Cyanosis
Methemoglobinemia
Osteoarthropathy, Secondary Hypertrophic
Heart Bypass, Right
Heart Defects, Congenital
Ebstein Anomaly
Arteriovenous Malformations
Tetralogy of Fallot
Heterotaxy Syndrome
Fontan Procedure
Pulmonary Artery
Methylene Blue
Pulmonary Veins
Vena Cava, Superior
Benzocaine
Cytochrome-B(5) Reductase
Hepatopulmonary Syndrome
Pulmonary Valve Stenosis
Tricuspid Atresia
Heart Septal Defects, Atrial
Arteriovenous Fistula
Oximetry
Transposition of Great Vessels
Heart Septal Defects, Ventricular
Decreased left ventricular filling pressure 8 months after corrective surgery in a 55-year-old man with tetralogy of Fallot: adaptation for increased preload. (1/188)
A 55-year-old man with tetralogy of Fallot underwent corrective surgery. Left ventricular filling pressure increased markedly with increased left ventricular volume one month after surgery, then decreased over the next 7 months, presumably due to increased left ventricular compliance. (+info)Left ventricle to pulmonary artery conduit in treatment of transposition of great arteries, restrictive ventricular septal defect, and acquired pulmonary atresia. (2/188)
Progressive cyanosis after banding of the pulmonary artery in infancy occurred in a child with transposition of the great arteries and a ventricular septal defect, and a Blalock-Taussig shunt operation had to be performed. At the time of correction a segment of pulmonary artery between the left ventricle and the band was found to be completely occluded so that continuity between the left ventricle and the pulmonary artery could not be restored. A Rastelli type of operation was not feasible as the ventricular septal defect was sited low in the muscular septum. Therefore, in addition to Mustard's operation, a Dacron conduit was inserted from the left ventricle to the main pulmonary artery to relieve the obstruction. Postoperative cardiac catheterization with angiocardiography indicated a satisfactory haemodynamic result. The patient remains well 11 months after the operation. This operation, a left ventricle to pulmonary artery conduit, may be used as an alternative procedure in patients with transposition of the great arteries, intact interventricular septum, and obstruction to the left ventricular outflow, if the obstruction cannot be adequately relieved. (+info)The myocardial profile of the cytosolic isozymes of creatine kinase is apparently not related to cyanosis in congenital heart disease. (3/188)
BACKGROUND: CKMB, the cardiac-specific heterodimer of cytosolic creatine-kinase (CK), is developmentally and physiologically regulated, tissue hypoxia being a proposed regulator. In patients with cyanotic heart disease the myocardium is perfused with partially saturated blood. We questioned whether the myocardium of cyanotic subjects contains higher proportions of CKMB. MATERIALS AND METHODS: CK activity, the distribution of cytosolic CK isozymes, activity of lactic dehydrogenase (LDH), and tissue protein content were determined in obstructive tissues removed at corrective surgery of patients with congenital heart defects. Cyanotic (n = 13) and acyanotic (n = 12) subjects were compared. RESULTS: In cyanotic and acyanotic patients, CK activity was 8.4 +/- 0.6 and 7.6 +/- 0.6 IU/mg protein and the proportion of CKMB was 21 +/- 1.4 and 22 +/- 2. 0% (mean +/- S.E.M), respectively. In the two groups of patients, the activity related to the B subunit corresponded to the steady-state level of the CKBmRNA. The tissue content of protein and the activities of CK and LDH were similar in cyanotic and acyanotic subjects and increased with the age. CONCLUSIONS: The lack of difference in CKMB distribution between the cyanotic and acyanotic patients may either indicate that hypooxygenation is not a regulator of CK isozyme expression, or may be attributed to the already high proportion of this isozyme in hypertrophied, obstructive tissues. Recruitment of additional CKMB, in the cyanotic hearts, may thus not be required. (+info)Controlled study of preschool development after surgery for congenital heart disease. (4/188)
