S1

Ddx: Normal

Phys: Caused by the closure of the mitral and tricuspid valves

Listen: 

- High pitched

- Apex 

S2

Ddx: Normal

Phys: Caused by the closure of the pulmonic & aortic valves

Listen:

- high pitched

- aortic

Accentuated S1

Ddx:

1) Shortened PR interval - time btwn atrial & ventricular contraction (e.g. preexcitation syndrome, junctional rhythm)

2) Mild mitral stenosis

3) High CO states and/or tachycardia

Phys:

Normally, the valve leaflets are forced wide open by atrial contraction, after which they begin to drift back towards one another (as ventricular pressure increases) until the ventricles contract & the leaflets are slammed shut. Anything that increases the distance btwn the leaflets when ventricular contraction occurs will increase the intensity of S1.

1) Shortened PR - less time for the leaflets to drift back

2) Mild mitral stenosis - prolonged diastolic pressure gradient between LA & LV (the pressure in the LA is increased) - keeps leaflets further apart than normal during diastole.

3) Increased CO/HR - shortened diastole means leaflets have less time to drift back

Listen:

- High pitched

- Apex

Diminished S1

Ddx:

1) Lengthened PR interval - time btwn atrial & ventricular contraction (e.g. AV nodal block)

2) Mitral regurgitation

3) Severe mitral stenosis

3) "Stiff" left ventricle (e.g. due to systemic HTN)

Phys:

Normally, the valve leaflets are forced wide open by atrial contraction, after which they begin to drift back towards one another until the ventricles contract & the leaflets are slammed shut. 

1) Lengthened PR - more time for the leaflets to drift back

2) Mitral regurgitation - mitral leaflets may never fully contact ea. other

3) Severe mitral stenosis - mitral leaflets are calcified &  nearly immobile (can't "slam shut" loudly)

4) "Stiff" LV - increased LV pressure at the end of diastole causes the drift-back of the leaflets to occur more quickly, meaning they are closer together when ventricular contraction occurs

Listen:

- High pitched

- Apex

S2 Split on Inspiration

Ddx:

Normal (physiologic splitting), A2 precedes P2

Phys:

As the chest expands during inspiration, pressure in the intrathoracic pulm. vessels falls --> increased capacitance in the pulm. vessels --> delay in "back pressure" on the pulm. valve --> delayed pulm. valve closing.

Also, increased capacitance in the pulm. vessels --> decreased venous return to L. heart --> decreased SV --> decreased LV emptying time --> earlier aortic valve closing

Listen:

- high pitched

- pulmonic

Widened Splitting of S2

(Split on both insp. & exp., but greater on insp.)

Ddx:

1) Right bundle branch block

2) Pulmonic stenosis (P2 also soft)

Phys:

Abnormally delayed closure of the pulmonic valve due to:

1) RBBB - impaired spread of electricity through RV --> delayed RV contraction --> delayed closure of pulm. valve

2) Stenosis of pulmonic valve - narrowing of RV outflow --> increased ejection time --> delayed closure of pulm. valve

Listen:

- high pitched

Splitting of S2 on Inspiration & Expiration

(Fixed Splitting)

Ddx:

Atrial septal defect 

Phys:

ASD causes L-R shunting --> chronic volume overload of right-sided (pulmonary) circulation --> delayed "back pressure" on pulm. valve --> delayed pulm. valve closure

Does not change with respiratory cycle because:

1) Inspiration can't significantly increase the already elevated pulm. vascular capacitance

2) Although inspiration does increase RA filling, this is counterbalanced by the fact that inspiration decreases the L-R shunt. As a result there is no respiratory variation in RV filling. 

Listen:

- high pitched

Splitting of S2 on Expiration & NOT on Inspiration

(Paradoxical Splitting)

Ddx:

1) Left bundle branch block

2) Advanced aortic stenosis

Phys:

In this case, P2 precedes A2. This is caused by an abnormal delay in the closure of the aortic valve. During expiration this delay causes A2 to come after P2. During inspiration, P2 is normally delayed, and so the two sounds coincide. The delay in aortic valve closure can be due to:

1) LBBB - spread of electricity through LV is impaired --> delayed LV contraction --> delayed closure of aortic valve

2) Aortic stenosis - narrowed outflow of LV --> greatly prolonged ejection time --> delayed closure of aortic valve

Listen:

- high pitched

Split S1

Ddx:

1)  Right bundle branch block

2) Normal

Phys:

Normally, mitral closure slightly precedes tricuspid closure, but the difference is not audible. To hear a split S1, the difference must be exaggerated.

