Pulmonary Veins
Catheter Ablation
Atrial Fibrillation
Pulmonary Veno-Occlusive Disease
Electrophysiologic Techniques, Cardiac
Heart Conduction System
Body Surface Potential Mapping
Tachycardia, Ectopic Atrial
Femoral Vein
Cardiac Catheters
Jugular Veins
Treatment Outcome
Vena Cava, Superior
Phlebography
Mesenteric Veins
Scimitar Syndrome
Constriction, Pathologic
Umbilical Veins
Iliac Vein
Atrial Septum
Anti-Arrhythmia Agents
Surgery, Computer-Assisted
Electrocardiography
Autonomic Denervation
Atrial Premature Complexes
Dogs
Imaging, Three-Dimensional
Popliteal Vein
Follow-Up Studies
Breath Holding
Echocardiography, Transesophageal
Atrial Flutter
Electrocardiography, Ambulatory
Cardiac Pacing, Artificial
Azygos Vein
Electrophysiological Phenomena
Cardiac Complexes, Premature
Catheterization
Subclavian Vein
Pulmonary Artery
Splenic Vein
Tomography, X-Ray Computed
Sinoatrial Node
Tachycardia
Heart Septal Defects, Atrial
Coronary Sinus
Tomography, Spiral Computed
Refractory Period, Electrophysiological
Magnetic Resonance Angiography
Retinal Vein
Pulmonary Atresia
Brachiocephalic Veins
Respiratory-Gated Imaging Techniques
Ganglia, Autonomic
Prospective Studies
Multidetector Computed Tomography
Feasibility Studies
Pericardium
Axillary Vein
Vascular Malformations
Transcatheter occlusion of a post-Fontan residual hepatic vein to pulmonary venous atrium communication using the Amplatzer septal occluder. (1/1323)
A residual hepatic vein to left atrial communication may result in progressive cyanosis after the Fontan procedure. This problem has usually been treated surgically by ligation or re-inclusion of the residual hepatic vein in the Fontan circulation. Previous attempts at transcatheter closure of such veins have been unsuccessful. An Amplatzer septal occluder was successfully used for transcatheter closure of a post-Fontan hepatic vein to pulmonary venous atrium fistula in an 8 year old boy. (+info)Effects of respiratory cycle on pulmonary venous flow and cardiac cycle on pulmonary venous diameter of dogs: a transesophageal echocardiography study. (2/1323)
We investigated 12 anesthetized normal dogs using transesophageal echocardiography to understand the effects of respiration on the pulmonary venous flow. Additionally, we observed whether the diameter of the pulmonary vein changes with the heart beat. The pulsed Doppler wave form of pulmonary venous flow predominantly demonstrated two backward flows, with one peak occurring during ventricular systole and another during ventricular diastole. Sometimes a small forward flow occurred during left atrial contraction. In comparison with expiration, the peak velocity and velocity-time integral of the flow wave under inspiration occurred during both systole and diastole were significantly smaller. The diameter of the pulmonary vein decreased during left atrial contraction and increased during left ventricular systole and diastole. (+info)Site of functional bronchopulmonary anastomoses in sheep. (3/1323)
The location of bronchopulmonary anastomoses has long been a topic of discussion, and pre-, post-, and capillary sites have all been demonstrated in postmortem examinations. However, there have been few studies that have provided insight into the patency and function of these anastomoses in the intact lung. To identify these functional sites where the bronchial circulation anastomoses with the pulmonary circulation, we studied sheep lungs in situ serial sectioned with high-resolution computed tomography (CT). Differences in radiodensities of blood, air, and nonionic contrast medium were used to differentiate and localize airways and vessels and to identify the effluent from the bronchial circulation. After an initial series of scans to identify the pulmonary arteries and veins adjacent to airways 2-12 mm in diameter, contrast material was infused into the bronchial artery. In three sheep, the major accumulation of contrast medium was found in pulmonary veins. In one of the sheep, a comparable number of pulmonary arteries and veins contained contrast medium. Serial histologic sections were able to identify small bronchial venules lying within subepithelial bronchial folds that drain directly into pulmonary veins. These results using serial CT and histologic images suggest that drainage from the intraparenchymal bronchial vasculature is predominantly into postcapillary pulmonary vessels. (+info)Pulmonary venous flow in hypertrophic cardiomyopathy as assessed by the transoesophageal approach. The additive value of pulmonary venous flow and left atrial size variables in estimating the mitral inflow pattern in hypertrophic cardiomyopathy. (4/1323)
