Aortic Valve Disease Lecture 3 PDF

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Summary

This lecture provides an overview of aortic valve disease, including aortic stenosis and regurgitation. It covers the anatomy, pathology, causes, clinical presentation, investigations, and treatment options for these conditions. The lecture material is suitable for undergraduate medical students or professionals studying cardiology.

Full Transcript

Aortic valve diseases Aortic valve anatomy 3 cusps and annulus (ring) attached to proximal Aorta (aortic root), with no sub valvular apparatus Opens during systole (ejection phase) allow flow of blood from LV to aorta. Closes during diastole (produce S2) so prevent backward flow from aor...

Aortic valve diseases Aortic valve anatomy 3 cusps and annulus (ring) attached to proximal Aorta (aortic root), with no sub valvular apparatus Opens during systole (ejection phase) allow flow of blood from LV to aorta. Closes during diastole (produce S2) so prevent backward flow from aorta into LV. Aortic valve pathology 1. stenosis (narrowing of AV opening) 2. regurgitation (backward flow of blood from aorta to LV due to improper closure of AV cusps or failure of cusps coaptation during diastole) Aortic stenosis Classification: - Valvular AS: Narrowing of AV opening. - Subvalvular AS: Stenosis below AV in LV outflow tract (membrane or ridge). - Supravalvular AS: Stenosis above AV in Aorta (narrowing in ascending aorta). Causes: 1. Congenital: Bicuspid AV, Subvalvular AS, Supravalvular AS. 2. Degenerative: old age, western countries. 3. Rheumatic: young age, developing countries. Pathology: thickening, fibrosis, calcification of the valve causing narrowing of opening. Pathophysiology: Progressive AV narrowing leads to progressive LV hypertrophy (LVH), increased LV systolic pressure with increased myocardial oxygen demand, this lead to myocardial ischemia and LV failure (pulmonary congestion). Presentation: A- History: - AS is typically asymptomatic until valvular stenosis is severe. - The hallmark of AS is the classical triad of exertional dyspnea, angina, and syncope (or near-syncope). 1- Exertional dyspnea is the most common symptom associated with severe AS. 2- Angina without significant obstructive CAD is caused by subendocardial ischemia due to increased total oxygen demand secondary to LVH. 3- Exertional syncope (or near syncope) occurs due to diminished cerebral perfusion secondary to low cardiac output − Symptoms may not develop simultaneously, may only one of the three is present. B- Physical Examination - Hallmarks of severe AS on physical examination include: − - Pulse: Reduction in the amplitude and delay of the carotid upstrokes (“parvus et tardus”). - Apical impulse: shifted downwards, outwards, heaving character, localized (LV apex). Cardiac auscultation: 1- Diminution or entire loss of the second heart sound (↓S2) 2- an opening ejection click in patients with a bicuspid valve 3- Ejection systolic crescendo-decrescendo murmur (radiates to the carotids, sometimes associated with a thrill. − Radiation may also occur across the precordium and to the apex (Gallavardin phenomenon) associated with a musical, high frequency quality. Investigations: a. Echocardiography: assess severity of AS, LV function. b. CXR: Lung congestion c. ECG: LVH Treatment: A. Prophylaxis against infective endocarditis, secondary prevention of rheumatic activity. B. Medical: Diuretics for HF symptoms. C. Interventional: Transcatheter AV Implantation (TAVI). D. Surgical: AV replacement either by mechanical or tissue prosthesis. Aortic regurge Aortic regurgitation Presentation: Acute AR: presented with Acute pulmonary edema, or cardiogenic shock Chronic AR A- History: - Symptoms are related to exaggerated cardiac output with increased stroke volume, including a sense of pounding in the chest. - Palpitations - Dyspnea. - Chest pain. B- Physical Examination - Blood pressure: High systolic BP, Low DBP, Wide pulse pressure. - Pulse: - Water hammer: characterized by exaggerated upstroke and fall of the arterial pulse, notable in the carotid pulse. Apical impulse: shifted downwards, outwards, hyperdynamic character (LV apex). Cardiac auscultation: 1- Diminution of the second heart sound (↓S2) with thickened calcific valve and accentuated S2 with dilated aortic root 2- The murmur of AR - high-pitched (“blowing”) in quality. - Radiation: along the left sternal border and is best heard with the patient sitting up and leaning forward after full expiration. If the murmur radiates along the right sternal border, it is suggestive of a dilated aortic root. -Ejection systolic Murmur (Functional AS; caused by ↑ systolic forward flow). - Very significant AR may be accompanied by a low pitched late mitral diastolic rumble (= MS; the “Austin-Flint” murmur) due to improper opening of the mitral valve by the aortic regurgitant jet. Investigations: a. Echocardiography: assess severity of AR, LV function, define the cause of AR. b. CXR: Lung congestion Treatment: A. Prophylaxis against infective endocarditis, secondary prevention of rheumatic activity. B. Medical: Diuretics for HF symptoms, Dilators. Good blood pressure control (afterload reduction) with calcium channel blockers and vasodilators (ACE inhibitors). C. Surgical: For Acute AR: treat the cause, hemodynamic support, AV replacement. For Chronic AR: 1- AV replacement (mechanical or biological prosthesis) ± Aortic root replacement. 2- AV repair. 3- Acute severe AR is associated with a high mortality and requires immediate intervention. Thank you

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