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How sleeping less than 6 hours affects your health After being awake for almost 14-16 hours, our body demands sleep. Minimum sleeping time required for a healthy mind and body is 7-8 hours. Although, this duration varies according to age. Because generally speaking, where a child can sleep for 12-14 hours, grownups can sleep for not more than 9 hours. Sound sleep is very essential otherwise, it can be harmful for our health. Let’s see how sleeping for less than 6 hours affects our health. Headache, weight gain and poor vision: When you sleep for less than 6 hours a day, it can not only give you headache all the time but can lead to a poor vision also. And if continued for a long time, may hamper your eyesight. The lesser you sleep the more weight you gain. And after-effects of gaining weight could be even more hazardous. Memory loss, heart disease, infection: Sleeplessness can have an adverse effect on one’s memory too. A person may find it difficult to remember even simple things. Also, infections can take a longer time to heal because sleep is something that stabilises and balances everything that goes wrong while we are awake. If we don’t get proper sleep, the process of healing takes longer. Lack of sleep can also elevate blood pressure which ultimately affects the heart. Urine overproduction, stammering and accident: Sleeping slows down urinating process but when you are awake for longer hours, you might have to urinate more than usual. Lack of sleep can also make you stammer while speaking. If lack of sleep continues, you may not be able to communicate properly. When you do not have sound sleep, your mental condition would not be stable because of declining concentration. You can be accident prone if you drive in such a condition. These are just a few of the ill effects. Sleeping for less than 5 hours is far more dangerous than you can even think. From behavioural to mental to physical effects, it can harm you in many more ways, So, have a sound sleep to avoid complications in life.
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
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,
HEART SPECIALISTS IN HEBBALABANGALORE Case-based learning: cardiovascular risk assessment Mr RF is 60 years old and presents for a check-up because he is concerned he may be at risk of heart disease. Objectives for the group to understand How should this type of request be managed What can be done to assess an individual’s future cardiac risk, and what can be done to improve the prognosis for those at increased risk Epidemiology and population health The presenter should ask the group to consider the concept of risk factors for cardiovascular disease and the differences between population risk factors and those for an individual. How did the concept of risk factors arise Presenting symptoms and clinical examination What questions should be asked of Mr RF to begin the risk factor assessment 1 Is there a history of ischaemic heart disease or symptoms of heart disease 2 Has his cholesterol level been checked in the past What was itHas it been treated with diet or drugs, or both Has the level improved 3 Is he a diabetic, or has he had an abnormal blood sugar measurement 4 Is there a history of high blood pressure Has this been treated If so, how 5 Is there a history of heart disease in the familIf so, who has been affected and at what age 6 Does he smoke? How many cigarettes a day If he has ceased smoking, when did he stop 7 Does he exercise regularly 8 Have any cardiac investigations been performed before What were the results 9 Is there a history of peripheral arterial disease (claudication) or erectile dysfunction The group should appreciate that considerable information about risk can be obtained by asking simple questions. What physical examination should be performed
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.