Tachycardia, Sinoatrial Nodal Reentry
Tachycardia, Atrioventricular Nodal Reentry
Sinoatrial Node
Tachycardia, Supraventricular
Tachycardia
Atrioventricular Node
Sinoatrial Block
Tachycardia, Ventricular
Catheter Ablation
Heart Conduction System
Electrocardiography
Tachycardia, Sinus
Tachycardia, Ectopic Atrial
Cardiac Pacing, Artificial
Electrophysiologic Techniques, Cardiac
Tachycardia, Reciprocating
Tachycardia, Ectopic Junctional
Bundle of His
Anti-Arrhythmia Agents
Arrhythmias, Cardiac
Heart Block
Postural Orthostatic Tachycardia Syndrome
Body Surface Potential Mapping
Ventricular Fibrillation
Bradycardia
Action Potentials
Arrhythmia, Sinus
Electrophysiology
Digitalis Glycosides
Cardiac Glycosides
Digoxin
Digitalis
Digitoxin
Glycosides
Cardenolides
Radiofrequency catheter ablation for sinoatrial node reentrant tachycardia: electrophysiologic features of ablation sites. (1/18)
The aim of this study was to investigate catheter ablation of sino-atrial reentrant tachycardia (SART) and the electrophysiologic characteristics of the ablation sites. From January 1990 to October 1997, 651 patients with supraventricular tachycardia were referred and 11 patients were found to have SART. Ablation was successful in all cases with a mean number of 3.3 radiofrequency (RF) current pulses. SART terminated during 22 of 36 RF pulses. In spite of prompt termination, tachycardia could be re-induced in 3 of 11 patients with its earliest activation site shifted. At effective ablation sites, the electrograms during tachycardia were characterized as fractionated (75+/-17 ms), and 38+/-16 ms prior to surface P wave, and 42+/-18 ms prior to the high right atrium. Unipolar electrograms revealed a sharp negative unipolar deflection, so called QS pattern, in 15 of 20 sites during SART and 15 of 15 sites during sinus rhythm. During effective applications, atrial premature beats (APB) with activation sequences identical to sinus rhythm appeared in 14 of 22 cases. Effective ablation sites of SART showed fractionated electrograms during tachycardia and sinus rhythm. Unipolar electrogram with a QS pattern and APB during energy application could be an indicator of the optimal ablation sites. (+info)Effect of intravenous amiodarone on electrophysiologic variables and on the modes of termination of atrioventricular reciprocating tachycardia in Wolff-Parkinson-White syndrome. (2/18)
Atrioventricular reciprocating tachycardia (AVRT) associated with the Wolff-Parkinson-White (WPW) syndrome, sometimes terminates spontaneously, generally sustains and eventually becomes drug resistant. Amiodarone is a potent antiarrhythmic drug that is sometimes effective in patients with AVRT which is resistant to conventional antiarrhythmic drugs. However, systematic studies concerning the effects of amiodarone on AVRT have not been reported. This study evaluated the effects of intravenous amiodarone on electrophysiologic variables, and on the sites and the modes of termination of AVRT. Fifteen WPW patients were studied. Nine had overt, and 6 had concealed WPW syndrome. Measurements of electrophysiologic variables and the induction of AVRT were performed by atrial and/or ventricular programmed stimulations. Amiodarone was then administered at a dose of 5 mg/kg over 5 min. The effective refractory periods (ERP) of the atrial, atrioventricular node, ventricular and accessory pathway were increased significantly by amiodarone. The conduction times of all the components were significantly lengthened by amiodarone, except for the His-ventricular (HV) interval in concealed WPW patients. AVRT was induced in all patients, and was terminated by amiodarone in 12 of 13 patients with sustained AVRT. After amiodarone, AVRT was induced in 9 patients. Spontaneous termination was observed 11 times in 3 of the 9 patients in whom AVRT was still induced. In these cases, the modes and sites of termination were the same as during the baseline state. The ERPs and conduction times of all components of AVRT, except the HV interval, were significantly lengthened by amiodarone. Amiodarone is efficacious for terminating AVRT wherever weak links exist. However, sites of spontaneous termination are not significantly affected by amiodarone. (+info)Experimental ablation study using a new long linear probe in isolated porcine hearts. (3/18)
We studied a new technique for creating long linear lesions in hearts using a custom-made linear probe. Radiofrequency (RF) energy applications using a 25-mm long stainless steel linear probe and a corresponding 500-kHz energy generator were tested, creating 90 lesions in isolated porcine hearts. The RF current was applied between the linear probe and a large patch electrode attached to the back of the specimen. Three parameters, comprising the power of the delivered energy, the pressure of contact between the probe and the specimen, and the duration of energy delivery were changed independently and the size of the resulting lesions was measured. All 90 lesions were transmural, well demarcated and created by a single stationary RF application. Lesion length and width increased with: 1) increasing power, when the other two parameters were maintained at constant levels, 2) increasing contact pressure, when the other two parameters were maintained at constant levels, and 3) increasing duration of energy delivery when the other two parameters were maintained at constant levels. The maximum width of the lesions was 3.7 mm. No overheating of any of the specimens was observed. In conclusion, the new original long linear probe used in this study was effective for creating transmural linear lesions, presenting the possibility of a worthwhile contribution to the maze surgical procedure applied to atrial fibrillation. (+info)The N + 1 difference: a new measure for entrainment mapping. (4/18)
