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Heart Sounds, Cardiac Cycle and Volume Changes


Heart Sounds

Phases of the Cardiac Cycle

Volume Changes

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Heart Sounds

The First Heart Sound

Special recording techniques enable us to differentiate four components of the first heart sound. The major audible components are the related to the closure of the Mitral (MV) and Tricuspid (TV) valves.

  • Mitral Valve close - slightly higher in intensity and frequency; best heard at the apex
  • Tricuspid Valve close - less intensity - best heard at the left sternal border
  • MV and TV  components are normally 20 - 30 milliseconds apart
  • A split of the first sound occurs when both events; are separately distinguishable.
  • A split of the first sound is heard in about 70% of normal subjects, and is heard best at the left lateral sternal border (LLSB).

Ausculation Areas


A physiological split occur when both components of the second sound are separately distinguishable. Normally this split sound is heard on inspiration and become single on expiration. The A2 and P2 components of the physiological split usually coincide, or are less than 30 milliseconds apart during expiration and often moved to around 50 to 60 milliseconds apart by the end of inspiration.


A physiological split occur when both components of the second sound are separately distinguishable. Normally this split sound is heard on inspiration and become single on expiration. The A2 and P2 components of the physiological split usually coincide, or are less than 30 milliseconds apart during expiration and often moved to around 50 to 60 milliseconds apart by the end of inspiration.

The physiological split is heard during during respiration because it is during that respiratory cycle that intrathoracic pressure drops. This drop permits more blood to return to the right heart. The increased blood volume  in the right ventricle results in a delayed pulmonic valve closure. At the same time, the capacity  of the pulmonary vessels in the lung is increased, which results in a slight decrease in the blood volume returning to the left heart.

With less blood in the left ventricle, its ejection takes less time, resulting in earlier closing of the aortic valve. Therefore, the net effect of inspiration, and a single second sound is heard during expiration. Listen to the second sound. The second sound will be split upon inspiration, and usually will be heard as single on expiation. The physiological split second is audible at base left, with the diaphragm chest piece.

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The Second Heart Sound

 The closure of the aortic and pulmonic valves contribute to the second sound production. In the normal sequence, the aortic valve closes before the pulmonic valve. The aortic (A2) component of the second sound is loudest of the two components and is discernible at all the ausculation sites. However, it is best heard at base right. The pulmonic component (P2) of the second sound is softer than A2, and may only be audible at the base left. Its high frequency is also best heard with the diaphragm of the chest piece firmly pressed.

The Third Heart Sound

The third heart sound is also of low frequency, but it is heard just after the second heart sound. It occurs in early diastole, during the time of rapid ventricular filling. This sound occurs about 140 to 160 milliseconds after the second sound. The S3 is often heard in normal children or young adults, but when heard in individuals over the age of 40 it is usually reflecting pathological heart disorders characterised by ventricular dilatation, decreased systolic function, and elevated ventricular diastolic filling pressure. Its nomoclature includes the term ventricular gallop, postdiastolic gallop, S3 gallop, and is usually heard past the age of forty. The abnormal, or pathological heart sound, may be heard in individuals with coronary artery disease, cardiomyopathies, incompetent vavles, left to right shunts, ventricular septal defects (VSD), or Patent Ductus Arteriosus (PDA).  Pathological S3 may be the first clinical appearance of congestive heart failure.

The Fourth Heart Sound

The fourth heart sound is a low frequency sound heard just before the first heart sound, usually proceeding this sound by a longer interval than separating  the two components of the normal first sound. It has also been known as an “atrial gallop” a “presystolic gallop” and an “S4” gallop. It is most commonly known as an S4 that is a diastolic sound, occuring during the late diastolic filling phase at the time when the atria contract. When the ventricles have a decreased compliance, or are receiving an increased diastolic volume, they generate a low frequency vibration. Some authorities believe the S4, may be normal in youth, but seldom considered normal after the age of 20. The pathological S is heard in primary myocardial disease, coronary artery disease, hypertension, and aortic and pulmonic stenosis.

The S4 may have its origin in either the left or right heart. The S4 of left ventricular origin is best heard at the apex, with the patient supine, or the left lateral position. Its causes include severe hypertension, aortic stenosis, cardiomyopathies, and left ventricular myocardial infarctions. In association with ischeamic heart disease the S4 is often loudest during episodes of angina pectoris or may occur early after an acute myocardial infarction, often becoming fainter as the patient improves.

