The cardiac cycle is the complete sequence of contraction and relaxation that your heart repeats roughly 100,000 times a day, and the sounds a stethoscope picks up are direct acoustic byproducts of that mechanical work. Each cycle has two major phases: systole, when the ventricles squeeze blood out, and diastole, when they relax and refill. Within those two broad categories sit several sub-phases, each defined by what the valves are doing and whether blood is actually moving. The familiar “lub-dub” maps neatly onto valve closures at the boundaries between those phases, but there is more going on acoustically than most people realize.
What Happens During Systole
Systole begins the instant the ventricles start contracting. The first thing that happens is a brief but important sub-phase called isovolumetric contraction. During this window, the muscle is generating force, pressure inside the ventricles is climbing rapidly, but no blood is going anywhere. That is because all four valves are shut: the mitral and tricuspid valves just closed (which is what you hear as the first heart sound), and the aortic and pulmonary valves have not opened yet because pressure inside the ventricles has not exceeded the pressure in the aorta and pulmonary artery. The ventricle is essentially a sealed chamber building up steam.
Once ventricular pressure surpasses aortic pressure on the left side and pulmonary artery pressure on the right, the semilunar valves pop open and the ejection phase begins. Blood rushes out into the aorta and pulmonary artery. Early ejection is fast, with most of the stroke volume leaving the ventricle in the first portion of this phase. As the ventricle empties and its contraction winds down, ejection slows. Eventually, ventricular pressure starts falling below the pressure in the great arteries, and blood briefly tries to reverse direction. That backflow snaps the aortic and pulmonary valves shut, producing the second heart sound and marking the end of systole.
What Happens During Diastole
Diastole mirrors the beginning of systole with its own sealed-chamber moment: isovolumetric relaxation. The semilunar valves have just closed, the mitral and tricuspid valves have not yet opened, and the ventricle is relaxing without changing its volume. Pressure drops sharply. How quickly that pressure falls matters clinically. The rate of relaxation is influenced by how hard the ventricle was working during systole; higher systolic loads tend to slow relaxation.1PubMed. Myocardial relaxation. II. Hemodynamic determinants of rate of left ventricular isovolumic pressure decline
When ventricular pressure drops below atrial pressure, the mitral and tricuspid valves open and the rapid filling phase begins. Blood pours into the ventricles largely under its own momentum and the pressure gradient between the atria and ventricles. This rapid filling phase accounts for the bulk of ventricular filling, delivering more than 70% of the stroke volume in a very short time.2European Journal of Cardio-Thoracic Surgery. Systolic ventricular filling After that initial rush, filling slows during a phase called diastasis, where pressures between the atria and ventricles nearly equalize and blood trickles in slowly. Finally, the atria contract (atrial systole, sometimes called the “atrial kick”), topping off the ventricles with the remaining volume just before the next ventricular contraction begins the cycle again.
At a normal resting heart rate, diastole lasts longer than systole. That extra time is not a luxury; the heart muscle gets most of its own blood supply during diastole, when the coronary arteries are not being squeezed by a contracting wall. When heart rate climbs during exercise, diastole shortens disproportionately, which is generally fine in a healthy heart but can cause problems when the ventricle is stiff or diseased.
The First Heart Sound
The first heart sound, known as S1, marks the transition from diastole to systole. It is produced primarily by the closure of the mitral and tricuspid valves. When the ventricles begin contracting, the pressure inside them rises above atrial pressure, and the valve leaflets snap shut. That abrupt halt of backward-moving blood and the resulting vibration of the leaflets, blood column, and surrounding cardiac structures produce the sound.3PLOS Computational Biology. Hemodynamics-driven mathematical model of first and second heart sound generation
S1 has two components: M1, from the mitral valve, and T1, from the tricuspid valve. In most people these occur so close together that they sound like a single event. But the loudness and frequency content of S1 are not fixed. Computational modeling has shown that the intensity of the first heart sound scales with how rapidly pressure is rising inside the ventricle at the moment the valve closes. A faster rate of pressure rise produces a louder sound. The pressure across the valve at the moment the leaflets come together also matters: higher transmitral pressure at coaptation produces a stronger acoustic signal.4PubMed. Haemodynamic determinants of the mitral valve closure sound: a finite element study This is one reason that a clinician’s ear can pick up clues about how forcefully the ventricle is contracting just from the quality of S1.