AIM: Research into intellectual impairment among children with congenital heart disease has focused mainly on older children. This study was designed to determine whether previous findings are applicable to preschool children. METHODS: Three groups of children under 31/2 years old were assessed immediately before treatment and 12 months later: a group with congenital heart disease awaiting surgery, another awaiting bone marrow transplantation, and a healthy comparison group. RESULTS: Although the means of the three groups were within the normal range, preoperatively the cardiac and transplant groups showed deficits compared with the healthy controls. Postoperatively, continuing developmental deficits were significant only in the children with cyanotic lesions. CONCLUSIONS: Conclusions about intellectual development in older children with congenital heart disease do not apply to preschool children. Before corrective surgery, chronic illness itself appears to be the predominant influence on development. Postoperatively, cyanotic and acyanotic lesions are associated with different short term outcomes. (+info)Malnutrition and growth failure in cyanotic and acyanotic congenital heart disease with and without pulmonary hypertension. (5/188)
AIM: To investigate the effect of several types of congenital heart disease (CHD) on nutrition and growth. PATIENTS AND METHODS: The prevalence of malnutrition and growth failure was investigated in 89 patients with CHD aged 1-45 months. They were grouped according to cardiac diagnosis: group aP (n = 26), acyanotic patients with pulmonary hypertension; group ap (n = 5), acyanotic patients without pulmonary hypertension; group cp (n = 42), cyanotic patients without pulmonary hypertension; and group cP (n = 16), cyanotic patients with pulmonary hypertension. Information on socioeconomic level, parental education status, birth weight and nutrition history, number of siblings, and the timing, quality, and quantity of nutrients ingested during weaning period and at the time of the examination were obtained through interviews with parents. RESULTS: There was no significant difference between groups in terms of parental education status, socioeconomic level, duration of breast feeding, and number of siblings (p > 0.05). Group cP patients ingested fewer nutrients for their age compared to other groups. 37 of the 89 patients were below the 5th centile for both weight and length, and 58 of 89 patients were below the 5th centile for weight. Mild or borderline malnutrition was more common in group aP patients. Most group cp patients were in normal nutritional state, and stunting was more common than wasting. Both moderate to severe malnutrition and failure to thrive were more common in group cP patients. CONCLUSION: Patients with CHD are prone to malnutrition and growth failure. Pulmonary hypertension appears to be the most important factor, and cyanotic patients with pulmonary hypertension are the ones most severely affected. This study shows the additive effects of hypoxia and pulmonary hypertension on nutrition and growth of children with CHD. (+info)Use of self expanding stents in stenotic aortopulmonary shunts in adults with complex cyanotic heart disease. (6/188)
OBJECTIVE: To describe the use of self expanding stents in treating long segment stenosis of aortopulmonary shunts (APS) in adults. DESIGN: Clinical records, catheterisation data, cineangiograms, and operation notes of four consecutive patients undergoing stent implantation since December 1994 were studied retrospectively. SETTING: A tertiary referral centre for cardiac disease. SUBJECTS: Four patients underwent cardiac catheterisation because of clinical deterioration. Their age ranged between 23 and 32 years. The underlying diagnosis was complex cyanotic heart disease in all. Three had a stenotic interposition graft, and one had a classic Blalock shunt. RESULTS: There was one technical failure owing to migration of the stent distal to an ostial stenosis. The ability index, resting oxygen saturation, and exercise tolerance improved in the remainder. Their medium term results have been excellent. CONCLUSIONS: This technique may further palliate adult patients with complex congenital heart disease, though the long term patency of stents is unknown. (+info)A case of methemoglobinemia after ingestion of an aphrodisiac, later proven as dapsone. (7/188)
Methemoglobin (MetHb) is an oxidation product of hemoglobin in which the sixth coordination position of ferric iron is bound to a water molecule or to a hydroxyl group. The most common cause of acquired MetHb-emia is accidental poisoning which usually is the result of ingestion of water containing nitrates or food containing nitrite, and sometimes the inhalation or ingestion of butyl or amyl nitrite used as an aphrodisiac. We herein report a case of MetHb-emia after ingestion of an aphrodisiac, later identified as dapsone by gas chromatograph/mass selective detector (GC/MSD). A 24-year old male was admitted due to cyanosis after ingestion of a drug purchased as an aphrodisiac. On arterial blood gas analysis, pH was 7.32, PaCO2 26.8 mmHg, PaO2 75.6 mmHg, and bicarbonate 13.9 mmol/L. Initial pulse oxymetry was 89%. With 3 liter of nasal oxygen supplement, oxygen saturation was increased to 90-92%, but cyanosis did not disappear. Despite continuous supplement of oxygen, cyanosis was not improved. On the fifth hospital day, MetHb was 24.9%. Methylene blue was administered (2 mg/kg intravenously) and the patient rapidly improved. We proved the composition of aphrodisiac as dapsone by the method of GC/MSD. (+info)Occlusion of azygos vein via direct percutaneous puncture of innominate vein following cavopulmonary anastomosis. (8/188)
