Cardiac Cycle

Introduction

The cardiac cycle is a precisely coordinated sequence of electrical and mechanical events that enables efficient pumping of blood by the heart. Understanding its phases reveals how changes in heart rate, ventricular filling, and myocardial function influence cardiac output and overall cardiovascular performance.

• The cardiac cycle is the sequence of electrical and mechanical events that occurs during one complete heartbeat.
• It includes coordinated changes in cardiac chamber pressure, blood volume, blood flow, and electrical activity.
• These events are repeated in a regular pattern with each heartbeat under normal physiological conditions.
• Electrical activity generated by the heart can be recorded using an electrocardiogram.
• Similar electromechanical events occur almost simultaneously in the right and left sides of the heart.
• The left side of the heart operates at much higher pressures than the right side, particularly in the left ventricle and aorta.
• For simplicity, the cardiac cycle is commonly described using events occurring in the left atrium, left ventricle, and aorta.

Phases of Cardiac Cycle

• The cardiac cycle consists of coordinated atrial and ventricular contraction and relaxation.
• It is commonly divided into three phases: atrial systole, ventricular systole, and ventricular diastole.
• Atrial relaxation occurs largely during ventricular systole and therefore is not usually described as a separate phase.

Atrial Systole

• Atrial systole begins near the end of the P wave and is completed before the onset of ventricular systole.
• During this phase, contraction of the atria propels blood into the ventricles and completes ventricular filling.
• Under resting conditions, atrial contraction contributes approximately 10–20% of the final ventricular filling volume.
• The remaining 80–90% of ventricular filling occurs passively due to the pressure gradient between the atria and ventricles during ventricular diastole.
• Consequently, ventricular volume increases only slightly during atrial systole.
• The contribution of atrial systole becomes more important when heart rate increases.
• In tachycardia, shortening of the cardiac cycle occurs mainly because ventricular diastole is reduced.
• Reduced diastolic duration limits passive ventricular filling.
• Under these conditions, atrial contraction provides a larger proportion of ventricular filling and helps maintain stroke volume.
• During exercise, increased sympathetic activity enhances atrial contractility.
• As a result, atrial systole may contribute up to 30–40% of ventricular filling.
• This additional filling supports the increase in cardiac output required to meet the metabolic demands of active tissues.
• Individuals with atrial fibrillation may have difficulty achieving an adequate rise in cardiac output during exercise because effective atrial contraction is absent.

Major events in atrial systole are:

• Atrial systole extends from the latter part of the P wave to the beginning of the QRS complex.
• Atrial contraction causes a mild increase in ventricular volume.
• Atrial pressure rises and produces the a wave in the atrial pressure and jugular venous pressure tracings.
• Atrial pressure temporarily exceeds ventricular pressure, facilitating blood flow into the ventricles.
• A fourth heart sound may be heard when atrial contraction forces blood into a less compliant ventricle.
• At the end of this phase, ventricular pressure begins to rise and ventricular systole subsequently leads to closure of the atrioventricular valves.

Atrial Diastole

• Atrial diastole begins immediately after atrial systole and is characterized by filling of the atria with venous blood.
• This phase occurs largely during ventricular systole.
• At the onset of ventricular contraction, the closed atrioventricular valves bulge slightly into the atria.
• This transient increase in atrial pressure produces the c wave in the atrial and jugular venous pressure tracings.
• Continuous venous return from the systemic and pulmonary circulations gradually increases atrial volume.
• Progressive atrial filling raises atrial pressure and generates the v wave in the venous pressure curve.
• The v wave reaches its peak just before the atrioventricular valves reopen during ventricular diastole.

Ventricular Systole

• Ventricular systole consists of the isovolumetric contraction phase followed by the ventricular ejection phase.
• It begins shortly after ventricular depolarization, represented by the QRS complex on the electrocardiogram.