AIMS: This study was conducted to assess the characteristics of the pattern of pulmonary venous flow and to document the interaction of this flow and left atrial function with the pattern of mitral inflow in hypertrophic cardiomyopathy. METHODS AND RESULTS: Pulmonary venous and mitral flows were evaluated by the transoesophageal approach in 80 patients with hypertrophic cardiomyopathy. Left atrial size and function were measured by the transthoracic approach. Their values were compared with those obtained from 35 normal controls. Twelve patients showed significant (> 2+) mitral regurgitation. As a group, hypertrophic cardiomyopathy patients showed increased atrial reversal flow and longer deceleration time of the diastolic wave, but a wide variability of pulmonary venous flow patterns were observed. Thirty patients (37.5%) had pseudonormal mitral flow patterns. Stepwise multilinear regression analysis identified the ratio of systolic to diastolic pulmonary venous flow velocity, the ratio of velocity-time integrals of both flow waves at atrial contraction, the left atrial minimal volume and the systolic fraction as independent predictive variables of the mitral E/A wave velocity ratio (r = 0.82). By logistic regression, the former three variables were selected as independent predictive covariates of a pseudonormal mitral flow pattern (sensitivity: 83%, specificity: 90%). The ratio of velocity-time integrals of both atrial waves was the most important predictive variable in both analyses. CONCLUSIONS: The observed variability in the configuration of pulmonary venous flow velocity waveform is related to what occurs in transmitral flow in patients with hypertrophic cardiomyopathy. Significant mitral regurgitation is not an independent correlate of pseudonormal mitral inflow patterns in these patients. Our results further emphasize the complementary, additive value of the pulmonary venous flow velocity pattern and left atrial size in the interpretation of the mitral flow velocity pattern, and indirectly suggest the underlying increased left ventricular filling pressures of patients with hypertrophic cardiomyopathy and pseudonormal mitral flow patterns. (+info)The functional anatomy of the bronchial circulation of the domestic fowl. (5/1323)
The bronchial circulation was studied in 25 adult domestic fowls. The right and left bronchial arteries originated caudal to the syrinx from a bronchoesophageal artery which is a branch of the right common carotid artery. Each bronchial artery ramified on the wall of the extrapulmonary part of the corresponding primary bronchus and finally anastomosed directly with a branch of the pulmonary artery at the hilus of the lung. Thr bronchial artery did not accompany the intrapulmonary part of the primary bronchus. The branches of each bronchial artery formed an anastomosing network on the wall of the extrapulmonary part of the primary bronchus. The calibre of the bronchial artery at its anastomosis with the branch of the pulmonary artery was greater than at its origin from the bronchoesophageal artery. Intravenous injections of Lycopodium spores indicated that the blood flows from the pulmonary artery into the bronchial artery. Small bronchial veins drained the extrapulmonary part of the primary bronchus into the pulmonary vein and the oesophageal veins. The intrapulmonary part of the primary bronchus was supplied by branches of the pulmonary artery and drained by tributaries of the pulmonary vein. The blood supply to the primary bronchus could constitute a shunt capable of passing blood from the pulmonary artery into the pulmonary vein without going through the exchange tissue. The parabronchial (atrial) muscles received a blood supply directly from the exchange tissue via septal venules which formed a network underneath the muscle bundles, without actually penetrating between the muscle cells. These venules drained into atrial veins which were tributaries of the pulmonary vein. The atrial muscles probably also received oxygen by direct diffusion from the parabronchial lumen. The pleura was supplied by the oesophageal branches of the bronchoesophageal artery, and by small twigs from the internal thoracic and intercostal arteries. (+info)Defibrillation-guided radiofrequency ablation of atrial fibrillation secondary to an atrial focus. (6/1323)
