A class in the phylum CNIDARIA, comprised mostly of corals and anemones. All members occur only as polyps; the medusa stage is completely absent.
Former state in north central Germany. Formally abolished March 1, 1947. Kingdom established 1701.
A progressive, degenerative neurologic disease characterized by a TREMOR that is maximal at rest, retropulsion (i.e. a tendency to fall backwards), rigidity, stooped posture, slowness of voluntary movements, and a masklike facial expression. Pathologic features include loss of melanin containing neurons in the substantia nigra and other pigmented nuclei of the brainstem. LEWY BODIES are present in the substantia nigra and locus coeruleus but may also be found in a related condition (LEWY BODY DISEASE, DIFFUSE) characterized by dementia in combination with varying degrees of parkinsonism. (Adams et al., Principles of Neurology, 6th ed, p1059, pp1067-75)
A characteristic symptom complex.
A synuclein that is a major component of LEWY BODIES that plays a role in neurodegeneration and neuroprotection.
A chromosome disorder associated either with an extra chromosome 21 or an effective trisomy for chromosome 21. Clinical manifestations include hypotonia, short stature, brachycephaly, upslanting palpebral fissures, epicanthus, Brushfield spots on the iris, protruding tongue, small ears, short, broad hands, fifth finger clinodactyly, Simian crease, and moderate to severe INTELLECTUAL DISABILITY. Cardiac and gastrointestinal malformations, a marked increase in the incidence of LEUKEMIA, and the early onset of ALZHEIMER DISEASE are also associated with this condition. Pathologic features include the development of NEUROFIBRILLARY TANGLES in neurons and the deposition of AMYLOID BETA-PROTEIN, similar to the pathology of ALZHEIMER DISEASE. (Menkes, Textbook of Child Neurology, 5th ed, p213)
A cluster of metabolic risk factors for CARDIOVASCULAR DISEASES and TYPE 2 DIABETES MELLITUS. The major components of metabolic syndrome X include excess ABDOMINAL FAT; atherogenic DYSLIPIDEMIA; HYPERTENSION; HYPERGLYCEMIA; INSULIN RESISTANCE; a proinflammatory state; and a prothrombotic (THROMBOSIS) state. (from AHA/NHLBI/ADA Conference Proceedings, Circulation 2004; 109:551-556)
An alkaloid found in the root of RAUWOLFIA SERPENTINA, among other plant sources. It is a class Ia antiarrhythmic agent that apparently acts by changing the shape and threshold of cardiac action potentials.
An autosomal dominant defect of cardiac conduction that is characterized by an abnormal ST-segment in leads V1-V3 on the ELECTROCARDIOGRAM resembling a right BUNDLE-BRANCH BLOCK; high risk of VENTRICULAR TACHYCARDIA; or VENTRICULAR FIBRILLATION; SYNCOPAL EPISODE; and possible sudden death. This syndrome is linked to mutations of gene encoding the cardiac SODIUM CHANNEL alpha subunit.
Recording of the moment-to-moment electromotive forces of the HEART as projected onto various sites on the body's surface, delineated as a scalar function of time. The recording is monitored by a tracing on slow moving chart paper or by observing it on a cardioscope, which is a CATHODE RAY TUBE DISPLAY.
Persistent and disabling ANXIETY.
Formed by the articulation of the talus with the calcaneus.
A form of heart block in which the electrical stimulation of HEART VENTRICLES is interrupted at either one of the branches of BUNDLE OF HIS thus preventing the simultaneous depolarization of the two ventricles.
Any disturbances of the normal rhythmic beating of the heart or MYOCARDIAL CONTRACTION. Cardiac arrhythmias can be classified by the abnormalities in HEART RATE, disorders of electrical impulse generation, or impulse conduction.

AV reentrant and idiopathic ventricular double tachycardias: complicated interactions between two tachycardias. (1/292)

An electrophysiological study was performed in a 61 year old man with Wolff- Parkinson-White (WPW) syndrome. At baseline, neither ventricular nor supraventricular tachycardias could be induced. During isoprenaline infusion, ventricular tachycardia originating from the right ventricular outflow tract (RVOT) with a cycle length of 280 ms was induced and subsequently atrioventricular reentrant tachycardia (AVRT) with a cycle length of 300 ms using an accessory pathway in the left free wall appeared. During these tachycardias, AVRT was entrained by ventricular tachycardia. The earliest ventricular activation site during the ventricular tachycardia was determined to be the RVOT site and a radiofrequency current at 30 W successfully ablated the ventricular tachycardia at this site. The left free wall accessory pathway was also successfully ablated during right ventricular pacing. The coexistence of WPW syndrome and cathecolamine sensitive ventricular tachycardia originating from the RVOT has rarely been reported. Furthermore, the tachycardias were triggered by previous tachycardias.  (+info)