Phase of Isovolumetric Contraction

• This phase starts with closure of the atrioventricular valves and ends with opening of the semilunar valves.
• All cardiac valves remain closed during this interval.
• Ventricular muscle fibers contract forcefully, but ventricular volume remains unchanged because no blood enters or leaves the ventricles.
• The first heart sound is produced mainly by closure of the mitral and tricuspid valves.
• Ventricular pressure rises rapidly from low diastolic values.
• In the left ventricle, pressure increases from approximately 5–10 millimeters of mercury to about 80 millimeters of mercury.
• No blood is ejected into the aorta or pulmonary trunk during this phase.
• The phase ends when ventricular pressure exceeds the pressure within the great arteries, causing the semilunar valves to open.

Phase of Ventricular Ejection

• The ventricular ejection phase begins when ventricular pressure exceeds arterial pressure, causing the semilunar valves to open.
• It is divided into a rapid ejection phase and a reduced ejection phase.
• During rapid ejection, a large volume of blood is expelled into the arteries within a short period.
• Ventricular and arterial pressures rise rapidly during this stage.
• Ventricular volume decreases markedly because of the high rate of blood flow.
• During reduced ejection, the rate of blood flow gradually declines as ventricular contraction weakens.

Rapid Ejection Phase

• The rapid ejection phase begins immediately after the semilunar valves open.
• During the preceding isovolumetric contraction phase, ventricular pressure rises sufficiently to overcome arterial pressure.
• Opening of the aortic and pulmonary valves allows blood to be expelled forcefully into the aorta and pulmonary trunk.
• Blood flow into the great arteries increases abruptly during this phase.
• Ventricular contraction remains strong, causing ventricular pressure to continue rising for a short period.
• Aortic and pulmonary arterial pressures also increase rapidly as blood enters these vessels.
• Throughout most of this phase, ventricular pressure remains slightly higher than arterial pressure, maintaining forward blood flow.
• Approximately two-thirds of the stroke volume is ejected during the rapid ejection phase.
• As a result, ventricular volume decreases sharply.
• This phase accounts for the greatest rate of ventricular emptying during systole.
• At the beginning of ventricular ejection, atrial pressure falls transiently.
• This fall occurs because downward movement of the atrioventricular junction enlarges the atrial cavities during ventricular contraction.
• After the initial decline, atrial pressure gradually rises as venous return continues to fill the atria.
• The c wave may be observed in the jugular venous pressure tracing during early ventricular systole.
• It is primarily produced by bulging of the closed tricuspid valve into the right atrium and, to a lesser extent, by transmission of adjacent arterial pulsations.

Important events in this phase are:

• The phase begins with opening of the semilunar valves.
• Arterial blood flow rises rapidly.
• Ventricular volume falls steeply due to rapid blood ejection.
• Ventricular and arterial pressures increase simultaneously.
• Atrial pressure shows an initial decline followed by a gradual rise.
• The phase corresponds mainly to the ST segment of the electrocardiogram.

Reduced Ejection Phase

• The reduced ejection phase is the latter and longer part of ventricular systole.
• During this phase, the force of ventricular contraction gradually declines.
• Ventricular pressure begins to decrease as myocardial fibers start to relax.
• Arterial pressure also falls because blood continues to flow from the arteries into the peripheral circulation.
• The decline in arterial pressure is slower than the decline in ventricular pressure.
• Consequently, aortic pressure becomes slightly higher than left ventricular pressure during the later part of this phase.
• Despite this reversal of the pressure gradient, forward blood flow continues for a short period because of the momentum of blood ejected during the rapid ejection phase and the elastic recoil of the large arteries.
• These factors help keep the semilunar valves open temporarily.
• The rate of blood ejection decreases markedly, giving rise to the term reduced ejection phase.
• Ventricular volume continues to fall, but at a slower rate than during rapid ejection.
• By the end of this phase, the ventricles reach the end-systolic volume, which represents the volume of blood remaining after systole.

Important events in this phase are:

• Ventricular and arterial pressures progressively decrease.
• Arterial pressure slightly exceeds ventricular pressure near the end of the phase.
• Blood flow through the semilunar valves is substantially reduced.
• Ventricular volume continues to decrease until end-systolic volume is reached.
• Atrial pressure gradually rises because venous return continues while the atria remain relaxed.
• The T wave, representing ventricular repolarization, appears during this phase.
• The phase ends with closure of the semilunar valves.

