Definition
Aortic insufficiency (AI), also known as aortic regurgitation (AR) is the return of blood to the left ventricle from the aorta during diastole (relaxation). Aortic insufficiency is a condition where there is reflux (backflow) of blood from the aorta into the left ventricle during relaxation. This causes backward flow of blood from the aorta (the largest blood vessel) into the left ventricle.
Etiology
Most common cause is rheumatic fever. Abnormalities of the aortic valve and the base could also lead to aortic insufficiency. On chronic aortic insufficiency seen fibrosis and retraction leaves or without valvular calcification, which is generally a sequela of rheumatic fever.
1. Rheumatic Fever
Rheumatic fever is a condition that results from infection by group A streptococcal bacteria that are not treated. Damage to the valve petals of rheumatic fever causes increased turbulence across the valve and more damage. Narrowing of rheumatic fever occurs from fusion of the edges (commissures) of the petals of the valve.
Under normal circumstances, the aortic valve closes to prevent blood in the aorta, from flowing back into the left ventricle. In aortic regurgitation, the valve that allows pain behind the leak of blood into the left ventricle when the ventricle relaxes muscles after pumping. These patients also have some degree of damage in rheumatic mitral valve.
2. Congenital Abnormalities
Congenital abnormalities which brought the baby from birth, such as valve disease which can not be shut down completely while in the womb, causing blood flow from the left ventricle can not flow properly.
3. The Aging Process
With aging, protein collagen of the valve petals destroyed, and calcium is deposited on the petals. Upheaval across the valves increase causes scarring and thickening. Progressive disease that causes aortic calcification had nothing to do with lifestyle choices are healthy, do not like to precipitate calcium in the coronary arteries to cause heart attacks.
Pathophysiology
Aortic insufficiency caused by inflammatory lesions that distort the shape of the aortic valve blade, so that each blade can not close the lumen of the aorta during diastole and consequently causes backflow of blood from the aorta into the left ventricle.
Because diastole when the aortic valve leaks, some blood in the aorta, which is usually high pressure, the left ventricle will flow, so that the left ventricle must cope with both the blood that normally sends received blood from the left atrium and the back of the aorta. Then dilated left ventricle and hypertrophy to accommodate the increased volume, as well as pushing the power due to more than normal to pump blood, causing blood pressure systolic increased. Cardiovascular system trying to compensate through reflex dilation of blood vessels and peripheral arterial limp, so the decreased peripheral resistance and diastolic pressure dropped drastically.
Hemodynamic changes in acute circumstances, can be distinguished with chronic conditions. Acute damage arising in patients without a history of previous insufficiency. The left ventricle did not have enough time to adapt to aortic insufficiency. Sudden increase of left ventricular end-diastolic pressure could arise with little ventricular dilatation.
Clinical Manifestations
Clients come with a complaint by a real carotid artery pulsation and pulsation at the apex when the client lying to the left. On the client chronic aortic insufficiency may develop symptoms of heart failure, including dypsnea during activity, orthopnea, paroxysmal nocturnal dyspnea, pulmonary edema and fatigue. Angina tends to arise only breaks the onset of bradycardia and longer disappear from the angina caused by coronary disease.
On physical examination found the carotid artery pulse rapid and substantial differences in blood pressure that can result in a hyperdynamic state with pulsus bisferiens. If severe insufficiency, arising noticeable effect on peripheral arterial pulsation. If severe heart failure, diastolic pressure may be normal due to the increase in left ventricular diastolic pressure. Can be normal-sized heart, if it when chronic mild aortic insufficiency or if acute insufficiency. In clients with moderate or severe insufficiency, heart looks enlarged, the apex impulse shifts to the inferolateral and is hyperdynamic.
Examination Support
1. Electrocardiogram
ECG is rarely normal in chronic aortic regurgitation and often exhibit significant changes in repolarization. On acute aortic regurgitation ECG may be normal. Visible image of left ventricular hypertrophy, increased amplitude QRS, ST-T-shaped type of diastolic overload, meaning that the average vector showed that ST is great, and and T wave vector parallel to the average of the QRS complex. Figure shows the P-R interval lengthening.
2. Thorax Radiography
Shows a progressive enlargement of the heart. Namely an enlarged left ventricle, left atrium, and aortic dilatation. The shape and size of the heart was unchanged in acute insufficiency but looks pulmonary edema.
3. Transthoracic Echocardiography
Exposing the base of the proximal aorta on imaging.
4. Aortography.
5. Increased cardiac isoenzyme (CPK and ck mb)
6. Cardiac catheterization
7. Transesophageal Echocardiography (TEE)
Visualize the entire aorta.
