http://WWW.HEARTDIABETESCARE.COM
SAMIKSHAHEARTCARE 57698d5b9ec66b0b6cfb5b6b False 573 1
OK
background image not found
Found Update results for
'different segments'
9
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.
Indications for Hemodynamic Monitoring in Patients with STEMI Management of complicated acute myocardial infarction Hypovolemia versus cardiogenic shock Ventricular septal rupture versus acute mitral regurgitation Severe left ventricular failure Right ventricular failure Refractory ventricular tachycadia Differentiating severe pulmonary disease from left ventricular failure Assessment of cardiac tamponade Assessment of therapy in selected individuals Afterload reduction in patients with severe left ventricular failure Inotropic agent therapy Beta-blocker therapy Temporary pacing (ventricular versus atrioventricular) Intraaortic balloon counterpulsation Mechanical ventilation
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
POPULAR CARDIOLOGISTS IN SAHAKARANAGAR 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 fSAor 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 QRS) In congenital heart disease conduction defects often come to obscure the hypertrophy patterns.
POPULAR CARDIOLOGISTS IN SAHAKARANAGAR Cardiomyopathies and valvular heart disease Regardless of the status of the coronary arterial tree, both primary and secondary heart muscle disease can produce anginal pain through the imbalance of the oxygen demand and supply. Hypertrophic cardiomyopathy is a relatively common cause of angina in the presence of normal coronary arteries. Aortic stenosis is the most common valvular cause of exertional chest tightness, which is probably due to myocardial ischaemia Exertional chest pain, which may be due to right ventricular angina, is a feature of pulmonary hypertension . Syndrome X There is some confusion regarding the ‘metabolic’ and ‘cardiac’ varieties. The former is a combination of insulin resistance, obesity, pro-inflammatory state and so on, leading to raised cardiovascular risk in the sufferers. The latter is, or should be, a form of stable effort angina that can be ascribed to coronary microvascular malfunction.23 The epicardial coronary tree is normal and the diagnosis is rather difficult to make except by exclusion. Acute coronary syndromes The terminology used to describe acute coronary syndromes (ACSs) continues to evolve as clinicians attempt to adjust to the accumulating evidence of the usefulness of modern cardiac markers and the treatment implications of different results. The most recent terminology is designed to help with treatment decisions based on the earliest clinical information from the patient. This comes from the history and the ECG. When the patient’s symptoms suggest an acute coronary syndrome, the first decisions about diagnosis and treatment are based on the ECG. If there is ST elevation present in a pattern to suggest myocardial infarction, the diagnosis is of ‘ST elevation myocardial infarction’ (STEMI). If there is no ST elevation, the initial diagnosis is of ‘non-ST elevation acute coronary syndrome’ (NSTEACS).24 This elegant phrase has replaced ‘non-ST elevation myocardial infarction’ (non- STEMI). The reason is that the diagnosis of infarction cannot be made in the absence of ST elevation until cardiac marker estimations are available. The decisions about treatment, however, need to be made immediately and are based on symptoms and ECG changes.
HEART DOCTORS IN YELAHANKA NEWTOWN, BANGALORE Management of ACS (NSTEACS) Patients with this diagnosis represent a rather heterogeneous group. Some have had the recent onset of angina at the extremes of exercise, others have angina at rest associated with ECG changes. This variation has made attempts to study the effects of different treatment rather difficult. Although the majority of patients with myocardial infarction have a preceding period of unstable angina, only about 5% of all patients admitted to hospital with a diagnosis of an ACS go on to infarct during that admission. The in-hospital mortality for these patients is low. Mortality rates of less than 2% are usual. Nevertheless, there is a real short-term and longerterm risk of infarction, recurrent admission with unstable symptoms and death which is higher than that of patients with stable angina. The diagnosis should therefore lead to admission to a CCU. The cardiac enzymes are, by definition, not elevated in these patients but the newer, more sensitive tests for troponin T and troponin I may be abnormal and indicate a worse prognosis . In the CCU, bed rest, oxygen and ECG monitoring are routinely enforced and any mobile phones taken away (allegedly to protect the monitoring equipment). Recurrence of chest pain can be assessed quickly and ECGs performed to look for changes suggesting infarction. The cardiac biomarkers can be checked regularly. All patients should receive aspirin (300 mg) unless there is a contraindication. Patients with an intermediate or a higher risk should also be given clopidogrel (usually a 300–600 mg loading dose). The use of intravenous heparin has become standard treatment. A typical starting dose is 5000 units as a bolus followed by 24, 000 units over 24 hours. The activated partial thromboplastin time (APPT) should be measured after about six hours of treatment and the infusion rate of heparin adjusted to maintain this at about twice normal. Heparin is generally safe when used in this way. Bleeding problems may sometimes occur and