A 2-year-10-month-old boy was diagnosed with a complex congenital heart disease: right atrial isomerism, left superior vena cava (LSVC), complete atrioventricular septal defect, secundum type atrial septal defect, transposition of the great arteries with pulmonary atresia, patent ductus arteriosus, absence of a right superior vena cava (RSVC), and dextrocardia. He had received a left Blalock-Taussig (BT) shunt at the age of 3 months and a left bidirectional Glenn shunt one year after BT shunt. Progressive cyanosis was noted after the second operation and cardiac catheterization showed a functional Glenn shunt with an engorged azygos vein, which was inadvertently skipped for ligation. Because of the absence of RSVC, transcatheter occlusion of the azygos vein was performed successfully via direct puncture of the innominate vein. (+info)In medicine, cyanosis is often used as an indication of the severity of a patient's condition. For example, a patient with severe cyanosis may have a more serious underlying condition than a patient with mild cyanosis. Additionally, cyanosis can be used to monitor the effectiveness of treatment and to determine when further interventions are necessary.
Cyanosis can be diagnosed through physical examination, blood tests, and other diagnostic procedures such as pulse oximetry or arterial blood gas analysis. Treatment for cyanosis depends on the underlying cause and may include oxygen therapy, medication, or surgical intervention.
In summary, cyanosis is a condition characterized by a bluish discoloration of the skin and mucous membranes due to inadequate oxygenation of the body's tissues. It is an important sign of underlying disease and can be used to assess the severity of a patient's condition and monitor the effectiveness of treatment.
There are several possible causes of methemoglobinemia, including:
1. Exposure to certain medications or chemicals, such as nitrates or aniline dyes.
2. Genetic disorders that affect the production or function of hemoglobin.
3. Infections, such as bacterial infections of the blood or respiratory tract.
4. Poor nutrition or malnutrition.
5. Certain chronic medical conditions, such as sickle cell anemia or thalassemia.
Methemoglobinemia can be diagnosed through a variety of tests, including:
1. Complete blood count (CBC) to measure the levels of methemoglobin in the blood.
2. Blood gas analysis to measure the partial pressure of oxygen and carbon dioxide in the blood.
3. Co-oximetry to measure the levels of methemoglobin and other forms of hemoglobin.
4. Urine tests to check for the presence of abnormal hemoglobin.
5. Genetic testing to identify inherited disorders that may be causing the condition.
Treatment of methemoglobinemia depends on the underlying cause and may include:
1. Administration of oxygen therapy to increase the amount of oxygen in the blood.
2. Use of medications to reduce the levels of methemoglobin and increase the levels of normal hemoglobin.
3. Transfusions of red blood cells to replace abnormal hemoglobin with normal hemoglobin.
4. Management of underlying medical conditions, such as infections or genetic disorders.
5. Dietary changes to address any nutritional deficiencies that may be contributing to the condition.
In severe cases of methemoglobinemia, hospitalization may be necessary to provide oxygen therapy and other treatments. In some cases, patients with methemoglobinemia may require long-term management and follow-up care to prevent complications and manage the underlying cause of the condition.
Symptoms of secondary hypertrophic osteoarthropathy may include:
1. Pain and stiffness in the hands and feet
2. Swelling and redness in the affected joints
3. Thickening and enlargement of the bones in the hands and feet
4. Limited range of motion in the affected joints
5. Warmth and erythema (redness) over the affected joints.
SHOA can be diagnosed through a combination of physical examination, X-rays, and other imaging tests such as CT or MRI scans. Treatment for SHOA may include medications to manage pain and inflammation, as well as surgery to remove any excess bone growth. In some cases, the underlying condition that is causing the bone growth may also be treated.
