Antibiotics Aortic Insufficiency
Aortic Insufficiency and Antibiotics - Aortic Insufficiency Treatment - Aortic valve prolapse - Aortic regurgitation
The aortic valve is between the heart's left ventricle (lower chamber that pumps blood to the body) and the aorta (the large artery that receives blood from the heart's left ventricle and distributes it to the body). Regurgitation means the valve doesn't close properly, and blood can leak backward through it. This means the left ventricle must pump more blood than normal, and will gradually get bigger because of the extra workload. Aortic regurgitation can range from mild to severe.
This is a condition in which the aortic valve has become disfigured to such an extent that its leaflets no longer are able to completely oppose each other during diastole
This condition allows blood to flow back into the left ventricle from the ascending aorta during diastole. Normally, there is no leakage of blood from the ascending aorta back into the left ventricle after systole.
Some people may have no symptoms for years. But as the condition worsens, symptoms will appear. These can include:
Causes of Aortic Regurgitation
Aortic valve regurgitation can be caused by infection of the aortic valve due to syphilis via unprotected coitus and bacteria, which have gained access to the blood stream and the aortic valve through the use of illicit drugs intravenously.
Treatment of Aortic Regurgitation
Patients with mild aortic regurgitation who have few or no symptoms need to see their physician regularly. As conditions worsen, medications may be used. These drugs can help regulate the heart rhythm, rid the body of fluids to control edema, and/or help the left ventricle pump better.
Serious cases may require surgical treatment. This involves replacing the diseased valve with an artificial one.
People with aortic regurgitation are at increased risk for developing an infection of the heart valve or lining of the heart (endocarditis). In the past, the American Heart Association has recommended that patients with aortic regurgitation take a dose of antibiotics before certain dental or surgical procedures. However, our association no longer recommends antibiotics before dental procedures except for patients at the highest level of risk for bad outcomes from endocarditis, such as:
Symptomatic patients with severe AR need medical and surgical treatment. Medical treatment consists of the administration of digitalis, diuretics, and vasodilators. Digitalis acts by increasing myocardial contractility, often reducing LV end-diastolic volume while increasing the LV ejection fraction and also the cardiac output if it is reduced in the resting state. Digitalis is clearly indicated in patients with symptoms.
Medical Treatment of Patients with Aortic Regurgitation
The need for and benefits of this therapy in asymptomatic patients have not been well documented. Diuretics are of value when the left atrial pressure is elevated and in the presence of heart failure.
Vasodilators are either arterial, venous, or both. Vasodilators act by reducing the peripheral arterial resistance, which favors forward cardiac output and reduces regurgitant volume; initially, the total LV stroke volume remains unchanged. If the left atrial pressure is elevated and LV ejection fraction reduced, vasodilators frequently result in an improvement in both. Long-term hydralazine therapy in symptomatic patients resuits in significant benefit in only 20 to 35 percent of patients.Those who are likely to benefit cannot be predicted. Vasodilators are indicated in patients who refuse surgery or are not operative candidates for any reason.
Vasodilators are also indicated for short-term therapy in patients awaiting valve replacement to optimize their hemodynamics (reduce filling pressures and increase cardiac output) and thus reduce their operative risks. If LV systolic function is normal, they can be given long-acting nifedipine. if they have abnormal LV systolic function, they should be treated with digitalis and ACE inhibitors; diuretics and hydralazine, with or without nitrates, can be used if needed. Small doses of hydralazine (50 mg) are without therapeutic effect in AR, and larger doses (approximately 100 mg) need to be given only twice daily; the twice-daily regimen reduces the incidence of side effects. Hydralazine should be started in small doses and gradually increased, depending on patient tolerance of the drug.
Vasodilators are of considerable short-term benefit in patients in functional classes III and IV or heart failure. All such patients need digitalis, diuretics, and ACE inhibitors. In patients in functional class IV with heart failure, vasodilators should ideally be started after the institution of beside henmodynamic monitoring-that is measuring of pulmonary artery wedge pressure and cardiac output with the use of ballon flotation catheters. Hemodynamic monitoring accurately identifies patients who need the therapy, since clinical judgments can be wrong. It establishes whether arterial dilators alone will suffice or whether additional venodilators are needed. Finally, it provides information on the optimum dosage of vasodilator therapy. After the initial hemodynamic measurements are made, arterial dilators are given in progressively increasing dosage until an optimum effect on cardiac output has been obtained. If cardiac output does not show any further increase but left atrial pressure is still very high, additional venodilator therapy should be given. If the patient is very ill or the hemodynamic abnormalities are marked, intravenous therapy (e.g., sodium nitroprusside) is the vasodilator of first choice. In this situation, intravenous vasodilator therapy should be used only with bedside hemodynamic monitoring. Inotropic agents, such as dobutamine, may be needed to improve LV function and increase cardiac output. Low-dose dopamine may be of value to increase urinary output.
Patients with severe chronic AR need valve surgery. The correct timing of surgical therapy is now better defined but is not fully clarified. Valve replacement should be performed before irreversible LV dysfunction occurs. The major problem, however, is identifying the precise point at which LV dysfunction will occur. Here, two major difficulties are encountered:
(1) patients may already have impaired LV systolic pump function at rest when they firstpresent or at the time of the first symptom and