Auscultation Of The Heart

Front 1

2 parts to a stethoscope; why two?

What sounds are best heard with each?

Back 1

Diaphragm--larger piece. Gets higher pitches. S1, S2, opening snaps, most murmers. Place with FIRM pressure.

Bell--smaller piece. Lower pitches. MS, S3 gallop. Place on chest wall with LIGHT pressure only.

Front 2

What locations will we listen to on the patient?

Back 2

A: right 2nd intercostal
P: left 2nd intercostal
-proceed down sternal border
T: lower left sternal border
-proceed out to mid-clavicular line
M: apex; 5th intercostal space at mid-clavicular line
-proceed out to axillary line

*Listen to neck for murmur radiation (for AS or sclerosis; pt can't be breathing if you want to hear this).

*One method: Neck to base, left sternal border, apex, axilla.

Front 3

What maneuvers help you hear heart sounds?

Back 3

*Hand grip:
*Squatting/standing: Not part of standard exam, but great for hypertrophic cardiomyopathy to alter preload.
*Valsalva: increases pressure inside chest; this decreases venous return and preload. Same effect as standing up from a squatting position.

Front 4

Discuss S1:

what factors make it sounds louder?

Back 4

*S1: closure of MV and TV (really just MV...there's no splitting of S1). Best heard in mitral area (apex). Diaphragm and bell can hear it.

*Factors that might increase S1 include any condition which would increase the rapidity of mitral valve closure.

*These factors would include:
1) Mitral stenosis – causing increased mitral gradient, and increased LA pressure
2) Increased trans-mitral flow --such as seen in left-to-right shunts (ASD, VSD) or high-output states, such as fever or thyrotoxicosis
3) Short PR-interval --causing early closure of the mitral valve

Front 5

What factors make S1 sound softer?

Back 5

*Factors that might decrease S1 include any factor which might cause the mitral leaflets not to “coapt” or come together properly, including fibrosis of the valve leaflets or any condition where the valve is not completely open prior to final closure.

*These conditions include:
1) Low cardiac output states, such as seen with dilated cardiomyopathy
2) Rheumatic mitral regurgitation with extensive valve leaflet destruction
3) Severe, acute aortic regurgitation, where there may be premature closure of the mitral valve
4) Long PR interval, causing delay in the mitral valve closure.

Front 6

Discuss S2:

Back 6

*The second heart sound, S2, is caused by the closure of the aortic and pulmonic valves – both of which are usually heard in the normal patient. The so-called “splitting” of the second heart sound should vary with normal respiration, such that the splitting becomes wider with inspiration.

*So, if we call the two components of the second heart sound A2 and P2 (aortic and pulmonic closure, respectively), then in the normal state, A2 precedes P2. During inspiration, P2 occurs even later, due to increased filling of the right ventricle during inspiration, and the splitting of S2 becomes wider.

*Remember it this way – “inspiratory splitting of the second heart sound” – more inspiration, more splitting.

Front 7

Describe wide splitting of S2:

Back 7

*“Wide splitting” of the second heart sound occurs when the splitting of S2 is wider both with expiration and with inspiration.

*This occurs with Right Bundle Branch Block (RBBB), because of delayed contraction of the right ventricle.

Front 8

Describe wide, fixed splitting of S2:

Back 8

*“Wide, fixed splitting” of S2 occurs when there is a large atrial septal defect with left-to-right shunting, causing increased RV volume and delayed closure of the pulmonic valve.

*IN this case, however, there is no change in splitting with inspiration, since the shunt continues to keep RV volume increased throughout changes in respiration.

*The major cause for wide, fixed splitting of S2 is a large ASD.

Front 9

What is paradoxical S2 splitting?

Back 9

*Reverse or “paradoxical” splitting of S2 is due to a significant delay of aortic valve closure, leading to P2 actually occurring before A2.

*In this scenario, the usual physiologic occurrence – the pulmonic valve closing slightly later during inspiration – leads to less splitting with inspiration, and this is called paradoxical splitting.

*This is usually due to Left Bundle Branch Block (LBBB), which causes delayed LV activation, delayed LV contraction, and delayed aortic valve closure.

Front 10

Discuss the opening snap:

Back 10

*The opening snap of the mitral valve may occur when the mitral valve is stenotic, and is caused by the sudden cessation of mitral valve opening, due to rheumatic deformity of the valve. Since this occurs just after the mitral valve opens, it also occurs just after the aortic valve closes, or just after S2.

*The opening snap is a high-pitched sound, just after S2, heard best with the diaphragm in the tricuspid or mitral positions.

*Ironically, the opening snap is best heard during the early stages of mitral stenosis, where the valve is somewhat rigid, but is still mobile. As the severity of mitral stenosis progresses, the S2 – OS interval (interval between S2 and the opening snap) becomes shorter, and the opening snap is less loud – eventually becoming inaudible when stenosis is severe.

