Diastole

Diastole is the phase of the cardiac cycle during which cardiac muscle relaxes and the chambers of the heart fill with blood. The term can refer to relaxation of either the atria or ventricles, but in descriptions of the cardiac cycle, ventricular diastole is usually the principal focus.

Ventricular diastole begins after ventricular ejection as the ventricular myocardium relaxes. It includes isovolumetric relaxation, rapid ventricular filling, diastasis, and atrial systole. These phases allow ventricular pressure to fall and ventricular volume to increase in preparation for the next contraction.

Normal diastolic function depends on active myocardial relaxation, ventricular compliance, atrial pressure, venous return, intact atrioventricular valves, and sufficient time for filling.

Phases of Ventricular Diastole

Phase	Major Event
Isovolumetric relaxation	Ventricles relax while all valves are closed
Rapid filling	AV valves open and blood enters ventricles rapidly
Diastasis	Ventricular filling slows as atrial and ventricular pressures approach equilibrium
Atrial systole	Atrial contraction provides the final active contribution to ventricular filling

Beginning of Ventricular Diastole

Ventricular diastole follows ventricular systole. Near the end of systole, ventricular repolarization is represented primarily by the T wave on the electrocardiogram.

As ventricular contraction ends, ventricular pressure falls and the semilunar valves close.

Ventricular Repolarization

Repolarization restores the electrical state of ventricular cardiomyocytes after depolarization.

Mechanical relaxation follows the electrical recovery process, although electrical and mechanical events are not exactly simultaneous.

T Wave

The T wave represents ventricular repolarization.

It occurs near the end of ventricular systole and precedes complete mechanical relaxation of the ventricles.

Semilunar Valve Closure

As ventricular pressure falls below pressure in the aorta and pulmonary trunk, the aortic and pulmonary valves close.

This prevents significant backward flow from the great arteries into the ventricles.

Second Heart Sound

Closure of the aortic and pulmonary valves contributes to the second heart sound (S2).

S2 marks the transition from ventricular ejection to early ventricular diastole.

Isovolumetric Relaxation

Isovolumetric relaxation is the initial phase of ventricular diastole.

During this period, the semilunar valves have closed, but ventricular pressure has not yet fallen sufficiently for the atrioventricular valves to open.

Valve Status During Isovolumetric Relaxation

All four cardiac valves are closed during isovolumetric relaxation.

Because no blood enters or leaves the ventricles, ventricular volume remains essentially unchanged while pressure falls rapidly.

End-Systolic Volume

The volume remaining within a ventricle after ejection is the end-systolic volume.

Ventricular volume remains at approximately this level throughout isovolumetric relaxation.

Decline in Ventricular Pressure

As the ventricular myocardium relaxes, ventricular pressure decreases rapidly.

When ventricular pressure falls below atrial pressure, the atrioventricular valves open and ventricular filling begins.

Opening of the Atrioventricular Valves

The mitral valve opens when left ventricular pressure falls below left atrial pressure.

The tricuspid valve opens when right ventricular pressure falls below right atrial pressure.

Rapid Ventricular Filling

Opening of the atrioventricular valves begins the rapid filling phase.

Blood that accumulated in the atria during ventricular systole flows rapidly into the relaxed ventricles because of the atrioventricular pressure gradient.

Passive Ventricular Filling

Most ventricular filling under normal resting conditions occurs passively rather than through active atrial contraction.

Ventricular relaxation and the pressure gradient between the atria and ventricles allow blood to move through the open atrioventricular valves.

Ventricular Suction

Active ventricular relaxation and elastic recoil contribute to the rapid decline in ventricular pressure during early diastole.

These properties can enhance the atrioventricular pressure gradient and facilitate early ventricular filling.

Rapid Filling and Ventricular Volume

Ventricular volume rises quickly during early diastole.

Ventricular pressure remains relatively low despite this increase in volume when ventricular relaxation and compliance are normal.

Third Heart Sound

A third heart sound (S3) may occur during early rapid ventricular filling.

It can be physiological in children, adolescents, young adults, and some pregnant individuals, but in older adults it may be associated with increased filling volume or ventricular dysfunction depending on the clinical context.

