Heart Sounds

Increased intensity of A2 in the right 2nd interspace

(where only A2 can usually be heard) occurs in systemic hypertension because of the increased pressure load. it also occurs when aortic root is dilated, probably because the aortic valve is then closer to chest wall.

Pathological Splitting: Paradoxical or reversed splitting

Refers to splitting that appears on expiration and disappears on inspiration. Closure of the aortic valve is abnormally delated so that A2 follows P2 in expiration. Normal inspiratory delay of P2 makes split disappear. The most common cause of paradoxical splitting is left bundle branch block.

Pathological Splitting: Fixed splitting

Refers to wide splitting that does not vary with respiration. It occurs in atrial septal defect and right ventricular failure.

Mitral Stenosis: associated findings

S1 accentuated and may be palpable at apex. opening snap often follows S2 and initiated murmur. if pulm hypertension develops, P2 is accentuated. mitral regurg and AoV diasease may be associated.

Accentuated S1

S1 is accentuated is 1) tachycardia, rhythms with a short PR interval, and high CO states (e.g. exercise, anemia, hyperthyroidism) and 2) mitral stenosis. In these conditions, the mitral valve is still open wide at the onset of ventricular systole and then closes quickly.

Diminished S1

S1 is diminished in first degree heart block (Delayed conduction from atria and ventricles). Here the mitral valve has had time after atrial contraction to float back into an almost closed position before ventricular contraction shuts it. it closes more quietly. S1 is also diminished 1) when mitral valve is calcified and relatively immobile, as in mitral regurgitation and 2) when left ventricular contractility is markedly reduced, as in heart failure or coronary heart disease.

normal variations

S1 is softer than S2 at the base (right and left 2nd interspaces) S1 is often but not aways louder than S2 at apex

Split S1

S1 may split normally along the lower left sternal border where tricuspid component, often too faint to be heard, becomes audible. this split may sometimes be heard at the apex, but consider also an S4, an aortic ejection sound, and an early systolic click. Abnormal splitting of both heart sounds may be heard in right bundle branch block and in premature ventricular contractions.

Mitral Regurgitation: associated findings

S1 normal, loud, soft apical S3 reflects volume overload of left ventricle. apical impulse is increased in amplitude, laterally displaced, and may be sustained.

Varying S1

S1 varies in intensity 1) in complete heart block, when atria and ventricles are beating independently of each other and 2) in any totally irregular rhythm (e.g atrial fib). in these situations, the mitral valve is in varying positions before being shut by ventricular contraction. Its closure sound, therefore, varies in loudness.

pulmonic stenosis: associated findings

S2 is widely split in severe stenosis and P2 is diminished/inaudible. early pulmonic ejection sound is common. may hear right sided S4. Rt ventric impulse often icnreased in amplitude and sustained.

Ventricular Septal Defect: associated findings

S2 may be obscured by loud murmur findings vary with severity of defect and with associated lesions.

hypertrophic cardiomyopathy: associated findings

S3 may be present. S4 often present at apex. apical impulse may be sustained and have 2 palpable components. carotid pulse rises quickly.

Pathological Splitting: Wide Splitting of S2

Wide splitting of S2 refers to an increase in usual splitting that persists throughout the respiratory cycle. Wide splitting can be caused by delayed closure of the pulmonic valve (As in pulmonic stenosis or right bundle branch block). RBBB also causes splitting of S1 into its mitral and tricuspid components. Wide splitting can also be caused by early closure of the aortic valve, as in mitral regurgitation.

Ventricular Septal Defect: mechanism

a ventricular septal defect is a congenital abnormality in which blood flows from relatively high pressure left ventricle into low pressure right ventricle through a hole.

S4

aka atrial sound or atrial gallop- occurs just before S1. dull, low in pitch, heard best with bell. occasionally normal in athletes and older age groups. due to increased resistance to ventricular filling following atrial contraction. this increased resistance is related to decreased compliance of ventricular myocardium. "Tennessee" left sided: heard best at apex in left lateral position. causes of left sided: hypertensive heart disease, myocardial ischemia, aortic stenosis, cardiomyopathy. right sided (less common): lower left sternal border or below xiphoid. causes of right sided: pulmonary hypertension and pulmonic stenosis S4 could also be associated with delayed conduction between atria and ventricles.

Extra heart sounds in diastole: S3, pathological

aka ventricular gallop- sounds like physiologic S3. over age 40 is pathologic, arising from high pressure and abrupt deceleration across mitral valve at end of rapid filling phase of diastole. causes include: decreased myocardial contractions, heart failure, volume overloading of ventricle (as in mitral or tricuspid regurgitation). left sided: heard at apex and left lateral decubitus. right sides: lower left sternal border or below xiphoid with patient supine, and louder on inspiration. "Kentucky"

Diastolic murmurs

almost always indicate heart disease. two basic types. early descres diastolic murmurs signify regurgitant flow through incompetent semilunar valve (more commonly AoV). Rumbling diastolic murmurs in mid or late diastole suggest stenosis of AV valve (usually mitral).

summation gallop

at rapid heart rates, S3 and S4 may merge into one loud extra sound.