OBJECTIVES: The purpose of this study was to develop and test a new entrainment mapping measurement, the N + 1 difference. BACKGROUND: Entrainment mapping is useful for identifying re-entry circuit sites but is often limited by difficulty in assessing: 1) changes in QRS complexes or P-waves that indicate fusion, and 2) the postpacing interval (PPI) recorded directly from the stimulation site. METHODS: In computer simulations of re-entry circuits, the interval from a stimulus that reset tachycardia to a timing reference during the second beat after the stimulus was compared with the timing of local activation at the site during tachycardia to define an interval designated the N + 1 difference. The N + 1 difference was compared with the PPI-tachycardia cycle length (TCL) difference in simulations and at 65 sites in 10 consecutive patients with ventricular tachycardia (VT) after myocardial infarction and at 45 sites in 10 consecutive patients with atrial flutter. RESULTS: In simulations, the N + 1 difference was equal to the PPI-TCL difference. During mapping of VT and atrial flutter, the N + 1 difference correlated well with the PPI-TCL difference (r > or = 0.91, p < 0.0001), identifying re-entry circuit sites with sensitivity of > or = 86% and specificity of > or = 90%. Accuracy was similar using either the surface electrocardiogram or an intracardiac electrogram (Eg) as the timing reference. CONCLUSIONS: The N + 1 difference allows entrainment mapping to be used to identify re-entry circuit sites when it is difficult to evaluate Egs at the mapping site or fusion in the surface electrocardiogram. (+info)Catheter ablation of sinoatrial re-entry tachycardia in a 2 month old infant. (5/18)
Successful catheter ablation of sinoatrial re-entry tachycardia in an infant has not been previously reported. This procedure is described in a 2 month old boy with tachycardia induced cardiomyopathy. (+info)A posteroseptal accessory pathway located in a coronary sinus aneurysm: diagnosis and radiofrequency catheter ablation. (6/18)
A coronary sinus aneurysm was diagnosed by means of echocardiography, coronary sinus contrast angiography, coronary angiography, and nuclear magnetic resonance imaging in a patient with Wolff-Parkinson-White syndrome caused by a posteroseptal accessory pathway. Percutaneous radiofrequency current catheter ablation performed in the isthmus of the coronary sinus aneurysm was successful. (+info)Effects of Na(+) channel and cell coupling abnormalities on vulnerability to reentry: a simulation study. (7/18)
The role of dynamic instabilities in the initiation of reentry in diseased (remodeled) hearts remains poorly explored. Using computer simulations, we studied the effects of altered Na(+) channel and cell coupling properties on the vulnerable window (VW) for reentry in simulated two-dimensional cardiac tissue with and without dynamic instabilities. We related the VW for reentry to effects on conduction velocity, action potential duration (APD), effective refractory period dispersion and restitution, and concordant and discordant APD alternans. We found the following: 1). reduced Na(+) current density and slowed recovery promoted postrepolarization refractoriness and enhanced concordant and discordant APD alternans, which increased the VW for reentry; 2). uniformly reduced cell coupling had little effect on cellular electrophysiological properties and the VW for reentry. However, randomly reduced cell coupling combined with decoupling promoted APD dispersion and alternans, which also increased the VW for reentry; 3). the combination of decreased Na(+) channel conductance, slowed Na(+) channel recovery, and cellular uncoupling synergistically increased the VW for reentry; and 4) the VW for reentry was greater when APD restitution slope was steep than when it was flat. In summary, altered Na(+) channel and cellular coupling properties increase vulnerability to reentrant arrhythmias. In remodeled hearts with altered Na(+) channel properties and cellular uncoupling, dynamic instabilities arising from electrical restitution exert important influences on the VW for reentry. (+info)Successful ablation of sinus node reentrant tachycardia using remote magnetic navigation system. (8/18)
(+info)Tachycardia is a heart rate that is faster than normal. In sinoatrial nodal reentry tachycardia (SANRT), the abnormally fast heart rhythm originates in the sinoatrial node, which is the natural pacemaker of the heart. This type of tachycardia occurs due to a reentry circuit within the sinoatrial node, where an electrical impulse travels in a circular pattern and repeatedly stimulates the node to fire off abnormal rapid heartbeats. SANRT is typically characterized by a heart rate of over 100 beats per minute, palpitations, lightheadedness, or occasionally chest discomfort. It is usually a benign condition but can cause symptoms that affect quality of life. In some cases, treatment may be required to prevent recurrences and manage symptoms.
Atrioventricular (AV) nodal reentrant tachycardia (AVNRT) is a type of supraventricular tachycardia (SVT), which is a rapid heart rhythm originating at or above the atrioventricular node. In AVNRT, an abnormal electrical circuit in or near the AV node creates a reentry pathway that allows for rapid heart rates, typically greater than 150-250 beats per minute.
In normal conduction, the electrical impulse travels from the atria to the ventricles through the AV node and then continues down the bundle branches to the Purkinje fibers, resulting in a coordinated contraction of the heart. In AVNRT, an extra electrical pathway exists that allows for the reentry of the electrical impulse back into the atria, creating a rapid and abnormal circuit.
AVNRT is classified based on the direction of the reentry circuit:
1. Typical or common AVNRT: The most common form, accounting for 90% of cases. In this type, the reentry circuit involves an "anterior" and a "posterior" loop in or near the AV node. The anterior loop has slower conduction velocity than the posterior loop, creating a "short" reentry circuit that is responsible for the rapid heart rate.
2. Atypical AVNRT: Less common, accounting for 10% of cases. In this type, the reentry circuit involves an "outer" and an "inner" loop around the AV node. The outer loop has slower conduction velocity than the inner loop, creating a "long" reentry circuit that is responsible for the rapid heart rate.
AVNRT can present with symptoms such as palpitations, dizziness, lightheadedness, shortness of breath, chest discomfort, or syncope (fainting). Treatment options include observation, vagal maneuvers, medications, and catheter ablation. Catheter ablation is a curative treatment that involves the destruction of the abnormal electrical pathway using radiofrequency energy or cryotherapy.