Ventricular Diastole

• Ventricular diastole is the phase during which the ventricles relax and prepare for the next cardiac cycle.
• It consists of two main phases: isovolumetric relaxation and ventricular filling.
• Ventricular filling is further divided into rapid filling and reduced filling (diastasis).

Phase of Isovolumetric Relaxation

• This phase begins immediately after closure of the semilunar valves.
• Ventricular muscle relaxation causes a rapid decline in ventricular pressure.
• Both the semilunar and atrioventricular valves remain closed during this interval.
• Because all valves are closed, no blood enters or leaves the ventricles.
• Consequently, ventricular volume remains constant throughout the phase.
• The term isovolumetric relaxation indicates that ventricular volume does not change while myocardial relaxation occurs.
• Closure of the aortic valve produces a characteristic notch, known as the dicrotic notch, on the descending limb of the aortic pressure curve.
• Vibrations generated by closure of the aortic and pulmonary valves produce the second heart sound.
• Arterial blood flow decreases markedly and forward flow from the ventricles ceases.
• During ventricular relaxation, venous return continues to fill the atria.
• As a result, atrial pressure gradually rises throughout this phase.
• The peak of the v wave in the atrial and jugular venous pressure tracings occurs near the end of this phase.

Important events in this phase are:

• Ventricular pressure falls rapidly.
• Ventricular volume remains unchanged.
• Semilunar valves are closed and atrioventricular valves have not yet opened.
• The second heart sound occurs early in the phase.
• Atrial pressure continues to increase.
• The phase ends when ventricular pressure falls below atrial pressure, causing the atrioventricular valves to open and ventricular filling to begin.

Phase of Ventricular Filling

The ventricular filling phase consists of rapid filling followed by reduced filling (diastasis) before atrial systole completes filling.

Rapid Filling Phase

• The rapid filling phase begins when ventricular pressure falls below atrial pressure, causing the atrioventricular valves to open.
• Blood accumulated in the atria during ventricular systole flows rapidly into the ventricles.
• This phase accounts for the largest portion of passive ventricular filling.
• Ventricular volume increases markedly because a substantial amount of blood enters the ventricles within a short period.
• Despite the rapid inflow of blood, ventricular pressure may continue to decrease briefly because ventricular relaxation is still ongoing.
• Atrial pressure falls as blood moves from the atria into the ventricles.
• The peak of the v wave in the atrial and jugular venous pressure tracings occurs at the beginning of this phase.
• A third heart sound may be produced during early rapid filling due to vibrations generated by rapid ventricular filling.
• In healthy children and young adults, this sound may be physiological, whereas in older adults it may indicate ventricular volume overload.

Important events in this phase are:

• Atrioventricular valves open.
• Ventricular volume increases rapidly.
• Atrial pressure decreases.
• Ventricular pressure remains low despite increasing volume.
• The third heart sound may occur in the early part of the phase.

Diastasis

• Diastasis is the period of slow ventricular filling that follows the rapid filling phase.
• As the pressure difference between the atria and ventricles decreases, the rate of blood flow into the ventricles slows considerably.
• Ventricular volume continues to increase, but at a much slower rate.
• Atrial and ventricular pressures remain nearly constant during this phase.
• Most ventricular filling occurs passively during rapid filling and diastasis.
• Atrial systole contributes the final 10–20% of ventricular filling under resting conditions.
• Toward the end of diastasis, the P wave appears, indicating the onset of atrial depolarization and the next atrial systole.

