FABROA, MARIA JESSICA ERLINDA P.

BSN III

AORTIC REGURGITATION NARRATIVE PATHOPHYSIOLOGY

The flow of blood back into the left ventricle from the aorta during diastole is called
Aortic Regurgitation. It can be caused by inflammatory lesions that deform aortic valve
leaflets or dilation of the aorta, preventing complete closure of the aortic valve (Cheever, H.
2018). It allows some of the blood that was pumped out of your heart's main pumping
chamber (left ventricle) to leak back into it. The leakage may prevent your heart from
efficiently pumping blood to the rest of your body. As a result, you may feel fatigued and
short of breath. Aortic valve regurgitation can develop suddenly or over decades. Once
aortic valve regurgitation becomes severe, surgery is often required to repair or replace the
aortic valve (Mayo Clinic, 2020).

Aortic Regurgitation causes left ventricular volume overload. Increase in LV end-

diastolic volume causes dilation and eccentric hypertrophy of the LV. This allows ejection of
a larger stroke volume. In patients with AR, the total stroke volume ejected by the LV is the
sum of effective stroke volume and the regurgitant volume. Thus, AR is associated with
increased preload. LV dilation increases the LV systolic tension in accordance with the law
of Laplace. This, in combination with the elevated systolic blood pressure that results from
the increase in total forward stroke volume, leads to increased afterload. LV function is
compensated due to the combination of LV dilation and hypertrophy. Over time, however,
wall thickening fails to keep pace with the hemodynamic load resulting in a decline in systolic
function and ejection fraction. Decompensation of the LV results in decreased compliance
and increased LV end-diastolic pressure and volume. In advanced stages, left atrial,
pulmonary artery wedge, pulmonary arterial, right ventricular (RV), and right atrial pressures
rise, and the effective (forward) cardiac output falls. Symptoms of heart failure develop,
including dyspnea, orthopnea, and paroxysmal nocturnal dyspnea due to pulmonary
congestion. An increase in LV mass leads to increased myocardial oxygen requirements.
Also, coronary perfusion pressure is reduced. This causes myocardial ischemia and
exertional chest pain. In patients with acute severe AR, compensatory mechanisms of the
LV do not develop rapidly enough to handle the regurgitant volume load. LV diastolic
pressures rise rapidly and may lead to acute pulmonary edema and cardiogenic shock. Even
diastolic mitral regurgitation can occur as a result of the sudden severe increase in LV
volume and pressure.

With treatment, the 10-year survival for patients with mild to moderate aortic
regurgitation is 80% to 95 %. With approximately timed valve replacement, long-term
prognosis for patients with moderate to severe AR is good. However, the prognosis for those
with severe AR is considerably poorer.

REFERENCES:

Cheever, K. H., & Hinkle, J. L. (2018). Brunner & Suddarth's textbook of medical-surgical
nursing. Philadelphia: Wolters Kluwer.

Aortic regurgitation: Background, pathophysiology, etiology. (2019, November 10). Diseases

& Conditions - Medscape Reference. Retrieved October 31, 2020, from
https://emedicine.medscape.com/article/150490-overview#a3

Aortic valve regurgitation - Symptoms and causes. (2020, August 7). Mayo Clinic. Retrieved
October 31, 2020, from https://www.mayoclinic.org/diseases-conditions/aortic-valve-
regurgitation/symptoms-causes/syc-20353129