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THE BEST CARDIOLOGISTS IN YELAHANKA nvestigations of possible or probable stable angina Electrocardiography A standard 12-lead ECG should be obtained in all patients. This is likely to be normal in almost half of patients with subsequently proven coronary artery disease. Nevertheless, an abnormal trace lends weight to the symptoms and favours further investigation. Chest X-ray Routine radiology is not essential but may reveal important co-morbidities. It should always be performed in those with clinical evidence of hypertension, pericarditis (p. 174), heart failure or valvular disease, if only as a baseline. It is similarly indicated for patients with suspected or known pulmonary or systemic disease such as rheumatoid arthritis, COPD or alcoholism. Routine blood tests All patients with suspected angina should have the following routine investigations at presentation (NHF grade A recommendation): n fasting lipids, including total cholesterol, LDLs, HDLs and triglycerides—risk factors n fasting blood sugar—risk factor n full blood count—anaemia exacerbates angina n serum creatinine—impaired renal function is a risk factor and can be worsened by some cardiac investigations. If indicated clinically, thyroid function
CARDIOLOGY DOCTORS IN HOSUR ROAD Pulmonary embolism This is not quite a cardiac condition and not quite a respiratory condition but it is often managed by cardiologists. Modern CT pulmonary angiography is very sensitive and specific for the diagnosis of PE. A negative scan that is of good quality effectively excludes the diagnosis. The scans are so sensitive that small distal emboli may be detected in patients who do not have convincing symptoms of embolism. This poses a therapeutic problem that may be avoided if scans are not ordered inappropriately. Some patients cannot have a CTPA, usually because of renal impairment that would make the injection of contrast risky. A V/Q nuclear scan is then a reasonable alternative to a CTPA. These scans are less accurate than CT pulmonary angiography but the clinical suspicion of PE and a lung scan reported as intermediate or high probability is an indication for treatment. Patients should be admitted to hospital and treatment begun with intravenous heparin or subcutaneous low molecular weight heparin. The latter has the advantage that the dose is determined by body weight and repeated measurements of clotting times are not required. In some cases it may be possible to treat patients with small pulmonary emboli at home with supervised low molecular weight heparin. Either way, soon after diagnosis patients should be started on oral anticoagulation treatment with warfarin. A stable INR may often be achieved within five days or so, the heparin ceased and the patient discharged. Most patients with dyspnoea as a result of PE begin to feel better within a few days of starting treatment. It is often difficult to know how long to continue treatment with warfarin. The usual recommendation for an uncomplicated first PE is three to six months. Recurrent PE may be an indication for lifelong treatment. It also suggests a need to investigate for clotting abnormalities (e.g. anti-thrombin III deficiency, protein S and protein C deficiency, abnormal Factor V and anti-nuclear antibody). A very large and life-threatening PE which is associated with the sudden onset of severe dyspnoea and hypotension may be an indication for thrombolytic treatment. An echocardiogram may show abnormal right ventricular function in these ill patients and help in the decision. Experience with this is limited and the optimum regimen is not really known. Tissue plasminogen activator (TPA) is now indicated for this purpose and current recommendations are for a 10 mg bolus over two minutes followed by 90 mg over two hours.
THE BEST CARDIOLOGISTS IN YELAHANKA Aortic regurgitation The incompetent aortic valve allows regurgitation of blood from the aorta to the left ventricle during diastole for as long as the aortic diastolic pressure exceeds the left ventricular diastolic pressure. Symptoms: Occur in the late stages of disease and include exertional dyspnoea, fatigue, palpitations (hyperdynamic circulation) and exertional angina. General signs: Marfan’s syndrome may be obvious. The pulse and blood pressure: The pulse is characteristically collapsing; there may be a wide pulse pressure. The neck: Prominent carotid pulsations (Corrigan’s sign). Palpation: The apex beat is characteristically displaced and hyperkinetic. A diastolic thrill may be felt at the left sternal edge when the patient sits up and breathes out. Auscultation): A2 (the aortic component of the second heart sound) may be soft; a decrescendo high-pitched diastolic murmur beginning immediately after the second heart sound and extending for a variable time into diastole—it is loudest at the third and fourth left intercostal spaces; a systolic ejection murmur is usually present (due to associated aortic stenosis or to torrential flow across a normal diameter aortic valve). Signs indicating severe chronic aortic regurgitation: Collapsing pulse; wide pulse pressure; long decrescendo diastolic murmur; left ventricular S3 (third heart sound); soft A2; signs of left ventricular failure. Causes of chronic aortic regurgitation: (i) Rheumatic (rarely the only murmur in this case), congenital; (ii) aortic root dilatation—Marfan’s syndrome, dissecting aneurysm. 8• THE PATIENT WITH A MURMUR 305 a b Valve cusps often thickened and calcified Left ventricle may be hypertrophied Ascending aorta may be dilated Systole Diastole S1 A2 P2 S1 Ejection click (Suggests congenital AS) Normal Mild S1 S1 Moderate S1 P2 A2 S1 Severe Reversed S2 Single (S2)
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.