Ventricular excitation maps using tissue Doppler acceleration imaging: potential clinical application. (2/292)

OBJECTIVES: The purpose of this study is to validate the use of tissue Doppler acceleration imaging (TDAI) for evaluation of the onset of ventricular contraction in humans. BACKGROUND: Tissue Doppler acceleration imaging can display the distribution, direction and value of ventricular acceleration responses to myocardial contraction and electrical excitation. METHODS: Twenty normal volunteers underwent TDAI testing to determine the normal onset of ventricular acceleration. Two patients with paroxysmal supraventricular tachycardia and 30 patients with permanent pacemakers underwent introduction of esophageal and right ventricular pacing electrodes, respectively, and were studied to visualize the onset of pacer-induced ventricular acceleration. Eight patients with dual atrioventricular (AV) node and 20 patients with Wolff-Parkinson-White (WPW) syndrome underwent TDAI testing to localize the abnormal onset of ventricular acceleration, and the results were compared with those of intracardiac electrophysiology (ICEP) tests. RESULTS: The normal onset and the onset of dual AV node were localized at the upper interventricular septum (IVS) under the right coronary cusp within 25 ms before the beginning of the R wave in the electrocardiogram (ECG). In all patients in the pacing group, the location and timing of the onset conformed to the positions and timing of electrodes (100%). In patients with WPW syndrome, abnormal onset was localized to portions of the ventricular wall other than the upper IVS at the delta wave or within 25 ms after the delta wave in the ECG. The agreement was 90% (18 of 20) between the abnormal onset and the position of the accessory pathways determined by ICEP testing. CONCLUSIONS: These results suggest that TDAI is a useful noninvasive method that frequently is successful in visualizing the intramural site of origin of ventricular mechanical contraction.  (+info)

Effect of intravenous amiodarone on electrophysiologic variables and on the modes of termination of atrioventricular reciprocating tachycardia in Wolff-Parkinson-White syndrome. (3/292)

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)

Importance of retrograde atrial activation in atrial fibrillation genesis in the initiation of atrial fibrillation in Wolff-Parkinson-White syndrome. Comparison of atrial electrophysiologic parameters between patients with different atrial fibrillation genesis (initiation sites) in atria. (4/292)

The changes in the duration of atrial electrograms during different atrial activation sequences from a sinus rhythm were evaluated to test the hypothesis that the prolongation of atrial electrogram duration caused by the different atrial activation sequence is more prominent at the site of atrial fibrillation (Afib) genesis (initiation site) than other areas. In 39 patients with single retrograde left-sided accessory connection who had inducible transient atrial fibrillation during an electrophysiologic study, the site of Afib genesis was determined and classified into three groups, i.e., 1) high right atrial genesis (HRA), 2) low right atrial genesis (LRA), and 3) left atrial genesis (LA). Single premature extrastimuli after 8 basic drive trains (600 ms) were delivered at the HRA and the right ventricular apex. Three atrial electrophysiologic parameters were evaluated at three atrial sites, i.e., 1) HRA, 2) LRA, and 3) coronary sinus. The atrial vulnerability parameters were as follows; 1) %A2/A1: % prolongation of atrial electrogram duration during premature beat (A2) in comparison with basic drive (A1), 2) wavelength index (WLI): calculated as [effective refractory period]/[A2], and 3) retrograde activation index (RAI): calculated as [A1 during retrograde activation; i.e., RVA pacing/[A1 during antegrade activation, i.e., HRA pacing], shown as a percentage. The Afib genesis was HRA in 20, LRA in 12 and LA in 7 patients. At the HRA recording site, %A2/A1 and RAI were the largest and WLI the shortest in the HRA genesis group in comparison with the other two groups. Similarly, at the LRA and LA recording sites, %A2/A1 and RAI were the largest and WLI the shortest in the groups with Afib genesis at these recording sites. In patients with inducible Afib, %A2/A1 and RAI were the highest and WLI the shortest at the atrial recording site close to the site of Afib genesis. Atrial wave prolongation during retrograde atrial activation, possibly the anisotropic conduction, was considered to play a role in initiating Afib as well as a conduction delay during the atrial premature beat.  (+info)

