Ventricular Systole and the Ejection Phase

The heart is a dynamic organ whose primary function is to pump blood efficiently throughout the body. This pumping occurs in a coordinated cycle known as the cardiac cycle, which consists of alternating phases of contraction (systole) and relaxation (diastole). Ventricular systole, in particular, is the period during which the ventricles contract, generating sufficient pressure to eject blood into the systemic and pulmonary circulations. The ejection phase is a critical part of ventricular systole, responsible for propelling oxygenated blood from the left ventricle into the aorta and deoxygenated blood from the right ventricle into the pulmonary artery.

Understanding ventricular systole and the ejection phase is essential for students, clinicians, and researchers in cardiology, as abnormalities in these processes underlie numerous cardiac disorders such as heart failure, cardiomyopathy, and valvular diseases.

1. Introduction to Ventricular Systole

Ventricular systole refers to the period of the cardiac cycle when the ventricles contract. This contraction increases intraventricular pressure, resulting in the opening of semilunar valves and ejection of blood. It follows atrial systole and occurs simultaneously with isovolumetric contraction and the ejection phase.

Key objectives of ventricular systole include:

Generating enough pressure to overcome arterial resistance
Ensuring effective stroke volume
Maintaining forward flow to systemic and pulmonary circuits

1.1 Components of Ventricular Systole

Ventricular systole can be divided into two main phases:

Isovolumetric contraction phase
- Occurs immediately after the AV valves close
- Ventricles contract without a change in volume
- Ventricular pressure rises sharply
Ejection phase
- Begins when ventricular pressure exceeds aortic/pulmonary artery pressure
- Semilunar valves open, and blood is ejected into circulation

2. Electrical Events During Ventricular Systole

The mechanical contraction of the ventricles is initiated and coordinated by electrical events in the heart.

2.1 Action Potential of Ventricular Myocytes

Ventricular contraction is triggered by action potentials generated in the sinoatrial (SA) node, conducted via the atrioventricular (AV) node, and propagated through the His-Purkinje system.

The ventricular action potential has distinct phases:

Phase 0 (Depolarization): Rapid Na⁺ influx
Phase 1 (Initial repolarization): Transient K⁺ efflux
Phase 2 (Plateau phase): Ca²⁺ influx balanced with K⁺ efflux
Phase 3 (Repolarization): K⁺ efflux predominates
Phase 4 (Resting membrane potential): Na⁺/K⁺ ATPase restores resting potential

The plateau phase is particularly important because Ca²⁺ entry triggers excitation-contraction coupling, leading to ventricular contraction.

2.2 Electrocardiogram (ECG) Correlates

Ventricular systole corresponds to:

QRS complex: Ventricular depolarization
ST segment: Ventricular contraction and plateau of action potential
T wave: Ventricular repolarization (marks the end of systole)

The ECG allows clinicians to assess the timing, duration, and abnormalities of ventricular systole.

3. Mechanical Events of Ventricular Systole

Mechanical events translate electrical signals into forceful contraction and ejection of blood.

3.1 Isovolumetric Contraction

Immediately following AV valve closure (mitral and tricuspid valves):

Ventricular pressure rises rapidly
No change in ventricular volume occurs
Semilunar valves remain closed until pressure exceeds arterial pressure

This phase is brief (≈0.05 seconds) but crucial for generating sufficient pressure to open the aortic and pulmonary valves.

3.2 Ejection Phase

Once ventricular pressure surpasses the pressure in the aorta and pulmonary artery:

Semilunar valves open
Blood is rapidly ejected (rapid ejection phase) followed by slower ejection (reduced ejection phase)
Ventricular volume decreases, stroke volume is ejected, and pressure peaks
Duration: ~0.2–0.25 seconds for left ventricle under normal conditions

Left ventricular ejection: Into the aorta, systemic circulation
Right ventricular ejection: Into the pulmonary artery, pulmonary circulation

4. Pressure-Volume Relationships

Pressure-volume (P-V) loops are an essential tool for understanding ventricular systole and the ejection phase.

