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CARDIOLOGISTS IN DEVARABESANAHALLI BANGALORE Complex congenital heart disease: Fontan repair Anatomy and physiology Babies with a single ventricle or equivalent defect are often treated during childhood with a palliative operation to connect venous return directly to the pulmonary arteries—a Fontan repair. The prognosis is usually good: 75% of these patients survive at least 20 years. Complications Problems develop because of failure of the systemic ventricle, obstruction of the venous to pulmonary connection, atrial enlargement and AV valve regurgitation. Atrial arrhythmias become increasingly common. Sinus node dysfunction may necessitate pacing, which requires an epicardial electrode in most cases. Follow-up Echocardiography allows assessment of ventricular function and the AV valve. Obstruction in the Fontan connections can be examined with Doppler. MRI is increasingly useful for this assessment. Treatment Severe AV valve regurgitation, cyanosis and ventricular dysfunction are indications for intervention, including transplant or revision of the Fontan. Atrial arrhythmias can be treated with radiofrequency ablation. Pregnancy and contraception Pregnancy is possible in some patients with excellent Fontan function, good LV function and minimal AV valve regurgitation. Maternal risk is high if the Fontan is failing. There may be problems with the need to withdraw ACE inhibitors and with anticoagulation.
CARDIOLOGISTS IN BANGALORE Arrhythmias during pregnancy Women with congenital heart disease are at increased risk of supraventricular arrhythmias during pregnancy. Anti-arrhythmic drug treatment may be necessary for recurrent episodes. Digoxin may be useful for the control of heart rate but is often not effective. Beta-blockers and verapamil have been used for these patients and appear to be free of teratogenic effects.27 Amiodarone is a more effective anti-arrhythmic drug than these but should be reserved for intractable cases and used at the lowest useful dose.28 Sustained tachycardias (atrial flutter is the most common) are not well tolerated in pregnancy and DC cardioversion should be performed without delay for these patients.
DIABETIC SPECIALIST IN YALAHANKA Syncope and dizziness The history Syncope is a transient loss of consciousness resulting from cerebral anoxia, usually due to inadequate blood flow. Syncope may represent a simple faint or be a symptom of cardiac or neurological disease. Establish whether the patient actually loses consciousness and under what circumstances the syncope occurs—for example, on standing for prolonged periods or standing up suddenly (postural syncope), while passing urine (micturition syncope), on coughing (tussive syncope) or with sudden emotional stress (vasovagal syncope). Find out whether there is any warning such as dizziness or palpitations, and how long the episodes last. Recovery may be spontaneous or require attention from bystanders. Bystanders may also have noticed abnormal movements if the patient has epilepsy, but these can also occur in primary syncope. If the patient’s symptoms appear to be postural, enquire about the use of anti-hypertensive or anti-anginal drugs and other medications that may induce postural hypotension. If the episode is vasovagal, it may be precipitated by something unpleasant like the sight of blood, or it may occur in a hot crowded room; patients often feel nauseated and sweaty before fainting and may have had prior similar episodes, especially during adolescence and young adulthood. The diagnosis of this relatively benign and very common cause of syncope can usually be made from the history. Patients with very typical symptoms rarely require extensive investigations. If syncope is due to an arrhythmia there is often sudden loss of consciousness regardless of the patient’s posture. A history of rapid and irregular palpitations or a diagnosis of atrial fibrillation in the past suggests the possibility of sick sinus syndrome. These patients have intermittent tachycardia, usually due to atrial fibrillation, and episodes of profound bradycardia, often due to complete heart block. Chest pain may also occur if the patient has aortic stenosis or hypertrophic cardiomyopathy. Exertional syncope may occur in these patients because of obstruction to left ventricular outflow by aortic stenosis or septal hypertrophy . Dizziness that occurs even when the patient is lying down or that is made worse by movements of the head is more likely to be of neurological origin (vertigo), although recurrent tachyarrhythmias may occasionally cause dizziness in any position. Try to decide whether the dizziness is really vertiginous (there is a sensation of movement or spinning of the surroundings or the patient’s head), or whether it is a presyncopal feeling. A family history of syncope or sudden death raises the possibility of an ion channel abnormality (long QT syndrome, Brugada syndrome or hypertrophic cardiomyopathy). Attempts should be made to find out what the diagnosis was for the affected relatives. A past history of severe structural heart disease, especially heart failure,
