Ventricular Systole
Ventricular systole is the phase of the cardiac cycle during which the right and left ventricles contract, first raising intraventricular pressure during isovolumetric contraction and then ejecting blood through the pulmonary and aortic valves.
Ventricular systole is the phase of the cardiac cycle during which the right and left ventricles contract. It begins shortly after ventricular depolarization and includes two major mechanical phases: isovolumetric contraction and ventricular ejection.
During isovolumetric contraction, ventricular pressure rises rapidly while all four cardiac valves are closed. When ventricular pressure exceeds the pressure in the pulmonary trunk and aorta, the semilunar valves open and blood is ejected from the right and left ventricles.
Ventricular systole converts the electrical activation of the ventricular myocardium into the mechanical pressure required to propel blood through the pulmonary and systemic circulations.
Position in the Cardiac Cycle
Ventricular systole follows ventricular filling and atrial systole. At the end of diastole, the ventricles contain their end-diastolic volume.
Ventricular depolarization then initiates excitation-contraction coupling, causing ventricular pressure to rise and beginning the mechanical systolic phase.
Major Phases
| Phase | Major Event |
|---|---|
| Isovolumetric contraction | Ventricular pressure rises while all valves are closed |
| Rapid ejection | Semilunar valves open and ventricular outflow is greatest |
| Reduced ejection | Ejection continues at a declining rate as ventricular contraction wanes |
Electrical Initiation
Ventricular systole is preceded by electrical activation of the ventricular myocardium.
After conduction through the atrioventricular node, the impulse travels through the atrioventricular bundle, bundle branches, and Purkinje network.
His-Purkinje System
The specialized ventricular conduction system distributes electrical excitation rapidly throughout the ventricles.
This coordinated activation helps the ventricular myocardium contract in an organized manner suitable for efficient ejection.
Ventricular Depolarization
Ventricular depolarization spreads rapidly through the myocardium and triggers contraction of ventricular cardiomyocytes.
The electrical event occurs before the full mechanical development of ventricular pressure.
QRS Complex
The QRS complex on the electrocardiogram represents ventricular depolarization.
Mechanical ventricular systole begins shortly after the onset of ventricular electrical activation.
Electrical and Mechanical Events
| Electrical Event | Mechanical Relationship |
|---|---|
| QRS complex | Ventricular depolarization followed by contraction |
| ST segment | Ventricular myocardium remains depolarized during much of ejection |
| T wave | Ventricular repolarization occurs as systole approaches completion |
Excitation-Contraction Coupling
Depolarization of ventricular cardiomyocytes opens voltage-dependent calcium channels in the cell membrane and transverse tubules.
Calcium entry promotes additional calcium release from the sarcoplasmic reticulum, increasing cytosolic calcium and initiating interaction between actin and myosin.
Calcium and Contraction
Calcium binds to troponin C, allowing the contractile proteins to generate force.
The coordinated development of force throughout the ventricular myocardium raises intraventricular pressure.
Isovolumetric Contraction
Isovolumetric contraction is the first mechanical phase of ventricular systole.
It begins when rising ventricular pressure closes the atrioventricular valves and ends when ventricular pressure becomes high enough to open the semilunar valves.
Closure of the Atrioventricular Valves
The mitral valve closes when left ventricular pressure exceeds left atrial pressure.
The tricuspid valve closes when right ventricular pressure exceeds right atrial pressure.
First Heart Sound
Closure and tensioning of the atrioventricular valve apparatus and associated cardiovascular structures at the onset of ventricular systole contribute to the first heart sound (S1).
S1 therefore occurs near the beginning of isovolumetric contraction.
Valve Status During Isovolumetric Contraction
All four cardiac valves are closed during isovolumetric contraction.
Because blood can neither enter nor leave the ventricles, ventricular volume remains essentially constant while pressure rises rapidly.
End-Diastolic Volume
The ventricular volume at the beginning of systole is the end-diastolic volume (EDV).