THE HYPERDYNAMIC STATE. MI with hyperdynamic state—that is, elevation of sinus rate, arterial pressure, and cardiac index, occurring singly or together in the presence of a normal or low left ventricular filling pressure—and if other causes of tachycardia such as fever, infection, and pericarditis can be excluded, treatment with beta blockers is indicated. Presumably, the increased heart rate and blood pressure are the result of inappropriate activation of the sympathetic nervous system, possibly secondary to augmented release of catecholamines, pain and anxiety, or some combination of these.
A risk factor is a demographic characteristic associated with an increased risk of ischaemic heart disease when other variables have been controlled. The presence of a risk factor in an individual increases his or her relative risk of a coronary event (angina, infarction or death). The absolute risk of a coronary event depends on the individual’s total number of risk factors and theirseverity (total risk). Important coronary risk factors are shown in Table 1.1. Risk assessment charts have been developed to estimate a patient’s cardiac risk over a number of years using easily identified risk factors. There are charts for different populations. The charts can be used to predict cardiovascular events or mortality (as in the NHF chart in Fig 1.1 on p. 4) or cardiac risk (systematic coronary risk evaluation system or SCORE charts). These charts can be very helpful in deciding when intervention to reduce risk is warranted; for example, when anti-hypertensive treatment should be commenced for a patient with mild blood pressure elevation. Risk factor reduction involves assessing the presence, severity and importance of risk factors for a
Average reductions in coronary events (benefits are greatest in patients with highest total risk) 1 Smoking cessation: 50% reduction in coronary events6 2 Low-dose aspirin in high-risk patients: 25% reduction in coronary events7 3 20% reduction in total cholesterol with statin treatment: 30% reduction in coronary events8 4 Treatment with pravastatin after acute coronary events: 22% reduction in mortality9 5 5–6 mmHg reduction in blood pressure: 15% reduction in coronary events (40% risk reduction for stroke)10 6 30 minutes of moderate exercise a day: 18% reduction in coronary events11 CARDIAC SPEACIALIST IN HEBBALA
THE BEST CARDIOLOGISTS NEAR HSR LAYOUT Coronary angiography (cardiac catheterisation) This procedure enables the cardiologist to visualise the coronary arteries . It is the standard against which other less-invasive investigations are assessed. Selective catheterisation of the right and left coronary ostia is performed. Contrast is then injected into the vessels and digital tape or disc storage of the images obtained. In most hospitals the patient is admitted on the morning of the test and allowed to go home that afternoon. The procedure is most often performed through the femoral artery (Judkins technique) . This artery can be punctured through the skin under local anaesthetic. A fine softtipped guide wire is then advanced into the artery and the needle withdrawn (Seldinger method). A short guiding sheath can then be placed over the wire and long cardiac catheters advanced through this sheath along a long guide wire into the femoral artery and up via the aorta to the aortic arch. The catheter and wire are advanced under X-ray control. Usually one catheter with a curved tip (pig-tail catheter; is advanced across the aortic valve into the left ventricle where left ventricular pressures are measured via a pressure transducer connected to the other end of the catheter. Measurement of the left ventricular end-diastolic pressure gives an indication of left ventricular function. Raised end-diastolic pressure (over 15 mmHg) suggests left ventricular dysfunction . The catheter is then connected to a pressure injector. This enables injection of a large volume of contrast over a few seconds; for example, 35 mL at 15 mL/second. X-ray recording during injection produces a left ventriculogram , Here left ventricular contraction can be assessed and the ejection fraction (percentage of end-diastolic volume ejected with each systole) estimated. The normal is 60% or more. The figure obtained by this method tends to be higher than that produced by the nuclear imaging method—gated blood pool scanning. The guide wire is reintroduced and the catheter withdrawn to be replaced by one shaped to fit into the right or left coronary orifice...
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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