Normal Heart Sounds
Stethoscope
Bell – Low frequency sounds. Apply lightly to the skin.
Diaphragm – High frequency sounds. Press firmly to the skin, thus eliminating low frequency sounds and accentuating high frequency sounds and murmurs.
Heart Sounds
(1) S1 (M1 + T1)
Source of sound: S1 is produced by the combined closure of the MV (M1) and TCV (T1) in early systole. It is a high frequency sound loudest near the apex of the heart. Softer component related to onset of ejection
Can M1 and T1 be distinguished?: Although the MV closes 0.01 sec before the TCV this is not usually appreciated.
- Exception: Right Bundle Branch Block, audible split is heard due to delayed closure of the TCV.
Three factors determining intesnity of S1: (contractility, the P-R interval, and changes in cardiac tissue)
(1) the distance between the open valve leaflets at the onset of ventricular systole
- Þ
the further the distance the louder the sound! Þ P-R interval
(2) the mobility of the leaflets (normal, or rigid because of stenosis) Þ cardiac tissue changes
(3) the rate of ventricular pressure elevation Þ contractility
Causes of Altered Intensity of S1:
- Accentuated S1
- (1) Shortened PR interval
– Diastole begins with the opening of the atrioventricular valves allowing the accumulated blood in the atria to flow into the ventricles (rapid filling). The P wave (i.e. atrial contraction) occurs only at the end of diastole, pushing the remaining blood from the atria into the ventricles, and triggering the QRS complex (ventricular contraction) which forces the valves shut thus creating S1. Under these normal conditions the valve leaflets are allowed some time to drift back together before they are forced shut. When the PR interval is shortened the leaflets have less time to drift back together and are thus shut at a farther distance from each other Þ accentuated S1.
- (2) Mild mitral stenosis
– MS is characterized by fibrosed MV leaflets which allow less blood through than normal. This results in an Ý diastolic pressure gradient which keeps the leaflets further apart than usual Þ accentuated S1.
- (3) High cardiac output states or tachycardia
(e.g., exercise or anemia) – The duration of systole is always constant, and the duration of diastole varies with HR. With Ý HR the leaflets shut at greater distances from each other because they didn’t have the time to drift back closer to each other before the onset of systole.
Diminished S1
- (1) Lengthened PR interval
(primary AV node block) – leaflets have additional time to float back together before being shut.
- (2) Mitral regurgitation
– leaflets do not come into full contact with one another as they close.
- (3) Severe mitral stenosis
– leaflets are nearly fixed in position throughout the cardiac cycle. ß movement = ß S1.
- (4)
"Stiff" left ventricle (e.g., systemic hypertension) - Ý LV diastolic pressure accelerates the drifting together of the mitral leaflets in diastole, so that upon systole the leaflets are forced together from a smaller than normal distance.
How to confirm S1:
- look for LV impulse (see chest moving)
- carotid pulse (not as good because only felt towards end of systole)
- move up to pulmonic area. If split it is really S.
(2) S2 (A2 + P2)
Source of sound: S2 is produced by the combined closure of the AV (A2) and PV (P2) at the end of systole. It is a high frequency sound loudest near the base of the heart. P2 normally heard only in the pulmonic area
S2 splitting: S2 normally splits during inspiration (A2 Þ P2). The negative intrathoracic pressure caused by inspiration transiently Ý capacitance (and ß impedance) of the pulmonary vessels. The lower pressure allows more blood to enter the lungs from the RV thus delaying the closure of the PV Þ delayed P2. Consequently, this results in ß pulmonary return to the LA and LV resulting in early AV closure Þ early A2.
Factors determining the intensity of S2: Intensity varies directly with the stroke volume, and the pressure in the great vessel at the time of valve closure.
Causes of Altered Intensity of Ss:
- Accentuated S2
– systemic or pulmonary arterial hypertension (diastolic pressure in the respective great artery is higher than normal
Þ Ý velocity)
Diminished S2 – severe aortic or pulmonary valve stenosis (valve commissures are nearly fixed Þ ß velocity)
(3) S3
Source of sound: S3 is produced by the tensing of the chordae tendinae as rapid filling of the ventricle causes expansion of the chamber. Heard in early diastole, following the opening of the atrioventricular valves. It is a low-pitched sound heard over the apex while the patient lies in the left lateral decubitus postion.
Is it a bad thing? S3 is normal in children and young adults (supple ventricle which undergoes normal rapid expansion in early diastole). Sign of disease in middle-aged or older adult (indicates volume overload owing to CHF, or Ý flow in mitral/tricuspid regurgitation). Referred to as a ventricular "gallop".
(4) S4
Source of sound: S4 is produced by the atria vigorously contracting against a stiffened ventricle. Heard in late diastole coinciding with contraction of the atria. Low pitched sound heard loudest at the apex with the patient lying the left lateral decubitus position. Referred to as an atrial "gallop".
Is it a bad thing? Though it can be audible in many normal people, it can indicate the presence of cardiac disease, specifically ß in ventricular compliance, usually due to ventricular hypertrophy or myocardial ischemia.
(5) Ejection Click
A loud, high frequency, brief sound coinciding with the onset of ejection (exaggerated ejection component of S1). Occurs with aortic or pulmonic stenosis when the leaflets are not thickened or calcified. Can be heard with dilation or altered compliance of either great vessel. A pulmonic ejection click usually varies with respiration.
(6) Non-ejection or Mid-Systolic Clicks
Brief, high frequency sound(s) that are associated with degenerative changes in mitral or tricuspid valve. The timing or position of the click(s) within systole is related to the ventricular volume. Often followed by a murmur of mitral (tricuspid) regurgitation.