SHOA is a rare condition, and it is estimated to affect only about 1 in 100,000 people. It can occur at any age but is more common in adults. The exact prevalence of SHOA is not known, as it is often misdiagnosed or underdiagnosed.
Secondary hypertrophic osteoarthropathy is a rare condition that causes excessive growth and thickening of the bones in the hands and feet. It is often associated with other conditions, such as inflammatory diseases or cancers. The exact cause of SHOA is not known, but it is thought to be related to an abnormal response to injury or inflammation. Treatment for SHOA typically focuses on managing the underlying condition that is causing the bone growth.
SHOA is a rare and often misdiagnosed condition that can cause significant pain and disability. It is important for individuals who are experiencing symptoms of SHOA to seek medical attention to receive an accurate diagnosis and appropriate treatment. With proper treatment, many people with SHOA can experience improvement in their symptoms and quality of life.
Types of congenital heart defects include:
1. Ventricular septal defect (VSD): A hole in the wall between the two lower chambers of the heart, allowing abnormal blood flow.
2. Atrial septal defect (ASD): A hole in the wall between the two upper chambers of the heart, also allowing abnormal blood flow.
3. Tetralogy of Fallot: A combination of four heart defects, including VSD, pulmonary stenosis (narrowing of the pulmonary valve), and abnormal development of the infundibulum (a part of the heart that connects the ventricles to the pulmonary artery).
4. Transposition of the great vessels: A condition in which the aorta and/or pulmonary artery are placed in the wrong position, disrupting blood flow.
5. Hypoplastic left heart syndrome (HLHS): A severe defect in which the left side of the heart is underdeveloped, resulting in insufficient blood flow to the body.
6. Pulmonary atresia: A condition in which the pulmonary valve does not form properly, blocking blood flow to the lungs.
7. Truncus arteriosus: A rare defect in which a single artery instead of two (aorta and pulmonary artery) arises from the heart.
8. Double-outlet right ventricle: A condition in which both the aorta and the pulmonary artery arise from the right ventricle instead of the left ventricle.
Causes of congenital heart defects are not fully understood, but genetics, environmental factors, and viral infections during pregnancy may play a role. Diagnosis is typically made through fetal echocardiography or cardiac ultrasound during pregnancy or after birth. Treatment depends on the type and severity of the defect and may include medication, surgery, or heart transplantation. With advances in medical technology and treatment, many children with congenital heart disease can lead active, healthy lives into adulthood.
The symptoms of Ebstein anomaly can vary depending on the severity of the defect and may include:
* Shortness of breath (dyspnea)
* Fatigue
* Swelling in the legs, feet, or abdomen (edema)
* Pale skin (cyanosis)
* Rapid breathing (tachypnea)
* A blue tint to the skin and mucous membranes (cyanosis)
Ebstein anomaly can be diagnosed through a variety of tests, including:
* Echocardiogram: This is a non-invasive test that uses sound waves to create images of the heart. It can help doctors visualize the tricuspid valve and determine the severity of the defect.
* Electrocardiogram (ECG): This test measures the electrical activity of the heart and can detect any abnormal rhythms or arrhythmias that may be associated with Ebstein anomaly.
* Chest X-ray: This test can provide images of the heart and lungs and can help doctors identify any other underlying conditions that may be contributing to the symptoms.
* Cardiac catheterization: This is a minimally invasive test in which a thin, flexible tube (catheter) is inserted into the heart through a vein in the leg. It can provide detailed information about the structure and function of the heart and its vessels.
Treatment for Ebstein anomaly may include:
* Medications to control symptoms such as high blood pressure, heart failure, or arrhythmias
* Surgery to repair or replace the tricuspid valve
* Catheter procedures to close any abnormal openings in the heart or to implant devices such as pacemakers or defibrillators
* In some cases, a heart transplant may be necessary.