Pressure–Volume Relationship

• The pressure–volume loop graphically represents changes in left ventricular pressure and volume during one cardiac cycle.
• It provides a useful overview of ventricular filling, contraction, ejection, and relaxation.
• Ventricular filling begins when the mitral valve opens and ends when it closes.
• During this phase, ventricular volume increases substantially, while pressure rises only slightly because the ventricle is relaxed and compliant.
• The isovolumetric contraction phase starts after mitral valve closure.
• Ventricular pressure rises rapidly, but ventricular volume remains constant because all cardiac valves are closed.
• When ventricular pressure exceeds aortic pressure, the aortic valve opens and ventricular ejection begins.
• Ventricular volume decreases as blood is expelled into the aorta.
• Pressure continues to rise during early ejection, reaches a peak, and then gradually declines during late ejection.
• At the end of systole, the aortic valve closes and isovolumetric relaxation begins.
• Ventricular pressure falls rapidly while ventricular volume remains unchanged because all valves are closed.
• When ventricular pressure becomes lower than atrial pressure, the mitral valve opens and a new filling phase starts.
• Completion of this sequence forms one complete cardiac cycle and one pressure–volume loop.

Effects of Ventricular Dysfunctions on Pressure-Volume Loop

Systolic Dysfunction

• Systolic dysfunction refers to impaired ventricular contraction and reduced pumping ability.
• Decreased myocardial contractility limits the amount of blood ejected during systole.
• As a result, the end-systolic volume increases because more blood remains in the ventricle after contraction.
• The pressure–volume loop becomes narrower, indicating a reduction in stroke volume.
• The end-systolic pressure–volume relationship shifts downward and to the right, reflecting reduced contractile performance.
• Cardiac output may decrease if compensatory mechanisms are inadequate.

Diastolic Dysfunction

• Diastolic dysfunction results from impaired ventricular relaxation or reduced ventricular compliance.
• Ventricular filling becomes restricted despite normal or near-normal contractile function.
• The diastolic pressure–volume relationship shifts upward and to the left.
• Higher filling pressures are required to achieve a given ventricular volume.
• End-diastolic volume decreases, leading to a reduction in stroke volume.
• Patients may develop elevated atrial and pulmonary venous pressures because ventricular filling is impaired.

Duration of Cardiac Cycle

• At a heart rate of approximately 75 beats per minute, one cardiac cycle lasts about 0.8 second.
• Ventricular systole occupies about 0.3 second, whereas diastole occupies about 0.5 second.
• Changes in heart rate affect the duration of diastole more than systole.
• During tachycardia, the cardiac cycle shortens predominantly because diastole becomes markedly shorter.
• Reduced diastolic duration limits ventricular filling and may decrease stroke volume and cardiac output.
• During bradycardia, the cardiac cycle lengthens mainly because of prolongation of diastole.
• The longer filling period allows greater ventricular filling and increased end-diastolic volume.
• Thus, variations in cardiac cycle length occur primarily through changes in the duration of ventricular diastole.

Jugular Venous Pulse

• The jugular venous pulse reflects pressure changes occurring in the right atrium.
• Clinical examination of the right internal jugular vein provides valuable information about right atrial pressure and cardiac function.

Waves of JVP

• The jugular venous pulse consists of three positive waves (a, c, and v) and two descents (x and y).
• These waveforms reflect pressure changes occurring in the right atrium during the cardiac cycle.
• The a wave is produced by right atrial contraction and represents atrial systole.
• The c wave occurs at the beginning of ventricular systole and results mainly from bulging of the closed tricuspid valve into the right atrium as right ventricular pressure rises.
• The v wave reflects progressive filling of the right atrium by venous return while the tricuspid valve remains closed.
• The x descent represents a fall in right atrial pressure due to atrial relaxation and downward displacement of the tricuspid valve during ventricular systole.
• The y descent occurs when the tricuspid valve opens and blood flows rapidly from the right atrium into the right ventricle.

Conditions that raise JVP

• Right-sided heart failure commonly causes elevation of jugular venous pressure.
• Obstruction of the superior vena cava impedes venous drainage and increases venous pressure.
• Increased circulating blood volume, such as during pregnancy, acute kidney inflammation, or excessive intravenous fluid administration, may raise jugular venous pressure.
• Congestive heart failure, constrictive pericarditis, and tricuspid valve regurgitation are additional important causes.
• Persistent elevation of jugular venous pressure is an important clinical sign of increased right atrial pressure and may indicate underlying cardiac dysfunction.