Decreased amplitude of left ventricular posterior wall motion with notch movement to determine the left posterior septal accessory pathway in Wolff-Parkinson-White syndrome. (5/292)

OBJECTIVE: To determine preoperatively, by analysing asynchronous left ventricular wall motion, whether to approach through the right ventricle or the left ventricle when carrying out catheter ablation of the accessory pathway in Wolff-Parkinson-White syndrome, especially in patients with the pathway located on the septum. METHODS: 73 patients with manifest Wolff-Parkinson-White syndrome who underwent successful catheter ablation were studied. Location of accessory pathway was classified as right ventricular side: right anterior paraseptum, right anterior, right lateral, right posterior, anterior septum, midseptum, right posterior septum; left ventricular side: left posterior septum, left posterior, left lateral, left anterior. Asynchronous systolic wall motion was analysed by cross sectional echocardiography. RESULTS: Echocardiography showed that the amplitude of left ventricular posterior systolic wall motion was reduced when the pathway was located on the left ventricular side as opposed to the right ventricular side (mean (SD), 11.1 (1.7) v 12.9 (1.1) mm, p < 0.001), especially in patients with left posterior septal accessory pathway (9.7 (0.8) mm). There were no overlapping values between the left posterior septal accessory pathway and the right ventricular side accessory pathway. Posterior wall notch motion was observed in all patients with a left posterior septal accessory pathway (9/9), but not at all in patients with pathways located on the right ventricular side of the septum. In patients with a septal accessory pathway, an ECG algorithm provided poor information (relatively low sensitivity, specificity, and predictive value) for determining whether the subsite faced either the left (left posterior septum) or the right ventricle (anterior septum, midseptum, right posterior septum). CONCLUSIONS: Decreased amplitude of left ventricular posterior wall motion with notch movement is an important finding for accessory pathways located on the left posterior septum. These findings provided clinically useful information for determining whether to approach catheter ablation from the right or the left ventricle.  (+info)

Gated blood-pool SPECT evaluation of changes after radiofrequency catheter ablation of accessory pathways: evidence for persistent ventricular preexcitation despite successful therapy. (6/292)

OBJECTIVES: This study was designed to prospectively evaluate the effects of radiofrequency ablation in Wolff-Parkinson-White (WPW) syndrome by scintigraphic analysis. BACKGROUND: The functional changes triggered by radiofrequency current ablation of atrioventricular accessory pathways are not fully known. METHODS: Forty-four patients with WPW syndrome were consecutively investigated before and 48 h after radiofrequency therapy. Fourteen patients had right sided atrioventricular pathways and 30 patients had left sided bypass-tracts. Planar gated imaging and gated blood pool tomography were performed in all of these patients. RESULTS: A significant increase in the left ventricular ejection fraction (LVEF) was demonstrated in patients with left preexcitation (62.2+/-7.9% before ablation against 64.4+/-6.3% after ablation, p = 0.02) but not for those with right sided anomalous pathway. Phase analysis only gave significant differences following ablation of right sided pathways (left-to-right phase difference = 14.4+/-13.8 degrees before ablation versus 7.5+/-7.2 degrees after ablation, p<0.05). Early abnormal ventricular contraction persisted in 12 patients with right accessory pathways and in 8 patients with left accessory pathways despite the complete disappearance of any abnormal conduction as proven electrophysiologically. CONCLUSIONS: Following catheter ablation of atrioventricular accessory pathways: 1) an improvement of left ventricular function may be seen, particularly in patients with left sided accessory pathways, and 2) unexpected persistence of local ventricular preexcitation at the site of successful ablation may be detected.  (+info)

Prediction of accessory pathway locations in Wolff-Parkinson-White syndrome with body surface potential Laplacian maps . A simulation study. (7/292)

An electrocardiographic computer simulation was conducted to study the feasibility of predicting accessory pathway locations in Wolff-Parkinson-White (WPW) syndrome with body surface potential Laplacian maps. Three-dimensional, realistically-shaped heart and torso models were used. Ten accessory pathways (APs) around the atrioventricular ring corresponding to Gallagher et al. were set in the heart model, and body surface Lapacian and potential maps of WPW syndrome with single or multiple APs were simulated and compared to each other. In simulations with a single AP in the anterior walls, the maximum-minimum pairs in Laplacian maps appeared to be similar to those in potential maps with respect to their locations and orientations, but the maximum-minimum pairs in Laplacian maps were sharper and more localized than in potential maps. In simulations with a posterior AP or multiple APs, the maximum-minimum pairs in the Laplacian maps showed features correlative to the AP locations, but no such features were found in potential maps. These results suggest the possibility of using Laplacian maps, as a non-invasive method for predicting accessory pathways locations in WPW syndrome.  (+info)