Overall, the prognosis for individuals with Ebstein anomaly varies depending on the severity of the defect and the presence of any other underlying conditions. With proper medical care and management, many people with this condition can lead active and fulfilling lives. However, it is important to carefully follow the recommended treatment plan and to attend regular follow-up appointments with a healthcare provider to monitor for any changes or complications.
AVMs are characterized by a tangle of abnormal blood vessels that can cause a variety of symptoms, including:
* Headaches
* Seizures
* Stroke-like episodes
* Neurological deficits such as weakness or numbness
* Vision problems
* Pain
AVMs can be diagnosed through a combination of imaging studies such as CT or MRI scans, and catheter angiography. Treatment options for AVMs include:
* Endovascular embolization, which involves using a catheter to inject materials into the abnormal blood vessels to block them off
* Surgery to remove the AVM
* Radiation therapy to shrink the AVM
The goal of treatment is to prevent bleeding, seizures, and other complications associated with AVMs. In some cases, treatment may not be necessary if the AVM is small and not causing any symptoms. However, in more severe cases, prompt treatment can significantly improve outcomes.
1. Ventricular septal defect (VSD): an opening in the wall between the two lower chambers of the heart, which allows oxygen-poor blood to mix with oxygen-rich blood.
2. Pulmonary stenosis: a narrowing of the pulmonary valve and pulmonary artery, which restricts blood flow to the lungs.
3. Overriding aorta: an aorta that grows over the ventricular septal defect, blocking the flow of oxygen-rich blood from the left ventricle to the rest of the body.
4. Right ventricular hypertrophy: enlargement of the right ventricle due to increased pressure caused by the backflow of blood through the VSD.
These abnormalities combine to reduce the amount of oxygen that reaches the body's tissues, leading to cyanosis (blue discoloration of the skin) and fatigue. Tetralogy of Fallot is usually diagnosed at birth or soon after, and treatment typically involves a combination of medications, surgery, and other interventions to repair the defects and improve blood flow to the body.
The term "heterotaxy" comes from the Greek words "heteros," meaning "different," and "taxis," meaning "arrangement." This condition is also known as situs inversus totalis or "complete reversal of internal organs." Heterotaxy syndrome can be diagnosed through imaging tests such as ultrasound, CT scan, or MRI.
The symptoms of heterotaxy syndrome vary depending on the severity of the condition and the specific organs affected. Common symptoms include difficulty breathing, swallowing, and digesting food, as well as abdominal pain, fatigue, and palpitations. Treatment options for heterotaxy syndrome may include surgery to correct any anatomical abnormalities, medication to manage symptoms, and close monitoring by a healthcare provider.
It is essential to seek medical attention if you or your child experiences any of the above symptoms, especially if they worsen over time. An early diagnosis can help prevent complications and improve the chances of successful treatment.
The exact prevalence of HPS is not well-established, but it is believed to affect approximately 30% to 50% of individuals with cirrhosis. Risk factors for developing HPS include alcohol consumption, viral hepatitis, and non-alcoholic fatty liver disease (NAFLD).
The diagnosis of HPS typically involves a combination of physical examination, imaging studies such as ultrasound or CT scans, and laboratory tests to evaluate liver function. Treatment options for HPS depend on the underlying cause of the condition and may include medications to manage portal hypertension, lung fibrosis, or other complications. In severe cases, liver transplantation may be necessary.
Prognosis for individuals with HPS is generally poor, with a 5-year survival rate of approximately 50%. However, early diagnosis and appropriate management can improve outcomes and reduce the risk of complications.
There are several causes of PVS, including:
1. Congenital heart defects: PVS can be present at birth due to abnormal development of the pulmonary valve or other structures near the valve.
2. Rheumatic fever: This is an inflammatory disease that can damage the heart valves, including the pulmonary valve.
3. Endocarditis: This is an infection of the heart valves, which can cause scarring and narrowing of the pulmonary valve.
4. Heart disease: PVS can be a complication of other heart conditions, such as hypertension or coronary artery disease.
5. Calcification: Over time, deposits of calcium can accumulate on the valve leaflets, causing them to become stiff and narrow.