The Second Heart Sound and Why It Splits
S2 marks the end of systole and the beginning of diastole. It is generated by the closure of the aortic valve (A2) and the pulmonary valve (P2). Under most conditions, these two closures happen nearly simultaneously, so you hear a single, crisp sound that is higher-pitched and shorter than S1.3PLOS Computational Biology. Hemodynamics-driven mathematical model of first and second heart sound generation
During inspiration, though, something changes. You might expect that the right ventricle simply takes longer to eject blood because more blood is returning to it from the veins during a breath in, and that is the explanation many people learn. The actual mechanism is more nuanced. Research measuring the timing of these valve closures found that the major contributor to inspiratory splitting is not a prolonged right ventricular contraction but rather a delay between the end of right ventricular systole and the moment the pulmonary valve actually closes. That delay is attributed to a drop in pulmonary vascular resistance during inspiration, which changes the impedance the right ventricle pumps against. A smaller contribution comes from the aortic valve closing slightly earlier during inspiration.5PubMed. Mechanism of normal splitting of the second heart sound The net result is that A2 and P2 separate enough to be heard as two distinct clicks during inspiration and fuse again on expiration. This is called physiologic splitting and is entirely normal.
When splitting persists throughout the respiratory cycle, widens abnormally, or paradoxically narrows during inspiration, it signals a timing mismatch between the two ventricles. Fixed splitting, for example, is a classic sign of an atrial septal defect. Clinicians and researchers have investigated using S2 splitting patterns as a noninvasive marker of interventricular dyssynchrony, the kind of timing mismatch that matters in conditions like heart failure.6PubMed Central. Second heart sound splitting as an indicator of interventricular mechanical dyssynchrony using a novel splitting detection algorithm
Extra Heart Sounds That Are Not Always Innocent
Beyond the normal S1 and S2, two additional heart sounds can sometimes be heard: the third heart sound (S3) and the fourth heart sound (S4). Neither is part of the standard “lub-dub,” and their presence tells you something specific about how the ventricle is handling blood during diastole.
S3 occurs during the rapid filling phase of diastole, shortly after the mitral valve opens. Research in animal models has demonstrated that it arises when a rush of incoming blood decelerates abruptly against the ventricular wall. The ventricle’s rising pressure reverses the transmitral pressure gradient, slamming the brakes on inflow, and that deceleration sets the ventricular wall vibrating.7JCI Insight. The genesis of the third and fourth heart sounds. A pressure-flow study in dogs In young, healthy people, an S3 can be normal because their ventricles fill rapidly and vigorously. In adults over about 40, an S3 is more concerning. Studies have found that patients with an audible S3 tend to have a higher and steeper rapid filling wave than normal adults, reflecting a ventricle that is overly compliant or volume-overloaded.8PubMed. Diastolic properties of the left ventricle in normal adults and in patients with third heart sounds An S3 in an older adult is a red flag for heart failure.
S4 occurs later in diastole, just before S1, during the atrial contraction phase. It arises from the same general mechanism as S3, deceleration of blood against the ventricular wall, but in this case the blood is being pushed by the atria rather than flowing passively. The fourth heart sound is thought to occur when atrial contraction drives blood into a ventricle that is abnormally stiff, producing a disproportionately sharp rise in end-diastolic pressure and the resulting vibration.9PubMed. Relationship of the fourth heart sound to atrial systolic transmitral flow deceleration Researchers have linked the S4 specifically to increased left ventricular end-diastolic stiffness, confirming the longstanding clinical suspicion that this sound indicates a ventricle that does not relax well.10PubMed Central. Association of the fourth heart sound with increased left ventricular end-diastolic stiffness Common causes include long-standing high blood pressure, aortic stenosis, and hypertrophic cardiomyopathy, all conditions that thicken or stiffen the ventricular wall.
Heart Murmurs and Turbulent Flow
Murmurs are different from heart sounds. Where S1 and S2 are brief, discrete events tied to valve closures, murmurs are sustained, whooshing or blowing sounds caused by turbulent blood flow. In a healthy resting person, turbulent flow is mostly limited to the area right around the aortic and pulmonary valves.11Clinical Hemorheology and Microcirculation. Clinical implications of turbulence in the cardiovascular system When flow becomes turbulent elsewhere, or when the degree of turbulence intensifies, a murmur becomes audible.
