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Front of thorax, showing surface relations of bones, lungs (purple), pleura (blue), and heart (red outline). Heart valves are labeled with "B", "T", "A", and "P".

First heart sound: caused by atrioventricular valves - Bicuspid/Mitral (B) and Tricuspid (T).

Second heart sound caused by semilunar valves -- Aortic (A) and Pulmonary/Pulmonic (P).

Diagram showing relations of opened heart to front of thoracic wall. Ant. Anterior segment of tricuspid valve. A O. Aorta. A.P. Anterior papillary muscle. In. Innominate artery. L.C.C. Left common carotid artery. L.S. Left subclavian artery. L.V. Left ventricle. P.A. Pulmonary artery. R.A. Right atrium. R.V. Right ventricle. V.S. Ventricular septum.

The heart sounds are the noises (sound) generated by the beating heart and the resultant flow of blood through it. This is also called a heartbeat. In cardiac auscultation, an examiner uses a stethoscope to listen for these sounds, which provide important information about the condition of the heart.

In healthy adults, there are two normal heart sounds often described as a lub and a dub (or dup), that occur in sequence with each heart beat. These are the first heart sound (S₁) and second heart sound (S₂), produced by the turbulent flow against the closed AV valves and semilunar valves respectively. In addition to these normal sounds, a variety of other sounds may be present including heart murmurs, adventitious sounds, and gallop rhythms S₃ and S₄.

Heart murmurs are also generated by turbulent flow of blood, which may occur inside or outside the heart, but the sound has different characteristics than normal heart sounds. Murmurs may be physiological (benign) or pathological (abnormal). Abnormal murmurs can be caused by stenosis restricting the opening of a heart valve, resulting in turbulence as blood flows through it. Abnormal murmurs may also occur with valvular insufficiency (or regurgitation), which allows backflow of blood when the incompetent valve closes with only partial effectiveness. Different murmurs are audible in different parts of the cardiac cycle, depending on the cause of the murmur.

Normal heart sounds

Normal heart sounds are associated with heart valves closing, causing changes in blood flow.

S₂

The second heart tone, or S₂, forms the "dub" of "lubb-dub" and is composed of components A₂ and P₂. It is caused by the sudden block of reversing blood flow due to closure of the aortic valve and pulmonary valve at the end of ventricular systole, i.e beginning of ventricular diastole. As the left ventricle empties, its pressure falls below the pressure in the aorta, aortic blood flow quickly reverses back toward the left ventricle, catching the aortic valve leaflets and is stopped by aortic (outlet) valve closure. Similarly, as the pressure in the right ventricle falls below the pressure in the pulmonary artery, the pulmonary (outlet) valve closes. The S₂ sound results from reverberation within the blood associated with the sudden block of flow reversal.

S₂ splitting

During inspiration, the increased negative intrathoracic pressure which allows lung expansion also induces both increased blood return from the body into the right ventricle and simultaneous reduced blood volume return from the lungs into the left ventricle. Because of the increased blood volume in the right atria, the pulmonary valve stays open longer during ventricular systole whereas the aortic valve closes slightly earlier due to slightly reduced left ventricular volume. Thus the P₂ component of S₂ is delayed relative to the A₂ component. This delay in P₂ versus A₂ is heard as a slight broadening or even "splitting" of the second heart sound, though usually only in the pulmonic area of the chest because the P₂ is soft and not heard in other areas. During expiration, the less negative (than during inspiration) intrathoracic pressure no longer increases blood return to the right ventricle versus the left ventricle, the right ventricle volume in no longer increased, the pulmonary valve closes earlier, P₂ occurs earlier and overlaps A₂. It is physiological to hear a "splitting" of the second heart tone in younger people, during inspiration and in the "pulmonary area", i.e. the 2nd ICS (intercostal space) at the left edge of the sternum. During expiration the interval between the two components normally shortens and the S2 sounds become merged.

A right bundle branch block will produce continuous splitting but the degree of splitting will still vary with respiration. If splitting does not vary with inspiration, it is termed a "fixed split S2" and is usually due to an atrial septal defect (ASD) or ventricular septal defect (VSD). The ASD or VSD creates a left to right shunt that increases the blood flow to the right side of the heart, thereby causing the pulmonic valve to close later than the aortic valve independent of inspiration/expiration.

Reverse splitting indicates pathology. Aortic stenosis, hypertrophic cardiomyopathy, left bundle branch block, and a ventricular pacemaker could all cause a reverse splitting of the second heart sound.

Extra heart sounds

The rarer extra heart sounds form gallop rhythms and are heard in both normal and abnormal situations.