1) RBBB - impaired electrical conduction through RV --> delayed RV contraction --> delayed tricuspid closure

(In LBBB the delayed mitral closure is inaudible because it is counterbalanced by the fact that mitral closure is usually earlier than tricuspid)

Listen:

- high pitched

- tri-cuspid (b/c tricuspid closure is softer than mitral closure)

Early Systolic Ejection Sound

(Ejection Click)

Ddx:

1) Aortic stenosis

2) Aortic dilatation

3) Pulmonic stenosis

4) Pulmonic dilatation

Phys:

1) Aortic stenosis -  As pressure builds up in the LV, the stenotic valve ascends into the aorta. Just before ejection the valve reaches its elastic limit and decelerates abruptly, causing the sound. 

2) Aortic dilatation - Sudden tensing of the aortic root with the onset of blood flow into the vessel causes the sound.

3) Pulmonic stenosis -  As pressure builds up in the RV, the stenotic valve ascends into the pulm artery. Just before ejection the valve reaches its elastic limit and decelerates abruptly, causing the sound. 

4) Pulmonic dilatation - Sudden tensing of the pulmonic root with the onset of blood flow into the vessel causes the sound.

Listen:

- sharp, high pitched

- Aortic sounds: heard at base & apex, no respiratory variation

- Pulmonic sounds heard at base, diminished during respiration

Mid or Late Systolic Click

Ddx:1) Mitral prolapse2) Tricuspid prolapse

Phys:Due to abnormal bulging of valve leaflets into the atrium during ventricular contraction

Listen:

- sharp, high pitched

- mitral & tricuspid

Diastolic "Opening Snap"

Ddx:

1) Mitral stenosis (more common)

2) Tricuspid stenosis 

Phys:The sound is caused by the opening of the stenotic valve. The more severe the stenosis, the shorter the time interval between S2 and the opening snap.  This is because the more severe the stenosis, the higher the atrial pressure will be. As the ventricle relaxes in diastole, the higher the atrial pressure, the earlier the A-V valve opens.  

Listen:

- sharp, high pitched

- between apex & left sternal border (for mitral stenosis)

S3

(Ventricular Gallop)

Heard in diastole, shortly after S2 (later than split S2 or OS)

Ddx:

1) Congestive heart failure

2) Advanced mitral regurgitation

3) Advanced tricuspid regurgitation

4) Normal (in children & young adults) 

Phys:

The sound results from the tensing of the chordae tendinae during rapid filling and expansion of the ventricle. This can be due to:

1) CHF - volume overload

2) & 3) Mitral/Tricuspid regurgitation - increased transvalvular flow

4) Healthy supple ventricle capable of rapid expansion

Listen:

- dull, low-pitched

- L-sided: heard best at apex in left lateral decubitus position

- R-sided: heard best at lower-left sternal border

S4

(Atrial Gallop)

Heard in late diastole, shortly before S1

Ddx:

1) HCM /  HOCM

2) Aortic or pulmonic stenosis

2) Myocardial ischemia

Phys:

The sound results from the L or R atria contracting vigorously against a stiffened ventricle. This occurs in states of decreased ventricular compliance such as hypertrophy (due to HCM or aortic/pulmonary stenosis) or ischemia.

Listen:

- dull, low-pitched

- L-sided: heard best at apex in left lateral decubitus position (L more common than R)

Quadruple Rhythm

(Summation Gallop)

Often heard as a long middiastolic, low-pitched sound

Ddx:

Phys:

This pattern is what you hear when a patient has S3 and S4 heart sounds (along with the normal S1 and S2) and becomes tachycardic. With a shortened diastole, the S3 and S4 coalesce into the "summation gallop"

Listen:

- low pitched

Pericardial Knock

Heard early in diastole, soon after S2 (later than an OS, earlier & louder than an S3)

Ddx:

Severe constrictive pericarditis 

Phys:

Pericarditis is marked by the presence of a rigid, scarred pericardium which inhibits the normal filling of the heart. The sound results from the abrupt cessation of ventricular filling in early diastole 

Listen:

- high pitched

Pericardial Friction Rub

A scratchy sound heard in both systole & diastole

Ddx:

1) Pericarditis

Phys:

The sound is caused by the movement of the inflamed pericardial layers against one another. The rub is heard during the phases of greatest cardiac movement: ventricular contraction, ventricular relaxation, and atrial contraction.

