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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
the best cardiac clinics in yelahanka new town bangalore Ventricular arrhythmias Ventricular ectopic beats Like SVEBs, VEBs are common and, by themselves, generally harmless. Past attempts to suppress them as harbingers of malignant arrhythmias have caused more harm than good. Nevertheless, recognition of their electrocardiographic morphology and behaviour remain important. VEBs that have a fixed coupling to the preceding beats are thought to represent a localised ventricular re-entry and are said to be extra-systolic (extra-systoles). In the top strip of they each replace a sinus beat, with a sinus P wave buried inside the ectopic QRS; their pauses are exactly (fully) compensatory. In the bottom strip, the pause cannot be quantified but, unlike the aberrant beats of Ashman’s phenomenon in , there is hint of a compensatory pause, even during AF. Also unlike aberrant beats in Figure 3.33, the VEBs do not come after the longest cycles in AF. VEBs with same morphology but variable coupling intervals usually represent a continuous discharge from an ectopic focus, like a fixed-rate electronic pacemaker. They capture the ventricles whenever the latter are not refractory and, when they occur at the right time, produce ventricular fusion beats. Fusion beats occur when impulses from two origins, in the case seen in from the sinus node and the parasystolic focus, occur at almost the same time. The resultant QRS complex has features of both types of beat. These VEBs are called parasystolic
the best cardiac clinics in yelahanka new town bangalore Ventricular arrhythmias Ventricular ectopic beats Like SVEBs, VEBs are common and, by themselves, generally harmless. Past attempts to suppress them as harbingers of malignant arrhythmias have caused more harm than good. Nevertheless, recognition of their electrocardiographic morphology and behaviour remain important. VEBs that have a fixed coupling to the preceding beats are thought to represent a localised ventricular re-entry and are said to be extra-systolic (extra-systoles). In the top strip of they each replace a sinus beat, with a sinus P wave buried inside the ectopic QRS; their pauses are exactly (fully) compensatory. In the bottom strip, the pause cannot be quantified but, unlike the aberrant beats of Ashman’s phenomenon in , there is hint of a compensatory pause, even during AF. Also unlike aberrant beats in Figure 3.33, the VEBs do not come after the longest cycles in AF. VEBs with same morphology but variable coupling intervals usually represent a continuous discharge from an ectopic focus, like a fixed-rate electronic pacemaker. They capture the ventricles whenever the latter are not refractory and, when they occur at the right time, produce ventricular fusion beats. Fusion beats occur when impulses from two origins, in the case seen in from the sinus node and the parasystolic focus, occur at almost the same time. The resultant QRS complex has features of both types of beat. These VEBs are called parasystolic
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.
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.
Cardiologist in Chikkajala, Bangalore • Electronic pacemakers Pacemakers come as temporary or permanent, fixed-rate (although only if they are faulty these days), demand or rate-responsive, atrial, ventricular, biventricular or dual chamber, unipolar or bipolar and as a combination of many of these features. In routine ECG reporting the pacemaker’s exact programming is not usually known, but it is still possible to diagnose the pacemaker type Acute inferolateral infarction with LBBB. Although ST elevation and depression in the limb leads are suggestive, the more discrete elevation in V6 proves the diagnosis (arrows). Within hours, it disappeared and all that was left were primary T wave changes in the inferior leads ). The same patient as in , showing residual primary T wave changes in the inferior leads 90 PRACTICAL CARDIOLOGY Pathological Q waves in all the LV leads in a 90-year-old man with known old anterior infarction Table 3.1 The North American Society of Pacing and Electrophysiology (NASPE) and the British Pacing and Electrophysiology Group (BPEG) generic (NBG) pacemaker codes Position I II III IV V Category Chamber(s) paced Chamber(s) sensed Response to sensing Programmability, rate modulation Anti- tachyarrhythmia function(s) O = none A = atrium V = ventricle D = dual (A + V) O = none A = atrium V = ventricle D = dual (A + V) O = none T = triggered I = inhibited D = dual (D + I) O = none P = simple programmable M = multiprogrammable C = communicating R = rate modulation O = none P = pacing (antitachyarrhythmia) S = shock D = dual (P + S) Manufacturers’ designation only S = single (A or V) S = single (A or V) Note: positions I–III are used exclusively for anti-bradyarrhythmia function. Source: and the all-important capacity to sense the native complexes and pace the appropriate chambers. An international letter code has evolved for describing pacemaker types, shown in Table 3.1. Thus: n VVI = ventricular pacing and sensing, inhibition (in response to sensing)—the pacemaker is inhibited and produces no impulse when it senses a ventricular impulse n AAI = atrial pacing and sensing 3• AN OVERVIEW OF CLINICAL ELECTROCARDIOGRAPHY 91 n VOO = fixed-rate (asynchronous) ventricular pacing, no sensing—this is used for pacemaker testing and is the usual response of a pacemaker when a magnet is placed over it; modern pacemakers are always demand (inhibited) devices n DDD = atrial and ventricular (dual) sensing and pacing n DDDR = same as universal (DDD) pacemaker, with rate-responsiveness—the device will change its pacing rate in response to the patient’s physical activity n VDD = ventricular pacing with dual-chamber sensing (through a single lead). The above codes include the implantable cardioverter-defibrillators. ‘Failed pacemaker’ is not a proper or complete diagnosis. Failure may be intermittent or complete and involve sensing or capture (pacing), or both. A few examples are shown in More examples and details of the pacemaker syndrome and arrhythmias Miscellaneous conditions Chamber hypertrophy Left ventricular hypertrophy Although the ECG is reasonably specific, it is not as sensitive as echocardiography in detecting LVH. The LVH voltage alone may be a normal finding in younger subjects, but in adults over 35 years it usually connotes true LVH, especially if corroboratory findings are present ). Unfortunately, LVH with ST/T changes may be impossible to separate from LVH voltage complicated by ST/T changes of different, especially ischaemic, origin Right ventricular hypertrophy The main criteria for detecting RVH are RAD over +110° and a dominant R wave in V1 (in the absence of its other causes and in the presence of normal-duration QR congenital heart disease conduction defects often come to obscure the hypertrophy patterns.