A wide "gap" in retrograde conduction through a concealed accessory atrioventricular pathway depending on ventricular pacing sites. (8/292)

We present a 57-year-old man with Wolff-Parkinson-White syndrome who exhibited a wide "gap" in retrograde conduction through a concealed atrioventricular accessory pathway. The appearance of the wide "gap" depended on the ventricular pacing sites. While ventricular extrastimuli at a basic cycle length of 600 msec from the right ventricular outflow tract consistently conducted to the atria, retrogradely through the accessory pathway, those from the right ventricular apex repeatedly revealed disappearance of the retrograde conduction at the wide coupling intervals from 550 to 380 msec. The mechanisms of this rare "gap"-like phenomenon are discussed in this paper.  (+info)

Anthozoa is a major class of marine animals, which are exclusively aquatic and almost entirely restricted to shallow waters. They are classified within the phylum Cnidaria, which also includes corals, jellyfish, sea anemones, and hydroids. Anthozoans are characterized by their lack of medusa stage in their life cycle, as they exist solely as polyps.

This class is divided into two main subclasses: Hexacorallia (also known as Zoantharia) and Octocorallia (also known as Alcyonaria). The primary differences between these subclasses lie in the structure of their polyps and the composition of their skeletons.

1. Hexacorallia: These are commonly referred to as 'stony' or 'hard' corals, due to their calcium carbonate-based skeletons. They have a simple polyp structure with six-fold symmetry (hence the name Hexacorallia), featuring 6 tentacles around the mouth opening. Examples of Hexacorallia include reef-building corals, sea fans, and black corals.
2. Octocorallia: These are also called 'soft' corals or 'leather' corals because they lack a calcium carbonate skeleton. Instead, their supporting structures consist of proteins and other organic compounds. Octocorallia polyps exhibit eight-fold symmetry (hence the name Octocorallia), with eight tentacles around the mouth opening. Examples of Octocorallia include sea fans, sea whips, and blue corals.

Anthozoa species are primarily found in tropical and subtropical oceans, but some can be found in colder, deeper waters as well. They play a crucial role in marine ecosystems by providing habitats and shelter for various other marine organisms, particularly on coral reefs. Additionally, they contribute to the formation of limestone deposits through their calcium carbonate-based skeletons.

I'm sorry for any confusion, but there seems to be a misunderstanding. "Prussia" is not a medical term or concept. It was a historic state in northern Europe, which existed from the late medieval period until the early 20th century. At its height, Prussia was a major power and included parts of what are now Germany, Poland, Russia, Denmark, Belgium, Czech Republic, and Lithuania.

If you have any medical questions or terms you'd like defined, I'd be happy to help!

Parkinson's disease is a progressive neurodegenerative disorder that affects movement. It is characterized by the death of dopamine-producing cells in the brain, specifically in an area called the substantia nigra. The loss of these cells leads to a decrease in dopamine levels, which results in the motor symptoms associated with Parkinson's disease. These symptoms can include tremors at rest, stiffness or rigidity of the limbs and trunk, bradykinesia (slowness of movement), and postural instability (impaired balance and coordination). In addition to these motor symptoms, non-motor symptoms such as cognitive impairment, depression, anxiety, and sleep disturbances are also common in people with Parkinson's disease. The exact cause of Parkinson's disease is unknown, but it is thought to be a combination of genetic and environmental factors. There is currently no cure for Parkinson's disease, but medications and therapies can help manage the symptoms and improve quality of life.

A syndrome, in medical terms, is a set of symptoms that collectively indicate or characterize a disease, disorder, or underlying pathological process. It's essentially a collection of signs and/or symptoms that frequently occur together and can suggest a particular cause or condition, even though the exact physiological mechanisms might not be fully understood.

For example, Down syndrome is characterized by specific physical features, cognitive delays, and other developmental issues resulting from an extra copy of chromosome 21. Similarly, metabolic syndromes like diabetes mellitus type 2 involve a group of risk factors such as obesity, high blood pressure, high blood sugar, and abnormal cholesterol or triglyceride levels that collectively increase the risk of heart disease, stroke, and diabetes.

