Heart Sounds


The first heart sound - S1 - is in time with the pulse in your carotid artery in your neck. The sound of the tricuspid valve closing may be louder in patients with pulmonary hypertension due to increased pressure beyond the valve. Non-heart-related factors such as obesity, muscularity, emphysema, and fluid around the heart can reduce both S1 and S2.
     The position of the valves when the ventricles contract can have a big effect on the first heart sound. If the valves are wide open when the ventricule contracts, a loud S1 is heard. This can occur with anemia, fever or hyperthyroid.
     When the valves are partly closed when the ventricule contracts, S1 is faint. Beta-blockers produce a fainter S1. Structural changes in the heart valves can also affect S1. Fibrosis and calcification of the mitral valve may reduce S1, while stenosis of the mitral valve may cause a louder S1.


The second heart sound marks the beginning of diastole - the heart's relaxation phase - when the ventricles fill with blood. In children and teenagers, S2 may be more pronounced. Right ventricular ejection time is slightly longer than left ventricular ejection time. As a result, the pulmonic valve closes a little later than the aortic valve.
     Higher closing pressures occur in patients with chronic high blood pressure, pulmonary hypertension, or during exercise or excitement. This results in a louder A2 (the closing sound of the aortic valve).
     On the other hand, low blood pressure reduces the sound. The second heart sound may be "split" in patients with right bundle branch block, which results in delayed pulmonic valve closing. Left bundle branch block may cause aortic valve closing (A2) to be slower than pulmonic valve closing (P2).


During diastole there are 2 sounds of ventricular filling: The first is from the atrial walls and the second is from the contraction of the atriums. The third heart sound is caused by vibration of the ventricular walls, resulting from the first rapid filling so it is heard just after S2. The third heart sound is low in frequency and intensity. An S3 is commonly heard in children and young adults. In older adults and the elderly with heart disease, an S3 often means heart failure.


The fourth heart sound occurs during the second phase of ventricular filling: when the atriums contract just before S1. As with S3, the fourth heart sound is thought to be caused by the vibration of valves, supporting structures, and the ventricular walls. An abnormal S4 is heard in people with conditions that increase resistance to ventricular filling, such as a weak left ventricle.

 Other Abnormal Heart Sounds
opening snap
is caused by a noncompliant valve, such as a mitral valve in a patient with a history of rheumatic fever
ejection click
is a high-pitched sound occurring shortly after S1. It is associated with a dilated pulmonary artery or septal defects
pericardial friction rub
is a to-and-fro sound that waxes and wanes with diastole and systole. It is present even when the patient holds his breath
is a vague sound associated with turbulent blood flow through a heart valve. Turbulent blood flow may be the result of:
  1. increased flow across a normal valve
  2. forward flow across an irregular or constricted valve, or into an enlarged heart chamber
  3. back-flow through an insufficient valve
is a vibration, high in frequency and sustained. If a vibration is felt but no murmur is heard, the vibration is not called a thrill
pericardial knock
is a high-pitched sound best heard during diastole. Pericardial knocks are caused by a thick pericardium limiting expansion of the ventricle during the filling phase (diastole)
 The Third Heart Sound - S3

October, 1999 - A third heart sound may be the earliest clue to heart failure. It predicts a high risk of complications in non-heart surgery. CHF patients with an S3 will probably respond well to digoxin. However, detecting S3 is inconsistent even among experienced doctors. While an S3 may have important implications for treatment, many doctors cannot detect it. The following is some history and the current thinking on heart sounds and their usefulness.
     In 1856, Potain first described "gallop rhythm" as a tripling or quadrupling of heart sounds sounding like the canter of a horse. That term is still used to describe a third or fourth heart sound. Gallops are diastolic events - they occur during the heart's relaxation phase, when it fills with blood. S3 seems to be related to the filling phase and S4 seems to be related to atrial contraction.
     S3 is well recognized as an early clue to the presence of heart disease. S3 may offer valuable information about diagnosis, prognosis, and treatment. It occurs 0.12 to 0.16 seconds after the second heart sound. Potain suggested that S3 results from the sudden stop of the ventricle's expansion as it fills with blood. It is agreed that S3 is associated with over-expansion of the ventricle during the filling phase.
     Coulshed and Epstein return to the original theory: "Our evidence supports the original concept that S3 occurs when the rapidly filling ventricle reaches a point when its expansion is halted by the resistance of its wall. The resulting vibrations are heard as the third heart sound." Pozzoli confirmed that the rapid slowing of the left ventricle at the end of filling is the most likely cause of S3.
     As the rush of blood into the heart's ventricles during filling comes to a sudden halt - when it reaches maximum filling - the kinetic energy of the blood's movement is converted to vibration. These vibrations can sometimes be heard. The higher the inflow rate and the higher the filling rate, the greater the blood's deceleration, and the more likely an S3 will occur.
     S3 in young adults may be explained by the relatively large motion of the heart and the thin chest wall. S3 disappears around age 40 in healthy people.