Research has demonstrated a direct, linear relationship between the energy in the turbulence and the energy in the resulting sound. When the power generated by turbulent flow exceeds a certain threshold, the murmur becomes audible through the chest wall, and louder turbulence produces a louder murmur on the traditional clinical grading scale.12PubMed. Turbulent blood flow in humans: its primary role in the production of ejection murmurs Conditions that generate murmurs include narrowed valves (stenosis), leaky valves (regurgitation), abnormal connections between chambers, and high-flow states like anemia or pregnancy where blood simply moves faster than usual through normal structures.
The timing of a murmur within the cardiac cycle is a critical diagnostic clue. A murmur heard during systole (between S1 and S2) could be an ejection murmur from a narrowed aortic or pulmonary valve, or a regurgitant murmur from a leaking mitral or tricuspid valve. A murmur heard during diastole (between S2 and the next S1) might point to aortic regurgitation or mitral stenosis. Some murmurs span the entire cycle. By placing the murmur in the correct phase and identifying where on the chest it is loudest, a clinician can narrow down the likely cause before any imaging is done.
How Exercise Reshapes the Cycle
When you start exercising, your heart rate climbs, and the cardiac cycle compresses. Both systole and diastole get shorter, but diastole takes the bigger hit. At rest, diastole might account for roughly two-thirds of each cycle. During intense exercise, it may shrink to less than half. In a healthy heart, this is manageable: the ventricle fills faster, the Frank-Starling mechanism ramps up contractile force, and cardiac output rises to meet the demand.
In a diseased heart, this compression of diastole can become a serious bottleneck. In patients with dilated cardiomyopathy, researchers have measured a progressive and disproportionate loss of diastolic time per beat as exercise intensity increases.13PubMed. Disproportionate shortening of left ventricular diastolic duration in patients with dilated cardiomyopathy A similar pattern appears in hypertrophic obstructive cardiomyopathy, where baseline abnormalities in the ratio of systolic to diastolic time worsen during exercise, restricting diastolic filling and impairing the heart’s efficiency.14PubMed. Effects of exercise on the duration of diastole and on interventricular phase differences in patients with hypertrophic cardiomyopathy For these patients, exercise intolerance is not just about a weak pump; it is partly about not having enough time between beats to fill the pump properly.
How Aging Alters the Cycle
Even in the absence of disease, aging gradually changes the mechanics of the cardiac cycle, particularly on the diastolic side. Relaxation slows. The time it takes for the ventricle to release its contraction and drop its internal pressure (the isovolumetric relaxation time) gets longer. The speed at which the mitral annulus moves during early filling decreases. These changes begin in early middle age and become most pronounced in people over 65.15PubMed Central. Effect of healthy aging on left ventricular relaxation and diastolic suction
The ventricle also becomes stiffer with age. There is a direct correlation between advancing age and increasing myocardial stiffness, and an inverse relationship between age and the rate of early filling.16PubMed. Age dependency of left ventricular diastolic function in pressure overload hypertrophy The heart compensates with a familiar trick: the atrial contraction becomes more vigorous, contributing a larger share of ventricular filling than it does in younger adults. In a young person, the rapid passive filling phase does most of the work. In an older person, the atrial kick picks up the slack, maintaining a normal total filling volume even though the pattern of filling has shifted.17European heart journal. Changes in cardiovascular function with aging
This compensation is effective but fragile. If an older person develops atrial fibrillation and loses the coordinated atrial contraction, the ventricle suddenly loses the filling mechanism it has come to depend on. That is one reason atrial fibrillation tends to cause more dramatic symptoms in elderly patients than in younger ones: their ventricles were already relying heavily on atrial systole to fill adequately.