EDV is determined by ventricular filling during the preceding diastole and is an important determinant of preload.
Preload
Preload reflects myocardial fiber stretch before contraction and is related to ventricular filling conditions.
Within physiological limits, greater preload can increase the force of ventricular contraction through the Frank-Starling mechanism.
Rise in Ventricular Pressure
During isovolumetric contraction, left and right ventricular pressures rise steeply.
The left ventricle must generate enough pressure to exceed aortic pressure, while the right ventricle must exceed pulmonary arterial pressure.
Opening of the Semilunar Valves
When left ventricular pressure exceeds aortic pressure, the aortic valve opens.
When right ventricular pressure exceeds pulmonary trunk pressure, the pulmonary valve opens.
Ventricular Ejection
Opening of the semilunar valves begins the ventricular ejection phase.
Blood moves from the ventricles into the pulmonary trunk and aorta as long as the appropriate pressure gradients support forward flow.
Rapid Ejection
Early in the ejection phase, blood leaves the ventricles rapidly.
Ventricular and arterial pressures rise toward their peak values while ventricular volume decreases substantially.
Reduced Ejection
Later in systole, the rate of ventricular ejection decreases.
Ventricular contraction begins to decline, ventricular pressure eventually falls, and ventricular repolarization occurs during this period.
Right Ventricular Systole
Right ventricular contraction propels blood through the pulmonary valve into the pulmonary trunk and pulmonary circulation.
The right ventricle operates against the relatively low resistance of the pulmonary vascular system.
Left Ventricular Systole
Left ventricular contraction propels blood through the aortic valve into the aorta and systemic circulation.
Because systemic vascular resistance and arterial pressure are substantially greater than those in the pulmonary circulation, the left ventricle must generate much higher systolic pressure.
Ventricular Wall Thickness
The left ventricular myocardium is considerably thicker than the right ventricular myocardium.
This anatomical difference reflects the greater pressure required to eject blood through the systemic circulation.
Pressure Differences Between Ventricles
| Ventricle | Outflow | Pressure Requirement |
|---|---|---|
| Right ventricle | Pulmonary trunk | Relatively low |
| Left ventricle | Aorta | Substantially higher |
Valve Status During Ejection
During ventricular ejection, the aortic and pulmonary valves are open.
The mitral and tricuspid valves remain closed, preventing backward movement of blood into the atria.
Valve Status During Ventricular Systole
| Phase | Mitral and Tricuspid Valves | Aortic and Pulmonary Valves |
|---|---|---|
| Isovolumetric contraction | Closed | Closed |
| Ventricular ejection | Closed | Open |
Papillary Muscles
The papillary muscles contract during ventricular systole along with the ventricular myocardium.
Through the chordae tendineae, they help prevent the atrioventricular valve leaflets from prolapsing excessively into the atria as ventricular pressure rises.
Chordae Tendineae
Chordae tendineae are fibrous cords connecting atrioventricular valve leaflets to papillary muscles.
They do not pull the valves open or closed. Instead, they stabilize the valve leaflets during ventricular contraction.
Atrial Filling During Ventricular Systole
While the atrioventricular valves are closed, venous blood continues to return to the atria.
The right atrium receives systemic venous blood, while the left atrium receives pulmonary venous blood.
V Wave
Progressive atrial filling during ventricular systole contributes to the v wave of the atrial pressure tracing.
When ventricular pressure later falls below atrial pressure, the atrioventricular valves open and accumulated atrial blood flows into the ventricles.
Stroke Volume
Stroke volume is the volume of blood ejected by one ventricle during a cardiac cycle.
It can be expressed as the difference between end-diastolic volume and end-systolic volume.
Stroke Volume Relationship
| Variable | Meaning |
|---|---|
| End-diastolic volume | Ventricular volume immediately before systole |
| End-systolic volume | Ventricular volume remaining after ejection |
| Stroke volume | EDV minus ESV |
End-Systolic Volume
The blood remaining in a ventricle after systolic ejection is the end-systolic volume (ESV).