The S4 of right ventricular origen is best heard at the left lateral sternal border. It is usually accentuated with inspiration, and may be due to pulmonary stenosis, pulmonary hypertension, or right myocardial infarction.

Systolic Murmurs

Early systolic murmurs begin with the first sound and peak in the first third of systole. Early murmurs have the greatest intensity in the early part of the cycle. The most frequent cause is innocent murmur of childhood. A small ventricular septal defect (VSD) occasionally causes an early systolic murmur. The early systolic murmur of a small VSD begin with S1 and stops in mid systole, because an ejection continues and ventricular size decreases, the small defect is sealed. This murmur is characteristic of the type of children’s VSD located in the muscular portion of the ventricular septum.

A late systolic murmur begins in the latter half of systole, peaks in the later third of systole, and extends to the second sound. It is a modified regurgitant murmur with a backward flow through an usually high in frequency (blowing in quality), and heard best with a diaphragm at the apex. It may radiate to the axilla or left sternal border.

Diastolic Murmur

Diastolic murmurs are sustained noises that are audible between S2 and the next S1. Unlike systolic murmurs, diastolic murmurs should usually be considered pathological, and not normal. Typical abnormailities causing diastolic murmurs are aortic regurgitation, pulmonic regurgitation, mitral stenosis, and tricuspid stenosis. An early diastolic murmur begins with a second sound, and peaks in the first third of astole. Common causes are aortic regurgitation and pulmonic regurgitation. Aortic regurgitation: high frequency quality, best heard - diaphragm at Erb’s point and radiates downward along the left sternal border. Pulmonic regurgitation: occurs after a slight delay after P2. Has a rough quality best heard with the bell lightly held at the base left, and radiated along the left sternal border. The murmur of pulmonic regurgitation tends to be short of duration, and heard best on inspiration. This respiratory variation is helpfull in differentiating pulmonic regurgitation from aortic regurgitation.

A late diastolic murmur occurs in the latter half of diastole, synchronus with atrial contraction, and extends to the first sound. Although occasionally ocuring alone, it is usually a component of frequency, and rumbling in qaulity. Ejection sounds are high frequency “clicky” sounds occuring shortly after the first sound with the onset of ventricular ejection. They are produced by the opening of the semilunar valves (aortic or pulmonic) either when one of these valves is diseased or when ejection is rapid through a normal valve. They are heard best at the base and may be of either aortic or pulmonic origin.


Phases of the Cardiac Cycle

Phases of the cardiac cycle, presents pressure changes and valves that govern the blood flow. A great amount of this knowledge is summarised in Figure Cardiac Cycle and Phases. The coloured areas indicate the different phases, that is completed in 1 second. The systolic period is the period of contraction and the diastolic period the relaxation.

Atrial Contraction

  • This is the first phase of the cardiac cycle and is initiated by the P-wave of the electrocardiogram (ECG), that represents electrical depolarization of the atria. Atrial depolarization then causes contraction of the atrial musculature. As the atria contract, the pressure within the atrial chambers increases so that a pressure gradient is generated across the open atrioventricular (AV) valves, thereby causing a rapid flow of blood into the ventricles. Retrograde atrial flow back into the vena cavae is impeded by venous return (inertial effect) and by the wave of contraction ("milking effect") throughout the atria. However, atrial contraction does produce a small increase in venous pressure that can be noted as the "a-wave" of the jugular pulse. Just following the peak of the a-wave is the x-descent.
  • Atrial contraction normally accounts for about 10% of left ventricular filling when a person is at rest because most of the ventricular filling occurs before the atria contract and therefore is passive. Atrial contribution to ventricular filling varies inversely with duration of ventricular diastole and directly with atrial contractility.
  • Once atrial contraction is complete, the atrial pressure begins to fall causing a pressure gradient reversal across the AV valves. This causes the valves to move upward before closure. The ventricular volumes are now maximal, and is termed the end-diastolic volume (EDV). The left ventricular EDV (LVEDV), that is about 120 ml, comprises the ventricular preload and is associated with an end-diastolic pressures of 8-12 mmHg and 3-6 mmHg in the left and right ventricles, respectively.
  • A heart sound is sometimes noted during atrial contraction (Fourth Heart Sound, S4). This sound is caused by vibration of the ventricular wall during atrial contraction.