Front 11

What are gallop sounds?

Back 11

The so-called gallop sounds, S3 and S4, are low pitched sounds heard best at the apex of the heart using the bell, with the patient in the left lateral decubitus position.

Front 12

Discuss the S3 gallop:

Back 12

*The S3 gallop is described as a “physiologic” (i.e. normal) finding in children and young adults, but in anyone over the age of forty, the S3 gallop is considered an abnormal finding associated with significant left ventricular dysfunction.

*It is a low pitched vibration occurring 120–200 milliseconds after S2, and is often very soft and difficult to hear, except in a quiet room with intent listening technique. The genesis of the S3 remains controversial. In general, an S3 is heard when there is a dilated, hypocontractile left ventricle with elevated filling pressures (i.e. congestive heart failure due to systolic dysfunction), and is an indicator of a poor prognosis.

*It may be due to “the dynamic interplay between the force of delivery of blood into the ventricle and the ability of the ventricle to accept this flow”or might be due to the dynamic impact of the heart against the chest wall.

*Bottom line: LV function is poor and filling pressure is very high.

Front 13

Discuss the S4 gallop:

Back 13

*The S4 gallop is a much more common finding than the S3, and is better understood. The S4 is associated with decreased LV compliance, and coincides with atrial systole, occurring just before S1 (just before the closure of the mitral valve). Because its presence coincides with atrial contraction, it therefore is not heard when atrial fibrillation is present, since there is no effective atrial contraction during atrial fibrillation.

*The S4 is a low-pitched sound, best heard with the bell, at the apex, with the patient in a left lateral decubitus position. However, it is easier to hear than the S3, and is often heard in the supine position.

*Common causes of the S4 gallop include any condition which leads to concentric LVH, including:
1) Hypertensive heart disease (with concentric LVH and normal LV systolic function)
2) Hypertrophic cardiomyopathy
3) Aortic stenosis

*An S4 can also occur transiently during myocardial ischemia or during MI, presumable related to suddenly increased LV diastolic pressure to due to abnormal LV compliance.

Front 14

What is pericardial knock?"

Back 14

The “pericardial knock” is an early diastolic sound occurring commonly in patients with constrictive pericarditis, which is slightly higher pitched and earlier than an S3 gallop. It often is heard best with inspiration at the left sternal border.

Front 15

What is mid-systolic click?

Back 15

*The “mid-systolic click” is a sound associated with prolapse of the mitral valve, and is, as described, a mid-systolic sound which is high-pitched, and is often followed by a late-systolic murmur.

*This is usually heard best at the apex, and the timing of the click, as well as the intensity, may vary with various maneuvers, as well as with a change in the patient’s volume status (i.e. LV filling).

*Anything that makes the heart smaller tends to accentuate the mitral prolapse, and cause the click to occur earlier. Thus standing up, performing the Valsalva maneuver, or administering amyl nitrate will cause the click to occur earlier (and any associated late-systolic murmur to begin earlier).

*Conversely, any maneuver which causes an increase in left ventricular end-diastolic volume (causing the left ventricle to enlarge) will cause the click to occur later – these maneuvers include squatting down and the hand-grip maneuver.

Front 16

What are the basic principles of listening for murmurs?

Back 16

*Most patients with significant valvular heart disease are first diagnosed based upon the finding of a murmur.

*Auscultation has a reported sensitivity of 70 percent and a specificity of 98 percent for detection of valvular heart disease.

*When describing a heart murmur, we must employ a systematic approach, and describe each murmur based upon its intensity, pitch, configuration, location and radiation, and timing.

Front 17

Discuss scales of murmur intensity:

Back 17

Front 18

Describe murmur pitch:

Back 18

*The frequency of the murmur determines the pitch, and is usually described as high-pitched or low-pitched.

*The quality of the murmur may also be described, for example, as “harsh”, “rumbling”, “blowing”, or “honking” to better define the character of the sound.

Front 19

Discuss murmur shape and configuration:

Back 19

*The time-course of murmur intensity helps to describe a “shape” of the murmur, which should approximate the appearance of the murmur as seen on a phonocardiogram.

*Descriptions of the murmur “shape” usually include: “Crescendo” (increasing), “Decrescendo” (decreasing), “Crescendo-decrescendo” or “ejection-type” (diamond-shaped) and “plateau” (unchanging in intensity).

Front 20

Discuss murmur Location and radiation:

Back 20

The location of the murmur’s greatest intensity, as well as the locations where it is also heard or where it “radiates” to are described – e.g. “a III/VI holo-systolic plateau murmur heard at the apex, with radiation to the left axilla.”

Front 21

Discuss murmur duration and timing:

Back 21

*The duration and timing of the murmur is described based on its location in the cardiac cycle.

*A murmur can be described as: early systolic, mid-systolic, late-systolic, holosystolic (throughout systole), early diastolic, mid-diastolic, late-diastolic or diastolic.