The sinoatrial (SA) node, also known as the sinus node, is the primary pacemaker of the heart. It is a small bundle of specialized cardiac conduction tissue located in the upper part of the right atrium, near the entrance of the superior vena cava. The SA node generates electrical impulses that initiate each heartbeat, causing the atria to contract and pump blood into the ventricles. This process is called sinus rhythm.
The SA node's electrical activity is regulated by the autonomic nervous system, which can adjust the heart rate in response to changes in the body's needs, such as during exercise or rest. The SA node's rate of firing determines the heart rate, with a normal resting heart rate ranging from 60 to 100 beats per minute.
If the SA node fails to function properly or its electrical impulses are blocked, other secondary pacemakers in the heart may take over, resulting in abnormal heart rhythms called arrhythmias.
Supraventricular tachycardia (SVT) is a rapid heart rhythm that originates above the ventricles (the lower chambers of the heart). This type of tachycardia includes atrial tachycardia, atrioventricular nodal reentrant tachycardia (AVNRT), and atrioventricular reentrant tachycardia (AVRT). SVT usually causes a rapid heartbeat that starts and stops suddenly, and may not cause any other symptoms. However, some people may experience palpitations, shortness of breath, chest discomfort, dizziness, or fainting. SVT is typically diagnosed through an electrocardiogram (ECG) or Holter monitor, and can be treated with medications, cardioversion, or catheter ablation.
Tachycardia is a medical term that refers to an abnormally rapid heart rate, often defined as a heart rate greater than 100 beats per minute in adults. It can occur in either the atria (upper chambers) or ventricles (lower chambers) of the heart. Different types of tachycardia include supraventricular tachycardia (SVT), atrial fibrillation, atrial flutter, and ventricular tachycardia.
Tachycardia can cause various symptoms such as palpitations, shortness of breath, dizziness, lightheadedness, chest discomfort, or syncope (fainting). In some cases, tachycardia may not cause any symptoms and may only be detected during a routine physical examination or medical test.
The underlying causes of tachycardia can vary widely, including heart disease, electrolyte imbalances, medications, illicit drug use, alcohol abuse, smoking, stress, anxiety, and other medical conditions. In some cases, the cause may be unknown. Treatment for tachycardia depends on the underlying cause, type, severity, and duration of the arrhythmia.
The atrioventricular (AV) node is a critical part of the electrical conduction system of the heart. It is a small cluster of specialized cardiac muscle cells located in the lower interatrial septum, near the opening of the coronary sinus. The AV node receives electrical impulses from the sinoatrial node (the heart's natural pacemaker) via the internodal pathways and delays their transmission for a brief period before transmitting them to the bundle of His and then to the ventricles. This delay allows the atria to contract and empty their contents into the ventricles before the ventricles themselves contract, ensuring efficient pumping of blood throughout the body.
The AV node plays an essential role in maintaining a normal heart rhythm, as it can also function as a backup pacemaker if the sinoatrial node fails to generate impulses. However, certain heart conditions or medications can affect the AV node's function and lead to abnormal heart rhythms, such as atrioventricular block or atrial tachycardia.
Sinoatrial block is a type of heart conduction disorder that affects the sinoatrial node, which is the natural pacemaker of the heart. In a sinoatrial block, the electrical impulses that originate in the sinoatrial node are delayed or blocked, resulting in a slower than normal heart rate or pauses between heartbeats.
A sinoatrial block can be classified as first-, second-, or third-degree, depending on the severity of the block. In a first-degree sinoatrial block, the electrical impulses are slowed but still conducted through to the atria. In a second-degree sinoatrial block, some of the electrical impulses are blocked, resulting in dropped beats or an irregular heart rhythm. In a third-degree sinoatrial block, also known as sinus node arrest, there is a complete failure of the sinoatrial node to generate impulses, resulting in a prolonged pause followed by a ventricular escape rhythm.
Sinoatrial blocks can be caused by various factors, including aging, heart disease, medication side effects, and electrolyte imbalances. In some cases, a sinoatrial block may not cause any symptoms and may only be detected during a routine electrocardiogram (ECG). However, in more severe cases, a sinoatrial block can lead to symptoms such as palpitations, dizziness, syncope (fainting), or shortness of breath. Treatment for a sinoatrial block depends on the underlying cause and may include medication adjustments, pacemaker implantation, or other interventions.
Ventricular Tachycardia (VT) is a rapid heart rhythm that originates from the ventricles, the lower chambers of the heart. It is defined as three or more consecutive ventricular beats at a rate of 120 beats per minute or greater in a resting adult. This abnormal heart rhythm can cause the heart to pump less effectively, leading to inadequate blood flow to the body and potentially life-threatening conditions such as hypotension, shock, or cardiac arrest.
VT can be classified into three types based on its duration, hemodynamic stability, and response to treatment:
1. Non-sustained VT (NSVT): It lasts for less than 30 seconds and is usually well tolerated without causing significant symptoms or hemodynamic instability.
2. Sustained VT (SVT): It lasts for more than 30 seconds, causes symptoms such as palpitations, dizziness, shortness of breath, or chest pain, and may lead to hemodynamic instability.
3. Pulseless VT: It is a type of sustained VT that does not produce a pulse, blood pressure, or adequate cardiac output, requiring immediate electrical cardioversion or defibrillation to restore a normal heart rhythm.
VT can occur in people with various underlying heart conditions such as coronary artery disease, cardiomyopathy, valvular heart disease, congenital heart defects, and electrolyte imbalances. It can also be triggered by certain medications, substance abuse, or electrical abnormalities in the heart. Prompt diagnosis and treatment of VT are crucial to prevent complications and improve outcomes.
