Physical examination Phonocardiograms from normal and abnormal heart sounds Upon auscultation of an individual with<unk> , the first heart sound is usually loud and may be palpable (tapping apex beat) because of increased force in closing the<unk>  valve. The first heart sound is made by the<unk>  and tricuspid heart valves closing. These are normally synchronous, and the sounds are termed M1 and T1, respectively. M1 becomes louder in<unk> . It may be the most prominent sign. If pulmonary hypertension secondary to<unk>  is severe, the P2 (pulmonic) component of the second heart sound (S2) will become loud. An opening snap that is a high-pitch additional sound may be heard after the A2 (aortic) component of the second heart sound (S2), which correlates to the forceful opening of the<unk>  valve. The<unk>  valve opens when the pressure in the left atrium is greater than the pressure in the left ventricle. This happens in ventricular diastole (after closure of the aortic valve), when the pressure in the ventricle precipitously drops. In individuals with<unk> , the pressure in the left atrium correlates with the severity of the<unk> . As the severity of the<unk>  increases, the pressure in the left atrium increases, and the<unk>  valve opens earlier in ventricular diastole. A mid-diastolic rumbling murmur with presystolic accentuation will be heard after the opening snap. The murmur is best heard at the apical region and is not radiated. Since it is a low-pitch sound, it is heard best with the bell of the stethoscope. Its duration increases with worsening disease. Rolling the patient toward left as well as isometric exercise will accentuate the murmur. A thrill might be present when palpating at the apical region of the precordium. Advanced disease may present with signs of right-sided heart failure such as parasternal heave, jugular venous distension, hepatomegaly, ascites and/or pulmonary hypertension, the latter often presenting with a loud P2. Almost all signs increase with exercise and pregnancy. Other peripheral signs include: * Malar flush - due to back pressure and buildup of carbon dioxide (CO2). CO2 is a natural vasodilator. * Atrial fibrillation - irregular pulse and loss of 'a' wave in jugular venous pressure * Left parasternal heave - presence of right ventricular hypertrophy due to pulmonary hypertension * Tapping apex beat that is not displaced Medical signs of atrial fibrillation include: Heart rate is about 100-150/min. Irregularly irregular pulse with a pulse deficit>10. Varying first heart sound intensity. Opening snap is not heard sometimes. Absent a waves in the neck veins. Presystolic accentuation of diastolic murmur disappears. Embolic manifestations may appear. Associated lesions With severe pulmonary hypertension, a pansystolic murmur produced by functional tricuspid regurgitation may be audible along the left sternal border. This murmur is usually louder during inspiration and diminishes during forced expiration (Carvallo’s sign). When the cardiac output is markedly reduced in<unk> , the typical auscultatory findings, including the diastolic rumbling murmur, may not be detectable (silent<unk> , but they may reappear as compensation is restored. The Graham Steell murmur of pulmonary regurgitation, a high-pitched, diastolic, decrescendo blowing murmur along the left sternal border, results from dilation of the pulmonary valve ring and occurs in patients with<unk>  valve disease and severe pulmonary hypertension. This murmur may be indistinguishable from the more common murmur produced by aortic regurgitation (AR), although it may increase in intensity with inspiration and is accompanied by a loud and often palpable P2. Echocardiography + Severity of<unk>  Degree of<unk>  Mean gradient<unk>  valve area Progressive<unk>  1.5 cm2 Severe<unk>  5–10 mmHg 1.0–1.5 cm2 Very severe<unk>  > 10 mmHg 2 In most cases, the diagnosis of<unk>  is most easily made by echocardiography, which shows left atrial enlargement, thick and calcified<unk>  valve with narrow and "fish-mouth"-shaped orifice and signs of right ventricular failure in advanced disease. It can also show decreased opening of the<unk>  valve leaflets, and increased blood flow velocity during diastole. The trans-mitral gradient as measured by Doppler echocardiography is the gold standard in the evaluation of the severity of<unk> . Cardiac chamber catheterization Another method of measuring the severity of<unk>  is the simultaneous left and right heart chamber catheterization. The right heart catheterization (commonly known as Swan-Ganz catheterization) gives the physician the mean pulmonary capillary wedge pressure, which is a reflection of the left atrial pressure. The left heart catheterization, on the other hand, gives the pressure in the left ventricle. By simultaneously taking these pressures, it is possible to determine the gradient between the left atrium and left ventricle during ventricular diastole, which is a marker for the severity of<unk> . This method of evaluating<unk>  tends to overestimate the degree of<unk> , however, because of the time lag in the pressure tracings seen on the right-heart catheterization and the slow Y descent seen on the wedge tracings. If a trans-septal puncture is made during right heart catheterization, however, the pressure gradient can accurately quantify the severity of<unk> . Other techniques Chest X-ray may also assist in diagnosis, showing left atrial enlargement. Electrocardiography may show P<unk> e, that is, broad, notched P waves in several or many leads with a prominent late negative component to the P wave in lead V1, and may also be seen in<unk>  regurgitation, and, potentially, any cause of overload of the left atrium. Thus, P-sinistrocardiale may be a more appropriate term.
Mitral stenosis
Aortic regurgitation
Mitral regurgitation
Tricuspid regurgitation
Aortic stenosis
Pulmonary valve stenosis
Tricuspid valve stenosis
Systolic hypertension