It's important to note that a syndrome is not a specific diagnosis; rather, it's a pattern of symptoms that can help guide further diagnostic evaluation and management.

Alpha-synuclein is a protein that is primarily found in neurons (nerve cells) in the brain. It is encoded by the SNCA gene and is abundantly expressed in presynaptic terminals, where it is believed to play a role in the regulation of neurotransmitter release.

In certain neurological disorders, including Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy, alpha-synuclein can form aggregates known as Lewy bodies and Lewy neurites. These aggregates are a pathological hallmark of these diseases and are believed to contribute to the death of nerve cells, leading to the symptoms associated with these disorders.

The precise function of alpha-synuclein is not fully understood, but it is thought to be involved in various cellular processes such as maintaining the structure of the presynaptic terminal, regulating synaptic vesicle trafficking and neurotransmitter release, and protecting neurons from stress.

Down syndrome is a genetic disorder caused by the presence of all or part of a third copy of chromosome 21. It is characterized by intellectual and developmental disabilities, distinctive facial features, and sometimes physical growth delays and health problems. The condition affects approximately one in every 700 babies born in the United States.

Individuals with Down syndrome have varying degrees of cognitive impairment, ranging from mild to moderate or severe. They may also have delayed development, including late walking and talking, and may require additional support and education services throughout their lives.

People with Down syndrome are at increased risk for certain health conditions, such as congenital heart defects, respiratory infections, hearing loss, vision problems, gastrointestinal issues, and thyroid disorders. However, many individuals with Down syndrome live healthy and fulfilling lives with appropriate medical care and support.

The condition is named after John Langdon Down, an English physician who first described the syndrome in 1866.

Metabolic syndrome, also known as Syndrome X, is a cluster of conditions that increase the risk of heart disease, stroke, and diabetes. It is not a single disease but a group of risk factors that often co-occur. According to the American Heart Association and the National Heart, Lung, and Blood Institute, a person has metabolic syndrome if they have any three of the following five conditions:

1. Abdominal obesity (waist circumference of 40 inches or more in men, and 35 inches or more in women)
2. Triglyceride level of 150 milligrams per deciliter of blood (mg/dL) or greater
3. HDL cholesterol level of less than 40 mg/dL in men or less than 50 mg/dL in women
4. Systolic blood pressure of 130 millimeters of mercury (mmHg) or greater, or diastolic blood pressure of 85 mmHg or greater
5. Fasting glucose level of 100 mg/dL or greater

Metabolic syndrome is thought to be caused by a combination of genetic and lifestyle factors, such as physical inactivity and a diet high in refined carbohydrates and unhealthy fats. Treatment typically involves making lifestyle changes, such as eating a healthy diet, getting regular exercise, and losing weight if necessary. In some cases, medication may also be needed to manage individual components of the syndrome, such as high blood pressure or high cholesterol.

Ajmaline is a type of medication known as a Class I antiarrhythmic agent, which is used to treat certain types of abnormal heart rhythms. It works by blocking the sodium channels in the heart muscle, which helps to slow down the conduction of electrical signals within the heart and can help to restore a normal heart rhythm.

Ajmaline is typically administered intravenously (through a vein) in a hospital setting, as it acts quickly and its effects can be closely monitored by healthcare professionals. It may be used to diagnose certain types of heart rhythm disturbances or to treat acute episodes of arrhythmias that are not responding to other treatments.

Like all medications, ajmaline can have side effects, including dizziness, headache, nausea, and chest pain. It is important for patients to be closely monitored while taking this medication and to report any unusual symptoms to their healthcare provider. Ajmaline should only be used under the close supervision of a qualified healthcare professional.

Brugada Syndrome is a genetic disorder characterized by abnormal electrocardiogram (ECG) findings and an increased risk of sudden cardiac death. It is typically caused by a mutation in the SCN5A gene, which encodes for a sodium channel protein in the heart. This mutation can lead to abnormal ion transport in the heart cells, causing changes in the electrical activity of the heart that can trigger dangerous arrhythmias.