Catheter ablation is a medical procedure in which specific areas of heart tissue that are causing arrhythmias (irregular heartbeats) are destroyed or ablated using heat energy (radiofrequency ablation), cold energy (cryoablation), or other methods. The procedure involves threading one or more catheters through the blood vessels to the heart, where the tip of the catheter can be used to selectively destroy the problematic tissue. Catheter ablation is often used to treat atrial fibrillation, atrial flutter, and other types of arrhythmias that originate in the heart's upper chambers (atria). It may also be used to treat certain types of arrhythmias that originate in the heart's lower chambers (ventricles), such as ventricular tachycardia.
The goal of catheter ablation is to eliminate or reduce the frequency and severity of arrhythmias, thereby improving symptoms and quality of life. In some cases, it may also help to reduce the risk of stroke and other complications associated with arrhythmias. Catheter ablation is typically performed by a specialist in heart rhythm disorders (electrophysiologist) in a hospital or outpatient setting under local anesthesia and sedation. The procedure can take several hours to complete, depending on the complexity of the arrhythmia being treated.
It's important to note that while catheter ablation is generally safe and effective, it does carry some risks, such as bleeding, infection, damage to nearby structures, and the possibility of recurrent arrhythmias. Patients should discuss the potential benefits and risks of the procedure with their healthcare provider before making a decision about treatment.
The heart conduction system is a group of specialized cardiac muscle cells that generate and conduct electrical impulses to coordinate the contraction of the heart chambers. The main components of the heart conduction system include:
1. Sinoatrial (SA) node: Also known as the sinus node, it is located in the right atrium near the entrance of the superior vena cava and functions as the primary pacemaker of the heart. It sets the heart rate by generating electrical impulses at regular intervals.
2. Atrioventricular (AV) node: Located in the interatrial septum, near the opening of the coronary sinus, it serves as a relay station for electrical signals between the atria and ventricles. The AV node delays the transmission of impulses to allow the atria to contract before the ventricles.
3. Bundle of His: A bundle of specialized cardiac muscle fibers that conducts electrical impulses from the AV node to the ventricles. It divides into two main branches, the right and left bundle branches, which further divide into smaller Purkinje fibers.
4. Right and left bundle branches: These are extensions of the Bundle of His that transmit electrical impulses to the respective right and left ventricular myocardium. They consist of specialized conducting tissue with large diameters and minimal resistance, allowing for rapid conduction of electrical signals.
5. Purkinje fibers: Fine, branching fibers that arise from the bundle branches and spread throughout the ventricular myocardium. They are responsible for transmitting electrical impulses to the working cardiac muscle cells, triggering coordinated ventricular contraction.
In summary, the heart conduction system is a complex network of specialized muscle cells responsible for generating and conducting electrical signals that coordinate the contraction of the atria and ventricles, ensuring efficient blood flow throughout the body.
Cryosurgery is a medical procedure that uses extreme cold, such as liquid nitrogen or argon gas, to destroy abnormal or unwanted tissue. The intense cold causes the water inside the cells to freeze and form ice crystals, which can rupture the cell membrane and cause the cells to die. Cryosurgery is often used to treat a variety of conditions including skin growths such as warts and tumors, precancerous lesions, and some types of cancer. The procedure is typically performed in a doctor's office or outpatient setting and may require local anesthesia.
Electrocardiography (ECG or EKG) is a medical procedure that records the electrical activity of the heart. It provides a graphic representation of the electrical changes that occur during each heartbeat. The resulting tracing, called an electrocardiogram, can reveal information about the heart's rate and rhythm, as well as any damage to its cells or abnormalities in its conduction system.
During an ECG, small electrodes are placed on the skin of the chest, arms, and legs. These electrodes detect the electrical signals produced by the heart and transmit them to a machine that amplifies and records them. The procedure is non-invasive, painless, and quick, usually taking only a few minutes.
ECGs are commonly used to diagnose and monitor various heart conditions, including arrhythmias, coronary artery disease, heart attacks, and electrolyte imbalances. They can also be used to evaluate the effectiveness of certain medications or treatments.
Sinus tachycardia is a type of rapid heart rate, characterized by an abnormally fast sinus rhythm, with a rate greater than 100 beats per minute in adults. The sinoatrial node (SA node), which is the natural pacemaker of the heart, generates these impulses regularly and at an increased rate.
Sinus tachycardia is usually a physiological response to various stimuli or conditions, such as physical exertion, strong emotions, fever, anxiety, pain, or certain medications. It can also be caused by hormonal imbalances, anemia, hyperthyroidism, or other medical disorders.
In most cases, sinus tachycardia is not harmful and resolves once the underlying cause is addressed. However, if it occurs persistently or is associated with symptoms like palpitations, shortness of breath, dizziness, or chest discomfort, further evaluation by a healthcare professional is recommended to rule out any underlying heart conditions or other medical issues.
Paroxysmal Tachycardia is a type of arrhythmia (abnormal heart rhythm) characterized by rapid and abrupt onset and offset of episodes of tachycardia, which are faster than normal heart rates. The term "paroxysmal" refers to the sudden and recurring nature of these episodes.
Paroxysmal Tachycardia can occur in various parts of the heart, including the atria (small upper chambers) or ventricles (larger lower chambers). The two most common types are Atrial Paroxysmal Tachycardia (APT) and Ventricular Paroxysmal Tachycardia (VPT).
APT is more common and typically results in a rapid heart rate of 100-250 beats per minute. It usually begins and ends suddenly, lasting for seconds to hours. APT can cause symptoms such as palpitations, lightheadedness, shortness of breath, chest discomfort, or anxiety.
VPT is less common but more serious because it involves the ventricles, which are responsible for pumping blood to the rest of the body. VPT can lead to decreased cardiac output and potentially life-threatening conditions such as syncope (fainting) or even cardiac arrest.
