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best cardiologists in bangalore Murmurs Murmurs are produced by turbulent blood flow, and are described according to their location, intensity, timing, frequency, and radiation (Tables 15.1 to 15.3 and Figure 15.1). Innocent murmurs are due to pulmonary flow and can be heard in children, pregnancy, and high-flow states, such as hyperthyroidism and anaemia. They are heard over the left sternal edge and are ejection systolic, and there are no added sounds or thrill. The cervical venous hum is a continuous murmur, common in children and typically reduced by turning the head laterally or bending the elbows back. The mammary soufflé is a continuous murmur that may be heard in pregnancy. Dynamic auscultation manoeuvres may help bedside diagnosis of systolic murmurs (Table 15.2). 4, 5 Murmurs originating within the right-sided chambers of the heart can be differentiated from all other murmurs by augmentation of their intensity with inspiration and diminution with expiration. The murmur of hypertrophic cardiomyopathy is distinguished from all other systolic murmurs by an increase in intensity with the Valsalva manoeuvre and during squatting-to-standing, and by a decrease in intensity during standing-to-squatting action, passive leg elevation, and handgrip. The murmurs of MR and VSD have similar responses but can be differentiated from other systolic murmurs by augmentation of their intensity with handgrip and during transient arterial occlusion.
VITAMIN, D, A diet deficient in vitamin D in conjunction with inadequate sun exposure causes osteomalacia (or rickets when it occurs in children), which is a softening of the bones. In the developed world, this is a rare disease. However, vitamin D deficiency has become a worldwide problem in the elderly and remains common in children and adults. Low blood calcifediol (hydroxy-vitamin D) can result from avoiding the sun.[1Deficiency results in impaired bone mineralization and bone damage which leads to bone-softening diseasesincluding rickets and osteomalacia.
POPULAR CARDIOLOGIST IN KATTIGENAHALLI, BANGALORE Cyanotic congenital heart disease Some of the more common cyanotic lesions are discussed below. There are, however, a number of problems common to patients with cyanotic heart disease. 1 Erythrocytosis. Chronic cyanosis causes an increase in red cell numbers as a way of increasing oxygen carrying capacity. The platelet count is sometimes reduced and the white cell count normal. The increased blood viscosity associated with the high red cell mass causes a slight increase in the risk of stroke.37 Most patients have a stable elevated haemoglobin level, but venesection is recommended if this is greater than 20 g/dL and the haematocrit is greater than 65%. Levels as high as this can be associated with the hyperviscosity syndrome: headache, fatigue and difficulty concentrating. Recurrent venesection can cause iron depletion and the production of microcytic red cells, which are stiffer than normal cells and so increase viscosity further. 2 Bleeding. Reduced platelet numbers, abnormal platelet function and clotting factor deficiencies mean these patients have an increased risk of haemorrhage. The most dangerous problem is pulmonary haemorrhage but bleeding from the gums and menorrhagia are more common. The use of anticoagulation must be restricted to those with a strong indication for treatment. 3 Gallstones. Chronic cyanosis and increased haem turnover are associated with an increased incidence of pigment gallstones. 4 Renal dysfunction and gout. Congestion of the renal glomeruli is associated with a reduced glomerular filtration rate and proteinuria. This and the increased turnover of red cells lead to urate accumulation and gout. 5 Pulmonary hypertension. Lesions associated with increased flow through the pulmonary circulation (e.g. a large atrial septal defect) can lead to a reactive rise in pulmonary arterial resistance. This is more likely to occur if the left to right shunt is large. Eventually these pulmonary vascular changes become irreversible, pulmonary pressures equal or exceed systemic pressures, and central cyanosis occurs because the intra-cardiac shunt reverses (Eisenmenger’s syndrome). Flow is now from right to left. There is then no benefit in attempting to correct the underlying cardiac abnormality. Earlier and more successful treatment of children with congenital heart disease has reduced the number of patients with this inexorable disease. Careful management of these conditions can nevertheless improve patients’ symptoms and survival. Reasonable exercise tolerance is usually maintained into adult life for most patients but progressive deterioration then occurs. Haemorrhagic complications, especially haemoptysis, are common. Thrombotic stroke, cerebral abscess and pulmonary infarction can also occur.
