Cardiac Cycle Phases: Systole, Diastole & Heart Sounds

The cardiac cycle is the complete sequence of mechanical and electrical events that occurs from the beginning of one heartbeat to the beginning of the next. Each cardiac cycle lasts approximately 0.8 seconds at a resting heart rate of 75 beats per minute, and it encompasses every contraction and relaxation phase of the atria and ventricles. Understanding the cardiac cycle is essential for students of anatomy, physiology, cardiology, and nursing, as it forms the basis for interpreting heart sounds, electrocardiograms, and hemodynamic measurements.

At its core, the cardiac cycle can be divided into two major periods: systole and diastole. Systole refers to the phase of ventricular contraction, during which blood is ejected from the ventricles into the pulmonary artery and aorta. Diastole refers to the phase of ventricular relaxation, during which the ventricles fill with blood from the atria. While these two terms capture the broad strokes, the cardiac cycle phases are more nuanced, involving distinct sub-phases that describe precise valve movements, pressure changes, and volume shifts within the heart chambers.

The cardiac cycle is driven by the intrinsic electrical conduction system of the heart, beginning with the sinoatrial (SA) node, which generates spontaneous action potentials. These electrical impulses propagate through the atria, the atrioventricular (AV) node, the bundle of His, and the Purkinje fibers, coordinating the sequential contraction of atrial and ventricular muscle. The mechanical events of the cardiac cycle are therefore tightly coupled to the electrical events recorded on an ECG, making the cardiac cycle a cornerstone concept in cardiovascular physiology.

The cardiac cycle phases can be broken down into seven distinct sub-phases that describe the precise mechanical events occurring in the heart. Understanding each phase in order is crucial for mastering hemodynamics and interpreting clinical findings.

Phase 1: Atrial Systole. The cardiac cycle begins with atrial contraction, triggered by the P wave on the ECG. The atria contract and push the final 20-30% of blood into the ventricles, a contribution sometimes called the "atrial kick." The AV valves (mitral and tricuspid) are open during this phase, and the semilunar valves (aortic and pulmonic) are closed. Phase 2: Isovolumetric Contraction. Once the ventricles begin to contract (following the QRS complex), pressure rises rapidly inside the ventricles. Both the AV valves and the semilunar valves are closed during this brief phase, meaning ventricular volume does not change. This phase marks the very beginning of systole.

Phase 3: Rapid Ventricular Ejection. When ventricular pressure exceeds the pressure in the aorta and pulmonary artery, the semilunar valves open, and blood is ejected forcefully. Approximately two-thirds of the stroke volume is expelled during this rapid ejection phase. Phase 4: Reduced Ventricular Ejection. Ejection slows as the pressure gradient between the ventricles and the great arteries diminishes. The T wave appears on the ECG during this phase, indicating ventricular repolarization.

Phase 5: Isovolumetric Relaxation. After the semilunar valves close (marking the end of systole), the ventricles relax, but the AV valves have not yet opened. All four valves are closed, and ventricular volume remains constant while pressure drops sharply. Phase 6: Rapid Ventricular Filling. When ventricular pressure falls below atrial pressure, the AV valves open, and blood rushes passively from the atria into the ventricles. This phase accounts for about 70-80% of ventricular filling during diastole. Phase 7: Reduced Ventricular Filling (Diastasis). Filling slows as the pressure gradient between atria and ventricles equilibrates. The cycle then repeats with the next atrial systole.

Heart sounds are the audible vibrations produced by the closure of heart valves during the cardiac cycle. The two primary heart sounds, S1 and S2, are fundamental to cardiac auscultation and serve as clinical landmarks for the timing of systole and diastole. Understanding the origin and timing of heart sounds is a core competency for medical students, nurses, and allied health professionals.

S1, the first heart sound, is produced by the closure of the atrioventricular valves (mitral and tricuspid) at the onset of ventricular systole. It corresponds to the beginning of isovolumetric contraction and is best heard at the apex of the heart. S1 is often described as a "lub" sound and has a lower pitch and longer duration than S2. The mitral component of S1 typically precedes the tricuspid component slightly, though this split is usually inaudible under normal conditions.

S2, the second heart sound, is produced by the closure of the semilunar valves (aortic and pulmonic) at the end of ventricular systole. It marks the transition from systole to diastole and is best heard at the base of the heart. S2 is described as a "dub" sound and is higher-pitched and shorter than S1. Physiological splitting of S2 occurs during inspiration, when increased venous return to the right heart delays pulmonic valve closure relative to aortic valve closure. The familiar "lub-dub" rhythm of S1 S2 defines the audible cardiac cycle and helps clinicians identify the boundaries between systole and diastole.

In addition to S1 and S2, two other heart sounds may be heard in certain clinical contexts. S3 is a low-pitched sound occurring during rapid ventricular filling in early diastole. In young adults, S3 may be a normal finding, but in older patients, it often indicates heart failure with volume overload. S4 is a late diastolic sound produced by atrial contraction against a stiff, non-compliant ventricle. S4 is always considered pathological in adults and suggests conditions such as ventricular hypertrophy or ischemic heart disease.