Symptoms of PVS may include:
1. Shortness of breath (dyspnea)
2. Fatigue or weakness
3. Chest pain (angina)
4. Swelling in the legs, ankles, or feet (edema)
5. Palpitations or irregular heartbeat
If PVS is suspected, a healthcare provider may perform several tests to confirm the diagnosis, including:
1. Echocardiogram: This is an ultrasound test that uses sound waves to create images of the heart and its valves.
2. Cardiac catheterization: A thin tube (catheter) is inserted into a blood vessel in the arm or leg and guided to the heart to measure pressure and oxygen levels in the chambers.
3. Chest X-ray: This test can help identify any enlargement of the heart or lungs that may be indicative of PVS.
4. Electrocardiogram (ECG): This test measures the electrical activity of the heart and can help identify irregular heart rhythms or other signs of PVS.
Treatment for PVS may include:
1. Medications to manage symptoms, such as diuretics to reduce fluid buildup in the body, and ACE inhibitors or beta blockers to lower blood pressure.
2. Lifestyle changes, such as a healthy diet, regular exercise, and stress reduction techniques.
3. Valve repair or replacement surgery: In severe cases of PVS, surgery may be necessary to repair or replace the affected valve.
If you suspect you may have PVS, it is important to seek medical attention as soon as possible to receive an accurate diagnosis and appropriate treatment. With prompt and proper treatment, many people with PVS are able to manage their symptoms and improve their quality of life.
Tricuspid atresia is a rare congenital heart defect that occurs when the tricuspid valve, which separates the right atrium and ventricle, does not develop properly and is absent or very small. This results in poor blood flow from the right atrium to the right ventricle, leading to inadequate oxygenation of the body.
Symptoms:
Children with tricuspid atresia may experience symptoms such as:
* Blue tinge to the skin (cyanosis)
* Shortness of breath
* Fatigue
* Poor feeding and growth
* Rapid breathing
* Pallor (pale skin)
Diagnosis:
Tricuspid atresia is diagnosed through a series of tests, including:
* Physical examination
* Chest X-ray
* Echocardiogram (echo)
* Electrocardiogram (ECG)
* Cardiac catheterization
Treatment:
The treatment for tricuspid atresia usually involves a series of surgeries and catheterizations to improve blood flow and oxygenation to the body. These may include:
* Balloon atrial septostomy: A procedure in which a balloon is inserted through a catheter into the atrial septum to create a hole between the atria to improve blood flow.
* Tricuspid valve replacement: A surgical procedure to replace the tricuspid valve with an artificial valve.
* Intracardiac repair: A surgical procedure to repair any other defects in the heart.
Prognosis:
The prognosis for children with tricuspid atresia varies depending on the severity of the defect and the presence of other congenital heart defects. With appropriate treatment, many children with tricuspid atresia can lead active and healthy lives. However, some may experience ongoing health problems and may require long-term monitoring and care.
The AVF is created by joining a radial or brachial artery to a vein in the forearm or upper arm. The vein is typically a radiocephalic vein, which is a vein that drains blood from the hand and forearm. The fistula is formed by sewing the artery and vein together with a specialized suture material.
Once the AVF is created, it needs time to mature before it can be used for hemodialysis. This process can take several weeks or months, depending on the size of the fistula and the individual patient's healing response. During this time, the patient may need to undergo regular monitoring and testing to ensure that the fistula is functioning properly.
The advantages of an AVF over other types of hemodialysis access include:
1. Improved blood flow: The high-flow path created by the AVF allows for more efficient removal of waste products from the blood.
2. Reduced risk of infection: The connection between the artery and vein is less likely to become infected than other types of hemodialysis access.
3. Longer duration: AVFs can last for several years, providing a reliable and consistent source of hemodialysis access.
4. Improved patient comfort: The fistula is typically located in the arm or forearm, which is less invasive and more comfortable for the patient than other types of hemodialysis access.
However, there are also potential risks and complications associated with AVFs, including:
1. Access failure: The fistula may not mature properly or may become blocked, requiring alternative access methods.
2. Infection: As with any surgical procedure, there is a risk of infection with AVF creation.
3. Steal syndrome: This is a rare complication that occurs when the flow of blood through the fistula interferes with the normal flow of blood through the arm.