OBJECTIVES: Our aim was to evaluate a potential focal source of atrial fibrillation (AF) by unmasking spontaneous early reinitiation of AF after transvenous atrial defibrillation (TADF), and to describe a method of using repeated TADF to map and ablate the focus. BACKGROUND: Atrial fibrillation may develop secondary to a rapidly discharging atrial focus that the atria cannot follow synchronously, with suppression of the focus once AF establishes. Focus mapping and radiofrequency (RF) ablation may be curative but is limited if the patient is in AF or if the focus is quiescent. Early reinitiation of AF has been observed following defibrillation, which might have a focal mechanism. METHODS: We performed TADF in patients with drug-refractory lone AF using electrodes in the right atrium (RA) and the coronary sinus. When reproducible early reinitiation of AF within 2 min after TADF was observed that exhibited a potential focal mechanism, both mapping and RF ablation were performed to suppress AF reinitiation. Clinical and ambulatory ECG monitoring was used to assess AF recurrence. RESULTS: A total of 44 lone AF patients (40 men, 4 women; 32 persistent, 12 paroxysmal AF) with a mean age of 58+/-13 years underwent TADF. Sixteen patients had early reinitiation of AF after TADF, nine (20%; 5 paroxysmal) exhibited a pattern of focal reinitiation. Earliest atrial activation was mapped to the right superior (n = 4) and the left superior (n = 3) pulmonary vein, just inside the orifice, in the seven patients who underwent further study. At the onset of AF reinitiation, the site of earliest activation was 86+/-38 ms ahead of the RA reference electrogram. The atrial activities from this site were fragmented and exhibited progressive cycle-length shortening with decremental conduction to the rest of the atrium until AF reinitiated. Radiofrequency ablation at the earliest activation site resulted in suppression of AF reinitiation despite pace-inducibility. Improved clinical outcome was observed over 8+/-4 months' follow-up. CONCLUSIONS: Transvenous atrial defibrillation can help to unmask, map, and ablate a potential atrial focus in patients with paroxysmal and persistent AF. A consistent atrial focus is the cause of early reinitiation of AF in 20% of patients with lone AF, and these patients may benefit from this technique. (+info)Prostanoid receptors involved in the relaxation of human pulmonary vessels. (7/1323)
1. To characterize the prostanoid receptors on human pulmonary smooth muscle involved in vasodilatations, isolated arteries and veins were contracted with norepinephrine (10 microM) and vessels were subsequently challenged with different prostanoid-receptor agonists in the absence or presence of selective antagonists. 2. Prostaglandin D2 (PGD2) and the selective DP-receptor agonist, BW245C, induced relaxations in the contracted human pulmonary venous preparations. The pD2 values were: 6.88+/-0.11 (n=17) and 7.31+/-0.12 (n=5), respectively. The relaxant responses induced by PGD2 were reduced by the selective DP-receptor antagonist, BWA868C, and the estimated pA2 value was 7.84+/-0.16 (n=4). PGD2 and BW245C did not relax contracted human pulmonary arteries. 3. The selective IP-receptor agonists, iloprost and cicaprost, both induced relaxations in the contracted human vascular preparations. The pD2 values for iloprost were: 7.84+/-0.08 (n=6) and 8.25+/-0.06 (n=4) and for cicaprost: 8.06+/-0.12 (n=5) and 8.11+/-0.09 (n=5) in arteries and veins respectively. 4. Prostaglandin E2 (PGE2) and the EP2/EP3-receptor agonist, misoprostol, partially relaxed the contracted venous preparations and the pD2 values were: 8.10+/-0.15 (n=15) and 6.24+/-0.33 (n=3), respectively. These relaxations suggest the presence of an EP receptor in the human pulmonary veins. The contracted human pulmonary arteries did not relax when challenged with PGE2. 