The pressure-volume (PV) loop is a graphical representation of the cardiac cycle phases that plots left ventricular pressure against left ventricular volume throughout one complete heartbeat. PV loops are indispensable tools for understanding cardiac mechanics, as they integrate the concepts of preload, afterload, contractility, and stroke volume into a single visual framework.

The PV loop begins at the bottom-right corner, where the ventricle is fully relaxed and filled with blood (end-diastolic volume). As isovolumetric contraction begins, pressure rises sharply along a vertical line because the volume does not change while all valves are closed. When ventricular pressure exceeds aortic pressure, the aortic valve opens, and the ejection phase begins. During ejection, the loop moves leftward and upward as volume decreases and pressure initially continues to rise. The peak of the loop corresponds to peak systolic pressure.

As ejection ends and the aortic valve closes, isovolumetric relaxation begins. Pressure drops rapidly along a second vertical line with no change in volume, bringing us to the bottom-left corner of the loop, which represents end-systolic volume. When ventricular pressure drops below atrial pressure, the mitral valve opens, and the filling phase carries the loop back toward the right along the bottom, completing the cycle. The width of the PV loop represents the stroke volume, which is the difference between end-diastolic volume and end-systolic volume.

Changes in cardiac cycle conditions shift the PV loop in predictable ways. Increased preload stretches the ventricle further during diastole, shifting the loop to the right and increasing stroke volume. Increased afterload requires the ventricle to generate more pressure before the aortic valve opens, making the loop taller and narrower. Enhanced contractility increases the rate and force of pressure development during systole, shifting the end-systolic pressure-volume relationship upward and to the left. These PV loop alterations are clinically relevant for understanding conditions such as heart failure, hypertension, and valvular disease, where the normal cardiac cycle is disrupted.

A thorough understanding of the cardiac cycle is directly applicable to clinical medicine, where deviations from normal hemodynamics underlie a wide range of cardiovascular diseases. Clinicians rely on knowledge of the cardiac cycle phases to interpret heart sounds, diagnose valvular disorders, and understand the pathophysiology of heart failure, arrhythmias, and shock.

Valvular heart disease provides a clear illustration of how disruptions in the cardiac cycle produce clinical findings. In aortic stenosis, the aortic valve does not open fully during systole, creating a harsh systolic murmur and increasing the afterload on the left ventricle. In mitral regurgitation, the mitral valve fails to close completely during systole, allowing blood to flow backward into the left atrium and producing a holosystolic murmur heard best at the apex. Both conditions alter the normal pattern of systole and diastole and can ultimately lead to heart failure if untreated.

Arrhythmias disrupt the normal timing of the cardiac cycle. Atrial fibrillation eliminates the organized atrial kick, reducing ventricular filling and cardiac output by up to 25%. Ventricular tachycardia shortens diastole so severely that filling time is inadequate, leading to decreased stroke volume and potential hemodynamic collapse. Understanding how these rhythm disturbances alter the cardiac cycle phases helps clinicians predict symptoms and guide treatment.

Heart failure represents a state in which the cardiac cycle cannot meet the metabolic demands of the body. In systolic heart failure (heart failure with reduced ejection fraction), the ventricle contracts weakly during systole, reducing stroke volume and ejection fraction. In diastolic heart failure (heart failure with preserved ejection fraction), the ventricle is stiff and does not relax properly during diastole, impairing filling. Both forms can be understood through the lens of altered PV loops and abnormal cardiac cycle dynamics. Familiarity with the cardiac cycle enables clinicians to select appropriate therapies, whether medications that reduce afterload, devices that restore normal rhythm, or surgical interventions that repair damaged valves.

The cardiac cycle is one of the most frequently tested topics in anatomy, physiology, and medical board examinations such as the USMLE and MCAT. Its complexity arises from the simultaneous mechanical, electrical, and hemodynamic events that must be understood together rather than in isolation. Here are strategies for studying the cardiac cycle phases effectively.

First, learn the cardiac cycle as a sequence of valve events. The opening and closing of valves dictate the transitions between phases. Create a table with columns for each phase, listing which valves are open, which are closed, what is happening to ventricular pressure, and what is happening to ventricular volume. This systematic approach ensures you can reconstruct the entire cycle from first principles rather than relying on memorization.

Second, master the Wiggers diagram. The Wiggers diagram is a composite graph that plots atrial pressure, ventricular pressure, aortic pressure, ventricular volume, the ECG, and heart sounds on a shared time axis. Drawing the Wiggers diagram by hand and labeling each cardiac cycle phase is one of the most effective study techniques for integrating all the moving parts. Pay special attention to the timing of S1 S2 relative to the ECG and pressure tracings, as this is a common exam question.

Third, use clinical correlations to anchor your understanding. For each phase of the cardiac cycle, ask yourself: what happens if this phase is disrupted? For example, what occurs during systole in aortic stenosis? What happens during diastole in mitral stenosis? Linking physiology to pathology makes the material more memorable and clinically relevant.

Finally, leverage active recall and spaced repetition tools. Platforms like LectureScribe can generate flashcards and practice questions from your cardiac cycle lecture notes, allowing you to test yourself on heart sounds, pressure tracings, and cardiac cycle phases repeatedly over time. The combination of visual learning, clinical integration, and self-testing will prepare you to answer even the most challenging cardiac cycle questions on any examination.