cardiovascular disorders
Aortic Stenosis
Symptoms and Signs of Aortic Stenosis
Congenital aortic stenosis is usually asymptomatic until age 10 or 20 years, when symptoms develop insidiously. In all forms, progressive untreated aortic stenosis ultimately results in exertional syncope, angina, and dyspnea (SAD triad). Other symptoms and signs may include those of Heart Failure (HF) and Exertional syncope occurs because cardiac output cannot increase enough to meet the demands of physical activity. Nonexertional syncope may result from altered baroreceptor responses or Ventricular Tachycardia (VT) . Exertional angina pectoris affects about two thirds of patients; about half have significant coronary artery atherosclerosis, and half have normal coronary arteries but have ischemia induced by LV hypertrophy and altered coronary flow dynamics. There are no visible signs of aortic stenosis. Palpable signs include carotid and peripheral pulses that are reduced in amplitude and slow rising (pulsus parvus et tardus) and an apical impulse that is sustained (thrusts with the first heart sound [S1] and relaxes with the second heart sound [S2]) because of left ventricular hypertrophy. The LV impulse may become displaced when systolic dysfunction develops. A palpable fourth heart sound (S4), felt best at the apex, and a systolic thrill, corresponding with the murmur of AS and felt best at the left upper sternal border, are occasionally present in severe cases. Systolic blood pressure (BP) may be high even when AS is severe but ultimately falls when the LV fails. Onauscultation,S1 is normal and S2 is single because aortic valve closing is delayed and merges with the pulmonic (P2) component of S2. The aortic component may also be soft. Paradoxical splitting of S2 may be heard. A normally split S2 is the only physical finding that reliably excludes severe AS. An S4 may be audible. An ejection click may also be audible early after S1 in patients with congenital bicuspid AS when valve leaflets are stiff but not completely immobile. The click does not change with dynamic maneuvers. The hallmark finding is a crescendo-decrescendo ejection murmur, heard best with the diaphragm of the stethoscope at the right and left upper sternal borders when a patient who is sitting upright leans forward. The murmur typically radiates to the right clavicle and both carotid arteries (left often louder than right) and has a harsh or grating quality. In older patients, vibration of the unfused cusps of calcified aortic valve leaflets may transmit a louder, more high-pitched, “cooing” or musical sound to the cardiac apex, with softening or absence of the murmur parasternally (Gallavardin phenomenon), thereby mimicking mitral regurgitation. The murmur is soft when stenosis is less severe, grows louder as stenosis progresses, and becomes longer and peaks in volume later in systole (ie, crescendo phase becomes longer and decrescendo phase becomes shorter) as stenosis becomes more severe. As LV contractility decreases in critical AS, the murmur becomes softer and shorter. The intensity of the murmur may therefore be misleading in these circumstances. The murmur of aortic stenosis typically increases with maneuvers that increase LV volume and contractility (eg, leg-raising, squatting, Valsalva release, after a ventricular premature beat) and decreases with maneuvers that decrease LV volume (Valsalva maneuver) or increase afterload (isometric handgrip). These dynamic maneuvers have the opposite effect on the murmur of hypertrophic cardiomyopathy, which can otherwise resemble that of AS. The murmur of mitral regurgitation due to prolapse of the posterior leaflet may also mimic AS. 