4. Thrombosis: The fistula may become occluded due to clotting, which can be treated with thrombolysis or surgical intervention.
In summary, an arteriovenous fistula (AVF) is a type of hemodialysis access that is created by connecting an artery and a vein, providing a high-flow path for hemodialysis. AVFs offer several advantages over other types of hemodialysis access, including improved blood flow, reduced risk of infection, longer duration, and improved patient comfort. However, there are also potential risks and complications associated with AVFs, including access failure, infection, steal syndrome, and thrombosis. Regular monitoring and testing are necessary to ensure that the fistula is functioning properly and to minimize the risk of these complications.
In a normal heart, the aorta arises from the left ventricle and the pulmonary artery arises from the right ventricle. In TGV, the positions of these vessels are reversed, with the aorta arising from the right ventricle and the pulmonary artery arising from the left ventricle. This can lead to a variety of complications, including cyanosis (blue discoloration of the skin), tachycardia (rapid heart rate), and difficulty breathing.
TGV is often diagnosed during infancy or early childhood, and treatment typically involves surgery to repair the defect. In some cases, a procedure called an arterial switch may be performed, in which the aorta and pulmonary artery are surgically reversed to their normal positions. In other cases, a heart transplant may be necessary. With proper treatment, many individuals with TGV can lead active and healthy lives. However, they may require ongoing monitoring and care throughout their lives to manage any potential complications.
There are several types of heart septal defects, including atrial septal defects, ventricular septal defects, and mitral valve defects. Ventricular septal defects are the most common type and occur when there is an abnormal opening in the wall between the right and left ventricles.
Symptoms of heart septal defects can include shortness of breath, fatigue, and swelling in the legs and feet. In some cases, the defect may not cause any symptoms at all until later in life.
Diagnosis of heart septal defects is typically made using echocardiography, electrocardiography (ECG), or chest X-rays. Treatment options vary depending on the severity of the defect and can include medication to manage symptoms, surgery to repair the defect, or catheter procedures to close the opening. In some cases, heart septal defects may be treated with a procedure called balloon atrial septostomy, in which a balloon is inserted through a catheter into the abnormal opening and inflated to close it.
Prognosis for patients with heart septal defects depends on the severity of the defect and the presence of any other congenital heart defects. In general, early diagnosis and treatment can improve outcomes and reduce the risk of complications such as heart failure, arrhythmias, and endocardrial infection.
In summary, heart septal defects, ventricular type, are congenital heart defects that occur when there is an abnormal opening in the wall between the right and left ventricles of the heart. Symptoms can include shortness of breath, fatigue, and swelling in the legs and feet. Diagnosis is typically made using echocardiography, electrocardiography (ECG), or chest X-rays. Treatment options vary depending on the severity of the defect and can include medication, surgery, or catheter procedures. Prognosis is generally good for patients with heart septal defects if they receive early diagnosis and treatment.