Measuring Phase Timing With Imaging
In clinical practice, the phases of the cardiac cycle are not just conceptual. They are measured with precision using echocardiography and Doppler techniques. Specific time intervals, such as isovolumetric contraction time, ejection time, and isovolumetric relaxation time, can be quantified and combined into an index of overall cardiac performance called the myocardial performance index (MPI). Studies establishing normal values for these intervals have found that isovolumetric relaxation time and MPI both increase with age in both men and women. Interestingly, women generally exhibit slightly better cardiac function on these measures, with differences in isovolumetric contraction time, ejection time, and MPI between the sexes reaching statistical significance.18PLoS One. Normal Values of Cardiac Time Intervals by TDI M-Mode
These timing measurements are not just academic exercises. Changes in specific intervals can reveal problems before structural damage shows up on imaging. A prolonged isovolumetric relaxation time, for example, can be an early marker of diastolic dysfunction, even when the heart looks structurally normal and the ejection fraction is preserved. Cardiologists use these intervals alongside standard measures like ejection fraction and strain imaging to build a more complete picture of how well the heart is functioning throughout its entire cycle, not just during the contraction phase that gets the most public attention.
The Cardiac Cycle Before Birth
The fetal heart operates under fundamentally different rules. Before birth, the lungs are filled with fluid, not air, so the pulmonary circulation carries very little flow. The fetus has structural shortcuts, including the foramen ovale (a hole between the right and left atria) and the ductus arteriosus (a vessel connecting the pulmonary artery to the aorta), that allow most blood to bypass the lungs entirely.19PubMed Central. The Transitional Heart: From Early Embryonic and Fetal Development to Neonatal Life
At birth, the transition is dramatic. The baby’s first breaths expand the lungs, pulmonary vascular resistance plummets, and blood suddenly floods into the pulmonary circuit. The pressure dynamics between the left and right sides of the heart reverse, and the fetal shunts begin to close. The foramen ovale is pushed shut by the new pressure differential, and the ductus arteriosus constricts in response to rising oxygen levels. Within hours to days, the newborn’s cardiac cycle starts to resemble the adult pattern, with fully separated right and left circulations. This transition is one of the more remarkable feats of human physiology, essentially rewiring the plumbing of the heart while it continues to beat.
The Stethoscope’s Two Centuries
Before 1816, physicians assessed the heart by pressing an ear directly to the patient’s chest. That changed when René Laënnec, examining a young woman with suspected heart disease, rolled a sheet of paper into a tube and discovered he could hear internal sounds far more clearly through it. That improvised tube became the stethoscope, and Laënnec went on to describe heart and lung sounds in extraordinary detail, correlating what he heard during life with what he found at autopsy.20PubMed Central. The first 200 years of cardiac auscultation and future perspectives
Two centuries later, auscultation remains a first-line diagnostic tool despite the availability of echocardiography, cardiac MRI, and digital sound analysis. A skilled clinician can identify valve disease, heart failure, and congenital abnormalities in seconds with a stethoscope, often triaging patients who need urgent imaging from those who do not. Digital stethoscopes and machine-learning algorithms that classify heart sounds are beginning to extend this capability, particularly in settings where echocardiography is not readily available. The acoustic fingerprint of the cardiac cycle, those vibrations set off by valve closures and turbulent flow, remains one of the most information-dense signals a clinician can access at the bedside.
Cardiac Cycles Across Species
The human cardiac cycle is just one version of a pattern shared across mammals, but the timing varies enormously with body size and habitat. Electrocardiographic studies comparing marine and terrestrial mammals have found that heart-rate scaling with body mass follows roughly the same power law across species, but the internal timing of the cycle differs in interesting ways. Marine mammals, for instance, have slower atrial and ventricular depolarization (longer P-waves and QRS intervals) but faster ventricular repolarization (shorter QT intervals) compared to terrestrial mammals of similar size.21PubMed Central. Electrocardiographic Scaling Reveals Differences in Electrocardiogram Interval Durations Between Marine and Terrestrial Mammals These differences likely reflect adaptations to diving, where the heart must function efficiently during prolonged breath-holds and dramatic swings in oxygen delivery.
At the extremes, a blue whale’s heart beats roughly five to six times per minute during a deep dive, with each cardiac cycle lasting around ten seconds. A hummingbird’s heart, by contrast, can exceed 1,200 beats per minute in flight, compressing the entire systole-diastole sequence into a tiny fraction of a second. The basic architecture of the cycle, contraction followed by relaxation, valves opening and closing, blood ejected and then refilled, is conserved. What varies is the tempo and the relative duration of each phase, tuned by evolution to match each species’ metabolic demands and environmental pressures.