the platelet count should be checked every few days so that heparin-induced thrombocytopenia (HITS), a rare but serious complication, can be detected early. Low molecular weight heparins are at least as effective as unfractionated heparin. These drugs have some advantages over heparin. Their dose response effect is more predictable and they cause less thrombocytopenia. They are effective given subcutaneously without APPT monitoring and are now cheaper than IV heparin when savings on APPT monitoring and the use of infusion sets are considered. A standard twice-daily dose is given according to the patient’s weight—1 mg/kg for enoxaparin (Clexane). The dose is reduced by half for those with moderate or severe renal impairment and for those over the age of 75. Additional treatment should include beta-blockers unless these are contraindicated. These drugs reduce the number of ischaemic episodes and probably the risk of myocardial infarction. Nitrates can be a useful adjunctive treatment. They may be given orally, topically or intravenously. The IV dose can be titrated up or down depending on the amount of pain the patient is experiencing and the severity of side effects such as hypotension and headache. The problem of tachyphylaxis with nitrates can be overcome by steady increases in the IV dose if necessary. Calcium antagonists are appropriate treatment for patients intolerant of beta-blockers and may sometimes be added to beta-blockers. Nifedipine, especially in its short-acting form, should not be used for patients with acute coronary syndromes unless they are already taking beta-blockers. Thrombolytic drugs have been disappointing when used for NSTEACS. In trials where they have been used for patients with ischaemic chest pain but without ST elevation there has been a trend towards an adverse outcome. This may be related to the rebound hypercoagulable state that can occur after their use. In general they should not be used for the treatment of NSTEACS. Glycoprotein IIb/IIIa inhibitors (p. 198) should be given for high-risk patients,
SAMIKSHA HEART AND DIABETIC CARE ''CONNECTIVE TISSUE DISORDERS'' ''Marfan Syndrome'' Marfan syndrome is a systemic connective tissue disorder with a frequency of 2 to 3 in 10, 000. The disorder is characterized by manifestations involving the cardiovascular, skeletal, and ocular systems. Current diagnostic criteria are based on involvement of above organ systems and family history. Cardiovascular manifestations include mitral valve prolapse, progressive aortic root enlargement, and ascending aortic aneurisms, possibly leading to aortic regurgitation, dissection, or rupture. Some characteristic skeletal manifestations of this syndrome include disproportional increase of linear bone growth resulting in malformations of the digits (arachnodactyly), craniofacial abnormalities, pectus excavatum/carinatum, and scoliosis. A common ocular involvement is severe myopia and lens dislocation in one or both eyes (ectopia lentis). Marfan syndrome is an autosomal dominant disorder caused by fibrillin-1 gene mutations encoding for the extracellular matrix protein fibrillin (Fbn-1). Fibrillin is an integral component of both elastic and nonelastic connective tissue. The mechanism of fibrillin mutation in Marfan syndrome remains unclear. However, animal models of Fbn-1 have demonstrated a role of TGF-beta signaling. In some patients with phenotypes similar to Marfan syndrome but without fibrillin- 1 gene mutations, TGF-beta receptor mutations have been identified, suggesting a significant role of TGF-beta pathway in the pathogenesis of Marfan syndrome features. Aortic root involvement remains the leading cause of death in patients with Marfan syndrome. Echocardiography is recommended to routinely screen and to follow aortic root dilation. In addition, all first-degree relatives of the family should have screening echocardiography. Patients should be advised against strenuous exercises. Medical therapy for Marfan syndrome includes beta-blockers to reduce myocardial contractility and pulse pressure. Animal models of Marfan syndrome have demonstrated a possible benefit of losartan in preventing progression of the disease by inhibiting the TGF-beta pathway, and this therapy is the subject of an active clinical trial. Elective aortic root replacement remains the therapy of choice once the aortic root becomes significantly enlarged. Marfan patients who become pregnant need to be counseled not only about the 50% chance of transmitting the disease but also the substantially increased risk of aortic rupture/dissection during and after pregnancy. Important components of Marfan syndrome counseling are consideration of contraception and pregnancy management. Loeys-Dietz Syndrome Recently, an aortic aneurysm syndrome has been identified with TGF-beta receptor mutations. Loeys-Dietz syndrome is an autosomal dominant condition with a characteristic triad of arterial tortuosity/aneurysm, hypertelorism, and bifid uvula or cleft palate. There is significant overlap with Marfan syndrome, and the management is similar in terms of cardiovascular manifestation. Early, elective, surgical intervention should be considered in patients with significant aneurysmal dilation of the aorta. Some clinicians have argued for much earlier surgical intervention for the dilated aorta in this condition, compared with Marfan syndrome, since there appears to be a much greater risk of rupture and dissection at earlier ages and smaller aortic sizes. Pregnancy