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First Heart Sound (s1) Produced by closure of mitral valve and tricuspid valve in early systole best heard at the apex of the heart. There are 3 types of abnormal splitting of S2: Extra Systolic heart Sounds (ejection clicks)
First Heart Sound (s1) Produced by closure of mitral valve and tricuspid valve in early systole best heard at the apex of the heart. There are 3 types of abnormal splitting of S2: Extra Systolic heart Sounds (ejection clicks)
First Heart Sound (s1) Produced by closure of mitral valve and tricuspid valve in early systole best heard at the apex of the heart. There are 3 types of abnormal splitting of S2: Extra Systolic heart Sounds (ejection clicks)
Produced by closure of mitral valve and tricuspid valve in early systole
Best heard at the apex of the heart. High frequency diaphragm Actually the mitral valve closes before tricuspid valve, separated by only 0,01s heard as a single sound 3 factors determine the intensity of S1: 1) The distance separating the leaflets of the open valves at the onset of ventricular contraction described by PR interval in the ECG period between onset of atrial and ventricular contraction. When atrial contraction occurs, the valve will open. As the ventricle contracts, the leaflets are drifted back together and forced to shut 2) Mobility of the leaflets 3) The rate of ventricular pressure Accentuated S1 short PR interval valve leaflets dont have sufficient time to drift back together forced to shut from relatively wide distance. Examples: mild stenosis, tachycardia Reduced intensity of S1 first degree AV block delays of the ventricular contraction valves have additional time to float back together softer sound
Second Heart Sound (S2) Results from the closure of aortic and pulmonic valves has aortic (A2) and pulmonic (P2) components The components of S2 vary with the respiratory cycle fused during expiration and separated during inspiration physiologic splitting At inspiration more negative intrathoracic pressure capacitance of intrathoracic pulmonary vessels temporary delay in diastolic back pressure of the pulmonary artery for the closure of pulmonary valve delayed P2 Inspiration more negative intrathoracic pressure capacitance of pulmonary vein venous return to LA and LV SV shortens valve closure Intensity of S2 depends on the velocity of blood coursing back toward the valves from aorta and pulmonary artery and the suddenness with which that motion is arrested by the closing of the valves Hypertension accentuated S2 because the pressure is each great artery is higher blood velocity Severe aortic or pulmonary valve stenosis valve commissures are nearly fixed in position diminished S2 There are 3 types of abnormal splitting of S2:
Extra Systolic Heart Sounds Early Extra Systolic Heart Sounds (Ejection Clicks) Occurs shortly after S1 coincide with the opening of the aortic or pulmonic valves Sharp, high pitched, best heard with diaphragm placed over the aortic and pulmonic areas Aortic and pulmonic stenosis deformed valve leaflets reach their maximal level of ascent into the great artery before the blood ejection reach their elastic limits decelerate abruptly ejection click Dilatation of the root of the aorta or pulmonary artery sudden tensing of the root with onset of blood flow into vessel ejection click Aortic ejection click: heard both at the base and apex of the heart, doesnt vary during respiration Pulmonic ejection click: heard only at base, intensity diminishes during inspiration
Mid or Late Extra Systolic Heart Sounds Result of systolic prolapsed of the mitral or tricuspid valves leaflets bulge abnormally into the atrium Loudest over the mitral or tricuspid regions
Extra Diastolic Heart Sounds Opening Snap Resulting from the opening of mitral and tricuspid valves Sharp, high-pitched, timing doesnt vary with respiration In mitral stenosis heard best between the apex and left sterna border, just after A2 Can be confused with P2. With careful auscultation, 3 sounds occurring in rapid successions A2, P2, OS Third Heart Sound (S3) Occurs in early diastole, following the opening of AV valves, during the ventricular rapid filling phase Dull, low-pitched, best heard with bell Production of S3 results from tensing of the chordae tendinae during rapid filling and expansion of the ventricle Normally found in children and young adults, abnormal in middle-aged or older adults When abnormally heard volume overload because CHF/ transvalvular flow that accompany advanced mitral/tricuspid regurgitation Pathologic S3 ventricular gallop Fourth Heart Sound Occurs in late diastole, coincides with the contraction of atria Generated by the left or right atrium vigorously contracting against a stiffened ventricle Thus, the presence of S4 usually indicates a in ventricular compliance ventricular hypertrophy or myocardial ischemia Dull, low-pitched sound, best heard with bell Also known as atrial gallop Quadruple Rhythm or Summation Gallop Patients with S3 and S4, in conjunction with S1 and S2 produce quadruple beat If patient with quadruple rhythm develops tachycardia shorter diastole duration S3 and S4 coalesce summation gallop Pericardial Knock Uncommon, high-pitched Hallmark of constrictive pericarditis Appears early in diastole, soon after S2, later than OS, louder and earlier than ventricular gallop Results from abrupt cessation of ventricular filling in early diastole