What is the difference between regurgitation and insufficiency

This condition can keep blood from flowing properly throughout your body , which can lead to symptoms such as shortness of breath, fatigue, dizziness or lightheadedness, fainting, and chest pain. There are different classifications of aortic regurgitation, including acute and chronic. Acute aortic regurgitation can develop suddenly.

Chronic aortic regurgitation persists for long periods of time. It can even continue for decades. Aortic regurgitation can result from abnormalities of the aortic valve leaflets or dilation of the aortic root, though an increase in afterload is not by itself a cause of aortic regurgitation. When the aortic leaflets are involved, a destructive process such as infective endocarditis or rheumatic valvular disease is frequently implicated.

Any disease process that leads to aortic root dilation eg, Marfan syndrome or aortic dissection may cause enlargement of the aortic valve annulus; this results in failure of the leaflets to coapt close properly in diastole loss of coaptation and aortic regurgitation.

Frequently, repairs to the aortic root and valve are required in these conditions. The most common causes of acute aortic dissection include bacterial endocarditis, aortic dissection and blunt trauma-induced aortic valve damage Hamirani YS, et al.

As chronic aortic regurgitation develops slowly over time, the left ventricle slowly dilates and hypertrophies, as described previously. The disease remains asymptomatic for a long period of time. The later symptoms of chronic AR are mostly due to congestive heart failure. Left heart failure results in passive elevation of pulmonary pressures with dyspnea. Physical activity may even cause transient pulmonary edema.

Right heart failure symptoms include lower extremity-dependent edema and hepatic congestion. At night, when patients are recumbent, the excess extracellular fluid redistributes centrally, causing orthopnea the need to sit up to breathe or paroxysmal nocturnal dyspnea. The large stroke volumes and forceful left ventricular contractions may cause head bobbing and awareness of the peripheral pulse. Angina may occur in the absence of atherosclerotic coronary disease, as the low diastolic pressures in severe aortic regurgitation compromise coronary filling, and the left ventricular hypertrophy increases oxygen demand.

Other symptoms related to low cardiac output include fatigue, weakness and, in extreme cases, cardiac cachexia. Unlike in chronic aortic regurgitation, almost all patients with significant acute aortic regurgitation are symptomatic.

Signs of acute left heart failure — including severe dyspnea, dyspnea at rest, orthopnea and paroxysmal nocturnal dyspnea PND — arise. Patients typically present with symptoms of low cardiac output and systemic vasoconstriction, including pallor and coolness in the distal extremities, peripheral cyanosis and tachycardia with a reduced peripheral pulse.

Hypotension, flash pulmonary edema and shock can also occur. In chronic aortic regurgitation, visible cardiac and arterial pulsations are common due to the large stroke volume.

The carotid pulse can commonly be seen. The point of maximal impulse PMI is displaced laterally and caudally due to the LV dilation and hypertrophy that occurs. This murmur may be difficult to distinguish from the Graham-Steele murmur of pulmonic insufficiency. As aortic regurgitation worsens, the murmur becomes shorter, as less time is needed for left ventricular and aortic pressure equalization. In addition, a systolic ejection murmur may be present at the right upper sternal border, simply due to the large stroke volume passing through the aortic valve with each left ventricular systolic contraction.

An early diastolic rumble the Austin-Flint murmur may also be heard at the apex, due to the regurgitant jet striking the anterior leaflet of the mitral valve and causing it to vibrate. A widened pulse pressure is often present due to increased stroke volume, as previously described. When heart failure develops, the pulse pressure decreases and the peripheral signs of aortic regurgitation, listed below, are lessened. A fourth heart sound S4 may develop when LV hypertrophy becomes severe and limits diastolic filling.

A third heart sound S3 is often present, due to increased early diastolic filling into a compliant, dilated left ventricle. Acute aortic regurgitation will cause a very short, early diastolic decrescendo murmur with the aortic and left ventricular pressures equalized quickly, as the left ventricle has not had time to dilate or hypertrophy.

The peripheral signs of aortic regurgitation are mostly due to the increased stroke volume and wide pulse pressure seen in aortic regurgitation. In 19th century Europe, syphilis was widespread. View current visitor policy. Aortic insufficiency is a heart valve disease in which the aortic valve does not close tightly. This leads to the backward flow of blood from the aorta the largest blood vessel into the left ventricle a chamber of the heart.

Aortic insufficiency can result from any condition that keeps the aortic valve from closing all the way. A small amount of blood comes back each time the heart beats. The condition causes widening dilation of the left lower chamber of the heart.

Larger amounts of blood leave the heart with each squeeze or contraction. This leads to a strong and forceful pulse bounding pulse. Over time, the heart becomes less able to pump blood to the body. In the past, rheumatic fever was the main cause of aortic insufficiency. Now that antibiotics are used to treat rheumatic fever, other causes are more commonly seen.

Aortic insufficiency often has no symptoms for many years. Symptoms may occur slowly or suddenly. A chest X-ray may show swelling of the left lower heart chamber. Lab tests cannot diagnose aortic insufficiency, but they may be used to rule out other disorders or causes. If there are no symptoms or if symptoms are mild, you may only need to get an echocardiogram from time to time and be monitored by a health care provider.

This elevates aortic systolic pressure mmHg in this example ; however, the aortic diastolic pressure 60 mmHg in this example is much lower than normal because blood more rapidly leaves the aorta due to regurgitation back into the ventricle. Therefore, a defining characteristic of aortic regurgitation is an increase in aortic pulse pressure systolic minus diastolic pressure. The elevation in LV end-diastolic pressure causes blood to back up into the left atrium and pulmonary veins, which leads to an increase in left atrial pressure and pulmonary capillary wedge pressure , which can result in pulmonary congestion and edema.

The backward flow of blood into the ventricular chamber during diastole results in a diastolic murmur. The figure at the right shows the changes in aortic pressure AP , left ventricular pressure LVP and left atrial pressure LAP that can be observed during the cardiac cycle with aortic regurgitation.

These pressures differ from those that normally occur compare with normal cardiac cycle in that the aortic pulse pressure is greatly increased because of a lower diastolic pressure and elevated systolic pressure.

Furthermore, the LAP and LVP pressures are elevated during ventricular filling because of the increased ventricular volume. Early in the course of regurgitant aortic valve disease, there is a large increase in left ventricular end-diastolic pressure and left atrial pressure.

The ventricle and atria function on a stiffer portion of their compliance curves so that the increased volume results in a large rise in pressure.

With long-standing regurgitation and volume overload of the chambers, the ventricles and atria dilate so that the increased volume does not result in an exceptionally large increase in pressure.