ESV is influenced by ventricular contractility, afterload, and the initial filling conditions of the ventricle.
Ejection Fraction
Ejection fraction is the fraction of end-diastolic ventricular volume ejected during systole.
For the left ventricle, it is commonly used as one measure of systolic pumping performance, although it does not describe every aspect of ventricular function.
Contractility
Contractility refers to the intrinsic ability of the myocardium to develop force at a given loading condition.
Increased contractility generally enhances ventricular emptying and can reduce end-systolic volume.
Sympathetic Stimulation
Sympathetic stimulation increases ventricular contractility through beta-adrenergic signaling.
Increased intracellular calcium availability allows the myocardium to develop greater force during systole.
Afterload
Afterload describes the load against which the ventricle contracts and ejects blood.
For the left ventricle, arterial pressure and systemic vascular properties are major contributors to afterload. The right ventricle ejects against the pulmonary circulation.
Increased Afterload
When afterload increases acutely, the ventricle must generate greater pressure before and during ejection.
If other factors remain unchanged, greater afterload can reduce the amount of blood ejected and increase end-systolic volume.
Frank-Starling Mechanism
The Frank-Starling mechanism helps match ventricular output to venous return.
Within physiological limits, greater ventricular filling increases myocardial fiber stretch and can increase the force of the subsequent systolic contraction.
Determinants of Stroke Volume
| Determinant | General Influence |
|---|---|
| Preload | Greater physiological filling can increase stroke volume |
| Contractility | Greater contractility tends to increase stroke volume |
| Afterload | Greater afterload tends to oppose ventricular ejection |
Aortic Pressure During Systole
Blood ejected from the left ventricle distends the aorta and raises aortic pressure.
The elastic properties of the aorta allow part of the energy of ventricular ejection to be stored in the arterial wall and released during diastole.
Pulmonary Arterial Pressure
Right ventricular ejection raises pressure in the pulmonary trunk and pulmonary arteries.
Pulmonary arterial pressure remains substantially lower than systemic arterial pressure under normal conditions.
Arterial Pulse
Left ventricular ejection generates a pressure wave that propagates through the systemic arterial tree.
This pressure wave produces the arterial pulse that can be palpated at superficial arteries.
Systolic Blood Pressure
Systolic blood pressure is the peak arterial pressure reached during the cardiac cycle.
It is influenced by stroke volume, arterial compliance, the rate of ventricular ejection, and other cardiovascular factors.
Ventricular Repolarization
As systole progresses, ventricular cardiomyocytes begin to repolarize.
Repolarization is represented primarily by the T wave and is followed by declining active tension and ventricular relaxation.
End of Ventricular Ejection
As ventricular pressure falls, forward flow through the semilunar valves slows.
When arterial pressure exceeds ventricular pressure, the aortic and pulmonary valves close.
Second Heart Sound
Closure of the aortic and pulmonary valves contributes to the second heart sound (S2).
This event marks the end of ventricular ejection and the transition into ventricular diastole.
Dicrotic Notch
Aortic valve closure produces a small feature in the aortic pressure tracing called the dicrotic notch, or incisura.
It reflects transient changes in pressure and flow associated with closure of the aortic valve.
Transition to Isovolumetric Relaxation
After the semilunar valves close, the ventricles begin isovolumetric relaxation.
All valves are again closed, ventricular pressure falls rapidly, and ventricular volume remains at end-systolic volume until the atrioventricular valves open.
Pressure-Volume Relationship
Ventricular systole can be represented on a pressure-volume loop by isovolumetric pressure development followed by ejection.
These relationships provide a useful framework for understanding ventricular loading conditions and mechanical performance.
Isovolumetric Contraction on the Pressure-Volume Loop
During isovolumetric contraction, ventricular pressure rises vertically on a pressure-volume representation because volume remains essentially constant.
The phase ends when ventricular pressure becomes sufficient to open the outflow valve.