The ECG findings associated with Brugada Syndrome include a distinct pattern of ST-segment elevation in the right precordial leads (V1-V3), which can appear spontaneously or be induced by certain medications. The syndrome is often classified into two types based on the presence or absence of symptoms:

* Type 1 Brugada Syndrome: This type is characterized by a coved-type ST-segment elevation of at least 2 mm in height in at least one right precordial lead, with a negative T wave. This pattern must be present to make the diagnosis, and it should not be transient or induced by any medication or condition. Type 1 Brugada Syndrome is associated with a higher risk of sudden cardiac death.
* Type 2 Brugada Syndrome: This type is characterized by a saddleback-type ST-segment elevation of at least 2 mm in height in at least one right precordial lead, with a positive or biphasic T wave. The ST segment should return to the baseline level or below within 0.08 seconds after the J point (the junction between the QRS complex and the ST segment). Type 2 Brugada Syndrome is associated with a lower risk of sudden cardiac death compared to Type 1, but it can still pose a significant risk in some individuals.

Brugada Syndrome can affect people of any age, gender, or ethnicity, although it is more commonly diagnosed in middle-aged men of Asian descent. The syndrome can be inherited in an autosomal dominant manner, meaning that a child has a 50% chance of inheriting the mutation from a parent who carries the gene. However, not all individuals with the genetic mutation will develop symptoms or have abnormal ECG findings.

Treatment for Brugada Syndrome typically involves implanting a cardioverter-defibrillator (ICD) to prevent sudden cardiac death. Medications such as quinidine or isoproterenol may also be used to reduce the risk of arrhythmias. Lifestyle modifications, such as avoiding alcohol and certain medications that can trigger arrhythmias, may also be recommended.

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.

Anxiety disorders are a category of mental health disorders characterized by feelings of excessive and persistent worry, fear, or anxiety that interfere with daily activities. They include several different types of disorders, such as:

1. Generalized Anxiety Disorder (GAD): This is characterized by chronic and exaggerated worry and tension, even when there is little or nothing to provoke it.
2. Panic Disorder: This is characterized by recurring unexpected panic attacks and fear of experiencing more panic attacks.
3. Social Anxiety Disorder (SAD): Also known as social phobia, this is characterized by excessive fear, anxiety, or avoidance of social situations due to feelings of embarrassment, self-consciousness, and concern about being judged or viewed negatively by others.
4. Phobias: These are intense, irrational fears of certain objects, places, or situations. When a person with a phobia encounters the object or situation they fear, they may experience panic attacks or other severe anxiety responses.
5. Agoraphobia: This is a fear of being in places where it may be difficult to escape or get help if one has a panic attack or other embarrassing or incapacitating symptoms.
6. Separation Anxiety Disorder (SAD): This is characterized by excessive anxiety about separation from home or from people to whom the individual has a strong emotional attachment (such as a parent, sibling, or partner).
7. Selective Mutism: This is a disorder where a child becomes mute in certain situations, such as at school, but can speak normally at home or with close family members.

These disorders are treatable with a combination of medication and psychotherapy (cognitive-behavioral therapy, exposure therapy). It's important to seek professional help if you suspect that you or someone you know may have an anxiety disorder.

The subtalar joint is a joint in the foot that is located between the talus and calcaneus (heel) bones. It is called a "joint" because it allows for movement, specifically inversion and eversion, which are the movements that allow the foot to roll inward or outward. The subtalar joint plays an essential role in the biomechanics of the foot and ankle, helping to absorb shock during walking and running, and contributing to the stability of the foot during standing and walking. Issues with the subtalar joint can lead to various foot and ankle problems, such as flatfoot or chronic ankle instability.

Bundle-branch block (BBB) is a type of conduction delay or block in the heart's electrical system that affects the way electrical impulses travel through the ventricles (the lower chambers of the heart). In BBB, one of the two main bundle branches that conduct electrical impulses to the ventricles is partially or completely blocked, causing a delay in the contraction of one of the ventricles.

There are two types of bundle-branch block: right bundle-branch block (RBBB) and left bundle-branch block (LBBB). In RBBB, the right bundle branch is affected, while in LBBB, the left bundle branch is affected. The symptoms and severity of BBB can vary depending on the underlying cause and the presence of other heart conditions.

In some cases, BBB may not cause any noticeable symptoms and may only be detected during a routine electrocardiogram (ECG). However, if BBB occurs along with other heart conditions such as coronary artery disease, heart failure, or cardiomyopathy, it can increase the risk of serious complications such as arrhythmias, syncope, and even sudden cardiac death.

Treatment for bundle-branch block depends on the underlying cause and the severity of the condition. In some cases, no treatment may be necessary, while in others, medications, pacemakers, or other treatments may be recommended to manage symptoms and prevent complications.

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.

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