Treatment options for Paroxysmal Tachycardia depend on the underlying cause, severity, and frequency of symptoms. These may include lifestyle modifications, medications, cardioversion (electrical shock to restore normal rhythm), catheter ablation (destroying problematic heart tissue), or implantable devices such as pacemakers or defibrillators.
Tachycardia is a heart rate that is faster than normal when resting. In adults, a normal resting heart rate is typically between 60 and 100 beats per minute (bpm). Tachycardia is generally considered to be a heart rate of more than 100 bpm.
Ectopic atrial tachycardia (EAT) is a type of supraventricular tachycardia (SVT), which means that the abnormal rapid heartbeats originate in the atria, the upper chambers of the heart. EAT is caused by an ectopic focus, or an abnormal electrical focus outside of the sinoatrial node (the heart's natural pacemaker). This ectopic focus can be located in one of the pulmonary veins or in other atrial tissue.
EAT may present with symptoms such as palpitations, lightheadedness, shortness of breath, chest discomfort, or syncope (fainting). In some cases, EAT may not cause any symptoms and can be an incidental finding on an electrocardiogram (ECG) or Holter monitor.
The diagnosis of EAT is typically made based on the ECG findings, which show a regular narrow QRS complex tachycardia with P waves that are inverted in the inferior leads and often dissociated from the QRS complexes. Treatment options for EAT include observation, pharmacologic therapy, cardioversion, or catheter ablation.
Artificial cardiac pacing is a medical procedure that involves the use of an artificial device to regulate and stimulate the contraction of the heart muscle. This is often necessary when the heart's natural pacemaker, the sinoatrial node, is not functioning properly and the heart is beating too slowly or irregularly.
The artificial pacemaker consists of a small generator that produces electrical impulses and leads that are positioned in the heart to transmit the impulses. The generator is typically implanted just under the skin in the chest, while the leads are inserted into the heart through a vein.
There are different types of artificial cardiac pacing systems, including single-chamber pacemakers, which stimulate either the right atrium or right ventricle, and dual-chamber pacemakers, which stimulate both chambers of the heart. Some pacemakers also have additional features that allow them to respond to changes in the body's needs, such as during exercise or sleep.
Artificial cardiac pacing is a safe and effective treatment for many people with abnormal heart rhythms, and it can significantly improve their quality of life and longevity.
Electrophysiologic techniques, cardiac, refer to medical procedures used to study the electrical activities and conduction systems of the heart. These techniques involve the insertion of electrode catheters into the heart through blood vessels under fluoroscopic guidance to record and stimulate electrical signals. The information obtained from these studies can help diagnose and evaluate various cardiac arrhythmias, determine the optimal treatment strategy, and assess the effectiveness of therapies such as ablation or implantable devices.
The electrophysiologic study (EPS) is a type of cardiac electrophysiologic technique that involves the measurement of electrical signals from different regions of the heart to evaluate its conduction system's function. The procedure can help identify the location of abnormal electrical pathways responsible for arrhythmias and determine the optimal treatment strategy, such as catheter ablation or medication therapy.
Cardiac electrophysiologic techniques are also used in device implantation procedures, such as pacemaker or defibrillator implantation, to ensure proper placement and function of the devices. These techniques can help program and test the devices to optimize their settings for each patient's needs.
In summary, cardiac electrophysiologic techniques are medical procedures used to study and manipulate the electrical activities of the heart, helping diagnose and treat various arrhythmias and other cardiac conditions.
Reciprocating tachycardia is a type of supraventricular tachycardia (SVT), which is a rapid heart rhythm originating in the atria or atrioventricular node. In reciprocating tachycardia, there are abnormal electrical connections between the atria and ventricles called "accessory pathways" that allow electrical impulses to bypass the normal conduction system.
In this type of tachycardia, an electrical impulse originates in one of the atria and travels down the normal conduction system to the ventricles, but then instead of following the normal route back up to the atria, it takes a shortcut through an accessory pathway. This creates a reentry circuit, where the electrical impulse continuously circulates between the atria and ventricles, causing a rapid heart rate.
Reciprocating tachycardia can be classified as either orthodromic or antidromic, depending on the direction of the electrical impulse through the accessory pathway. In orthodromic reciprocating tachycardia, the electrical impulse travels down the normal conduction system to the ventricles and then returns up the accessory pathway to the atria. This type of reciprocating tachycardia is more common than antidromic reciprocating tachycardia, which occurs when the electrical impulse travels down the accessory pathway to the ventricles and then returns up the normal conduction system to the atria.
Symptoms of reciprocating tachycardia may include palpitations, lightheadedness, shortness of breath, chest discomfort, or syncope (fainting). Treatment options for reciprocating tachycardia include medications, cardioversion, catheter ablation, and surgery.
Tachycardia refers to a rapid heart rate, typically defined as over 100 beats per minute in adults. Ectopic junctional tachycardia (EJT) is a specific type of abnormal heart rhythm that originates from the junction between the atria (the upper chambers of the heart) and ventricles (the lower chambers).
In EJT, the electrical impulse arises from an ectopic focus (an area outside of the normal conduction system) located in or near the atrioventricular (AV) node. This results in a rapid heart rate that can range from 100 to 250 beats per minute.
EJT is often seen in patients after cardiac surgery, and it can also occur in other conditions such as myocarditis, digoxin toxicity, or following congenital heart disease repair. It may cause symptoms such as palpitations, shortness of breath, chest discomfort, or dizziness. Treatment options for EJT include medications, cardioversion, or ablation therapy, depending on the underlying cause and severity of symptoms.
The heart atria are the upper chambers of the heart that receive blood from the veins and deliver it to the lower chambers, or ventricles. There are two atria in the heart: the right atrium receives oxygen-poor blood from the body and pumps it into the right ventricle, which then sends it to the lungs to be oxygenated; and the left atrium receives oxygen-rich blood from the lungs and pumps it into the left ventricle, which then sends it out to the rest of the body. The atria contract before the ventricles during each heartbeat, helping to fill the ventricles with blood and prepare them for contraction.
