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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.
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
This ordinarily consists of monitoring of  is suspected. heart rate and rhythm,  repeated measurement of systemic arterial pressure by cuff,  obtaining chest radiographs to detect heart failure,  repeated auscultation of the lung fields for pulmonary congestion,  measurement of urine flow,  examination of the skin and mucous membranes for evidence of the adequacy of perfusion, and
It may also improve arterial oxygenation by reducing pulmonary vascular congestion DIURETICS. Mild heart failure responds well to diuretics such as furosemide, Dose - 10 to 40 mg, repeated at 3- to 4-hour intervals if necessary. It reduces pulmonary capillary pressure reduces dyspnea. Decreased LVDV↓ LV wall tension - ↓ myocardial oxygen requirements and may lead to improvement of contractility and augmentation of the ejection fraction, stroke volume, and cardiac output. The reduction of elevated left ventricular filling pressure may also enhance myocardial oxygen delivery by diminishing the impedance to coronary perfusion attributable to elevated ventricular wall tension. .
Left Ventricular Failure Single most important predictor of mortality following STEMI in patients with STEMI Systolic dysfunction alone or both systolic and diastolic dysfunction can occur. LVDD leads to pulmonary venous hypertension and pulmonary congestion. Systolic dysfunction - ↓ cardiac output and of the ejection fraction. Predictors of LVF infarct size, advanced age and diabetes.[190] Mortality increases in association with the severity of the hemodynamic deficit.
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
THE BEST CARDIOLOGISTS IN YELAHANKA Indications for coronary angiography 1 Angina not responding to medical treatment in a patient without contraindications (e.g. extreme old age—usually older than about 85 these days—or severe co-morbidities) to cardiac surgery or angioplasty. 2 Continuing chest pain whose cause is not clear despite non-invasive investigations. The procedure may well be worthwhile if it reveals normal coronary arteries and prevents a patient being treated unnecessarily with more and more anti-anginal drugs. Non-invasive investigations are more often equivocal in women, and more women than men are found to have normal coronaries at angiography. 3 Preparation of a patient older than 35 or so for some other cardiac surgery (e.g. valve replacement). The surgeon needs to know whether significant coronary disease is present so that coronary grafting can be performed at the time of valve surgery. Otherwise, patients are at risk of ischaemic problems in the post-operative period. 4 Diagnosis of cardiomyopathy (p. 267) by excluding coronary artery disease and infarction as the cause of angina or cardiac failure. These patients may benefit from revascularisation if significant coronary disease is also present (‘ischaemic cardiomyopathy’). 5 Investigation of patients following myocardial infarction. Routine transfer to a centre with angiographic facilities after successful thrombolytic treatment is a grade D recommendation. There is no proof that a patient without continuing ischaemia has an improved prognosis when angiography and revascularisation are carried out routinely after infarction. The Open Artery Trial results suggest there is no benefit compared with optimal medical treatment for patients without ischaemic symptoms in having an occluded vessel opened five days or more after an infarction. However, spontaneous or induced ischaemia (by modified stress testing or perfusion imaging) leads to a grade B recommendation for angiography and intervention. The management of post-infarct patients is definitely easier if the coronary anatomy is known, and many units adopt the policy of early (within a week) angiography of infarct patients without contraindications to revascularisation. 6 Non-ST elevation acute coronary syndromes (p. 156). 7 Acute myocardial infarction in a unit where primary angioplasty can be performed
POPULAR CARDIOLOGISTS IN H S R LAYOUT Ventricular tachycardia Ventricular tachycardia is defined as three or more ventricular ectopic beats at a rate over 100/minute. It is said to be sustained if it lasts more than 30 seconds. Most broad-complex tachycardias are ventricular (rather than supraventricular with aberrant conduction). The diagnosis of VT is greatly strengthened if there is a history of myocardial infarction or cardiac failure but, oddly enough, the patient’s haemodynamics are of no help. A number of criteria have evolved over the years to help ascertain the diagnosis of VT over aberrancy. These include: evidence of AV dissociation—P waves can be seen unrelated to the QRS complexes (they are usually visible only at relatively slow VT rates) the presence of supraventricular capture or fusion beats visible retrograde conduction with 2:1 block (P waves visible following every second complex) the presence of monophasic R, qR or QR patterns in V1, provided a septal infarction has not modified a RBBB a taller left rabbit ear in RR' or qRR' complexes in V1 n QS complexes in V1 with a slow S descent and sharp upstroke—the opposite of LBBB—or a broad small primary R wave in rS morphology (the Rosenbaum pattern) RAD in the frontal plane with LBBB-like QRS complexes
IHEART SPECIALISTS IN HEBBALA ndications for coronary angiography 1 Angina not responding to medical treatment in a patient without contraindications (e.g. extreme old age—usually older than about 85 these days—or severe co-morbidities) to cardiac surgery or angioplasty. 2 Continuing chest pain whose cause is not clear despite non-invasive investigations. The procedure may well be worthwhile if it reveals normal coronary arteries and prevents a patient being treated unnecessarily with more and more anti-anginal drugs. Non-invasive investigations are more often equivocal in women, and more women than men are found to have normal coronaries at angiography. 3 Preparation of a patient older than 35 or so for some other cardiac surgery (e.g. valve replacement). The surgeon needs to know whether significant coronary disease is present so that coronary grafting can be performed at the time of valve surgery. Otherwise, patients are at risk of ischaemic problems in the post-operative period. 4 Diagnosis of cardiomyopathy (p. 267) by excluding coronary artery disease and infarction as the cause of angina or cardiac failure. These patients may benefit from revascularisation if significant coronary disease is also present (‘ischaemic cardiomyopathy’). 5 Investigation of patients following myocardial infarction. Routine transfer to a centre with angiographic facilities after successful thrombolytic treatment is a grade D recommendation. There is no proof that a patient without continuing ischaemia has an improved prognosis when angiography and revascularisation are carried out routinely after infarction. The Open Artery Trial results suggest there is no benefit compared with optimal medical treatment for patients without ischaemic symptoms in having an occluded vessel opened five days or more after an infarction. However, spontaneous or induced ischaemia (by modified stress testing or perfusion imaging) leads to a grade B recommendation for angiography and intervention. The management of post-infarct patients is definitely easier if the coronary anatomy is known, and many units adopt the policy of early (within a week) angiography of infarct patients without contraindications to revascularisation. 6 Non-ST elevation acute coronary syndromes . 7 Acute myocardial infarction in a unit where primary angioplasty can be performed . Risks of cardiac catheterisation Cardiac catheterisation is an invasive procedure and patients must be aware of
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