Aortic insufficiency

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Aortic insufficiency ( AI ), also known as aortic regurgitation ( AR ), is the leaking of the heart aortic valve that causes blood to flow in the opposite direction during ventricular diastole, from the aorta to the left ventricle. As a result, the heart muscle is forced to work harder than usual.

Video Aortic insufficiency

Signs and symptoms

Symptoms of aortic insufficiency are similar to heart failure and include the following:

• Dyspnea while on the move
• Ortopnea
• Paroxysmal nocturnal dyspnea
• Palpitations
• Angina pectoris
• Cyanosis (in acute cases)

Maps Aortic insufficiency

Cause

In the case of aortic insufficiency, it is often caused by aortic root dilatation ( annuloaortic ectasia), which is idiopathic in more than 80% of cases, but may occur from aging, syphilis aortitis, osteogenesis imperfecta, aortic dissection, BehÃÆ'§et disease, reactive arthritis and systemic hypertension. Opening of the aortic root is the most common cause of aortic insufficiency in developed countries. In addition, aortic insufficiency has been associated with the use of several drugs, particularly drugs containing fenfluramine or dexfenfluramine isomers and dopamine agonists. Other potential causes affecting the valve directly include Marfan syndrome, Ehlers-Danlos syndrome, ankylosing spondylitis, and systemic lupus erythematosus. In the case of acute aortic insufficiency, the main cause is infective endocarditis, aortic dissection or trauma.

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Pathophysiology

The mechanism of aortic insufficiency (AI), consisting of pressure in the left ventricle that falls under pressure in the aorta, the aortic valve can not completely close. This causes leaking of blood from the aorta into the left ventricle. This means that some blood that has been thrown from the liver is spewing back to the heart. The percentage of blood that regurgitates through the aortic valve because AI is known as the regurgitant fraction. This regurgitant flow causes a decrease in diastolic blood pressure in the aorta, and therefore an increase in pulse pressure. Because some blood released during sistole regurgitates returns to the left ventricle during diastole, there is an effective forward flow reduction in AI .

While diastolic blood pressure is reduced and pulse pressure widens, systolic blood pressure is generally normal or even slightly increased, this is because the sympathetic nervous system and the renal renin-angiotensin-aldosterone axis compensate for a decrease in cardiac output. Catecholamines will increase heart rate and increase the strength of ventricular contraction, which directly increases cardiac output. Catecholamines will also cause peripheral vasoconstriction, leading to increased systemic vascular resistance and ensuring that organs are adequately perfused. Renin, a proteolytic enzyme, breaks angiotensinogen into angiotensin I, which is converted to angiotensin II. In the case of chronic aortic inadequacy with cardiac remodeling produced, heart failure will develop, and it is possible to see reduced systolic pressure. Aortic insufficiency leads to excess volume (increased preload) and excessive pressure (increased afterload) of the heart.

Excessive volume, due to increased pulse pressure and systemic effects of neuroendocrine hormone leads to left ventricular hypertrophy (LVH). There are both concentric hypertrophy and eccentric hypertrophy in AI. Concentric hypertrophy is caused by increased left ventricular pressure associated with AI, whereas eccentric hypertrophy is caused by excess volume caused by the regurgitant fraction.

Physiologically, in individuals with a functioning normal aortic valve, the valve is only open when the pressure in the left ventricle is higher than the pressure in the aorta. This allows the blood to be removed from the left ventricle into the aorta during ventricular systole. The amount of blood released by the heart is known as the volume of stroke . Under normal circumstances, & gt; 50% of the blood in the left ventricle is charged to the aorta for use by the body. After ventricular systole, pressure in the left ventricle decreases as it relaxes and begins to fill with blood from the left atrium. This left ventricular relaxation (early ventricular diastole) causes a decrease in pressure. When the pressure in the left ventricle falls under pressure in the aorta, the aortic valve closes, preventing blood in the aorta from returning to the left ventricle.

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Diagnosis

In the case of aortic regurgitation diagnosis a common test for evaluation of severity is transthoracic echocardiography, which can provide a two dimensional view of the regurgitant jet, allowing velocity measurements, and estimating jet volume. Findings in severe aortic regurgitation, according to American College of Cardiology/American Heart Association 2012 guidelines include:

Chest x-rays may be helpful in making the diagnosis, indicating left ventricular hypertrophy and dilated aorta. The ECG usually shows left ventricular hypertrophy. Cardiac catheterization helps in assessing the severity of regurgitation and left ventricular dysfunction.

Physical exam

The physical examination of an individual with aortic insufficiency involves auscultation of the heart to listen to aortic insuffer murmurs and S3 heart sounds (S3 galop correlates with progression of LV dysfunction). Chronic aortic insufficiency murmurs are usually described as diastolic and early decrescendo, which are best heard in the third left intercostal space and may spread along the left sternal border.

If there is an increase in the volume of left ventricular stroke due to excessive volume, the ejection 'systole' murmur flow may also occur when auscultation in the same aortic area. Unless there is a simultaneous aortic valve stenosis, murmurs should not begin with ejection clicks. There can also be an Austin Flint murmur, a soft mid-diastolic rumble heard in apical areas, appearing when the jet regurgitant from severe aortic insufficiency. partial closure of the anterior mitral membrane. The physical signs of aortic insufficiency are associated with high pulse pressure and rapid blood pressure drop during diastole because blood returns to the heart from the aorta through an incompetent aortic valve, although the usefulness of some eponymous signs has been questioned: Phonocardiograms detect AI by having the electrical voltage that mimics the sound produced by the heart.

