Presentation on theme: "Diagnosis of valvular diseases Dr. Szathmári Miklós Semmelweis University First Department of Medicine 24. Oct. 2011."— Presentation transcript:
Diagnosis of valvular diseases Dr. Szathmári Miklós Semmelweis University First Department of Medicine 24. Oct. 2011.
Normal heart sounds First heart sound (S1) Lub Closure of the mitral and tricuspidal valves Second heard sound (S2) Dub Closure of semilunar valves Start of the systoleStart of the diastole
Identification of heart sounds The systolic sound (S1) longer, deeper and softer, than S2 (beat-like, dobbanás-szerű). The diastolic sound (S2) is shorter, higher, and sharp (clicking-like, koppanás-szerű) The diastolic interval (S2 – S1) is longer, than the systolic (S1-S2) The carotid artery pulse or apical impulse occur in early systole, right after the first heart sound S1 is usually louder than S2 at the apex, and S2 is usually louder than S1 at the base.
Extra heart sounds in diastole S 3 - ventricular galopp – It is heard best at the apex in the left lateral position.It is louder on inspiration. Dull, low – pitched. Over 40 year of age is almost certainly pathologic. Causes: decreased myocardial contractility, myocardial failure, and volume ovarload of a ventricle, as from mitral or tricuspid regurgitation.
Global burden of valvular heart disease Primary valvular heart disease ranks below coronary heart disease, stroke, hypertension, obesity, and diabetes as major threats to the public health. Rheumatic fever is the dominant cause of valvular heart disease in developing countries. Prevalence and mortality rates vary according to the availability of medical resources and population-wide programs for detection and treatment of group A streptococcal pharyngitis. Valve disease in developed countries is dominated by degenerative or inflammatory processes that lead to valve tickening, calcification, and dysfunction. Left-sided valve disease may affect as many as 12-13% of adults over the age of 75.
Mitral stenosis Presystolic murmur –Low pitched, rumbling –In left lateral position, during exersice, and after complete exhalation is heard better. S1 is accentuated and delayed: –The mitral valve is still open wide at the onset of ventricular systole and closes quickly P2 is accentuated: –Pulmonary hypertension develops Opening snap –Very early diastolic sound produced by the opening of a stenotic mitral valve. –It is heard best just medial to the apex –High pitch and snapping quality, it is heard better with the diaphragma Middiastolic murmur) –Usually limited to the apex –Little or non radiation
Mitral stenosis Associated signs: –Malar flush with perioral pallor –In case of right-sided heart failure peripheral edema, hepatomegaly, ascites and pleural effusion –With severe pulmonary hypertension, a pansystolic murmur produced by functional tricuspidal regurgitation. –Graham-Steel murmur of PR, a high-pitched, diastolic, decrescendo blowing murmur along the left sternal border because of dilatation of the pulmonary valve ring –Atrial fibrillation –The left ventricle is smaller, the right ventricle is hypertrophic. –The systemic arterial pressure is normal or slightly low.
Mitral regurgitation Holosystolic murmur –Maximal intensity at the apex –Blowing quality, medium to high pitch. If loud associated with an apical thrills –Radiation to the left axilla, less often to the left sternal border –An apical S3 reflects the volume overload on the left ventricle –The S1 is often decreased (calcified and relatively inmobile mitral valve) –Unlike the murmur of tricuspid regurgitation, it does not become louder in inspiration –Wide splitting of 2nd heart sound because of the early closure of aortic valve
Causes of mitral regurgitation Acute mitral regurgitation: –acute myocardial infarction with papillary muscle rupture, or during the course of infective endocarditis Transient, acute mitral regurgitation: –during periods of acute ischaemia and bouts of angina pectoris Chronic mitral regurgitation can result from –rheumatic disease (more frequently in males) –extensive mitral annular calcification (among patients with advanced renal disease, and is commonly observed in elderly women with hypertension and diabetes) –hypertrophic obstructive cardiomyopathy –dilated cardiomyopathy (The annular dilatation and ventricular remodeling causes papillary muscle displacement and fibrosis)
Symptoms of mitral regurgation Chronic mild-to-moderate MR is usually asymptomatic (well tolerated volume overload of LV) Severe MR: fatique, exertional dyspnea, orthopnea, palpitation In case of marked pulmonary hypertension: painful hepatic congestion, anckle edema, distended neck veins, ascites In case of acute MR the acute pulmonary edema is common
Aortic stenosis May be due to degenerative calcification of aortic cusps, or congenital in origin, or it may be secondary to rheumatic inflammation. Calcific AS is progressive disease, with an annual reduction in valve area averaging 0.1 cm2/year.