Cardiologist in Chikkajala, Bangalore • Electronic pacemakers Pacemakers come as temporary or permanent, fixed-rate (although only if they are faulty these days), demand or rate-responsive, atrial, ventricular, biventricular or dual chamber, unipolar or bipolar and as a combination of many of these features. In routine ECG reporting the pacemaker’s exact programming is not usually known, but it is still possible to diagnose the pacemaker type Acute inferolateral infarction with LBBB. Although ST elevation and depression in the limb leads are suggestive, the more discrete elevation in V6 proves the diagnosis (arrows). Within hours, it disappeared and all that was left were primary T wave changes in the inferior leads ). The same patient as in , showing residual primary T wave changes in the inferior leads 90 PRACTICAL CARDIOLOGY Pathological Q waves in all the LV leads in a 90-year-old man with known old anterior infarction Table 3.1 The North American Society of Pacing and Electrophysiology (NASPE) and the British Pacing and Electrophysiology Group (BPEG) generic (NBG) pacemaker codes Position I II III IV V Category Chamber(s) paced Chamber(s) sensed Response to sensing Programmability, rate modulation Anti- tachyarrhythmia function(s) O = none A = atrium V = ventricle D = dual (A + V) O = none A = atrium V = ventricle D = dual (A + V) O = none T = triggered I = inhibited D = dual (D + I) O = none P = simple programmable M = multiprogrammable C = communicating R = rate modulation O = none P = pacing (antitachyarrhythmia) S = shock D = dual (P + S) Manufacturers’ designation only S = single (A or V) S = single (A or V) Note: positions I–III are used exclusively for anti-bradyarrhythmia function. Source: and the all-important capacity to sense the native complexes and pace the appropriate chambers. An international letter code has evolved for describing pacemaker types, shown in Table 3.1. Thus: n VVI = ventricular pacing and sensing, inhibition (in response to sensing)—the pacemaker is inhibited and produces no impulse when it senses a ventricular impulse n AAI = atrial pacing and sensing 3• AN OVERVIEW OF CLINICAL ELECTROCARDIOGRAPHY 91 n VOO = fixed-rate (asynchronous) ventricular pacing, no sensing—this is used for pacemaker testing and is the usual response of a pacemaker when a magnet is placed over it; modern pacemakers are always demand (inhibited) devices n DDD = atrial and ventricular (dual) sensing and pacing n DDDR = same as universal (DDD) pacemaker, with rate-responsiveness—the device will change its pacing rate in response to the patient’s physical activity n VDD = ventricular pacing with dual-chamber sensing (through a single lead). The above codes include the implantable cardioverter-defibrillators. ‘Failed pacemaker’ is not a proper or complete diagnosis. Failure may be intermittent or complete and involve sensing or capture (pacing), or both. A few examples are shown in More examples and details of the pacemaker syndrome and arrhythmias Miscellaneous conditions Chamber hypertrophy Left ventricular hypertrophy Although the ECG is reasonably specific, it is not as sensitive as echocardiography in detecting LVH. The LVH voltage alone may be a normal finding in younger subjects, but in adults over 35 years it usually connotes true LVH, especially if corroboratory findings are present ). Unfortunately, LVH with ST/T changes may be impossible to separate from LVH voltage complicated by ST/T changes of different, especially ischaemic, origin Right ventricular hypertrophy The main criteria for detecting RVH are RAD over +110° and a dominant R wave in V1 (in the absence of its other causes and in the presence of normal-duration QR congenital heart disease conduction defects often come to obscure the hypertrophy patterns.
Diabetologists in Vidyaranyapura, Bangalore • Postmenopausal changes The lower incidence of coronary heart disease in women under 60 has been thought to be related to the protective effect of oestrogens. This has led to trials of hormone replacement therapy (HRT) in postmenopausal women.23 The results of these trials were surprising to many of the investigators. HRT provided no protection to postmenopausal women. In some groups there was an increased risk of myocardial infarction, especially in the first year. There was a definite increase in the risk of stroke and venous thromboembolism, and there was a probable increased risk of breast cancer. At the moment HRT has no role in the prevention of cardiovascular disease.
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