5. In human pulmonary venous preparations, the PGE2-induced relaxations were neither modified by treatment with TP/EP4-receptor antagonist, AH23848B (10 and 30 microM, n=6), nor by the DP/EP1/EP2-receptor antagonist, AH6809 (3 microM, n=6). 6. These data suggest that the relaxation induced by prostanoids involved DP-, IP-receptors and to a lesser extent an EP-receptor on human pulmonary venous smooth muscle. In contrast, only the IP-receptor is involved in the prostanoid induced relaxations on human pulmonary arterial smooth muscle. (+info)Fetal pulmonary venous flow into the left atrium relative to diastolic and systolic cardiac time intervals. (8/1323)
OBJECTIVE: To establish the nature and gestational age dependency of the pulmonary venous flow velocity pattern into the left atrium relative to systolic and diastolic phases of the cardiac cycle. DESIGN: This was a cross-sectional study of Doppler measurements of fetal pulmonary venous inflow velocities, which were correlated with simultaneous recordings of transmitral and aortic flow velocity waveforms based on an equal cardiac cycle length (+/- 5%). RESULTS: Successful recordings were obtained in 28 out of 60 (47%) normal singleton pregnancies at 20-36 weeks of gestation. Reproducibility of waveform analysis of the various phases of the cardiac cycle was satisfactory, within-patient variance ranging between 1.7% and 6.5%. A statistically significant increase (p < 0.05) in pulmonary venous time average velocity and velocity integral with advancing gestational age was established. A statistically significant increase (p < 0.05) of the pulmonary flow velocity integral was also found when related to each of the systolic and diastolic segments of the cardiac cycle, with the exception of isovolemic relaxation time. The duration of each of the diastolic and systolic segments of the cardiac cycle, as well as the pulmonary venous velocity integral expressed as a percentage of the cardiac cycle, remained constant with advancing gestational age. CONCLUSIONS: The second half of pregnancy is characterized by pulmonary venous inflow into the left atrium throughout the cardiac cycle. Pulmonary venous inflow into the left atrium occurs predominantly during the filling and ejection phases of the cardiac cycle. Absolute cardiac diastolic and systolic time intervals as well as the percentage distribution of pulmonary venous flow velocity integrals between these cardiac time intervals remain unchanged with advancing gestational age. (+info)There are several risk factors for developing AF, including:
1. Age: The risk of developing AF increases with age, with the majority of cases occurring in people over the age of 65.
2. Hypertension (high blood pressure): High blood pressure can damage the heart and increase the risk of developing AF.
3. Heart disease: People with heart disease, such as coronary artery disease or heart failure, are at higher risk of developing AF.
4. Diabetes mellitus: Diabetes can increase the risk of developing AF.
5. Sleep apnea: Sleep apnea can increase the risk of developing AF.
6. Certain medications: Certain medications, such as thyroid medications and asthma medications, can increase the risk of developing AF.
7. Alcohol consumption: Excessive alcohol consumption has been linked to an increased risk of developing AF.
8. Smoking: Smoking is a risk factor for many cardiovascular conditions, including AF.
9. Obesity: Obesity is a risk factor for many cardiovascular conditions, including AF.
Symptoms of AF can include:
1. Palpitations (rapid or irregular heartbeat)
2. Shortness of breath
3. Fatigue
4. Dizziness or lightheadedness
5. Chest pain or discomfort
AF can be diagnosed with the help of several tests, including:
1. Electrocardiogram (ECG): This is a non-invasive test that measures the electrical activity of the heart.
2. Holter monitor: This is a portable device that records the heart's rhythm over a 24-hour period.
3. Event monitor: This is a portable device that records the heart's rhythm over a longer period of time, usually 1-2 weeks.
4. Echocardiogram: This is an imaging test that uses sound waves to create pictures of the heart.
5. Cardiac MRI: This is an imaging test that uses magnetic fields and radio waves to create detailed pictures of the heart.
