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Auscultation (Abnormal Heart Sounds (S4 (heard in late diastole, just…
Auscultation
Abnormal Heart Sounds
S1 and S2
intensity
S1
depends on
the greater the force of contraction, the louder the sound
the lesser the blood in the LV, the louder the sound
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Loud: tachycardia, short PR intervals [probably don't allow the Vs to fill in adequately], Mitral stenosis with pliable valve
Soft: Long PR interval Mitral regurgitation Poor left ventricular function Mitral stenosis with rigid valve Thick chest wall
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respiratory splitting
S2
SINGLE S2: Pulmonic stenosis Systemic hypertension Coronary artery disease Any condition that can lead to paradoxical splitting of S2
WIDELY SPLIT S2 WITH NORMAL RESPIRATORY VARIATION: Right bundle branch block R side failure Left ventricular pacing Pulmonic stenosis Pulmonary embolism Idiopathic dilation of the pulmonary artery Mitral regurgitation Ventricular septal defect
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PARADOXICALLY SPLIT S2: Left bundle branch block Right ventricular pacing Angina, myocardial infarction Aortic stenosis Hypertrophic cardiomyopathy Aortic regurgitation
S4
heard in late diastole, just before S1; best recognized with the use of a bell at the apex (also S3 bc these are low pitch sounds)
a result of active ejection of blood into a noncompliant LV--> when atrial contraction is absent, such as in atrial fibrillation, an S4 cannot be heard.
LV diastolic dysfunction/ heart failure w/ preserved ejection fraction (LV can't relax enough, therefore not typically filled enough, to preserve ejection fraction, the atria contract to increase the end diastolic pressure)
S3
occurs during the rapid filling phase of diastole, thought to indicate a sudden limitation of the expansion of the LV; can be seen in cases of volume overload (chronic aortic regurgitation) or tachycardia. Maneuvers that increase venous return accentuate an S3, whereas those that reduce venous return diminish the intensity
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Ejection sounds: typically heard in early systole and involve the aortic and pulmonic valves. (high-frequency heard with a diaphragm shortly after S1)
Ejection clicks: Midsystolic to late systolic; most commonly associated with mitral valve prolapse; Any maneuver that decreases venous return will cause the click to occur earlier in systole, whereas increasing ventricular volume will delay the click
Opening snap: opening of abnormal mitral or tricuspid valves heard in early diastole; most frequently associated with rheumatic mitral stenosis; the shorter the interval between S2 and the opening snap, the more severe the degree of mitral stenosis, because this is a reflection of higher left atrial pressure
Normal Heart Sounds
S1
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Normal splitting in young patients and those w/ RBBB, in whom tricuspid valve closure is relatively delayed
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S3
physiologic: sometimes heard in healthy children and young adults. occurs during the rapid filling phase of diastole
S4
caused by forceful atrial contraction into a noncompliant ventricle; rarely audible in normal young patients but relatively common among older individuals (در سنین پایین غیر طبیعی نیست به خصوص در افراد بلند و لاغر) (در سنین بالاتر معادل با دومین عامل نارسایی قلب(
Murmurs: auditory vibrations generated by high flow across a normal valve or normal flow across an abnormal valve or structure; Right-sided murmurs become louder with inspiration because of increased venous return. This can help differentiate them from left-sided murmurs, which are unaffected by respiration
systolic
non pathologic
physiologic murmurs: high-flow states such as fever, anemia, thyroid disease, and pregnancy
innocent murmurs: occur early in systole + soft + brief in duration + not typically pathologic; u. caused by flow across normal LV or RV outflow tracts + found in children and young adults
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Techniques
Standing
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↑ HCM ↓ AS, MR MVP click earlier in systole; murmur prolongs
Squatting
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↑ AS, MR, AI ; ↓ HCM MVP click delayed; murmur shortens
Valsalva (initial ↑ BP, phase I; followed by ↓ BP, phase II)
↓ BP, ↓ venous return, ↓ LV size (phase II)
↓ HCM ↓ AS, MR MVP click earlier in systole; murmur prolongs
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Murmurs
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CONTINUOUS
continuous flow from a vessel or chamber with high pressure into a vessel or chamber with lower pressure. They are referred to as machinery murmurs and are caused by aortopulmonary connections such as a patent ductus arteriosus, AV malformations, or disturbances of flow in arteries or veins.
SYSTOLIC
Mid: begin after S1 end before S2, crescendo-decrescendo
obstruction to LV outflow, accelerated flow through the aortic or pulmonic valve, or enlargement of the aortic root or pulmonary trunk (aortic stenosis, pulmonic stenosis, HCM)
pulmonic stenosis: resistance to blood flow in systole results in the classic harsh crescendo-decrescendo systolic murmur. Although it is typically heard best in the aortic position, the murmur may radiate to the cardiac apical region (known as Gallivardin’s phenomenon). Because the stiff, calcified, and restricted aortic valve leaflets make little excursion in systole, their closing no longer produces a sound; this results in an inaudible aortic component of S2
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Early: begin w/ S1, decrescendo, end typically before midsystole, often high pitched
VSDs, acute mitral regurgitation,
late
more severe aortic stenosis, mitral valve prolapse