Characteristics - indications of aortic regurgitation are as follows:

Classification

The hemodynamic sequelae of AI depends on the level of onset of AI. Therefore, it can be acute or chronic as follows:

• Acute aortic insufficiency In acute AI, as can be seen with acute perforation of the aortic valve due to endocarditis, there will be a sudden increase in blood volume in the left ventricle. Ventricles can not handle sudden volume changes. Left ventricle filling pressure will increase. This causes the pressure in the left atrium to increase, and the individual will experience pulmonary edema. Severe acute aortic references are considered a medical emergency. There is a high mortality rate if the individual does not have immediate surgery for aortic valve replacement.
Acute AI usually appears as reddish congestive heart failure, and there will be no signs associated with chronic AI because the left ventricle has not developed eccentric hypertrophy and dilatation that allows an increase in stroke. volume, which in turn causes limiting peripheral pulses. In auscultation, there may be a short diastolic murmur and a mild S ₁ . S ₁ soft because high fill pressure closes the mitral valve in diastole.
• Chronic aortic insufficiency If the individual survives the initial hemodynamic disturbances arising from acute AI, the left ventricle adapts to eccentric hypertrophy and dilatation of the left ventricle , and the excess volume is compensated. The left ventricle filling pressure will return to normal and the individual will not experience heart failure blatantly. In this compensatory phase, the individual may be completely asymptomatic and may have normal exercise tolerance. Finally (usually after a latent period) the left ventricle will become decompensated, and the filling pressure will increase. Some individuals enter this decompensation phase asymptomatically, treatment for AI involves the replacement of the aortic valve prior to this decompensation phase.



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Treatment

Aortic insufficiency or aortic regurgitation can be treated either medically or surgically, depending on the sharpness of presentation, symptoms and signs associated with the disease process, and the level of left ventricular dysfunction. Surgical treatment in asymptomatic patients has been recommended if the ejection fraction drops by 50% or below, in the face of progressive and severe left ventricular dilatation, or with abnormal symptoms or responses to the exercise test. For both groups of patients, surgery before the development of a worsening ejection fraction/left ventricular dilatation is expected to reduce the risk of sudden death, and is associated with lower perioperative mortality. Also, surgery is performed optimally in an acute case.

Medical care

The chronic and asymptomatic therapy of chronic aortic insufficiency involves the use of vasodilators. Experiments have demonstrated short-term benefits in the use of ACE inhibitors or angiotensin II, nifedipine, and hydralazine receptor antagonists in increasing left ventricular wall pressure, ejection fraction, and mass. The goal in using this pharmacological agent is to reduce the afterload so that the left ventricle is somewhat spared. The regurgitant fraction may not change significantly, as the gradient between aortic and left ventricular pressure is usually quite low at the start of treatment. Other medical treatments are somewhat conservative for stable and asymptomatic cases including low-sodium diet, diuretics, digoxin, calcium blockers and avoiding very heavy activity.

In 2007, the American Heart Association no longer recommends antibiotics for the prophylaxis of endocarditis prior to certain procedures in patients with aortic insufficiency. Prophylactic antibiotics to prevent endocarditis before gastrointestinal or genitourinary procedures are no longer recommended for any patient with valvular disease. Heart stress tests are useful in identifying individuals who may be best suited for surgical intervention. Radionuclide angiography is recommended and useful when systolic wall stress is calculated and combined with results.

Surgery

Surgical treatment for AI is the replacement of the aortic valve; this is currently an open heart procedure. In the case of severe aortic insufficiency acute , all individuals should undergo surgery, if there is no absolute contraindication (for surgery). Individuals with bacteremia with aortic valve endocarditis should not wait for treatment with antibiotics to take effect, given the high mortality associated with acute AI. Replacement with aortic valve homograft should be performed where possible.



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Prognosis

The risk of death in individuals with aortic insufficiency, ventricular dilation, the normal ejection fraction is asymptomatic about 0.2 percent per year. The risk increases if the ejection fraction decreases or if the individual develops symptoms.

Individuals with chronic (heavy) aortic regurgitation follow courses that once symptoms appear, surgical intervention is necessary. AI is fatal in 10 to 20% of individuals who are not undergoing surgery for this condition. Left ventricular dysfunction determines the extent to which the prospect of severity of aortic regurgitation cases.



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References




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Further reading

• Hamirani, Yasmin S.; Dietl, Charles A.; Voyles, Wyatt; Peralta, Mel; Start, Darlene; Raizada, Veena (2012-08-28). "Acute Aortic Regurgitation". Circulation . 126 (9): 1121-1126. doi: 10.1161/CIRCULATIONAHA.112.113993. ISSNÃ, 0009-7322. PMID 22927474.
• Dujardin, Karl S.; Enriquez-Sarano, Maurice; Schaff, Hartzell V.; Bailey, Kent R.; Seward, James B.; Tajik, A. Jamil (1999-04-13). "Mortality and Morbidity of Aortic Regurgitation in Clinical Practice of Long-Term Follow-Up Study". Circulation . 99 (14): 1851-1857. doi: 10.1161/01.CIR.99.14.1851. ISSNÃ, 0009-7322. PMIDÃ, 10199882.



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External links




• "DMOZ - Hasil Pencarian". www.dmoz.org . Diperoleh 31 Mei 2016 .

Source of the article : Wikipedia