CARDIOLOGISTS IN H S R LAYOUT BANGALORE Cyanotic congenital heart disease Some of the more common cyanotic lesions are discussed below. There are, however, a number of problems common to patients with cyanotic heart disease. 1 Erythrocytosis. Chronic cyanosis causes an increase in red cell numbers as a way of increasing oxygen carrying capacity. The platelet count is sometimes reduced and the white cell count normal. The increased blood viscosity associated with the high red cell mass causes a slight increase in the risk of stroke.37 Most patients have a stable elevated haemoglobin level, but venesection is recommended if this is greater than 20 g/dL and the haematocrit is greater than 65%. Levels as high as this can be associated with the hyperviscosity syndrome: headache, fatigue and difficulty concentrating. Recurrent venesection can cause iron depletion and the production of microcytic red cells, which are stiffer than normal cells and so increase viscosity further. 2 Bleeding. Reduced platelet numbers, abnormal platelet function and clotting factor deficiencies mean these patients have an increased risk of haemorrhage. The most dangerous problem is pulmonary haemorrhage but bleeding from the gums and menorrhagia are more common. The use of anticoagulation must be restricted to those with a strong indication for treatment. 3 Gallstones. Chronic cyanosis and increased haem turnover are associated with an increased incidence of pigment gallstones. 4 Renal dysfunction and gout. Congestion of the renal glomeruli is associated with a reduced glomerular filtration rate and proteinuria. This and the increased turnover of red cells lead to urate accumulation and gout. 5 Pulmonary hypertension. Lesions associated with increased flow through the pulmonary circulation (e.g. a large atrial septal defect) can lead to a reactive rise in pulmonary arterial resistance. This is more likely to occur if the left to right shunt is large. Eventually these pulmonary vascular changes become irreversible, pulmonary pressures equal or exceed systemic pressures, and central cyanosis occurs because the intra-cardiac shunt reverses (Eisenmenger’s syndrome). Flow is now from right to left. There is then no benefit in attempting to correct the underlying cardiac abnormality. Earlier and more successful treatment of children with congenital heart disease has reduced the number of patients with this inexorable disease. Careful management of these conditions can nevertheless improve patients’ symptoms and survival. Reasonable exercise tolerance is usually maintained into adult life for most patients but progressive deterioration then occurs. Haemorrhagic complications, especially haemoptysis, are common. Thrombotic stroke, cerebral abscess and pulmonary infarction can also occur. 364 PRACTICAL CARDIOLOGY In a recent European survey, survival for patients with simple defects and Eisenmenger’s was to 32.5 years, but only 25.8 years for those with Eisenmenger’s resulting from complex abnormalities.38 There is a 50% maternal mortality risk with pregnancy. Quite minor surgical procedures are associated with high risk. Trials with endothelin antagonists are being conducted and continuous oxygen treatment can provide symptomatic relief. Lung and heart lung transplant should be considered for some of these patients. 6 Endocarditis. Most patients with congenital heart disease have a lifelong risk of infective endocarditis. Constant reminders of this risk should be given to the patients and their usual doctors. As well as appropriate antibiotic prophylaxis . before procedures, a high index of suspicion is very important. A febrile illness should not be treated with antibiotics until at least two sets of blood cultures have been taken. Early referral
Cardiologist in Chikkajala, Bangalore • Cyanotic congenital heart disease Some of the more common cyanotic lesions are discussed below. There are, however, a number of problems common to patients with cyanotic heart disease. 1 Erythrocytosis. Chronic cyanosis causes an increase in red cell numbers as a way of increasing oxygen carrying capacity. The platelet count is sometimes reduced and the white cell count normal. The increased blood viscosity associated with the high red cell mass causes a slight increase in the risk of stroke.37 Most patients have a stable elevated haemoglobin level, but venesection is recommended if this is greater than 20 g/dL and the haematocrit is greater than 65%. Levels as high as this can be associated with the hyperviscosity syndrome: headache, fatigue and difficulty concentrating. Recurrent venesection can cause iron depletion and the production of microcytic red cells, which are stiffer than normal cells and so increase viscosity further. 2 Bleeding. Reduced platelet numbers, abnormal platelet function and clotting factor deficiencies mean these patients have an increased risk of haemorrhage. The most dangerous problem is pulmonary haemorrhage but bleeding from the gums and menorrhagia are more common. The use of anticoagulation must be restricted to those with a strong indication for treatment. 3 Gallstones. Chronic cyanosis and increased haem turnover are associated with an increased incidence of pigment gallstones. 4 Renal dysfunction and gout. Congestion of the renal glomeruli is associated with a reduced glomerular filtration rate and proteinuria. This and the increased turnover of red cells lead to urate accumulation and gout. 5 Pulmonary hypertension. Lesions associated with increased flow through the pulmonary circulation (e.g. a large atrial septal defect) can lead to a reactive rise in pulmonary arterial resistance. This is more likely to occur if the left to right shunt is large. Eventually these pulmonary vascular changes become irreversible, pulmonary pressures equal or exceed systemic pressures, and central cyanosis occurs because the intra-cardiac shunt reverses (Eisenmenger’s syndrome). Flow is now from right to left. There is then no benefit in attempting to correct the underlying cardiac abnormality. Earlier and more successful treatment of children with congenital heart disease has reduced the number of patients with this inexorable disease. Careful management of these conditions can nevertheless improve patients’ symptoms and survival. Reasonable exercise tolerance is usually maintained into adult life for most patients but progressive deterioration then occurs. Haemorrhagic complications, especially haemoptysis, are common. Thrombotic stroke, cerebral abscess and pulmonary infarction can also occur.
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