Aortic Regurgitation: associated findings

ejection sound may be present. S3 or S4, if present, means severe regurg. progressive changes in apical impulse include increased amp, displacement laterally and downward, widened diameter, and increased duration. pulse pressure increases, arterial pulses are often bounding.

aortic stenosis: mechanism

impairs blood flow across the valve, causing turbulence, and increased left ventricular afterload. causes are congenital, rheumatic, and degenerative calcification on leaflets.

Extra heart sounds in diastole: S3, physiologic

in children and young adults to 35-40. common during last trimester of pregnancy. occurring early in diastole during rapid ventricular filling, later than an opening snap, dull, low in pitch, and heard best at apex in left lateral decubitus position. bell should be used.

Aortic Regurgitation: mechanism

leaflets of AoV fail to close completely during diastole, and blood regurgs fro aorta back to left vent. volume overload on left vent results. 2 murmurs may be associated: 1. midsystolic murmur from increased forward flow across AoV. 2. mitral diastole (Austin Flint) murmur.

Mitral Stenosis: mechanism

leaflets of mitral valve thicken, stiffen and become distorted from rheumatic gever, the mitral valve fails to open sufficicently in diasotle. two components: 1. middiastolic and 2. presystolic.

physiological splitting

listen for physiological splitting of S2 in the 2nd or 3rd left interspace. the pulmonic component of S2 is usually too faint to be heard at the apex or aortic area, where S2 is a single sound derived from aortic valve closure alone. Normal splitting is accentuated by inspiration and usually disappears on expiration. In some patients, especially younger ones, S2 may not become single on expiration. It may merge when the patient sits up.

innocent murmurs

location: 2nd to 4th interspaces between the left sternal border and apex little radiation grade 1, 2, possibly 3 soft to medium pitch variable quality aids: usually decreases or disappears on sitting mechanism: turbulent blood flow, probably generated by ventricular ejection of blood into aorta from the left and occasionally the right ventricle. very common in children and adults.

physiologic murmurs

location: 2nd to 4th interspaces between the left sternal border and apex little radiation grade 1, 2, possibly 3 soft to medium pitch variable quality aids: usually decreases or disappears on sitting mechanism: turbulence due to a temporary increase in blood flow in predisposing conditions such as anemia, pregnancy, fever, hyperthyroidism.

Aortic Regurgitation

location: 2nd to 4th left interspaces radiation: if loud, to apex, perhaps rt sternal border intensity: grade 1-3 pitch: high- use diaphragm. quality: blowing decrescendo, may be mistaken for breath sounds. aids: murmur is heard best with patient sitting, leaning forward, and breath held.

pulmonic stenosis

location: 2nd, 3rd left interspaces radiation: if loud, toward left shoulder and neck intensity: soft to loud, if loud- thrill pitch: medium; cresc-descre quality: often harsh

Ventricular Septal Defect

location: 3rd, 4th, and 5th left interspaces radiation: often wide intensity: often very loud, with thrill pitch: high, holosystolic quality: often harsh

hypertrophic cardiomyopathy

location: 3rd, 4th, left interspaces radiation: down left sternal border to apex, possibly to base, but not neck. intensity: variable pitch: medium quality: harsh aids: decreased with squatting, increases with straining down from Valsalva and standing

Mitral Regurgitation

location: apex radiation: to left axilla, less often to left sternal border intensity: soft to loud; if loud, associated with an apical thrill pitch: medium to high quality: harsh, holosystolic aids: does not become louder during inspiration (tricuspid regurgitation does)

Mitral Stenosis

location: limited to apex radiation: little or none intensity: grade 1-4 pitch: descresc low pitched rumble. BELL. aids: placing bell exactly on apical impulse, turning patient to left lateral position, and mild exercise all help to make murmur audible.

Tricuspid Regurgitation

location: lower left sternal border radiation: to the right of sternum, to the xiphoid area, and perhaps to the left midclavicular line, not not into axilla. intensity: variable pitch:medium quality: blowing, holosystolic aids: unlike mitral regurg, intensity may increase slightly with inspiration.

aortic stenosis

location: right 2nd interspace radiation: often to carotids, down to left sternal border, sometimes apex intensity: sometimes soft but often loud with thrill pitch: medium, harsh, cres-decres may be higher at apex quality: often harsh aids: heard best with patient sitting and leaning forward

hypertrophic cardiomyopathy: mechanism

massive ventricular hypertrophy is associated with unusually rapid ejection of blood from left ventricle during systole.

Midsystolic Ejection Murmurs

most common kind of heart murmur. they be 1. innocent or 2. physiologic- from changes in body mechanism. 3. pathologic- arising from a structural abnormality in heart of great vessels. tend to peak midsystole and usually stop before S2. the gap between murmur and S2 helps distinguish midsystolic from pansystolic murmurs.