S₃

Rarely, there may be a third heart sound also called a protodiastolic gallop, ventricular gallop, or informally the "Kentucky" gallop as an onomatopoeic reference to the rhythm and stress of S1, S2, and S3 together (S1=ken; S2=tuc; S3=ky). It occurs at the beginning of diastole after S2 and is lower in pitch than S1 or S2 as it is not of valvular origin. The third heart sound is benign in youth and some trained athletes, but if it re-emerges later in life it may signal cardiac problems like a failing left ventricle as in dilated congestive heart failure (CHF.)S3 is thought to be caused by the oscillation of blood back and forth between the walls of the ventricles initiated by inrushing blood from the atria. The reason the third heart sound does not occur until the middle third of diastole is probably because during the early part of diastole, the ventricles are not filled sufficiently to create enough tension for reverberation. It may also be a result of tensing of the chordae tendineae during rapid filling and expansion of the ventricle..

S₄

The rare fourth heart sound is sometimes audible in healthy children and again in trained athletes, but when audible in an adult is called a presystolic gallop or atrial gallop. This gallop is produced by the sound of blood being forced into a stiff/hypertrophic ventricle. It is a sign of a pathologic state, usually a failing left ventricle. The sound occurs just after atrial contraction ("atrial kick") at the end of diastole and immediately before S1, producing a rhythm sometimes referred to as the "Tennessee" gallop where S4 represents the "tenn-" syllable. The combined presence of S3 and S4 is a quadruple gallop. At rapid heart rates, S3 and S4 may merge to produce a summation gallop.

Murmurs

Heart murmurs are produced as a result of turbulent flow of blood, turbulence sufficient to produce audible noise. They are usually heard as a whooshing sound. The term murmur only refers to a sound believed to originate within blood flow through or near the heart; rapid blood velocity is necessary to produce a murmur. Though not fully reliable, soft murmurs are less likely to reflect a serious, if any, health problem; loud murmurs essentially always reflect a problem. Yet most heart problems do not produce any murmur and most valve problems also do not produce an audible murmur.

The following paragraphs overview the murmurs most commonly heard in adults who do not have major congenital heart abnormalities.

Regurgitation through the mitral valve is by far the most commonly heard murmur, sometimes fairly loud to a practiced ear, even though the volume of regurgitant blood flow may be quite small. Yet, though obvious using echocardiography visualization, probably about 20% of cases of mitral regurgitation do not produce an audible murmur.
Stenosis of the aortic valve is typically the next most common heart murmur, a systolic ejection murmur. This is more common in older adults or in those individuals having a two, not a three leaflet aortic valve.
Regurgitation through the aortic valve, if marked, is sometimes audible to a practiced ear with a high quality, especially electronically amplified, stethoscope. Generally, this is a very rarely heard murmur, even though aortic valve regurgitation is not so rare. Aortic regurgitation, though obvious using echocardiography visualization, usually does not produce an audible murmur.
Stenosis of the mitral valve, if severe, also rarely produces an audible, low frequency soft rumbling murmur, best recognized by a practiced ear using a high quality, especially electronically amplified, stethoscope.
Either regurgitation through, or stenosis of, the tricuspid or pulmonary valves essentially never produces audible murmurs.
Other audible murmurs are associated with abnormal openings between the left ventricle and right heart or from the aortic or pulmonary arteries back into a lower pressure heart chamber.

Gradations of Murmurs^[1]
Grade	Description
Grade 1	Very faint, heard only after listener has "tuned in"; may not be heard in all positions.
Grade 2	Quiet, but heard immediately after placing the stethoscope on the chest.
Grade 3	Moderately loud.
Grade 4	Loud, with palpable thrill (ie, a tremor or vibration felt on palpation)^[1]
Grade 5	Very loud, with thrill. May be heard when stethoscope is partly off the chest.
Grade 6	Very loud, with thrill. May be heard with stethoscope entirely off the chest.

As noted, several different cardiac conditions can cause heart murmurs. However, the murmurs produced often change in complex ways with the severity of the cardiac disease. An astute physician can sometimes diagnose cardiac conditions with some accuracy based largely on the murmur, related physical examination and experience with the relative frequency of different heart conditions. However, with the advent of better quality and wider availability of echocardiography and other techniques, heart status can be recognized and quantified much more accurately than formerly possible with only a stethoscope, examination and experience.

Effects of inhalation/expiration

Inhalation pressure causes an increase in the venous blood return to the right side of the heart. Therefore, right-sided murmurs generally increase in intensity with inspiration. The increased volume of blood entering the right sided chambers of the heart restricts the amount of blood entering the left sided chambers of the heart. This causes left-sided murmurs to generally decrease in intensity during inspiration.

With expiration, the opposite haemodynamic changes occur. This means that left-sided murmurs generally increase in intensity with expiration. Having the patient lie supine and raising their legs up to a 45 degree angle facilitates an increase in venous return to the right side of the heart producing effects similar to inhalation-increased blood flow.