Etiology of aortic stenosis Due to degenerative calcification of aortic cusps –Congenital –Secondary to rheumatic inflammation Age-related degenerative –About 30% of persons >65 years exhibit aortic valve sclerosis –Many of these have a systolic murmur of AS without obstruction –2% exhibit frank stenosis
Aortic stenosis –Frequently, an S4 is audable at the apex, and reflects the presence of left ventricle hypertrophy and an elevated left ventricle end-diastolic pressure; –Protosystolic ejection sound (aortic stenosis,dilated aorta, pulmonic stenosis). Relatively high in pitch with a sharp, clicking quality – crescendo-decrescendo ejection murmur -Loud, harsh murmur. Maximal intensity at the right 2nd interspace Often accompanies by palpable thrills Radiation often to the neck Heard best with the patient sitting and leaning forward, after complete exhalation. The intensity of the murmur decreases in upright position and during exercise
Extra heart sounds in diastole S 4 – atrial galopp – just before S1. It is heard best at the apex in the left lateral postion. Dull, low- pitched sound. It is due to increased resistance to ventricular filling following atrial contraction. (increased stiffness of ventricular myocardium) Hypertensive heart diasese, coronary artery disease, aortic stenosis, and cardiomyopathy.
Symptoms of aortic stenosis Associated signs (even severe AS may exist for many years without producing any symptoms because of the ability of the hypertrophied left ventricle to generate the elevated intraventricular pressures required for a normal stroke volume) –Dyspnea results from elevation of the pulmonary capillary pressure –Angina pectoris partly because of the compression of the coronary vessels by the hypertrophied myocardium –Exertional syncope: result from a decline in arterial pressure –The peripheral pulse rises slowly to a delayed sustained peak (pulsus parvus et tardus) –In the late stages, when stroke volume declines, the systolic pressure may fall and the pulse pressure narrow –Functional aortic regurgitation,with early decrescendo diastolic murmur.
Causes of aortic regurgitation Primary valve disease (3/4 of patients with pure valvular AR are males) –Rheumatic origin (mostly with associated mitral valve diasease) –Infective endocarditis Primary aortic root disease –Due to marked aortic dilatation (widening of the aortic annulus and separation of the aortic leaflets) Idiopathic Marfan’s syndrome Osteogenesis imperfecta Syphilis Ankylosing spondylitis
Aortic regurgitation S4 –Midsystolic murmur (relative aortic stenosis) increased forward flow across the aortic valve Early diastolic decrescendo murmur Blood regurgitates from the aorta back into the left ventricle 2nd to 4th left interspaces parasternally Radiation to the apex (if loud) High pitch It is heard best with the patient sitting, leaning forward, with breath held in exhalation –Mitral diastolic (Austin Flint) murmur Diastolic impingement of the regurgitant flow on the anterior leaflet of the mitral valve (mitral stenosis)
Aortic regurgitation The arterial pulse pressure is widened, and there is an elevation of systolic pressure, and a depression of the diastolic pressure. Rapidly rising pulse, which collapses suddenly as arterial pressure falls rapidly during late systole and diastole (Corrigan’s pulse, (pulsus celer et altus) Bobbing motion of the head with each systole (Musset’s sign) Capillary pulsations, an alternate flushing and paling of the skin at the root of the nail while pressure is applied to the tip of the nail is characteristic (Quincke’s pulse) If the femoral artery is lightly compressed with the stethoscope a systolo-diastolic murmur is audible (Duroziez’s sign)