Cyanosis
1-Octanethiol
1924 Los Angeles pneumonic plague outbreak
Rokhsareh Ghaemmaghami
Blue baby syndrome
Raghib syndrome
List of Equinox episodes
Atelectasis
Bufotenin
Diphtheria
Atrial septal defect
Heart murmur
List of dog diseases
Salt water aspiration syndrome
Dennis Embleton
Right-to-left shunt
Situs ambiguus
Hemoglobin M disease
Chiari malformation
Sulfhemoglobinemia
Elongated soft palate
Smoke screen
Choking
Smoke composition
Obligate nasal breathing
Food allergy
Hypoplastic left heart syndrome
Oxygen saturation (medicine)
Hypoxia (medical)
Perchloryl fluoride
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Tricuspid Atresia - Seattle Children's HospitalDyspnea1
- Dyspnea, a low FVC, and/or physical examination findings typical of interstitial fibrosis (rales, clubbing, or cyanosis) raised the risk of subsequent death from asbestos is by 2- to 6-fold. (cdc.gov)
Peripheral2
- Cyanosis may be classified as central or peripheral, referring to the etiology of the hemoglobin desaturation, not to the observed anatomic location of the cyanosis. (medscape.com)
- Peripheral cyanosis is a manifestation of diminished tissue perfusion with resultant increased local oxygen extraction leading to high levels of desaturated hemoglobin. (medscape.com)
Discoloration2
- Lack of oxygen in the blood causes a bluish discoloration in the skin or mucous membranes called cyanosis. (medlineplus.gov)
- The distinctive blue or purple skin discoloration of cyanosis indicates the presence of at least 5 g/dL of desaturated hemoglobin. (medscape.com)
Pulmonary2
- Most cyanosis is seen as a result of congenital heart disease, pulmonary disease, or as a terminal event as in cardiopulmonary arrest. (medlineplus.gov)
- Central cyanosis is often a manifestation of congenital heart disease characterized by right-to-left pulmonary shunts. (medscape.com)
Lips1
- Cyanotic heart disease is a congenital heart defect which results in low oxygen levels in the blood and causes the child's lips, fingers, and toes to look blue (cyanosis). (mountsinai.org)
Oxygen3
- Cyanosis is a medical condition characterized by blue colored skin and mucous membranes, which occurs as the result of inadequate amounts of oxygenated hemoglobin -- the molecule which carries oxygen to the body tissues -- or due to hemoglobin abnormalities. (petmd.com)
- It is classified as a cyanotic heart defect because the condition leads to cyanosis, a bluish-purple coloration to the skin, and shortness of breath due to low oxygen levels in the blood. (mountsinai.org)
- Less oxygen delivered to the body can make the skin look blue ( cyanosis ). (mountsinai.org)
Skin2
- Central cyanosis typically involves the entire body but may be best appreciated on warm areas of the body (eg, tongue, oral mucosa, conjunctiva, skin). (medscape.com)
- Cyanosis refers to a bluish color of the skin and mucous membranes. (mountsinai.org)
Depending1
- Depending on what underlying illness is causing the cyanosis, drugs may be prescribed to treat the condition, or surgery and/or further therapy ordered. (petmd.com)
Severe1
- Unfortunately, dogs that are suffering from cyanosis caused by advanced lung/airway disease and severe heart disease have a poor long-term prognosis. (petmd.com)
Signs1
- After the company switched to a replacement adhesive, Thixon-521, a followup study was performed to check workers for signs of cyanosis or other pertinent adverse health effects. (cdc.gov)
Disease1
- A blood chemical profile, complete blood count, urinalysis, electrocardiograph (EKG), thoracic radiographs (and echocardiogram with Doppler, if heart or lung disease is suspected), and an electrolyte panel should be ordered to determine the underlying cause of the disease that is causing cyanosis. (petmd.com)
Patients1
- Severely anemic patients (regardless of the degree of desaturation) are, therefore, unable to manifest cyanosis. (medscape.com)
Mucous2
- Lack of oxygen in the blood causes a bluish discoloration in the skin or mucous membranes called cyanosis. (medlineplus.gov)
- Cyanosis is a bluish or purplish tinge to the skin and mucous membranes. (medscape.com)
Hypoxemia5
- Facial cyanosis in a patient with chronic hypoxemia. (medscape.com)
- Before the era of rapid blood gas analysis, clinicians often assessed hypoxemia on clinical grounds alone, primarily by looking for cyanosis in the perioral area and fingers. (medscape.com)
- At this level of hypoxemia, the patient would also have other manifestations of hypoxemia (eg, respiratory symptoms, mental status changes) apart from cyanosis. (medscape.com)
- With a hemoglobin content of less than 9 g/dL, the patient would likely succumb from hypoxemia before cyanosis became evident. (medscape.com)
- [ 6 ] At the same time, one should not rely on the absence of cyanosis as reassurance that hypoxemia is not present. (medscape.com)
Manifest1
- For example, central cyanosis can manifest when SaO2 is 79% in a patient with a hemoglobin of 15 g/dL. (medscape.com)
Condition1
- A case report of Eisenmenger syndrome (interrupted aortic arch with ventricular septal defect) in a 31-year-old pregnant woman discusses the rare condition of differential cyanosis. (medscape.com)