Listen:

With patient leaning forward while exhaling (to bring pericardium closer to the chest wall)

Systolic Ejection Murmur

[image]

Crescendo-Decrescendo murmur

Ddx:

1) Aortic stenosis

2) Pulmonic stenosis

3) Obstructive hypertrophic cardiomyopathy

4) Normal (in young adults, often lessens on sitting upright)

Phys:

1) Aortic stenosis - (The murmur may be preceded by an ejection click, especially in mild AS). The murmur is separated from S1 by a short gap (isovolumetric contraction, before valve opens). The murmur becomes more intense as LV pressure rises and flow across the valve increases, then less intense as the LV relaxes. The murmur ends prior to S2. The more severe the stenosis, the later the murmur peaks (because it takes longer to force blood across the valve). A2 softens in severe AS.

2) Pulmonic stenosis (The murmur may be preceded by an ejection click). The murmur begins after S1, increases as RV pressure rises and then decreases as the RV relaxes. The murmur may extend into S2 (overlapping A2) and ending just before P2.

3) Hypertrophy of IV septum causes transient obstruction of LV outflow tract during systole. Usually accompanied by murmur of MR. Differentiated from AS by maneuvers: HOCM murmur increases with valsalve & standing & decreases with squatting.

Listen:

Aortic stenosis - high pitched, best heard at aortic area, radiates widely

Pulmonic stenosis - best heard at 2nd or 3rd left intercostal space, close to sternum, may radiate, but not as widely

HOCM - best heard at left lower sternal border

Holosystolic (Pansystolic) Murmur

[image]

Constant murmur of uniform intensity from S1 to S2. (No gap before S1)

Ddx:

1) Mitral regurgitation

2) Tricuspid regurgitation

3) Ventricular septal defect

Phys:

1) MR - continues through A2 (because LV pressure still greater than LA pressure). 

2) TR - intensity increases with inspiration because decreased intrathoracic pressure increases venous return to the R. heart

3) VSD - No change with inspiration. The smaller the VSD, the louder the murmur because of increased turbulence

Listen:

Mitral regurgitation - high pitched & "blowing," Heard best at the apex, often radiates toward left axilla

Tricuspid regurgitation - high pitched & "blowing." Heard best at left lower sternal border, often radiates to the right of the sternum

VSD - high pitched. Heard best at left intercostal spaces 4-6, does not radiate

Late Systolic Murmur

[image]

Begins in mid to late systole and continues to S2, often preceded by a mid-systolic click 

Ddx:

Mitral valve prolapse

Phys:

Murmur caused by the bowing into the LV of redundant & elongated valve leaflets during LV contraction. Click caused by sudden tensing of leaflet or chordae tendinae as leaflet is forced back toward the LA.

Maneuvers that increase venous return (e.g. squatting) delay the click & murmur

Listen:

- Apex

 Early Diastolic Decrescendo Murmur

[image]

Ddx:

1) Aortic regurgitation (more common)

2) Pulmonic regurgitation (usually due to pulmonary HTN)

Phys:

1) AR - Murmur begins at A2 at maximum intensity due to high pressure differential between aorta and lower-pressure ventricle. Decreases thereafter as LV pressure rises (LV fills) and aortic pressure falls.

2) PR - similar to AR

Listen:

- AR: high pitched, best heard at left sternal border with patient sitting, leaning forward, & exhaling

- PR: best heard at the pulmonic area, may increase with inhaling

Mid-to-Late Diastolic

Rumbling Murmur

[image]

Preceded by OS, begins at a maximum, declines in intensity (or disappears) & then re-intensifies at the end of diastole

Ddx:

1) Mitral stenosis (more common)

2) Tricuspid stenosis

Phys:

The murmur is at its loudest right after the OS because this is when the pressure gradient btwn atria & ventricle is greatest. As the ventricles fill, the gradient (& the murmur) lessens. At the end of diastole, the murmur re-intensifies upon atrial contraction.

In mild stenosis, the murmur disappears entirely during mid-diastole.

Listen:

- MS: low pitched, heard best at apex in left lateral decubitus

- TS: heard best at lower sternum near xiphoid process

Continuous Murmur

[image]

A murmur that continues throughout the cardiac cycle

Ddx:

e.g. Patent ductus arteriosus 

Phys:

An abnormal connection persists between the aorta & the pulmonary artery. Throughout the cardiac cycle aortic pressure is higher than pulmonic, so blood continuously flows through the PDA (from the aorta into the pulm. artery) causing a murmur. The murmur is at a maximum just before S2 (when the pressure gradient is greatest, and declines during diastole. At S1, it begins to increase again.  

Listen:

To-and-Fro Murmur

[image]

Two different murmurs that can sound like one continuous murmur

Ddx:

1) Aortic stenosis & aortic regurgitation

2) Pulmonic stenosis & pulmonic regurgitation

Phys:

A crescendo-decrescendo murmur is present in systole (stenosis) and a decrescendo murmur is present in diastole (regurgitation). The sound does not, however extend through S2.

Listen: