Introduction

Heart sounds are created from blood flowing through the heart chambers as the cardiac valves open and close during the cardiac cycle. Vibrations of these structures from the blood flow create audible sounds — the more turbulent the blood flow, the more vibrations that get created. The same variables determine the turbulence of blood flow as all fluids. These are fluid viscosity, density, velocity, and the diameter of the column through which the fluid is traveling. Auscultation of the heart sounds with a stethoscope is a cornerstone of physical medical exams and a valuable first-line tool to evaluate a patient. Some sounds are very characteristic of significant pathological lesions that have major pathophysiological consequences, and these first present on auscultation. These type of lesions can be heard in systole, diastole, or continuously through the cardiac cycle.

Organ Systems Involved

Cardiac Valves

Anatomy:

There are four chambers of the heart: the right atrium, the right ventricle, the left atrium, and the left ventricle. The atrioventricular valves are located on the floor of the atria and empty into the ventricles. These valves are composed of leaflets attached to papillary muscles in the ventricle via thin cord-like structures called chordae tendineae. The leaflets also attach to a fibrous ring, known as the valve annulus, that supports the valve between the atria and ventricles. The tricuspid valve separates the right atrium from the right ventricle, and the mitral valve separates the left atrium from the left ventricle. The tricuspid valve consists of three leaflets, while the mitral valve consists of two leaflets.

The semilunar valves separate the ventricles from the great arteries. These valves are composed of three sinus-like leaflets also attached to a valve annulus. The pulmonic valve separates the right ventricle from the pulmonary artery, and the aortic valve separates the left ventricle from the aorta. The superior aspects of the right and left aortic valve leaflets contain the origins of the coronary arteries. The aortic valve on average opens and closes 100000 times a day.[1]

Cellular:

A single layer of endothelial cells called the endocardium lines the surface of the heart valves. The subendocardium contains a vast population of cells types. It contains fibroblasts, myofibroblasts, smooth muscle cells, nerves, elastic and collagenous fibers. The connective tissue of the subendocardium is continuous with the connective tissue of the myocardial layer.[2]

The endothelial cells of the valves are genotypically and phenotypically unique from other endothelial cells found in the body. Research has shown these cells are very functionally active and can alter the mechanical properties of the aortic valve, which in turn alters its function. They modulate the elastic modulus of the valve, which is the valve’s strain for a given amount of stress. Endothelial cells accomplish this via communication with myofibroblast and smooth muscle cells in the subendocardial layer.[3]

Function:

The heart valves permit forward flow of blood while preventing backward regurgitant flow.[4] During systole, the tension provided by the chordae tendineae keep the atrioventricular valve leaflets together. The rise in pressure pushes the aortic and pulmonic valves open, allowing blood to flow forward. As the ventricle stops contracting and pressures fall in diastole, elastic recoil of the great arteries will cause blood to fall back toward the heart. The sinus-like leaflets will begin to fill with blood, which will distend the valve cusp toward one another for closure. Tension on the chordae tendineae also decreases. The atria fill with blood then contract, causing the atrioventricular valves to open so the ventricles can fill with blood.[5]

Function

Flow

Flow can be laminar or turbulent. Laminar flow is smooth with low resistance. It is conceptualized as layers neatly stacked in parallel as they flow through a column. In contrast, turbulent flow is rough with high resistance and has a chaotic, unorganized structural pattern. Reynold’s number can quantify the likelihood of a fluid demonstrating turbulent flow. It states this likelihood is related to fluid viscosity, density, velocity, and the diameter of the column through which the fluid is traveling. Flow becomes more turbulent as velocity increases and the diameter of the column becomes smaller.

Heart sounds are primarily generated from vibrations of cardiac structures caused by changes that create turbulent flow.[6] Under normal conditions, blood flow is laminar. With structural or hemodynamic changes turbulent flow results, which causes vibrational waves. These waves are transmitted through the chest wall and are the sounds practitioners auscultate with their stethoscopes. The sound transmits in the same direction as the blood flow.[7]

Physiologic Heart Sounds

The S1 heart sound is produced as the mitral and tricuspid valves close in systole.[8][9] This structural and hemodynamic change creates vibrations that are audible at the chest wall. The mitral valve closing is the louder component of S1. It also occurs sooner because of the left ventricle contracts earlier in systole. Thus, changes in the intensity of S1 are more attributable to forces acting on the mitral valve. Such causes include a change in left ventricular contractility, mitral structure, or the PR interval. However, under normal resting conditions, the mitral and tricuspid sounds occur close enough together not to be discernable. The most common reasons for a split S1 are things that delay right ventricular contraction, like a right bundle branch block.[8]

The S2 heart sound is produced with the closing of the aortic and pulmonic valves in diastole.[8][10] The aortic valve closes sooner than the pulmonic valve, and it is the louder component of S2; this occurs because the pressures in the aorta are higher than the pulmonary artery. Unlike the S1, under normal conditions, the closure sound of the aortic and pulmonic valves can be discernable, which occurs during inspiration due to the increase in venous return. The increase in volume means the right ventricle will take longer to pump out blood, which slightly delays the pressure increase in the pulmonic artery that leads to the pulmonic valve closure. So, the later sound in a physiologic split S2 is the closure of the pulmonic valve.[8] S2 can provide a lot of useful clinical information. Some have referred to it as the “auscultatory anchor point” pointing to its use as a reliably discernable sound that orients the listener to the other sounds.[11]

Different heart sounds exist aside from S1 and S2 that hold no pathologic consequence. The factors involved in the production of these sounds are the same factors involved with all heart sounds: turbulent flow and vibration of cardiac structures. These physiologic murmurs occur in systole, typically early systole, with a short duration. They are characterized as soft sounds affecting maximally 60% of systole and do not propagate well. These murmurs have also been called innocent, harmless, irrelevant, evolving, benign, habitual, infantile, growth murmurs, accidental, non-pathological, non-organic, normal, false, meaningless, ‘’functional’’, supine position, nonsignificant, transitory, and dynamic murmurs. Some specific examples are Still’s murmur, venous hum, and pulmonic flow murmur.[12]

Related Testing

The classic tool for evaluating heart sounds is the stethoscope. The stethoscope has been around for decades with many changes in design, but the function has always remained the same-to amplify the noise created by the heart and blood for better evaluation. The basic components are a headset with earpieces connected to a chest piece via tubing. The chest piece can act as a bell for low-frequency sounds and a diaphragm for high-frequency sounds. Most chest pieces incorporate both the bell and diaphragm, usually through a two-sided model, or a one-sided model where changing the amount of pressure applied to the chest piece allows for switching between each. The headpiece and earpieces are designed to optimize hearing by creating a seal around the ear canal to decrease ambient noise. The external ear canal travels in an anterior angle towards the tympanic membrane. The angle of the headset facilitates alignment with the external ear canal anatomy to create a complete seal. The correct size of the earpieces is also important for creating a proper seal.[11]

The stethoscope can be used to auscultate all four cardiac valves. The aortic valve is best heard in the 2nd right intercostal space. The pulmonic valve is best auscultated in the 2nd left intercostal space. The tricuspid valve is loudest in the 4th left intercostal space, and the mitral valve is loudest in the left 5th intercostal space at the midclavicular line.[13] Other areas of the body can also be auscultated for significant clinical data such as the neck, clavicles, supraclavicular fossa, axilla, sternal boarders, and abdomen.[7]

The digital age has spawned the creation of phonocardiography, which is the use of a phonocardiogram to record sounds made by the blood and heart. One example of these is commercially available electronic stethoscopes.[14] Their main features are their ambient noise canceling technology, and the ability to filter out and amplify specific noises. Some can also record, visually display, store, and playback sounds.[8][11] Recent research on the accuracy amongst different kinds of commercially available electronic stethoscopes suggests no significant difference between them in identifying pathological heart sounds. There was a significant difference between models with identifying normal heart sounds. [15] The future trend in electronic stethoscopes is an automatic interpretation of recorded sounds for diagnosis. This technology is being developed based on evidence-based algorithms and artificial intelligence.[15]

Clinical Significance

Auscultation of heart sounds is a foundational component in clinical physical examination. An abundant amount of on-going research has been produced on the proper technique and interpretation of heart auscultation. Heart sounds and murmurs have been described in terms of their timing in the cardiac cycle, intensity, how intensity changes during the cardiac cycle, sound wave shape, pitch, location where the sound is audible, radiation, rhythm, and response to physical exam maneuvers. These different characteristics are utilized to differentiate between physiologic and pathologic sounds.