Treatment for AF depends on the underlying cause and may include medications, such as:
1. Beta blockers: These medications slow the heart rate and reduce the force of the heart's contractions.
2. Antiarrhythmics: These medications help regulate the heart's rhythm.
3. Blood thinners: These medications prevent blood clots from forming and can help reduce the risk of stroke.
4. Calcium channel blockers: These medications slow the entry of calcium into the heart muscle cells, which can help slow the heart rate and reduce the force of the heart's contractions.
In some cases, catheter ablation may be recommended to destroy the abnormal electrical pathway causing AF. This is a minimally invasive procedure that involves inserting a catheter through a vein in the leg and guiding it to the heart using x-ray imaging. Once the catheter is in place, energy is applied to the abnormal electrical pathway to destroy it and restore a normal heart rhythm.
It's important to note that AF can increase the risk of stroke, so anticoagulation therapy may be recommended to reduce this risk. This can include medications such as warfarin or aspirin, or in some cases, implantable devices such as a left atrial appendage closure device.
In conclusion, atrial fibrillation is a common heart rhythm disorder that can increase the risk of stroke and heart failure. Treatment options depend on the underlying cause and may include medications, cardioversion, catheter ablation, or anticoagulation therapy. It's important to work closely with a healthcare provider to determine the best course of treatment for AF.
The exact cause of PVOD is unknown, but it is believed to be related to inflammation and scarring in the lungs. The disease can be associated with other conditions such as systemic sclerosis (SSc), rheumatoid arthritis (RA), and graft-versus-host disease (GVHD).
Symptoms of PVOD include shortness of breath, fatigue, chest pain, and coughing up blood. The disease can be diagnosed through a combination of physical examination, imaging tests such as CT or MRI scans, and lung biopsy.
Treatment options for PVOD are limited, and the primary goal of therapy is to manage symptoms and slow the progression of the disease. Medications such as calcium channel blockers, anticoagulants, and diuretics may be used to manage high blood pressure in the lungs and reduce fluid buildup in the body. Lung transplantation may be considered for patients with advanced stages of the disease.
Prognosis for PVOD is poor, with a five-year survival rate of approximately 50%. The disease can progress rapidly, and early diagnosis and aggressive treatment are essential to improve outcomes.
In summary, Pulmonary Veno-Occlusive Disease (PVOD) is a rare and severe lung disorder characterized by the obstruction of veins in the lungs, which can lead to high blood pressure, heart failure, and death. While treatment options are limited, early diagnosis and aggressive management can improve outcomes for patients with this condition.
In TEA, the abnormal electrical focus in the atria can be caused by various factors, including damage to the heart tissue due to coronary artery disease, high blood pressure, or other underlying conditions. The condition can be diagnosed using electrocardiography (ECG) and can be treated with medications such as beta blockers or antiarrhythmics, or in some cases, catheter ablation may be necessary to destroy the abnormal electrical focus in the atria.
The term "ectopic" refers to the fact that the abnormal electrical activity originates from an unusual location within the heart, specifically in the atria near the cavo-tricuspid isthmus. The term "tachycardia" refers to the rapid and irregular heartbeat.
In summary, Tachycardia, Ectopic Atrial (TEA) is a type of arrhythmia that originates from an abnormal electrical focus in the atria near the cavo-tricuspid isthmus, leading to rapid and irregular atrial contractions and potentially causing symptoms such as palpitations and shortness of breath.
Recurrence can also refer to the re-emergence of symptoms in a previously treated condition, such as a chronic pain condition that returns after a period of remission.
In medical research, recurrence is often studied to understand the underlying causes of disease progression and to develop new treatments and interventions to prevent or delay its return.
The symptoms of PAT can vary in severity and may include:
* Rapid heartbeats (tachycardia)
* Palpitations or pounding sensation in the chest
* Shortness of breath (dyspnea)
* Dizziness or lightheadedness
* Chest pain or discomfort
During an episode of PAT, the heart rate may exceed 100 beats per minute and can reach as high as 200-300 beats per minute. The episodes can last from a few seconds to several hours and may occur randomly throughout the day.
