The cardiac cycle is the continuous, rhythmic sequence of mechanical and electrical events that occurs during a single heartbeat. This process ensures the unidirectional flow of blood from the body and lungs, through the heart chambers, and back into the circulatory systems. The cycle’s purpose is to efficiently circulate blood, delivering oxygen and nutrients while removing metabolic waste. A typical cycle lasts approximately 0.8 seconds at a resting heart rate of 75 beats per minute. This highly regulated process involves precise changes in pressure and volume within the heart’s four chambers, allowing the heart to function as an effective pump.
Foundational Concepts: Systole, Diastole, and Valve Action
The cardiac cycle is fundamentally divided into two main states: systole and diastole. Systole refers to the period of contraction, during which the heart muscle tightens to push blood out of the chambers. Diastole, conversely, is the relaxation phase, allowing the chambers to expand and refill with blood. At a normal resting rate, diastole occupies roughly two-thirds of the total cycle duration, emphasizing the importance of filling time.
The actions of four distinct valves control the path of blood flow during these two states. The Atrioventricular (AV) valves (tricuspid and mitral) lie between the atria and the ventricles, preventing backflow into the atria during ventricular contraction. The Semilunar valves (aortic and pulmonary) sit between the ventricles and the major arteries. These valves prevent backflow from the arteries into the ventricles during relaxation. The coordinated opening and closing of these valves is driven entirely by pressure differences.
The Sequential Breakdown of the 5 Phases
Phase 1: Atrial Systole
The cardiac cycle begins with atrial systole. This phase occurs at the end of ventricular diastole, as the atria contract following electrical depolarization. The contraction forces the remaining blood from the atria into the relaxed ventricles through the open AV valves. While the ventricles are already 70–80% full from passive flow, this atrial “kick” contributes the final 20–30% of blood volume.
Phase 2: Isovolumetric Contraction
Immediately following atrial systole, the ventricles begin to contract, initiating isovolumetric contraction. As ventricular pressure quickly exceeds the pressure in the relaxed atria, the AV valves snap shut, producing the first heart sound (S1). Since ventricular pressure is still lower than the pressure in the aorta and pulmonary artery, the semilunar valves remain closed. With all four valves closed, the volume of blood inside the ventricle is fixed, but muscle contraction causes a sharp spike in intraventricular pressure. This brief phase builds the necessary force to overcome the arterial pressure.
Phase 3: Ventricular Ejection
Ventricular ejection begins when ventricular pressure surpasses the pressure in the great arteries (approximately 80 mmHg in the aorta). The semilunar valves are forced open, and blood is rapidly pushed into the aorta and pulmonary artery. Ejection is initially rapid, driven by the maximal force of contraction, followed by a slower, reduced ejection as the muscle repolarizes. The AV valves remain closed throughout this phase to prevent backflow into the atria. The left ventricle achieves a much higher peak pressure (up to 120 mmHg) than the right ventricle (up to 25 mmHg) because it pumps against systemic pressure.
Phase 4: Isovolumetric Relaxation
Once ventricular repolarization is complete, the ventricles begin to relax, and their internal pressure falls below the pressure in the aorta and pulmonary artery. This pressure reversal causes blood in the arteries to flow back toward the heart, forcing the semilunar valves to close and creating the second heart sound (S2). With all four valves momentarily closed, the volume of blood in the ventricles is fixed. This isovolumetric relaxation allows the ventricular muscle to drop its pressure rapidly, preparing for the next filling cycle.
Phase 5: Ventricular Filling
Ventricular filling begins when the pressure inside the relaxing ventricles falls below the pressure in the atria. This pressure gradient causes the AV valves to open, allowing blood that has collected in the atria to rush into the ventricles. This initial rush is termed rapid filling and accounts for the majority of the ventricular volume. As filling continues, the rate slows down, entering a period called diastasis or reduced filling. The cycle then concludes with atrial systole (Phase 1), which contributes the final volume before the next contraction.
Understanding Pressure and Volume Dynamics
The efficiency of the cardiac cycle is quantified by specific volume measurements, which are influenced by pressure changes throughout the five phases. End-Diastolic Volume (EDV) is the maximum volume of blood present in the ventricle at the end of the filling phase, typically around 130 milliliters in a resting adult. Conversely, End-Systolic Volume (ESV) is the volume of blood remaining in the ventricle immediately after ejection, usually about 50 to 60 milliliters.
The difference between these two values is the Stroke Volume (SV), which represents the amount of blood ejected by the ventricle in a single beat. For example, a ventricle with an EDV of 130 mL and an ESV of 60 mL has a Stroke Volume of 70 mL. Pressure gradients are the fundamental forces that drive these volume changes.
A subtle pressure fluctuation, the dicrotic notch, is visible in the aortic pressure tracing during isovolumetric relaxation. This small upward deflection is caused by the momentary backward flow of blood toward the heart as the aortic valve snaps shut. The dicrotic notch marks the end of systole and the beginning of diastole in the large arteries.