The Bundle of His is a bundle of specialized cardiac muscle fibers that conduct electrical impulses to the Purkinje fibers, which then stimulate contraction of the ventricles in the heart. It is named after Wilhelm His, Jr., who first described it in 1893.
The Bundle of His is a part of the electrical conduction system of the heart that helps coordinate the contraction of the atria and ventricles to ensure efficient pumping of blood. The bundle originates from the atrioventricular node, which receives electrical impulses from the sinoatrial node (the heart's natural pacemaker) and transmits them through the Bundle of His to the Purkinje fibers.
The Bundle of His is divided into two main branches, known as the right and left bundle branches, which further divide into smaller fascicles that spread throughout the ventricular myocardium. This ensures a coordinated contraction of the ventricles, allowing for efficient pumping of blood to the rest of the body.
Anti-arrhythmia agents are a class of medications used to treat abnormal heart rhythms or arrhythmias. These drugs work by modifying the electrical activity of the heart to restore and maintain a normal heart rhythm. There are several types of anti-arrhythmia agents, including:
1. Sodium channel blockers: These drugs slow down the conduction of electrical signals in the heart, which helps to reduce rapid or irregular heartbeats. Examples include flecainide, propafenone, and quinidine.
2. Beta-blockers: These medications work by blocking the effects of adrenaline on the heart, which helps to slow down the heart rate and reduce the force of heart contractions. Examples include metoprolol, atenolol, and esmolol.
3. Calcium channel blockers: These drugs block the entry of calcium into heart muscle cells, which helps to slow down the heart rate and reduce the force of heart contractions. Examples include verapamil and diltiazem.
4. Potassium channel blockers: These medications work by prolonging the duration of the heart's electrical cycle, which helps to prevent abnormal rhythms. Examples include amiodarone and sotalol.
5. Digoxin: This drug increases the force of heart contractions and slows down the heart rate, which can help to restore a normal rhythm in certain types of arrhythmias.
It's important to note that anti-arrhythmia agents can have significant side effects and should only be prescribed by a healthcare professional who has experience in managing arrhythmias. Close monitoring is necessary to ensure the medication is working effectively and not causing any adverse effects.
Heart rate is the number of heartbeats per unit of time, often expressed as beats per minute (bpm). It can vary significantly depending on factors such as age, physical fitness, emotions, and overall health status. A resting heart rate between 60-100 bpm is generally considered normal for adults, but athletes and individuals with high levels of physical fitness may have a resting heart rate below 60 bpm due to their enhanced cardiovascular efficiency. Monitoring heart rate can provide valuable insights into an individual's health status, exercise intensity, and response to various treatments or interventions.
Cardiac arrhythmias are abnormal heart rhythms that result from disturbances in the electrical conduction system of the heart. The heart's normal rhythm is controlled by an electrical signal that originates in the sinoatrial (SA) node, located in the right atrium. This signal travels through the atrioventricular (AV) node and into the ventricles, causing them to contract and pump blood throughout the body.
An arrhythmia occurs when there is a disruption in this electrical pathway or when the heart's natural pacemaker produces an abnormal rhythm. This can cause the heart to beat too fast (tachycardia), too slow (bradycardia), or irregularly.
There are several types of cardiac arrhythmias, including:
1. Atrial fibrillation: A rapid and irregular heartbeat that starts in the atria (the upper chambers of the heart).
2. Atrial flutter: A rapid but regular heartbeat that starts in the atria.
3. Supraventricular tachycardia (SVT): A rapid heartbeat that starts above the ventricles, usually in the atria or AV node.
4. Ventricular tachycardia: A rapid and potentially life-threatening heart rhythm that originates in the ventricles.
5. Ventricular fibrillation: A chaotic and disorganized electrical activity in the ventricles, which can be fatal if not treated immediately.
6. Heart block: A delay or interruption in the conduction of electrical signals from the atria to the ventricles.
Cardiac arrhythmias can cause various symptoms, such as palpitations, dizziness, shortness of breath, chest pain, and fatigue. In some cases, they may not cause any symptoms and go unnoticed. However, if left untreated, certain types of arrhythmias can lead to serious complications, including stroke, heart failure, or even sudden cardiac death.
Treatment for cardiac arrhythmias depends on the type, severity, and underlying causes. Options may include lifestyle changes, medications, cardioversion (electrical shock therapy), catheter ablation, implantable devices such as pacemakers or defibrillators, and surgery. It is essential to consult a healthcare professional for proper evaluation and management of cardiac arrhythmias.
Heart block is a cardiac condition characterized by the interruption of electrical impulse transmission from the atria (the upper chambers of the heart) to the ventricles (the lower chambers of the heart). This disruption can lead to abnormal heart rhythms, including bradycardia (a slower-than-normal heart rate), and in severe cases, can cause the heart to stop beating altogether. Heart block is typically caused by damage to the heart's electrical conduction system due to various factors such as aging, heart disease, or certain medications.
There are three types of heart block: first-degree, second-degree, and third-degree (also known as complete heart block). Each type has distinct electrocardiogram (ECG) findings and symptoms. Treatment for heart block depends on the severity of the condition and may include monitoring, medication, or implantation of a pacemaker to regulate the heart's electrical activity.
Postural Orthostatic Tachycardia Syndrome (POTS) is a condition characterized by an abnormally rapid heart rate (tachycardia) that occurs upon standing, leading to symptoms such as dizziness, lightheadedness, and fainting. The diagnostic criteria for POTS include:
1. A heart rate increase of 30 beats per minute or more within the first 10 minutes of standing or a heart rate of 120 beats per minute or more within the first 10 minutes of standing, measured by a heart rate monitor.
