Aortic stenosis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
When the aortic valve becomes stenosed, it can result in the formation of a pressure gradient between the left ventricle (LV) and the aorta | When the aortic valve becomes stenosed, it can result in the formation of a pressure gradient between the left ventricle (LV) and the aorta <ref name=Lilly>{{cite book | author = Lilly LS (editor) | title = Pathophysiology of Heart Disease | edition = 3rd ed. | publisher = Lippincott Williams & Wilkins | year = 2003 | id = ISBN 0-7817-4027-4 }}</ref>. The more constricted the valve, the higher the gradient between the LV and the aorta. For instance, with a mild AS, the gradient may be 20 [[mmHg]]. This means that, at peak systole, while the LV may generate a pressure of 140 mmHg, the pressure that is transmitted to the aorta will only be 120 mmHg. So, while a [[Sphygmomanometer|blood pressure cuff]] may measure a normal [[systole|systolic]] [[blood pressure]], the actual pressure generated by the LV would be considerably [[hypertension|higher]]. | ||
In individuals with AS, the left ventricle (LV) has to generate an increased pressure in order to overcome the increased [[afterload]] caused by the stenotic aortic valve and eject blood out of the LV. The more severe the aortic stenosis, the higher the gradient is between the left ventricular systolic pressures and the aortic systolic pressures. Due to the increased pressures generated by the left ventricle, the [[myocardium]] (muscle) of the LV undergoes [[left ventricular hypertrophy|hypertrophy]] (increase in muscle mass). This is seen as thickening of the walls of the LV. The type of hypertrophy most commonly seen in AS is concentric hypertrophy, meaning that all the walls of the LV are (approximately) equally thickened. | In individuals with AS, the left ventricle (LV) has to generate an increased pressure in order to overcome the increased [[afterload]] caused by the stenotic aortic valve and eject blood out of the LV. The more severe the aortic stenosis, the higher the gradient is between the left ventricular systolic pressures and the aortic systolic pressures. Due to the increased pressures generated by the left ventricle, the [[myocardium]] (muscle) of the LV undergoes [[left ventricular hypertrophy|hypertrophy]] (increase in muscle mass). This is seen as thickening of the walls of the LV. The type of hypertrophy most commonly seen in AS is concentric hypertrophy, meaning that all the walls of the LV are (approximately) equally thickened. | ||
Revision as of 16:28, 29 September 2011
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Aortic Stenosis Microchapters |
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Diagnosis |
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Treatment |
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Percutaneous Aortic Balloon Valvotomy (PABV) or Aortic Valvuloplasty |
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Transcatheter Aortic Valve Replacement (TAVR) |
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Case Studies |
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Aortic stenosis pathophysiology On the Web |
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American Roentgen Ray Society Images of Aortic stenosis pathophysiology |
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Directions to Hospitals Treating Aortic stenosis pathophysiology |
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Risk calculators and risk factors for Aortic stenosis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editors-In-Chief: Claudia P. Hochberg, M.D. [2], Abdul-Rahman Arabi, M.D. [3], Keri Shafer, M.D. [4], Priyamvada Singh, MBBS [5], Mohammed A. Sbeih, M.D. [6]; Assistant Editor-In-Chief: Kristin Feeney, B.S. [7]
Overview
Aortic stenosis results in the onset of a chronic pressure overload of the left ventricle. As the disease progresses, an aortic stenosis can result in compromised functional integrity of the surrounding mitral valve. The most common complication of aortic stenosis is left ventricular hypertrophy. Aortic stenosis could be subvalvular, supravalvular or at the level of the aortic valve.
Pathophysiology
When the aortic valve becomes stenosed, it can result in the formation of a pressure gradient between the left ventricle (LV) and the aorta [1]. The more constricted the valve, the higher the gradient between the LV and the aorta. For instance, with a mild AS, the gradient may be 20 mmHg. This means that, at peak systole, while the LV may generate a pressure of 140 mmHg, the pressure that is transmitted to the aorta will only be 120 mmHg. So, while a blood pressure cuff may measure a normal systolic blood pressure, the actual pressure generated by the LV would be considerably higher.
In individuals with AS, the left ventricle (LV) has to generate an increased pressure in order to overcome the increased afterload caused by the stenotic aortic valve and eject blood out of the LV. The more severe the aortic stenosis, the higher the gradient is between the left ventricular systolic pressures and the aortic systolic pressures. Due to the increased pressures generated by the left ventricle, the myocardium (muscle) of the LV undergoes hypertrophy (increase in muscle mass). This is seen as thickening of the walls of the LV. The type of hypertrophy most commonly seen in AS is concentric hypertrophy, meaning that all the walls of the LV are (approximately) equally thickened.
References
- ↑ Lilly LS (editor) (2003). Pathophysiology of Heart Disease (3rd ed. ed.). Lippincott Williams & Wilkins. ISBN 0-7817-4027-4.