Diastasis

After rapid filling, the rate of blood movement into the ventricles decreases. This slower phase is called diastasis.

Atrial and ventricular pressures become more similar, reducing the pressure gradient responsible for passive filling.

Duration of Diastasis

The duration of diastasis depends strongly on heart rate.

At slower heart rates it may occupy a substantial portion of diastole, while at faster rates it becomes markedly shortened.

Atrial Systole

Near the end of ventricular diastole, the atria contract.

This atrial systole provides an additional volume of blood to the ventricles before ventricular systole begins.

Atrial Kick

The additional ventricular filling produced by atrial contraction is often called the atrial kick.

Its relative importance increases in some conditions where ventricular relaxation or compliance is impaired.

End-Diastolic Volume

At the completion of ventricular filling, each ventricle contains its end-diastolic volume (EDV).

EDV represents the ventricular volume immediately before ventricular systole begins.

Preload

Ventricular filling during diastole determines an important component of preload.

Greater filling generally produces greater myocardial fiber stretch before contraction, within physiological limits.

Frank-Starling Mechanism

The Frank-Starling mechanism describes the relationship between ventricular filling and the force of subsequent contraction.

Within physiological limits, increased end-diastolic fiber length can increase the force developed during the following systole.

Valve Status During Diastole

Diastolic Phase	Mitral and Tricuspid Valves	Aortic and Pulmonary Valves
Isovolumetric relaxation	Closed	Closed
Rapid filling	Open	Closed
Diastasis	Open	Closed
Atrial systole	Open	Closed

Atrial Filling During Ventricular Systole

While the ventricles contract and the atrioventricular valves are closed, venous blood continues to enter the atria.

This produces progressive atrial filling and contributes to the pressure gradient that opens the atrioventricular valves when ventricular pressure falls sufficiently.

Atrial Pressure and the V Wave

Atrial filling while the atrioventricular valves are closed produces the v wave in atrial pressure tracings.

After the AV valves open, atrial pressure falls as blood empties into the ventricles.

Atrial Pressure Waves

Wave	Major Cause
a wave	Atrial contraction
c wave	Early ventricular systolic events and AV valve movement
v wave	Atrial filling while the AV valves are closed

Ventricular Compliance

Ventricular compliance describes the change in ventricular volume produced by a given change in filling pressure.

A highly compliant ventricle can accommodate an increase in volume with relatively little increase in pressure.

Reduced Ventricular Compliance

A stiff ventricle requires higher filling pressure to achieve a given end-diastolic volume.

Reduced compliance can therefore elevate atrial and venous pressures even when systolic contraction is preserved.

Myocardial Relaxation

Diastole is not simply a passive absence of contraction. Early ventricular relaxation is an active cellular process requiring energy.

Calcium must be removed from the cytosol and returned to intracellular stores or transported out of the cardiomyocyte so that actin-myosin interaction declines.

Calcium Handling During Relaxation

Removal of cytosolic calcium allows cardiac muscle fibers to relax.

ATP-dependent mechanisms, including calcium uptake by the sarcoplasmic reticulum, are important for efficient myocardial relaxation.

Lusitropy

Lusitropy refers to the relaxation properties of the myocardium.

Changes in lusitropy influence how rapidly ventricular pressure falls and therefore affect early diastolic filling.

Sympathetic Effects on Relaxation

Sympathetic stimulation can enhance myocardial relaxation as well as contraction.

Improved relaxation helps the ventricles fill efficiently even when heart rate is increased and diastolic time is shortened.

Coronary Perfusion During Diastole

Coronary blood flow, particularly to the left ventricular myocardium, is strongly favored during diastole.

During systole, contraction of the left ventricular myocardium compresses intramyocardial coronary vessels and limits flow, especially in the subendocardial region.

Left Coronary Flow

When the left ventricle relaxes during diastole, compression of intramyocardial vessels decreases.

Aortic pressure then drives blood through the coronary arteries into the myocardial microcirculation.

Aortic Diastolic Pressure

Aortic pressure does not immediately fall to zero after ventricular ejection because elastic recoil of the aortic wall maintains pressure during diastole.