CARDIOLOGIST IN DODDABOMMASANDRA, BANGALORE Cardiac rehabilitation Although rehabilitation has been a part of the management of patients following a myocardial infarction since the beginning of the last century, ideas have changed radically about the form this should take. In the early 1900s Sir Thomas Lewis insisted his patients remain in bed and be ‘guarded by day and night nursing and helped in every way to avoid voluntary movement or effort’. These severe restrictions were continued for at least six to eight weeks. The thinking was that complete rest would reduce the risk of aneurysm formation and avoid hypoxia that might cause arrhythmias. Even after discharge mild exertion was discouraged for up to a year and return to work was most unusual. In the 1970s periods of bed rest of between one and four weeks were enforced and patients remained in hospital for up to four weeks. It is now clear that this de-conditioning has many adverse physical and psychological effects. Patients with uncomplicated infarcts are now mobilised in hospital within a day or so of admission and are often discharged on the third day if successful primary angioplasty has been performed. Many hospitals provide a supervised rehabilitation program for patients who have had an infarct or episode of unstable angina. The program begins in hospital as soon as possible after admission. It includes a graded exercise regimen and advice about risk factor control. Such programs have many benefits for patients to help them to return quickly to normal life, including work and sexual activity. The supervised exercise regimen helps restore the patient’s confidence. There is clear evidence of the benefits of exercise for patients with ischaemic heart disease.54 Rehabilitation programs have been shown to be cost-effective. Well-conducted programs are tailored to individual patients’ needs and are very popular with many patients.55 There are often long-term exercise groups available for people who have completed the formal classes. Non-cardiac causes of chest pain Pulmonary embolism
BEST CARDIOLOGY HOSPITALS IN BANGALORE Cardiac failure Cardiac failure is an increasingly common condition affecting about 1% of the population but much higher proportions of older people. It is responsible for an increasing number of hospital admissions. The various aetiologies have been discussed above, but the most common cause is now ischaemic heart disease rather than hypertensive heart disease. This reflects the improved modern management of hypertension in the population. The definition of heart failure has always included reference to the inability of the heart to meet the metabolic needs of the body. The earliest concepts of heart failure were of inadequate cardiac pump function and associated salt and water retention. Treatment was aimed at improving cardiac contractility and removing salt and water from the body. In the 1970s the concept of after-load reduction was introduced. This was based partly on the realisation that vasoconstriction was part of the problem. This has led to the modern neuro-hormonal concept of heart failure. It is clear that many of the features of cardiac failure are a result of stimulation of the renin-angiotensin-aldosterone system and sympathetic stimulation. These responses of the body to the fall in cardiac output temporarily increase cardiac performance and blood pressure by increasing vascular volumes, cardiac contractility and systemic resistance. In the medium and longer term these responses are maladaptive. They increase cardiac work and left ventricular volumes and lead to myocardial fibrosis with further loss of myocytes. Most recently it has become clear that heart failure is also an inflammatory condition, with evidence of cytokine activation. Work is underway to establish a role for treatment of this part of the condition. Current drug treatment has been successful in blocking many of the maladaptive aspects of neuro-hormonal stimulation. Many of these treatments have become established after benefits have been ascertained in large randomised controlled trials. These trials have also led to the abandoning of certain drugs (often those that increase cardiac performance) that were shown to have a detrimental effect on survival (e.g. Milrinone). The principles of treatment of heart failure are as follows: 1 Remove the exacerbating factors. 2 Relieve fluid retention. 3 Improve left ventricular function and reduce cardiac work; improve prognosis. 4 Protect against the adverse effects of drug treatment. 5 Assess for further management (e.g. revascularisation, transplant). 6 Manage complications (e.g. arrhythmias). 7 Protect high-risk patients from sudden death.
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