Prominent ‘a’ Wave

• A prominent a wave indicates forceful right atrial contraction against increased resistance to right ventricular filling.
• It may occur in pulmonary valve stenosis, pulmonary hypertension, tricuspid valve stenosis, right atrial myxoma, atrial septal defect with right atrial enlargement, and certain cardiomyopathies.
• The underlying mechanism is increased right atrial pressure generated during atrial contraction.

Cannon Wave

• A cannon a wave is an unusually large a wave produced when the right atrium contracts against a closed tricuspid valve.
• It is commonly observed in complete atrioventricular block and some junctional rhythms where atrial and ventricular contractions occur simultaneously.

Absence of ‘a’ Wave

The a wave is absent in atrial fibrillation because organized atrial contraction is lost.

Prominent ‘v’ Wave

• A prominent v wave is characteristic of tricuspid valve regurgitation.
• During ventricular systole, blood flows backward from the right ventricle into the right atrium through the incompetent tricuspid valve.
• This regurgitant flow markedly increases right atrial pressure and enlarges the v wave.

Heart Sounds

• Four heart sounds are recognized: first, second, third, and fourth heart sounds.
• The first and second heart sounds are normally audible in healthy individuals.

First Heart Sound

• The first heart sound marks the onset of ventricular systole.
• It is produced primarily by closure of the mitral and tricuspid valves.
• Additional vibrations arise from rapid development of ventricular wall tension and movement of blood within the ventricles.
• The sound is low-pitched, has a duration of approximately 0.10–0.15 second, and is typically heard as “lub.”
• Its frequency generally ranges between 25 and 45 hertz.

Significance

• The first heart sound indicates closure of the atrioventricular valves and the beginning of ventricular contraction.
• It may become louder in conditions associated with increased cardiac output, such as exercise, anemia, systemic hypertension, and other hyperdynamic circulatory states.
• It may become softer in shock, acute myocardial infarction, constrictive pericarditis, pericardial effusion, advanced cardiomyopathy, obesity, and emphysema.

Splitting of S1

• The first heart sound contains separate mitral and tricuspid valve closure components.
• Under normal conditions, the mitral valve closes slightly before the tricuspid valve.
• Physiological splitting is usually not audible because the two components occur very close together and merge into a single sound.
• Clearly audible splitting of the first heart sound is generally considered abnormal and may indicate delayed closure of one atrioventricular valve.

Second Heart Sound

• The second heart sound is produced primarily by closure of the aortic and pulmonary valves at the end of ventricular systole.
• It marks the beginning of ventricular diastole and the end of mechanical systole.
• The sound is relatively short, lasting about 0.12 second, and has a higher frequency than the first heart sound.
• It is commonly described as “dup.”

Significance

• The aortic component (A2) becomes louder in systemic hypertension and dilatation of the ascending aorta.
• A2 may become softer in aortic valve stenosis and severe aortic valve regurgitation because valve closure is impaired.
• The pulmonary component (P2) becomes louder in pulmonary hypertension and pulmonary artery dilatation.
• P2 is diminished in pulmonary valve stenosis due to restricted valve movement.

Splitting of S2

• The second heart sound normally consists of separate aortic and pulmonary valve closure components.
• Under normal conditions, the aortic valve closes slightly before the pulmonary valve.
• Physiological splitting is most evident during inspiration and is best heard over the pulmonary area.
• The phenomenon is often more easily appreciated in children and young adults.

Mechanism of Splitting

• During inspiration, increased venous return to the right side of the heart increases right ventricular stroke volume.
• This prolongs right ventricular systole and delays closure of the pulmonary valve.
• Simultaneously, a slight reduction in left ventricular filling shortens left ventricular systole, causing earlier closure of the aortic valve.
• As a result, the interval between A2 and P2 widens during inspiration.
• During expiration, this interval narrows.

Reverse Splitting

• Reverse splitting occurs when aortic valve closure is delayed and follows pulmonary valve closure.
• It is seen in left bundle branch block and conditions associated with prolonged left ventricular ejection, such as left ventricular failure.