counseling is also an integral part of therapy. Ehlers-Danlos Syndrome Ehlers-Danlos syndrome is a group of disorders that affect connective tissue development due to defects in collagen and connective tissue biosynthesis. Prevalence of the disease is about 1 in 400, 000 people in the United States. Cardiac manifestations include spontaneous rupture of medium to large sized arteries including the aorta. Frequently, extracardiac presentations include hyperextensible skin and hypermobile joints. To date, 11 types of the disorder have been recognized, but collagen defects have been described in only 6 types. Although all types of Ehlers-Danlos syndrome affect the joints and the skin, clinical features vary by type. Different features characterize each type of the syndrome. Type IV carries the poorest prognosis, especially due to spontaneous ruptures of arteries and organs. Extreme caution needs to be taken if surgical intervention is needed due to weakened connective tissue structures. Many genes, including ADAMTS2, COL1A1, COL1A2, COL3A1, COL5A1, COL5A2, PLOD1, and TNXB, have been implicated in the pathogenesis of Ehlers- Danlos syndrome, but the predominant cardiovascular concern exists in the Type IV vascular form of Ehlers-Danlos associated with mutations in the COL3A1 gene and aortic dilation/aneurysms. Other less commonly associated anomalies include ventricular septal defect, patent ductus arteriosus, bicuspid pulmonic valve, and Ebstein’s anomaly. Bicuspid aortic valve has been shown to demonstrate familial clustering. However, identifying culprit genes have been difficult due to variable penetrance and the common nature of the disorder.
the best cardiologists in yelahanka new town bangalore 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 QRS) . In congenital heart disease conduction defects often come to obscure the hypertrophy patterns. An atrial (AAI) pacemaker in a patient with anterior myocardial infarction of uncertain age. There is sensing (inhibition) only after some native or paced P waves. The pacemaker captures the atria whenever the latter are not refractory: there is no failure to pace. The middle capture beat is earlier than the other two and has a longer PR interval and aberrant RBBB-type ventricular conduction. This is a pacemaker sensing problem. Reprogramming may enable the pacemaker to sense a smaller atrial amplitude and be inhibited correctly. A DDD pacemaker in trouble: there is no atrial capture and the ventricular complexes are capturing the atria on their own. The retrograde P wave interrupts the T wave and triggers another paced QRS whose retrograde conduction is blocked by the original retrograde P wave. Were it not for this block, an endless loop re-entry (paced) tachycardia would occur. The paced complexes have the typical LBBB/left-axis deviation expected from right ventricular apical pacing. Failure to capture may mean the lead has been displaced or that scarring has developed between the tip of the lead and the myocardium. Sometimes, reprogramming an increase in the output of the pacemaker will fix the problem. a = atrial pacing spike (not followed by a P wave); b = ventricular pacing spike (produced after the atrial spike after a programmed AV delay and followed by a paced ventricular beat); c = retrograde P wave following ventricular paced beat; d = pause caused by blocked retrograde conduction of the previo A DDD or VDD pacemaker with intermittent failure to pace. A 4:3 pacemakerventricular block results in trigeminy even though normal sinus rhythm continues throughout. The normal
the best cardiologists in yelahanka new town bangalore 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 QRS) . In congenital heart disease conduction defects often come to obscure the hypertrophy patterns. An atrial (AAI) pacemaker in a patient with anterior myocardial infarction of uncertain age. There is sensing (inhibition) only after some native or paced P waves. The pacemaker captures the atria whenever the latter are not refractory: there is no failure to pace. The middle capture beat is earlier than the other two and has a longer PR interval and aberrant RBBB-type ventricular conduction. This is a pacemaker sensing problem. Reprogramming may enable the pacemaker to sense a smaller atrial amplitude and be inhibited correctly. A DDD pacemaker in trouble: there is no atrial capture and the ventricular complexes are capturing the atria on their own. The retrograde P wave interrupts the T wave and triggers another paced QRS whose retrograde conduction is blocked by the original retrograde P wave. Were it not for this block, an endless loop re-entry (paced) tachycardia would occur. The paced complexes have the typical LBBB/left-axis deviation expected from right ventricular apical pacing. Failure to capture may mean the lead has been displaced or that scarring has developed between the tip of the lead and the myocardium. Sometimes, reprogramming an increase in the output of the pacemaker will fix the problem. a = atrial pacing spike (not followed by a P wave); b = ventricular pacing spike (produced after the atrial spike after a programmed AV delay and followed by a paced ventricular beat); c = retrograde P wave following ventricular paced beat; d = pause caused by blocked retrograde conduction of the previo A DDD or VDD pacemaker with intermittent failure to pace. A 4:3 pacemakerventricular block results in trigeminy even though normal sinus rhythm continues throughout. The normal
1
false