Ejection on the Pressure-Volume Loop
During ejection, ventricular volume decreases as blood leaves the chamber.
Pressure initially rises and then falls as the ventricle progresses through systole.
Cardiac Work
The ventricles perform mechanical work by generating pressure and ejecting blood.
The left ventricle performs substantially greater pressure work than the right ventricle because it pumps against the higher resistance and pressure of the systemic circulation.
Myocardial Oxygen Demand
Ventricular contraction requires substantial energy and oxygen.
Myocardial oxygen demand is influenced by heart rate, contractility, wall stress, ventricular pressure, and ventricular dimensions.
Coronary Blood Flow and Systole
Contraction of the left ventricular myocardium compresses intramyocardial coronary vessels during systole.
For this reason, perfusion of much of the left ventricular myocardium is favored during diastole.
Clinical Significance
Systolic Dysfunction
Systolic dysfunction occurs when the ventricle has impaired ability to generate force or eject blood effectively.
This can reduce stroke volume and may increase end-systolic and end-diastolic volumes.
Heart Failure With Reduced Ejection Fraction
Heart failure with reduced ejection fraction is characterized by impaired left ventricular systolic performance and a reduced proportion of end-diastolic blood being ejected.
Its causes include several forms of myocardial injury and chronic ventricular remodeling.
Myocardial Infarction
Myocardial infarction can destroy or impair contracting ventricular myocardium.
The resulting reduction in regional or global contractile function can decrease systolic performance.
Aortic Stenosis
Aortic stenosis creates an obstruction between the left ventricle and aorta during systole.
The left ventricle must generate elevated pressure to eject blood through the narrowed valve.
Pulmonary Stenosis
Pulmonary stenosis obstructs right ventricular outflow during systole.
This increases the pressure required for right ventricular ejection.
Mitral Regurgitation
In mitral regurgitation, the mitral valve does not prevent backward flow during ventricular systole.
Part of the left ventricular stroke volume can therefore move into the left atrium instead of entering the aorta.
Tricuspid Regurgitation
Tricuspid regurgitation allows backward flow from the right ventricle into the right atrium during systole.
Severe regurgitation can produce prominent systolic pressure waves in the systemic venous circulation.
Ventricular Septal Defect
A ventricular septal defect creates an abnormal communication between the ventricles.
During systole, the pressure difference between the ventricles can drive abnormal blood flow across the defect.
Hypertension
Systemic hypertension increases the pressure against which the left ventricle must eject.
Chronic pressure loading can contribute to left ventricular hypertrophy and changes in both systolic and diastolic function.
Key Features of Ventricular Systole
| Feature | Key Point |
|---|---|
| Electrical precursor | Ventricular depolarization represented by the QRS complex |
| Initial phase | Isovolumetric contraction |
| AV valves | Closed during ventricular systole |
| Semilunar valves | Open during ventricular ejection |
| Beginning volume | End-diastolic volume |
| Ending volume | End-systolic volume |
| Volume ejected | Stroke volume |
| Beginning heart sound | S1 near AV valve closure |
| Ending heart sound | S2 near semilunar valve closure |
Anatomical and Physiological Importance
Ventricular systole is the mechanical pumping phase that generates the pressure required to move blood through the pulmonary and systemic circulations. Rapid electrical conduction through the ventricular conduction system coordinates activation of the myocardium, while calcium-dependent excitation-contraction coupling converts this electrical signal into force.
The atrioventricular valves remain closed throughout ventricular systole, while the semilunar valves open only after ventricular pressure exceeds pressure in the great arteries. This pressure-dependent valve sequence ensures that ventricular contraction produces predominantly forward blood flow.
The effectiveness of ventricular systole depends on preload, myocardial contractility, afterload, valve competence, ventricular geometry, and coordinated electrical activation. Disturbance of any of these factors can impair stroke volume and cardiac output, demonstrating the close relationship between cardiac anatomy, electrical conduction, and mechanical pumping function.
Last updated on September 29, 2026