*This can be hard to describe.

Front 22

Describe the murmur in AS:

Back 22

*Aortic stenosis usually causes an easy to recognize, easy to hear murmur which occurs during systole, during the time when then aortic valve is open. The reduced opening of the stenotic valve leads to abnormal flow and turbulence above the valve.

*The murmur of aortic stenosis is usually a harsh, systolic murmur, often diamond-shaped (crescendo-decrescendo) which radiates from the second right intercostal space (the aortic area) upwards to the carotid arteries. It is sometimes associated with a thrill (grade IV murmur).

*As aortic stenosis progresses, the contour of the murmur changes, and it becomes more late-peaking, eventually blending in to the second heart sound, and may be associated with a single or absent second heart sound. Perhaps most importantly, as the severity of aortic stenosis progresses, there is a diminishment of the carotid pulses, leading to delayed and reduced carotid upstrokes, described as “pulsus parvus et tardus”.

*Therefore, a late-peaking, harsh systolic murmur heard at the base, radiating to the carotids, associated with decreased S2 and delayed, weak carotid upstrokes is highly suggestive of severe aortic stenosis.

Front 23

Describe the murmur of Aortic insufficiency:

Back 23

*Aortic insufficiency may actually lead to several murmurs. The characteristic murmur is described as a soft, high-pitched diastolic decrescendo blowing murmur best heard at the left sternal border, which is easiest to hear with the diaphragm of the stethoscope, with the patient sitting up and leaning forward, at the end of expiration. (It can easily be missed, unless the patient is asked to exhale and hold their breath in end-expiration, while firm pressure is held on the stethoscope against the left sternal border).

*Because aortic insufficiency leads to a substantial increase in the volume of blood ejected from the left ventricle during systole, there is almost always an associated systolic ejection murmur heard at the left sternal border and at the aortic area, due to increased flow through the LV outflow tract and the aortic valve. This tends to be early-to-mid peaking, rather than late-peaking as in severe aortic stenosis.

*Finally, a second diastolic murmur, which sounds more like the apical diastolic rumbling murmur of mitral stenosis (see below), can sometimes be heard with aortic insufficiency, and is termed the murmur of Austin Flint. This murmur is thought to occur related to the aortic regurgitant jets which are directed at the LV free wall, causing a low pitched pre-systolic sound, heard at the apex.

Front 24

Describe the murmur of chronic mitral regurgitation:

Back 24

*Mitral insufficiency or regurgitation (MR) may occur chronically or acutely (due to chordal or papillary muscle rupture.) Classically, in chronic mitral regurgitation the murmur is described as a high-pitched, holosystolic apical murmur, best heard with the diaphragm of the stethoscope in the left lateral decubitus position. This murmur may radiate laterally, to the axillary region, or posteriorly, to the left scapular area, depending on the location and direction of the regurgitant jet.

*Unfortunately, the loudness or duration of the murmur does not correlate well with the severity of the MR, and therefore auscultation is not that helpful in determining prognosis with MR.

Front 25

Describe the murmur of acute mitral regurgitation:

Back 25

*Acute mitral regurgitation is associated with a shorter, more ejection quality (crescendo/decrescendo) murmur, which can be mistaken for aortic stenosis. This murmur ends well before the second heart sound, and is often associated with an S4 gallop and sometimes an increased pulmonic component of S2, related to pulmonary hypertension. It may be best heard along the left sternal border, as opposed to chronic MR, which is best heard at the LV apex.

Front 26

Discuss the murmur due to MVP:

Back 26

*Mitral insufficiency due to mitral valve prolapse usually causes a late systolic blowing murmur, which may or may not be preceded by a mid-systolic click. This murmur may occasionally have a “whooping” or “honking” character to it, and this may be intermittently heard. This murmur can be lengthened or shortened based on diagnostic maneuvers.

Front 27

Describe the murmur due to Mitral Stenosis:

Back 27

*Mitral stenosis leads to obstruction of diastolic flow from the left atrium into the left ventricle, and the murmur is characteristically a low-pitched diastolic “rumbling” murmur which is best heard at the apex, with the bell portion of the stethoscope, in the left lateral decubitus position.

*In early mitral stenosis, there is often a prominent opening snap, followed by a short diastolic rumble, which does not extend all the way to S1. As mitral stenosis becomes more severe, the opening snap occurs earlier, and the diastolic rumble becomes longer, with pre-systolic accentuation – the longer the murmur, the worse the stenosis.

*The shorter the interval between S2 and the opening snap – the worse the stenosis.

*Finally, at the end stage of mitral stenosis, as pulmonary hypertension develops and the flow across the mitral valve is reduced, the murmur may become softer and almost inaudible, just as the opening snap becomes almost inaudible – resulting in virtually “silent” mitral stenosis. In this situation, clinical judgement and echocardiography will help to make the correct diagnosis.