Decreased or absent A2 in right 2nd interspace

noted in calcific aortic stenosis because of valve immobility. If A2 is inaudible, no splitting is heard.

early systolic ejection sounds

occur shortly after S1, coincident with opening of the aortic and pulmonic valves. they are relatively high in pitch, have sharp, clicking quality, and are heard better with diaphragm. Ejection sound indicates CVD. aortic ejection sound: at base and apex. it may be louder at apex and usually does not vary with respiration. an aortic ejection sound may accompany a dilated aorta, or aortic valve disease from congenital stenosis or bicuspid aortic valve. pulmonic ejection sound is heard best at 2nd and 3rd left interspaces. When S1, usually relatively soft in this area, appears to be loud, you may be hearing a pulm ejection sound. its intensity often decreases with inspiration. causes include: dilation of pulmonary artery, pulmonary hypertension, and pulmonic stenosis.

Extra heart sounds in diastole: opening snap

opening snap is a very early diastolic sound usually produced by the opening of a stenotic mitral valve. it is heard best just medial to apex and along the left sternal border. when it is loud, and opening snap radiates to apex and pulmonic area, where it could be mistaken for pulmonic component of split S2. its high pitch and snapping quality help to distinguish it from S2. heard best with diaphragm.

Pansystolic (Holosystolic) Murmurs

pathological, arising from blood flow from a chamber with high pressure to one of lower pressure, through a valve or other structure that should be closed. the murmur begins immediately with S1 and continues to S2.

pulmonic stenosis: mechanism

pulmonic valve stenosis impairs flow across valve, increasing Rt ventricular afterload. congenital and usually found in children. in an atrial septal defect, systolic murmur from pathologically increased flow across pulm valve may mimic pulm stenosis.

Tricuspid Regurgitation: associated findings

right ventricular impulse is increased in amplitude and may be sustained. an S3 may be audible along lower left sternal border. the jugular venous pressure is often elevated, with large v waves in jugular veins.

Venous Hum

timing continuous murmur without silent interval. loudest in diastole. location: above medial 3rd of clavicles, especially on right radiation: 1st and 2nd interspaces intensity: soft to moderate. quality: humming, roaring pitch: low- BELL.

Pericardial Friction Rub

timing: 3 short components, each associated with friction from cardiac movement in pericardial sac. 1. atrial systole 2. vent systole, 3. vent diastole. usually only 2 are present. location: variable, heard best in 3rd left interspace radiation: little intensity: variable. may increase when patient leans forward, exhales, and holds. quality: scratchy pitch: high

Patent Ductus Arteriosis

timing: continuous murmur in systole and diastole, often with silent interval late in diastole. loudest in late systole, obscures S2, fades in diastole location: left 2nd interspace radiation: toward left clavicle intensity: loud, sometimes thrill quality: harsh, machine like pitch: medium

systolic clicks

usually caused by mitral valve prolapse- an abnormal systolic ballooning of part of MV into left atrium from both leaflet redundancy and elongation of chordate tendinea. The clicks are usually mid or late systole. prolapse of mitral valve is common cardiac conditions, affecting 2-3% of population. squatting: click is usually single, but you may hear more than one usually at or medial to apex, but also lower left sternal border. high pitched, listen with diaphragm. click is often followed by late systolic murmur from regurgitation. the murmur usually crescendos up to S2. auscultatory findings are notably variable. most patients have only a click, some have only a murmur, and some have both. systolic clicks may be extracardial or mediastinal origin. standing: in mitral valve prolapse, findings vary from time to time and often change with body position. several positions are recommended to identify the syndrome: seated, squatting, and standing. squatting delays click and murmur, standing moves them closer to S1

Decreased or absent P2

usually from increased anteroposterior diameter of chest associated with aging. It can also result from pulmonic stenosis. If P2 is inaudible, no splitting is heard.

Increased intensity of P2

when P2 is equal to or louder than A2, suspect pulmonary hypertension. other causes include a dilated pulmonary artery and an atrial septal defect. When a split in S2 is heard widely, even at the apex and the right base, P2 is accentuated.

Mitral Regurgitation: mechanism

when mitral valve fails to close fully in systole, blood regurgitates from left ventricle to left atrium, causing a murmur. this leakage creates volume overload on left ventricle, with subsequent dilation.

Tricuspid Regurgitation: mechanism

when tricuspid valve fails to close fully in systole, blood regurgitates from right ventricle to right atrium, causing a murmur. most common cause is right ventricular failure and dilation, with resulting enlargement of the tricuspid orifice, often initiated by pulmonary hypertension or left ventricular failure.

aortic stenosis: associated findings

worsens A2 decreased and murmur peaks later in diastole. A2 may be delayed and merge with P2. carotid upstroke may be delayed. hypertrophied left ventricle may --> sustained apical impulse and an S4 from decreased compliance.