Interventions that change murmurs

There are a number of interventions that can be performed that alter the intensity and characteristics of abnormal heart sounds. These interventions can differentiate the different heart sounds to more effectively obtain a diagnosis of the cardiac anomaly that causes the heart sound.

Other abnormal sounds

Clicks: With the advent of newer, non-invasive imaging techniques, the origin of other, so-called adventitial sounds or "clicks" has been appreciated. These are short, high-pitched sounds.

The atrioventricular valves of patients with mitral stenosis may open with an opening snap on the beginning of diastole.
Patients with mitral valve prolapse may have a mid-systolic click along with a murmur.
Aortic and pulmonary stenosis may cause an ejection click immediately after S₁.

Rubs: Patients with pericarditis, an inflammation of the sac surrounding the heart (pericardium), may have an audible pericardial friction rub. This is a characteristic scratching, creaking, high-pitched sound emanating from the rubbing of both layers of inflammated pericardium. It is the loudest in systole, but can often be heard at the beginning and at the end of diastole. It is very dependent on body position and breathing, and changes from hour to hour.

Surface anatomy

The aortic area, pulmonic area, tricuspid area and mitral area are areas on the surface of the chest where the heart is auscultated. The opening and closing of the valves is usually much less loud than the sound of the blood rushing through the valve and "colliding" with the subsequent barrier. Because of this, auscultation to determine function of a valve is usually not performed at the position of the valve, but at a downstream position where the listener can best hear the blood colliding after the valve is closed.

Pulmonary valve (to pulmonary trunk)	second intercostal space	left upper sternal border
Aortic valve (to aorta)	second intercostal space	right upper sternal border
Mitral valve (to left ventricle)	fifth intercostal space	lateral to left midclavicular line
Tricuspid valve (to right ventricle)	fourth intercostal space	lower left sternal border

Recording heart sounds

Using electronic stethoscopes, it is possible to record heart sounds via direct output to an external recording device, such as a laptop or MP3 recorder. The same connection can be used to listen to the previously-recorded auscultation through the stethoscope headphones, allowing for more detailed study of murmurs and other heart sounds, for general research as well as evaluation of a particular patient's condition.

Notes and references

^ "Medline Plus Medical Dictionary, definition of "cardiac thrill"".

External links

Diagram, with associated sounds at University of Michigan
Flash tutorials at blaufuss.org
Overview at University of Dundee
Overview at University of Washington
Recorded heart sounds at Auscultation Assistant at UCLA

[1] "Medline Plus Medical Dictionary, definition of "cardiac thrill"".

[1]

@@ Line 19: / Line 19: @@
 During inspiration, the increased negative [[intrathoracic]] pressure which allows lung expansion also induces both increased blood return from the body into the right ventricle and simultaneous reduced blood volume return from the lungs into the left ventricle. Because of the increased blood volume in the right atria, the pulmonary valve stays open longer during ventricular systole whereas the aortic valve closes slightly earlier due to slightly reduced left ventricular volume. Thus the P<sub>2</sub> component of S<sub>2</sub> is delayed relative to the A<sub>2</sub> component. This delay in P<sub>2</sub> versus A<sub>2</sub> is heard as a slight broadening or even "splitting" of the second heart sound, though usually only in the pulmonic area of the chest because the P<sub>2</sub> is soft and not heard in other areas. During expiration, the less negative (than during inspiration) intrathoracic pressure no longer increases blood return to the right ventricle versus the left ventricle, the right ventricle volume in no longer increased, the pulmonary valve closes earlier, P<sub>2</sub> occurs earlier and overlaps A<sub>2</sub>. It is physiological to hear a "splitting" of the second heart tone in younger people, during inspiration and in the "pulmonary area", i.e. the 2nd ICS (intercostal space) at the left edge of the sternum. During expiration the interval between the two components normally shortens and the S2 sounds become merged.
-A [[bundle branch block]] will produce continuous splitting but the degree of splitting will still vary with respiration. If splitting does not vary with inspiration, it is termed a "fixed split S2" and is usually due to an [[atrial septal defect]] (ASD) or [[ventricular septal defect]] (VSD).  The ASD or VSD creates a left to right shunt that increases the blood flow to the right side of the heart, thereby causing the pulmonic valve to close later than the aortic valve independent of inspiration/expiration.
+A right [[bundle branch block]] will produce continuous splitting but the degree of splitting will still vary with respiration. If splitting does not vary with inspiration, it is termed a "fixed split S2" and is usually due to an [[atrial septal defect]] (ASD) or [[ventricular septal defect]] (VSD).  The ASD or VSD creates a left to right shunt that increases the blood flow to the right side of the heart, thereby causing the pulmonic valve to close later than the aortic valve independent of inspiration/expiration.
 Reverse splitting indicates pathology. Aortic stenosis, hypertrophic cardiomyopathy, left bundle branch block, and a ventricular pacemaker could all cause a reverse splitting of the second heart sound.