2. The presence of symptoms such as lightheadedness, dizziness, blurred vision, weakness, fatigue, headache, shortness of breath, or chest pain upon standing that are relieved by lying down.
3. Symptoms must be present for at least three months and occur in the absence of other medical conditions that could explain them.
POTS is thought to be caused by a dysfunction of the autonomic nervous system, which controls involuntary functions such as heart rate and blood pressure. Treatment may include lifestyle modifications, such as increasing fluid and salt intake, wearing compression stockings, and avoiding prolonged standing or sitting. Medications that help regulate blood pressure and heart rate may also be prescribed.
Body Surface Potential Mapping (BSPM) is a non-invasive medical technique used to record and analyze the electrical activity of the heart from the surface of the body. It involves placing multiple electrodes on the skin of the chest, back, and limbs to measure the potential differences between these points during each heartbeat. This information is then used to create a detailed, visual representation of the electrical activation pattern of the heart, which can help in the diagnosis and evaluation of various cardiac disorders such as arrhythmias, myocardial infarction, and ventricular hypertrophy.
The BSPM technique provides high-resolution spatial and temporal information about the cardiac electrical activity, making it a valuable tool for both clinical and research purposes. It can help identify the origin and spread of abnormal electrical signals in the heart, which is crucial for determining appropriate treatment strategies. Overall, Body Surface Potential Mapping is an important diagnostic modality that offers unique insights into the electrical functioning of the heart.
Ventricular Fibrillation (VF) is a type of cardiac arrhythmia, which is an abnormal heart rhythm. In VF, the ventricles, which are the lower chambers of the heart, beat in a rapid and unorganized manner. This results in the heart being unable to pump blood effectively to the rest of the body, leading to immediate circulatory collapse and cardiac arrest if not treated promptly. It is often caused by underlying heart conditions such as coronary artery disease, structural heart problems, or electrolyte imbalances. VF is a medical emergency that requires immediate defibrillation to restore a normal heart rhythm.
Bradycardia is a medical term that refers to an abnormally slow heart rate, typically defined as a resting heart rate of less than 60 beats per minute in adults. While some people, particularly well-trained athletes, may have a naturally low resting heart rate, bradycardia can also be a sign of an underlying health problem.
There are several potential causes of bradycardia, including:
* Damage to the heart's electrical conduction system, such as from heart disease or aging
* Certain medications, including beta blockers, calcium channel blockers, and digoxin
* Hypothyroidism (underactive thyroid gland)
* Sleep apnea
* Infection of the heart (endocarditis or myocarditis)
* Infiltrative diseases such as amyloidosis or sarcoidosis
Symptoms of bradycardia can vary depending on the severity and underlying cause. Some people with bradycardia may not experience any symptoms, while others may feel weak, fatigued, dizzy, or short of breath. In severe cases, bradycardia can lead to fainting, confusion, or even cardiac arrest.
Treatment for bradycardia depends on the underlying cause. If a medication is causing the slow heart rate, adjusting the dosage or switching to a different medication may help. In other cases, a pacemaker may be necessary to regulate the heart's rhythm. It is important to seek medical attention if you experience symptoms of bradycardia, as it can be a sign of a serious underlying condition.
An action potential is a brief electrical signal that travels along the membrane of a nerve cell (neuron) or muscle cell. It is initiated by a rapid, localized change in the permeability of the cell membrane to specific ions, such as sodium and potassium, resulting in a rapid influx of sodium ions and a subsequent efflux of potassium ions. This ion movement causes a brief reversal of the electrical potential across the membrane, which is known as depolarization. The action potential then propagates along the cell membrane as a wave, allowing the electrical signal to be transmitted over long distances within the body. Action potentials play a crucial role in the communication and functioning of the nervous system and muscle tissue.
Sinus arrhythmia is a type of heart rhythm disorder (arrhythmia) where the normal rhythm generated by the sinus node in the heart varies in rate or pattern. The sinus node is the natural pacemaker of the heart and usually sets a steady pace for heartbeats. However, in sinus arrhythmia, the heart rate may speed up or slow down abnormally during breathing in (inspiration) or breathing out (expiration).
When the heart rate increases during inspiration, it is called "inspiratory sinus arrhythmia," and when the heart rate decreases during expiration, it is called "expiratory sinus arrhythmia." Most people experience a mild form of inspiratory sinus arrhythmia, which is considered normal, especially in children and young adults.
However, if the variation in heart rate is significant or accompanied by symptoms such as palpitations, dizziness, shortness of breath, or chest discomfort, it may require medical evaluation and treatment. Sinus arrhythmia can be caused by various factors, including lung disease, heart disease, electrolyte imbalances, or the use of certain medications.
Electrophysiology is a branch of medicine that deals with the electrical activities of the body, particularly the heart. In a medical context, electrophysiology studies (EPS) are performed to assess abnormal heart rhythms (arrhythmias) and to evaluate the effectiveness of certain treatments, such as medication or pacemakers.
During an EPS, electrode catheters are inserted into the heart through blood vessels in the groin or neck. These catheters can record the electrical activity of the heart and stimulate it to help identify the source of the arrhythmia. The information gathered during the study can help doctors determine the best course of treatment for each patient.
In addition to cardiac electrophysiology, there are also other subspecialties within electrophysiology, such as neuromuscular electrophysiology, which deals with the electrical activity of the nervous system and muscles.
Digitalis glycosides are a type of cardiac glycoside that are derived from the foxglove plant (Digitalis purpurea) and related species. These compounds have a steroidal structure with a lactone ring attached to the molecule, which is responsible for their positive inotropic effects on the heart.
