tachycardiac and Wolff-Parkinson-White syndrome. Lorcainide was developed by Janssen Pharmaceutica (Belgium) in 1968 under the commercial name Remivox and is designated by code numbers R-15889 or Ro 13-1042/001. It has a half-life of 8.9 +- 2.3 hrs which may be prolonged to 66 hrs in people with cardiac disease.

An accessory pathway is an additional electrical connection between two parts of the heart. These pathways can lead to abnormal heart rhythms or arrhythmias associated with symptoms of palpitations. Some pathways may activate a region of ventricular muscle earlier than would normally occur, referred to as pre-excitation, and this may be seen on an electrocardiogram. The combination of an accessory pathway that causes pre-excitation with arrhythmias is known as Wolff-Parkinson-White syndrome.

Right axis deviation

The electrical axis of the heart is the net direction in which the wave of depolarisation travels. It is measured using an electrocardiogram (ECG). Normally, this begins at the sinoatrial node ; from here the wave of depolarisation travels down to the apex of the heart. The hexaxial reference system can be used to visualise the directions in which the depolarisation wave may travel.

An ectopic pacemaker is an excitable group of cells that causes a premature heart beat outside the normally functioning SA node of the heart. It is thus a cardiac pacemaker that is ectopic, producing an ectopic beat. Acute occurrence is usually non-life-threatening, but chronic occurrence can progress into tachycardia, bradycardia or ventricular fibrillation. In a normal heart beat rhythm, the SA node usually suppresses the ectopic pacemaker activity due to the higher impulse rate of the SA node. However, in the instance of either a malfunctioning SA node or an ectopic focus bearing an intrinsic rate superior to SA node rate, ectopic pacemaker activity may take over the natural heart rhythm. This phenomenon is called an escape rhythm, the lower rhythm having escaped from the dominance of the upper rhythm. As a rule, premature ectopic beats indicate increased myocyte or conducting tissue excitability, whereas late ectopic beats indicate proximal pacemaker or conduction failure with an escape 'ectopic' beat.

The following outline is provided as an overview of and topical guide to cardiology, the branch of medicine dealing with disorders of the human heart. The field includes medical diagnosis and treatment of congenital heart defects, coronary artery disease, heart failure, valvular heart disease and electrophysiology. Physicians who specialize in cardiology are called cardiologists.

Junctional ectopic tachycardia

Junctional ectopic tachycardia (JET) is a rare syndrome of the heart that manifests in patients recovering from heart surgery. It is characterized by cardiac arrhythmia, or irregular beating of the heart, caused by abnormal conduction from or through the atrioventricular node. In newborns and infants up to 6 weeks old, the disease may also be referred to as His bundle tachycardia or congenital JET.

Arrhythmia Group of conditions in which the heartbeat is irregular, too fast, or too slow

Arrhythmia, also known as cardiac arrhythmia or heart arrhythmia, is a group of conditions in which the heartbeat is irregular, too fast, or too slow. The heart rate that is too fast – above 100 beats per minute in adults – is called tachycardia, and a heart rate that is too slow – below 60 beats per minute – is called bradycardia. Some types of arrhythmias have no symptoms. Symptoms, when present, may include palpitations or feeling a pause between heartbeats. In more serious cases, there may be lightheadedness, passing out, shortness of breath or chest pain. While most types of arrhythmia are not serious, some predispose a person to complications such as stroke or heart failure. Others may result in sudden death.

Cardiac physiology or heart function is the study of healthy, unimpaired function of the heart: involving blood flow; myocardium structure; the electrical conduction system of the heart; the cardiac cycle and cardiac output and how these interact and depend on one another.

Cardiac Contractility Modulation is a therapy which is intended for the treatment of patients with moderate to severe heart failure with symptoms despite optimal medical therapy who can benefit from an improvement in cardiac output. The short- and long-term use of this therapy enhances the strength of ventricular contraction and therefore the heart's pumping capacity by modulating (adjusting) the myocardial contractility. This is provided by a pacemaker-like device that applies non-excitatory electrical signals adjusted to and synchronized with the electrical action in the cardiac cycle.

In cardiology, ventricular dyssynchrony is a difference in the timing, or lack of synchrony, of contractions in different ventricles in the heart. Large differences in timing of contractions can reduce cardiac efficiency and is correlated with heart failure.

References

  1. Denes P. et al. "Electrophysiological observations in patients with rate dependent bundle branch block."[ sic ]Journal of the American Heart Association. 51 (1975) 244-250
  2. Rausenbaum M.B. et al. "The Mechanism of Intermittent Bundle Branch Block: Relationship to Prolonged Recovery, Hypopolarization and Spontaneous Diastolic Depolarization". Chest. 63 (1973) 666-677
  3. Chiale P. A. et al. "Contrasting Effects of Verapamil and Procainamide on Rate-Dependent Bundle Branch Block: Pharmacologic Evidence for The Role of Depressed Sodium Channel Responses". American College of Cardiology. 15 (1990) 633-639
  4. Kumar V, Venkataraman R, Aljaroudi W, Osorio J, Heo J, Iskandrian AE, Hage FG. "Implications of Left Bundle Branch Block in Patient Treatment", Am J Cardiol 2013;111:291-300.
  5. 1 2 3 Shlipak M. G. et al. "Treatment and outcomes of left bundle-branch block patients with myocardial infarction who present without chest pain". Journal of the American College of Cardiology. 36 (2000) 706-712
  6. 1 2 Hayes D. L. "Advances in pacing therapy for bradycardia". International Journal of Cardiology. 32 (1991) 183-196