Detecting Heart Sounds

To detect heart sounds, the patient should be lying down and examined in a quiet room. Left-sided S3 is best heard at the apex of the heart (the lower pointed end of the heart) with the patient lying on his left side. It is a low-pitched sound and heard best using the bell of the stethoscope with light pressure. It follows the second heart sound in timing. S4 is more easily heard after mild exertion in the presence of a fast heart rate, and also with the legs elevated.
     Things that usually prevent S3 detection are surrounding noise, obesity, emphysema, failure to use the stethescope properly, and examining the patient in a seated position. Simple maneuvers like closing the door to the exam room to reduce surrounding noise helps in detecting S3.
     If heart rate is higher than 100 beats per minute, finding third and fourth heart sounds is impossible. Unless the heart rate is slowed, the examiner can only guess at telling S3 from S4 unless there is a-fib, which eliminates the possibility of an S4.

 What Does An S3 Mean For Me?

S3 is heard in several illnesses. It can normally be heard in healthy children and adults up to age 40. Authors have reported it in 20 to 93% of healthy volunteers. S3 heard after 40 years of age usually indicates illness. S3 is more often heard in adults who are very lean. S3 is heard normally in 80% of pregnant women. The most useful importance of S3 is in detecting left-sided heart failure, especially in the early stages when other signs may be normal.
     In 1968, Shah studied patients with heart disease and found that an S3 identified patients with high end-diastolic pressure and low heart output. In a later study of patients with aortic valve disease, the same authors again found that S3 is associated with left ventricular failure.
     Harvey and Stapleton first noted that an S3 alone identified patients who are prone to pulmonary edema after a surgury. More recently, an S3 identified which CHF patients would respond well to digoxin.
     Patel compared stethescope findings of S3 with MUGA testing of heart function. They found that an S3 predicted an abnormal EF. The absence of S3, however, is not uncommon in patients with a mildly reduced EF.
     Mitral valve regurgitation can cause S3 without heart failure. It is also common to hear an S3 after an acute heart attack. This usually disappears several days or weeks afterward. Persistent S3 after this time may mean more severe heart damage. In a study of patients awaiting heart transplant, an S3 was one of 7 risk factors predicting a poor prognosis.

 Finding That Heart Sound

Held compared the ability of 4 groups of observers - cardiologists, residents, nurses, and students - to detect third heart sounds. He found that the detection rate increased with the experience of the observer. While success was highest for cardiologists, the ability varied a lot even among experienced cardiologists.
     Another study of inpatients with heart conditions studied S3 detection by 4 observer groups - a board certified internist, an internist trainee, a cardiologist trainee, and a board certified cardiologist. Each patient was seen by at least one pair of the above. They found that if one observer heard an S3, the chance that another observer hearing an S3 was only 34 to 38%. Gadsboll also reported poor agreement between observers on S3 in examining heart attack patients for CHF.


The third heart sound is a low-pitched sound after the second heart sound. S3 is caused by rapid ventricular filling during diastole. It is best heard at the mitral area, with the patient lying down on his left side. While it may be heard normally in people under 40 years old, its presence beyond this age usually means a heart problem.
     Presence of an S3 may be important. It may be the earliest clue to left ventricular failure. It predicts higher risk of complications in surgery and predicts a good response to digoxin in CHF patients. In patients with aortic valve regurgitation, S3 indicates left ventricular dysfunction and may be useful for selecting patients for heart cath and valve replacement. A persistent S3 after heart attack indicates a poor prognosis.
Author: Nirmal Joshi, MD
General Internal Medicine, Milton S. Hershey Medical Center, Pennsylvania State University
Source: South Med J 92(8):756-761, 1999

All information on this site is opinion only. All concepts, explanations, trials, and studies have been re-written in plain English and may contain errors. I am not a doctor. Use the reference information at the end of each article to search MedLine for more complete and accurate information. All original copyrights apply. No information on this page should be used by any person to affect their medical, legal, educational, social, or psychological treatment in any way. I am not a doctor. This web site and all its pages, graphics, and content copyright © 1997, 1998, 1999, 2000, 2001, 2002, 2003, 2004 Jon C.

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