Systolic Sounds

Clinically significant systolic heart murmurs can be further broken down into ejection and regurgitant murmurs.  Ejection murmurs are crescendo-decrescendo murmurs that occur as blood flows through an obstruction. The sound intensity increases as the pressure gradient across the obstruction increases.[16] Common causes of obstruction include pathology like aortic valve stenosis, pulmonary valve stenosis, ventricular septal defect, and hypertrophic cardiomyopathy. The regurgitant murmurs are mitral and tricuspid insufficiency. They are classically described as harsh, loud, holosystolic murmurs, which means the murmur lasts the entire duration of systole and covers up S2. The noise is due to the regurgitant flow through the incompetent valve. Systolic clicks are loud mid-systolic noises due to prolapse of either the mitral or tricuspid valve leaflets into the atria during ventricular contraction. Depending on the severity, these prolapses can have pathologic consequences. Variations in S1 and S2 intensity or character can be suggestive of a pathologic lesion but can also be physiological.[8][17]

Diastolic Sounds

Examples of diastolic murmurs are aortic and pulmonic valve regurgitation (AR & PR), tricuspid and mitral valve stenosis (TS & MS), S3 sounds, and S4 sounds. Diastolic heart sounds are more clinically significant because all diastolic murmurs are pathologic, except for some S3.[18] The mechanism for sound creation is the same in AR, PR, MS, and TS as their systole counterparts. Turbulent flow from the stenosis is due to a pressure gradient the obstruction creates. The sound created in regurgitation murmurs is from regurgitant flow through the incompetent valve. The AR and PR sounds have a blowing character that occurs in early diastole and decreases in intensity as the phase progresses, resulting in a decrescendo configuration. AR has a high pitch while PR has a low to medium pitch.[8] MS occurs in mid to late diastole and begins with a loud opening snap followed by a rumble. TS has a similar sound, but it is softer and best heard in the tricuspid area. The S3 heart sound correlates to conditions of increased left atrial volume and/or increased ventricular filling pressure. The exact mechanism for the creation of the S3 has been more controversial than most of the other heart sounds.[19][20][21] It is classically taught this sound is created from blood filling a volume-overloaded ventricle., like during an acute heart failure exacerbation. Recent research suggests that mitral valve annulus diameter is one of the more important factors in creating the sound.[21] The sound can be physiologic in some children and athletes. It is a low frequency early diastolic sound best heard at the cardiac apex in the left lateral decubitus position. The S4 sound is created when someone has a less compliant ventricle. As the atria contracts in late diastole against a stiffened ventricle, it must increase its force-production, which creates turbulent blood flow. It is the hallmark of diseases that decrease ventricular compliance, like left ventricular hypertrophy.[8]

Continuous Sounds

Continuous sounds are created when there is a connection between two chambers or vessels that have differences in pressure. These sounds can be heard throughout the body, such as in the renal arteries from renal artery stenosis, or with the formation of an arteriovenous fistula, like those common in pregnancy. The cardiac lesion that creates a continuous murmur is a patent ductus arteriosus. This is a connection between the pulmonary artery and the aorta that is needed only for fetal development but sometimes persist after birth. It is said to be a “machine-like” sound best heard in the left upper sternal border.[8]

Review Questions

• Access free multiple choice questions on this topic.
• Comment on this article.

References

1.

Rozeik M, Wheatley D, Gourlay T. The aortic valve: structure, complications and implications for transcatheter aortic valve replacement. Perfusion. 2014 Jul;29(4):285-300. [PubMed: 24570076]

2.

Simmons CA. Aortic valve mechanics: an emerging role for the endothelium. J Am Coll Cardiol. 2009 Apr 21;53(16):1456-8. [PubMed: 19371830]

3.

El-Hamamsy I, Balachandran K, Yacoub MH, Stevens LM, Sarathchandra P, Taylor PM, Yoganathan AP, Chester AH. Endothelium-dependent regulation of the mechanical properties of aortic valve cusps. J Am Coll Cardiol. 2009 Apr 21;53(16):1448-55. [PubMed: 19371829]

4.