PAT is often diagnosed through a physical examination, electrocardiogram (ECG), or holter monitor. Treatment options for PAT may include medications to control heart rate and rhythm, lifestyle changes such as avoiding triggers, and in severe cases, implantable devices such as pacemakers or cardioverter-defibrillators.
In summary, paroxysmal tachycardia is a type of arrhythmia that is characterized by rapid heartbeats that come and go in episodes, and it can be triggered by various factors. It can cause symptoms such as palpitations, shortness of breath, and chest pain, and may require treatment with medications or implantable devices.
Scimitar syndrome can be diagnosed through a combination of clinical evaluation, ultrasound imaging, and genetic testing. Treatment for the condition typically involves monitoring the child's growth and development, as well as managing any associated health problems such as portal hypertension or liver failure. In some cases, a liver transplant may be necessary.
The prognosis for Scimitar syndrome varies depending on the severity of the condition and the presence of any other underlying health issues. With appropriate medical management, many individuals with Scimitar syndrome can lead active and productive lives into adulthood. However, the condition can be life-threatening if left untreated or if complications arise.
Some examples of pathologic constrictions include:
1. Stenosis: A narrowing or constriction of a blood vessel or other tubular structure, often caused by the buildup of plaque or scar tissue.
2. Asthma: A condition characterized by inflammation and constriction of the airways, which can make breathing difficult.
3. Esophageal stricture: A narrowing of the esophagus that can cause difficulty swallowing.
4. Gastric ring constriction: A narrowing of the stomach caused by a band of tissue that forms in the upper part of the stomach.
5. Anal fissure: A tear in the lining of the anus that can cause pain and difficulty passing stools.
Pathologic constrictions can be caused by a variety of factors, including inflammation, infection, injury, or genetic disorders. They can be diagnosed through imaging tests such as X-rays, CT scans, or endoscopies, and may require surgical treatment to relieve symptoms and improve function.
APCs can be diagnosed with an electrocardiogram (ECG), which records the electrical activity of the heart. The ECG will show a premature beat in the atria, followed by a normal heartbeat. APCs can also be detected using other tests such as Holter monitor or event monitor, which record the heart's rhythm over a longer period of time.
Treatment for APCs depends on the underlying cause and can range from medications to control the heart rate, cardioversion to restore a normal heart rhythm, or catheter ablation to destroy the abnormal electrical pathway causing the premature beats. In some cases, no treatment may be necessary if the APCs are benign and not causing any symptoms.
Symptoms of atrial flutter may include palpitations, shortness of breath, fatigue, and dizziness. In some cases, atrial flutter can lead to more serious complications such as stroke or heart failure if left untreated. Diagnosis is typically made through a combination of physical examination, electrocardiography (ECG), and other tests such as echocardiography or stress testing.
Treatment for atrial flutter depends on the underlying cause and may include medications to control the heart rate or restore a normal heart rhythm, cardioversion (a procedure that uses electrical shock to restore a normal heart rhythm), or in some cases, catheter ablation (a minimally invasive procedure that destroys the abnormal electrical pathway in the heart).
There are several types of premature complexes, including:
1. Premature atrial complex (PAC): An extra heartbeat that originates in the atria, usually due to a rapid or irregular heart rate.
2. Premature ventricular complex (PVC): An extra heartbeat that originates in the ventricles, which can be more serious than PACs and may require further evaluation.
3. Premature nodal rhythm: A condition where the AV node (the electrical pathway between the atria and ventricles) fires prematurely, causing a rapid heart rate.
PCCs can be diagnosed using electrocardiography (ECG), which records the electrical activity of the heart. Treatment options for PCCs depend on the underlying cause and may include medications to regulate the heart rhythm, cardioversion (a procedure that restores a normal heart rhythm using electrical shock), or catheter ablation (a minimally invasive procedure that destroys the abnormal electrical pathway).