The two main digitalis glycosides used clinically are digoxin and digitoxin. They work by inhibiting the sodium-potassium pump in cardiac muscle cells, leading to an increase in intracellular calcium levels and a subsequent enhancement of myocardial contractility. This makes them useful in the treatment of heart failure and atrial arrhythmias such as atrial fibrillation.
However, digitalis glycosides have a narrow therapeutic index, meaning that there is only a small difference between their therapeutic and toxic doses. Therefore, they must be administered with caution and patients should be closely monitored for signs of toxicity such as nausea, vomiting, visual disturbances, and cardiac arrhythmias.
Cardiac glycosides are a group of naturally occurring compounds that have a toxic effect on the heart. They are found in certain plants, including foxglove and lily of the valley, as well as in some toads and beetles. The most well-known cardiac glycoside is digoxin, which is derived from the foxglove plant and is used as a medication to treat heart failure and atrial arrhythmias.
Cardiac glycosides work by inhibiting the sodium-potassium pump in heart muscle cells, leading to an increase in intracellular calcium levels. This increases the force of heart contractions, which can be beneficial in treating heart failure. However, if the dose is too high, cardiac glycosides can also cause dangerous arrhythmias and even death.
It's important for healthcare professionals to carefully monitor patients taking cardiac glycosides, as the therapeutic and toxic doses are very close together. Additionally, certain medications and medical conditions can interact with cardiac glycosides and increase the risk of toxicity.
Digoxin is a medication that belongs to a class of drugs called cardiac glycosides. It is used to treat various heart conditions, such as heart failure and atrial fibrillation, by helping the heart beat stronger and more regularly. Digoxin works by inhibiting the sodium-potassium pump in heart muscle cells, which leads to an increase in intracellular calcium and a strengthening of heart contractions. It is important to monitor digoxin levels closely, as too much can lead to toxicity and serious side effects.
'Digitalis' is a medication that is derived from the foxglove plant (Digitalis purpurea). It contains cardiac glycosides, primarily digoxin and digitoxin, which have positive inotropic effects on the heart muscle, increasing its contractility. Digitalis is primarily used to treat various types of heart failure and atrial arrhythmias. It works by inhibiting the sodium-potassium pump in heart muscle cells, leading to an increase in intracellular calcium and enhanced cardiac muscle contraction.
It's important to note that digitalis has a narrow therapeutic index, meaning that the difference between a therapeutic and toxic dose is small. Therefore, it requires careful monitoring of serum drug levels and clinical response to ensure safe and effective use. Common side effects include gastrointestinal symptoms such as nausea, vomiting, and diarrhea, as well as visual disturbances and cardiac arrhythmias.
Digitoxin is a cardiac glycoside drug that is derived from the foxglove plant (Digitalis lanata). It is used in the treatment of various heart conditions, particularly congestive heart failure and certain types of arrhythmias. Digitoxin works by increasing the force of heart muscle contractions and slowing the heart rate, which helps to improve the efficiency of the heart's pumping action.
Like other cardiac glycosides, digitoxin inhibits the sodium-potassium pump in heart muscle cells, leading to an increase in intracellular calcium levels and a strengthening of heart muscle contractions. However, digitoxin has a longer half-life than other cardiac glycosides such as digoxin, which means that it stays in the body for a longer period of time and may require less frequent dosing.
Digitoxin is available in tablet form and is typically prescribed at a low dose, with regular monitoring of blood levels to ensure safe and effective use. Common side effects of digitoxin include nausea, vomiting, diarrhea, and dizziness. In rare cases, it can cause more serious side effects such as arrhythmias or toxicity, which may require hospitalization and treatment with medications or other interventions.
Glycosides are organic compounds that consist of a glycone (a sugar component) linked to a non-sugar component, known as an aglycone, via a glycosidic bond. They can be found in various plants, microorganisms, and some animals. Depending on the nature of the aglycone, glycosides can be classified into different types, such as anthraquinone glycosides, cardiac glycosides, and saponin glycosides.
These compounds have diverse biological activities and pharmacological effects. For instance:
* Cardiac glycosides, like digoxin and digitoxin, are used in the treatment of heart failure and certain cardiac arrhythmias due to their positive inotropic (contractility-enhancing) and negative chronotropic (heart rate-slowing) effects on the heart.
* Saponin glycosides have potent detergent properties and can cause hemolysis (rupture of red blood cells). They are used in various industries, including cosmetics and food processing, and have potential applications in drug delivery systems.
* Some glycosides, like amygdalin found in apricot kernels and bitter almonds, can release cyanide upon hydrolysis, making them potentially toxic.
It is important to note that while some glycosides have therapeutic uses, others can be harmful or even lethal if ingested or otherwise introduced into the body in large quantities.
Cardenolides are a type of steroid compound that are found in certain plants and animals. These compounds have a characteristic structure that includes a five-membered lactone ring, which is attached to a steroid nucleus. Cardenolides are well known for their toxicity to many organisms, including humans, and they have been used for both medicinal and poisonous purposes.
One of the most famous cardenolides is digitoxin, which is derived from the foxglove plant (Digitalis purpurea). Digitoxin has been used as a medication to treat heart conditions such as congestive heart failure, as it can help to strengthen heart contractions and regulate heart rhythm. However, because of its narrow therapeutic index and potential for toxicity, digitoxin is not commonly used today.
Other cardenolides include ouabain, which is found in the seeds of the African plant Acokanthera ouabaio, and bufadienolides, which are found in the skin and parotid glands of toads. These compounds have also been studied for their potential medicinal uses, but they are not widely used in clinical practice due to their toxicity.
It is important to note that cardenolides can be highly toxic to humans and animals, and exposure to these compounds can cause a range of symptoms including nausea, vomiting, diarrhea, seizures, and even death. As such, it is essential to use caution when handling or coming into contact with plants or animals that contain cardenolides.