Third Heart Sound

• The third heart sound is a low-frequency sound that occurs during early ventricular diastole.
• It follows the second heart sound and coincides with the rapid filling phase of the ventricles.
• Although it can be recorded on phonocardiography, it is usually not audible in healthy adults.
• It may be heard normally in children, adolescents, young adults, and pregnant women because of enhanced ventricular filling.
• The sound most commonly originates from the left ventricle and is best heard over the cardiac apex.

Causes

• The third heart sound is produced by vibrations generated during rapid passive filling of the ventricle.
• Sudden deceleration of blood entering the ventricle contributes to these vibrations.
• Oscillation of the ventricular wall, chordae tendineae, and atrioventricular valve apparatus also plays a role.
• The sound is low-pitched, lasts approximately 0.1 second, and occurs shortly after the second heart sound.

Significance

• In young individuals, the third heart sound may be a normal physiological finding.
• It is often associated with hyperdynamic circulation, where ventricular filling is increased.
• Conditions such as mitral valve regurgitation and ventricular septal defect may produce an audible third heart sound because of increased diastolic blood flow.
• In middle-aged and older adults, the presence of a third heart sound commonly suggests ventricular volume overload or heart failure.
• It may also occur after myocardial infarction or in disorders that alter ventricular compliance and filling dynamics.

Fourth Heart Sound

• The fourth heart sound is produced during atrial contraction and occurs in late ventricular diastole.
• It is generated by vibrations created when blood is forced into a stiff or poorly compliant ventricle.
• The sound is low-pitched and occurs immediately before the first heart sound.
• It is usually not audible in healthy adults and is generally considered a pathological finding when heard.

Significance

• The fourth heart sound indicates decreased ventricular compliance or increased ventricular stiffness.
• It develops when atrial contraction causes a sudden rise in ventricular pressure.
• Common causes include left ventricular hypertrophy associated with systemic hypertension.
• It may also occur following myocardial infarction and in conditions causing ventricular hypertrophy or impaired ventricular relaxation.
• Right-sided fourth heart sounds may be heard in pulmonary hypertension and pulmonary embolism.
• The sound is absent in atrial fibrillation because effective atrial contraction is required for its production.

Triple Heart Sound

• A triple heart sound consists of the first and second heart sounds together with either a third or a fourth heart sound.
• In some healthy children and young adults, a triple rhythm associated with a physiological third heart sound may be normal.
• When a triple rhythm occurs in association with cardiovascular disease, it often indicates significant cardiac dysfunction.
• If the heart rate exceeds approximately 100 beats per minute, the triple rhythm may merge into a gallop rhythm.
• Gallop rhythm produces a cadence that resembles the galloping sound of a horse.
• A gallop caused by the third heart sound is termed a protodiastolic gallop or ventricular gallop.
• A gallop caused by the fourth heart sound is termed a presystolic gallop or atrial gallop.
• Gallop rhythms are commonly associated with ventricular dysfunction, heart failure, or reduced ventricular compliance.

Murmurs

• A murmur is an abnormal sound produced by turbulent blood flow within the heart or great vessels.
• Murmurs may result from valvular stenosis, valvular regurgitation, increased blood flow, or abnormal intracardiac communications.
• Compared with heart sounds, murmurs are generally longer in duration and contain higher-frequency components.

Site of Origin:

• The location where a murmur is heard most clearly helps identify its likely origin.
• The point of maximal intensity often corresponds to the affected valve or structure.

Timing and duration:

• Murmurs are classified as systolic, diastolic, or continuous according to their occurrence within the cardiac cycle.
• They may also be described as early, mid, late, or pansystolic, depending on their duration.

Character:

• Murmurs may be soft, blowing, harsh, rough, musical, or rumbling.
• Harsh murmurs often indicate structural cardiac abnormalities.

Radiation (Conduction):

• Some murmurs remain localized, whereas others are transmitted to distant areas.
• For example, mitral valve regurgitation commonly radiates toward the axilla.

Relation with respiration:

• Right-sided murmurs generally become louder during inspiration because right ventricular filling increases.
• Left-sided murmurs usually become more prominent during expiration as left ventricular filling increases.