4.1 Phases on the P-V Loop

Isovolumetric contraction: Vertical rise in pressure with no volume change
Rapid ejection: Steep decline in ventricular volume, slight pressure increase
Reduced ejection: Slower volume decline, ventricular pressure gradually falls
Isovolumetric relaxation: Pressure falls rapidly, volume constant

4.2 Stroke Volume and Ejection Fraction

Stroke Volume (SV): Volume of blood ejected per beat SV=EDV−ESVSV = EDV – ESVSV=EDV−ESV Where EDV = end-diastolic volume, ESV = end-systolic volume
Ejection Fraction (EF): Fraction of EDV ejected EF=SVEDV×100EF = \frac{SV}{EDV} \times 100EF=EDVSV×100 Normal left ventricular EF: 55–70%
P-V loops show how increased contractility, afterload, or preload affects stroke volume and ejection efficiency.

5. Hemodynamic Considerations

The ejection phase is influenced by several hemodynamic factors:

5.1 Preload

Definition: Initial stretching of ventricular fibers at end-diastole
Effect: Higher preload increases stroke volume (Frank-Starling mechanism)

5.2 Afterload

Definition: Resistance the ventricle must overcome to eject blood (aortic/pulmonary pressure)
Effect: High afterload reduces stroke volume and prolongs ejection time

5.3 Contractility (Inotropy)

Definition: Intrinsic strength of ventricular contraction
Influence: Sympathetic stimulation, catecholamines, calcium availability
Effect: Increased contractility enhances stroke volume and ejection velocity

5.4 Heart Rate

Higher heart rate reduces diastolic filling time, which may influence preload and stroke volume
Ejection phase duration shortens at higher rates but contractility increases

6. Phases of Ejection in Detail

The ejection phase can be subdivided:

6.1 Rapid Ejection

Begins immediately after semilunar valve opening
Ventricular pressure exceeds arterial pressure
Accounts for the majority of stroke volume (~70%)
Peak aortic and pulmonary pressures are reached

6.2 Reduced Ejection

Occurs in the latter part of systole
Ventricular pressure gradually declines as contraction weakens
Stroke volume continues to decrease slowly
Marks transition toward isovolumetric relaxation

7. Role of Valves

7.1 Semilunar Valves

Aortic and Pulmonary Valves: Open when ventricular pressure exceeds arterial pressure
Ensure unidirectional blood flow
Prevent backflow during diastole

7.2 AV Valves

Mitral and Tricuspid Valves: Closed during systole to prevent regurgitation

Valve dysfunction, such as stenosis or regurgitation, significantly alters the ejection phase and hemodynamics.

8. Regulation of Ventricular Systole

8.1 Autonomic Nervous System

Sympathetic stimulation: Increases contractility, heart rate, and stroke volume
Parasympathetic stimulation: Slightly affects atria, minimal effect on ventricles

8.2 Hormonal Regulation

Catecholamines (adrenaline, noradrenaline) enhance contractility
Thyroid hormones increase heart rate and systolic performance

8.3 Intrinsic Regulation

Frank-Starling mechanism: Stretching myocardial fibers increases contraction strength
Afterload sensitivity: Ventricles adjust ejection based on arterial resistance

9. Clinical Implications

Understanding ventricular systole and ejection phase is vital for diagnosing and managing cardiovascular diseases.

9.1 Heart Failure

Systolic dysfunction: Impaired contractility reduces stroke volume and ejection fraction
Diastolic dysfunction: Ejection phase may be normal, but filling is impaired

9.2 Valvular Heart Disease

Aortic stenosis: Increased afterload prolongs ejection phase
Aortic regurgitation: Early systolic ejection may be compromised

9.3 Hypertension

Increased afterload reduces efficiency of ejection and increases myocardial oxygen demand

9.4 Arrhythmias

Ventricular systolic timing is altered in tachyarrhythmias, reducing stroke volume
ECG monitoring aids in assessing ejection phase abnormalities

10. Advanced Concepts

10.1 Ventricular-Vascular Coupling

The relationship between ventricular contractility and arterial compliance
Optimal coupling maximizes stroke work and efficiency

10.2 Myocardial Mechanics

Fiber orientation, torsion, and wall stress influence ejection efficiency
Left ventricular twist contributes to rapid ejection and diastolic recoil

10.3 Imaging and Measurement

Echocardiography: Measures stroke volume, ejection fraction, and wall motion
Cardiac MRI: Provides detailed volumetric and functional analysis
Hemodynamic monitoring: Invasive pressure catheters assess systolic pressure and ejection dynamics