Voin V, Oskouian RJ, Loukas M, Tubbs RS. Auscultation of the heart: The Basics with Anatomical Correlation. Clin Anat. 2017 Jan;30(1):58-60. [PubMed: 27576554]

5.

Spicer DE, Bridgeman JM, Brown NA, Mohun TJ, Anderson RH. The anatomy and development of the cardiac valves. Cardiol Young. 2014 Dec;24(6):1008-22. [PubMed: 25647375]

6.

Kupari M. Aortic valve closure and cardiac vibrations in the genesis of the second heart sound. Am J Cardiol. 1983 Jul;52(1):152-4. [PubMed: 6858903]

7.

Conn RD, O'Keefe JH. Cardiac physical diagnosis in the digital age: an important but increasingly neglected skill (from stethoscopes to microchips). Am J Cardiol. 2009 Aug 15;104(4):590-5. [PubMed: 19660617]

8.

Chizner MA. Cardiac auscultation: rediscovering the lost art. Curr Probl Cardiol. 2008 Jul;33(7):326-408. [PubMed: 18513577]

9.

Prakash R, Moorthy K, Aronow WS. First heart sound: a phono-echocardiographic correlation with mitral, tricuspid, and aortic valvular events. Cathet Cardiovasc Diagn. 1976;2(4):381-7. [PubMed: 1000626]

10.

Prakash R. Second heart sound: a phono-echocardiographic correlation in 20 cardiac patients. J Am Geriatr Soc. 1978 Aug;26(8):372-4. [PubMed: 670625]

11.

Shindler DM. Practical cardiac auscultation. Crit Care Nurs Q. 2007 Apr-Jun;30(2):166-80. [PubMed: 17356358]

12.

Begic E, Begic Z. Accidental Heart Murmurs. Med Arch. 2017 Aug;71(4):284-287. [PMC free article: PMC5585808] [PubMed: 28974851]

13.

Morgan S. How to auscultate for heart sounds in adults. Nurs Stand. 2017 Sep 27;32(5):41-43. [PubMed: 29094542]

14.

Mondal H, Mondal S, Saha K. Development of a Low-Cost Wireless Phonocardiograph With a Bluetooth Headset under Resource-Limited Conditions. Med Sci (Basel). 2018 Dec 17;6(4) [PMC free article: PMC6313612] [PubMed: 30563004]

15.

Pinto C, Pereira D, Ferreira-Coimbra J, Portugues J, Gama V, Coimbra M. A comparative study of electronic stethoscopes for cardiac auscultation. Annu Int Conf IEEE Eng Med Biol Soc. 2017 Jul;2017:2610-2613. [PubMed: 29060434]

16.

Constant J. How to differentiate ejection murmurs from systolic regurgitant murmurs. Keio J Med. 1995 Sep;44(3):85-7. [PubMed: 7474646]

17.

Luisada AA. The first heart sound in normal and pathological conditions. Jpn Heart J. 1987 Mar;28(2):143-56. [PubMed: 3298709]

18.

Mehta NJ, Khan IA. Third heart sound: genesis and clinical importance. Int J Cardiol. 2004 Nov;97(2):183-6. [PubMed: 15458681]

19.

Vancheri F, Gibson D. Relation of third and fourth heart sounds to blood velocity during left ventricular filling. Br Heart J. 1989 Feb;61(2):144-8. [PMC free article: PMC1216631] [PubMed: 2923750]

20.

Shah SJ, Michaels AD. Hemodynamic correlates of the third heart sound and systolic time intervals. Congest Heart Fail. 2006 Jul-Aug;12 Suppl 1:8-13. [PubMed: 16894268]

21.

Omar HR, Guglin M. Mitral annulus diameter is the main echocardiographic correlate of S3 gallop in acute heart failure. Int J Cardiol. 2017 Feb 01;228:834-836. [PubMed: 27888763]

Disclosure: Sean Dornbush declares no relevant financial relationships with ineligible companies.

Disclosure: Andre Turnquest declares no relevant financial relationships with ineligible companies.