Isovolumetric Contraction

  • This phase of the cardiac cycle is initiated by the QRS complex that represents ventricular depolarization. As the ventricles depolarize, excitation-contraction coupling leads to myocyte contraction and the development of ventricular wall tension and a rapid increase in intra-ventricular pressure. Early in this phase, the rate of pressure development becomes maximal.
  • The abrupt rise in pressure causes the A-V valves to close as intra-ventricular pressure exceeds atrial pressure. Contraction of the papillary muscles with attached chordae tendineae prevent the A-V valve leaflets from bulging back into the atria and becoming incompetent (i.e., “leaky”). Closure of the A-V valves results in the First Heart Sound (S1). This sound is normally split (~0.04 sec) because mitral valve closure precedes tricuspid closure.
  • During the time period between the closure of the AV valves and the opening of the semilunar valves, ventricular pressure rises rapidly without a change in ventricular volume. Contraction is said to be "isovolumic" or "isovolumetric." Individual myocyte contraction, however, is not necessarily isometric. Individual fibers contract isotonically and others contract isometrically or eccentrically. Therefore, ventricular chamber geometry changes considerably as the heart becomes more spheroid in shape. The circumference increases and atrial base-to-apex length decreases.
  • Atrial pressures increase due to continued venous return and possible bulging of AV valves back into the atrial chambers.

Rapid Ejection

  • When the intraventricular pressures exceed the pressures within the aorta and pulmonary artery, the aortic and pulmonic valves open and blood is ejected from the ventricles. Blood is ejected as the total energy of the blood within the ventricle exceeds the total energy of blood within the aorta. During this phase, ventricular pressure normally exceeds outflow tract pressure by only a few mmHg. Although blood flow across the valves is very high, the relatively large valve opening requires only on few mmHg of a pressure gradient to propel flow across the valve. Maximal outflow velocity is reached early in the ejection phase, and maximal (systolic) aortic and pulmonary artery pressures are achieved. 
  • Atrial pressure initially decreases as the atrial base is pulled downward, expanding the atrial chamber. Blood continues to flow into the atria from their respective venous inflow tracts.

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Reduced Ejection

  • Approximately 150-200 msec after the QRS, ventricular repolarization occurs (T-wave). This causes ventricular active tension to decrease and the rate of ejection (ventricular emptying) to fall. Ventricular pressure falls slightly below outflow tract pressure; however, outward flow still occurs due to kinetic (or inertial) energy of the blood.
  • Atrial pressures gradually rise due to venous return. 

Isovolumetric Relaxation

  • As the ventricles continue to relax and intraventricular pressures fall, a point is reached when the total energy of blood within the ventricles is less than the energy of blood in the outflow tracts. When this occurs, the pressure reversal causes the aortic and pulmonic valves to abruptly close (aortic precedes pulmonic) causing the Second Heart Sound (S2). Valve closure is associated with a small backflow of blood into the ventricles and a characteristic notch (incisura or dicrotic notch) in the aortic and pulmonary artery pressure tracings. The decline in aortic and pulmonary artery pressures is not as abrupt as in the ventricles because of potential energy stored in outflow vessel walls.
  • Ventricular pressures decrease; however, volumes remain constant because all valves are closed. The volume of blood that remains in a ventricle is called the end-systolic volume and is ~50 ml in the left ventricle. The difference between the end-diastolic volume and the end-systolic volume is ~70 ml and represents the stroke volume.
  • Atrial pressures continue to rise due to venous return.

Rapid Filling

  • When the ventricular pressures fall below atrial pressures, the AV valves open and ventricular filling begins. The ventricles continue to relax despite the inflow, which causes intraventricular pressure to continue to fall by a few additional mmHg.
  • The opening of the AV valves causes a rapid fall in atrial pressures and a fall in the jugular pulse. The peak of the jugular pulse just before the valve opens is the v-wave. This is followed by the y-descent of the jugular pulse.
  • If the AV valves are healthy, no prominent sounds will be heard during filling. When a Third Heart Sound (S3) is audible, it may represent tensing of chordae tendineae and AV ring during ventricular relaxation and filling.

Reduced filling

  • As the ventricles continue to fill with blood and expand, they become less compliant and the intraventricular pressures rise. This reduces the pressure gradient across the AV valves so that the rate of filling falls.
  • Aortic pressure (and pulmonary arterial pressure) continues to fall during this period.


Volume Changes


    To maintain homeostasis, the two ventricles must have equal output.

Left Ventricle Volume Shifts

End-systolic volume (ESV, left from previous heartbeat)

60 mL

Pasively added - atrial diastole

+ 30 mL

Atrial Systole

+ 40 mL

Total: end-diastolic volume (EDV)

130 mL

Stroke volume (SV) ejected by ventricular systole

- 70 mL

Leaves: end-systolic volume (ESV)

60 mL


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