READ MORE - Nursing Care Plan for Aortic Insufficiency (Regurgitation)
Aortic insufficiency (AI), also known as aortic regurgitation (AR) is the return of blood to the left ventricle from the aorta during diastole (relaxation). Aortic insufficiency is a condition where there is reflux (backflow) of blood from the aorta into the left ventricle during relaxation. This causes backward flow of blood from the aorta (the largest blood vessel) into the left ventricle.
Etiology
Most common cause is rheumatic fever. Abnormalities of the aortic valve and the base could also lead to aortic insufficiency. On chronic aortic insufficiency seen fibrosis and retraction leaves or without valvular calcification, which is generally a sequela of rheumatic fever.
1. Rheumatic Fever
Rheumatic fever is a condition that results from infection by group A streptococcal bacteria that are not treated. Damage to the valve petals of rheumatic fever causes increased turbulence across the valve and more damage. Narrowing of rheumatic fever occurs from fusion of the edges (commissures) of the petals of the valve.
Under normal circumstances, the aortic valve closes to prevent blood in the aorta, from flowing back into the left ventricle. In aortic regurgitation, the valve that allows pain behind the leak of blood into the left ventricle when the ventricle relaxes muscles after pumping. These patients also have some degree of damage in rheumatic mitral valve.
2. Congenital Abnormalities
Congenital abnormalities which brought the baby from birth, such as valve disease which can not be shut down completely while in the womb, causing blood flow from the left ventricle can not flow properly.
3. The Aging Process
With aging, protein collagen of the valve petals destroyed, and calcium is deposited on the petals. Upheaval across the valves increase causes scarring and thickening. Progressive disease that causes aortic calcification had nothing to do with lifestyle choices are healthy, do not like to precipitate calcium in the coronary arteries to cause heart attacks.
Pathophysiology
Aortic insufficiency caused by inflammatory lesions that distort the shape of the aortic valve blade, so that each blade can not close the lumen of the aorta during diastole and consequently causes backflow of blood from the aorta into the left ventricle.
Because diastole when the aortic valve leaks, some blood in the aorta, which is usually high pressure, the left ventricle will flow, so that the left ventricle must cope with both the blood that normally sends received blood from the left atrium and the back of the aorta. Then dilated left ventricle and hypertrophy to accommodate the increased volume, as well as pushing the power due to more than normal to pump blood, causing blood pressure systolic increased. Cardiovascular system trying to compensate through reflex dilation of blood vessels and peripheral arterial limp, so the decreased peripheral resistance and diastolic pressure dropped drastically.
Hemodynamic changes in acute circumstances, can be distinguished with chronic conditions. Acute damage arising in patients without a history of previous insufficiency. The left ventricle did not have enough time to adapt to aortic insufficiency. Sudden increase of left ventricular end-diastolic pressure could arise with little ventricular dilatation.
Clinical Manifestations
Clients come with a complaint by a real carotid artery pulsation and pulsation at the apex when the client lying to the left. On the client chronic aortic insufficiency may develop symptoms of heart failure, including dypsnea during activity, orthopnea, paroxysmal nocturnal dyspnea, pulmonary edema and fatigue. Angina tends to arise only breaks the onset of bradycardia and longer disappear from the angina caused by coronary disease.
On physical examination found the carotid artery pulse rapid and substantial differences in blood pressure that can result in a hyperdynamic state with pulsus bisferiens. If severe insufficiency, arising noticeable effect on peripheral arterial pulsation. If severe heart failure, diastolic pressure may be normal due to the increase in left ventricular diastolic pressure. Can be normal-sized heart, if it when chronic mild aortic insufficiency or if acute insufficiency. In clients with moderate or severe insufficiency, heart looks enlarged, the apex impulse shifts to the inferolateral and is hyperdynamic.
Examination Support
1. Electrocardiogram
ECG is rarely normal in chronic aortic regurgitation and often exhibit significant changes in repolarization. On acute aortic regurgitation ECG may be normal. Visible image of left ventricular hypertrophy, increased amplitude QRS, ST-T-shaped type of diastolic overload, meaning that the average vector showed that ST is great, and and T wave vector parallel to the average of the QRS complex. Figure shows the P-R interval lengthening.
2. Thorax Radiography
Shows a progressive enlargement of the heart. Namely an enlarged left ventricle, left atrium, and aortic dilatation. The shape and size of the heart was unchanged in acute insufficiency but looks pulmonary edema.
3. Transthoracic Echocardiography
Exposing the base of the proximal aorta on imaging.
4. Aortography.
5. Increased cardiac isoenzyme (CPK and ck mb)
6. Cardiac catheterization
7. Transesophageal Echocardiography (TEE)
Visualize the entire aorta.