There are several causes of lymphangiectasis, including:
1. Genetic mutations
2. Infections such as filariasis or tularemia
3. Inflammatory conditions such as rheumatoid arthritis or sarcoidosis
4. Trauma to the lymph vessels
5. Tumors that block the flow of lymph fluid
6. Radiation therapy or chemotherapy
7. Infectious diseases such as HIV/AIDS
8. Vitamin deficiencies such as vitamin C or B12 deficiency
The diagnosis of lymphangiectasis is based on a combination of physical examination, medical history, and diagnostic tests such as imaging studies (e.g., CT or MRI scans), lymphoscintigraphy, and biopsy.
Treatment for lymphangiectasis depends on the underlying cause and may include:
1. Antibiotics to treat infections
2. Pain management medications
3. Anti-inflammatory drugs to reduce swelling
4. Compression garments or bandaging to reduce swelling
5. Elevation of the affected limb to reduce swelling
6. Surgery to remove blockages or repair damaged lymph vessels
7. Physical therapy to improve lymphatic drainage
8. Medications to treat underlying conditions such as rheumatoid arthritis or HIV/AIDS
Prognosis for patients with lymphangiectasis varies depending on the underlying cause and severity of the condition. In general, early diagnosis and treatment can improve outcomes and reduce the risk of complications such as infection, fibrosis, and lymphedema.
There are several types of tachycardia, including:
1. Sinus tachycardia: This is the most common type and is caused by an increase in the rate of the normal sinus node. It is often seen in response to physical activity or stress.
2. Atrial fibrillation: This is a type of arrhythmia where the heart's upper chambers (atria) contract irregularly and rapidly, leading to a rapid heart rate.
3. Ventricular tachycardia: This is a type of arrhythmia where the heart's lower chambers (ventricles) contract rapidly, often with a rate above 100 bpm.
4. Premature ventricular contractions (PVCs): These are early or extra beats that originate in the ventricles, causing a rapid heart rate.
Tachycardia can cause a range of symptoms, including palpitations, shortness of breath, chest pain, and dizziness. In severe cases, it can lead to cardiac arrhythmias, heart failure, and even death.
Diagnosis of tachycardia typically involves a physical examination, electrocardiogram (ECG), and other tests such as stress tests or echocardiography. Treatment options vary depending on the underlying cause, but may include medications to regulate the heart rate, cardioversion to restore a normal heart rhythm, or in severe cases, implantation of a pacemaker or defibrillator.
Symptoms of pulmonary atresia may include:
* Blue tint to the skin (cyanosis)
* Rapid breathing
* Shortness of breath
* Fatigue
* Difficulty feeding in infants
Diagnosis is typically made through echocardiography, electrocardiography, or cardiac catheterization. Treatment involves a series of surgeries to repair or replace the valve and may include:
* Balloon atrial septostomy to create a hole in the wall between the atria to allow blood to flow from the right atrium to the left atrium and lungs
* Intracardiac repair, where a surgical patch is used to close the atrial septal defect and repair or replace the pulmonary valve
* Heart transplantation in severe cases
Prognosis for pulmonary atresia depends on the severity of the condition and the presence of other cardiac defects. With appropriate treatment, many individuals with pulmonary atresia can lead active and productive lives.
There are several types of vascular malformations, including:
1. Arteriovenous malformations (AVMs): These are abnormal connections between arteries and veins that can cause bleeding, seizures, and other neurological symptoms.
2. Capillary malformations (CMs): These are abnormalities in the tiny blood vessels that can cause redness, swelling, and other skin changes.
3. Venous malformations (VMs): These are abnormalities in the veins that can cause swelling, pain, and other symptoms.
4. Lymphatic malformations: These are abnormalities in the lymphatic system that can cause swelling, pain, and other symptoms.
Vascular malformations can be diagnosed using a variety of imaging tests, such as ultrasound, CT scans, and MRI scans. Treatment options vary depending on the type and location of the malformation, and may include surgery, embolization, or sclerotherapy.
In summary, vascular malformations are abnormalities in the blood vessels that can cause a range of symptoms and can be diagnosed using imaging tests. Treatment options vary depending on the type and location of the malformation.