This diastolic pressure is important for continued systemic and coronary perfusion between ventricular contractions.

Dicrotic Notch

Closure of the aortic valve produces a small feature in the aortic pressure tracing called the dicrotic notch, or incisura.

It marks the end of ventricular ejection and the beginning of the diastolic decline in aortic pressure.

Diastolic Blood Pressure

Diastolic blood pressure is the lowest arterial pressure reached during the cardiac cycle before the next ventricular ejection.

It is influenced by systemic vascular resistance, heart rate, arterial compliance, and the rate at which blood leaves the arterial system.

Heart Rate and Diastole

The duration of the cardiac cycle decreases as heart rate increases.

Diastole shortens proportionally more than systole, reducing the time available for ventricular filling and coronary perfusion.

Tachycardia

During tachycardia, shortened diastolic duration can reduce ventricular filling time.

Very rapid rates may also compromise coronary perfusion, particularly when myocardial oxygen demand is simultaneously increased.

Bradycardia

During bradycardia, diastole is prolonged.

This generally provides more time for passive ventricular filling, although cardiac output also depends on stroke volume and the number of cardiac cycles per minute.

Diastole and the ECG

ECG Event	Mechanical Relationship
T wave	Ventricular repolarization and transition toward relaxation
TP interval	Electrical baseline during much of ventricular filling
P wave	Atrial depolarization near the end of ventricular diastole

Diastole and Heart Sounds

Several clinically important heart sounds are related to events occurring at the beginning of or during diastole.

S2 is associated with semilunar valve closure, while S3 and S4, when present, occur during ventricular filling.

Heart Sounds During Diastole

Heart Sound	Timing	Association
S2	Beginning of ventricular diastole	Closure of aortic and pulmonary valves
S3	Early diastole	Rapid ventricular filling
S4	Late diastole	Atrial contraction against a relatively stiff ventricle

Diastolic Filling of the Right Ventricle

Right ventricular filling occurs when right ventricular pressure falls below right atrial pressure and the tricuspid valve opens.

Systemic venous return then passes from the right atrium into the right ventricle.

Diastolic Filling of the Left Ventricle

Left ventricular filling occurs when left ventricular pressure falls below left atrial pressure and the mitral valve opens.

Blood returning from the pulmonary circulation then moves from the left atrium into the left ventricle.

Respiratory Effects on Filling

Respiration influences venous return and therefore ventricular filling.

During inspiration, reduced intrathoracic pressure generally increases systemic venous return to the right side of the heart, producing normal respiratory variation in right-sided filling and valve events.

Diastole and Stroke Volume

Diastolic filling contributes to end-diastolic volume, which influences the amount of blood available for ejection during the subsequent systole.

Abnormal filling can therefore affect stroke volume even when myocardial contractility itself is not primarily impaired.

Clinical Significance

Diastolic Dysfunction

Diastolic dysfunction occurs when ventricular relaxation, compliance, or filling is abnormal.

The ventricle may require elevated filling pressures to achieve an adequate end-diastolic volume.

Heart Failure With Preserved Ejection Fraction

Heart failure can occur despite a preserved left ventricular ejection fraction.

In many such patients, abnormalities of relaxation, ventricular stiffness, vascular function, and filling pressures contribute to symptoms and congestion.

Left Ventricular Hypertrophy

Hypertrophied ventricular myocardium can become relatively stiff and relax abnormally.

This can increase dependence on atrial contraction and raise left atrial filling pressure.

Myocardial Ischemia

Myocardial relaxation requires energy and can be impaired by ischemia.

Ischemia can therefore disturb diastolic function before or along with abnormalities of systolic contraction.

Atrial Fibrillation

Atrial fibrillation eliminates coordinated atrial systole.

Loss of the atrial contribution to late diastolic filling can be particularly important when ventricular compliance is reduced.

Mitral Stenosis

Mitral stenosis obstructs blood flow from the left atrium into the left ventricle during diastole.

This increases the pressure gradient across the mitral valve and can elevate left atrial and pulmonary venous pressures.

Aortic Regurgitation

In aortic regurgitation, the aortic valve does not close effectively during diastole.

Blood can therefore flow backward from the aorta into the left ventricle while the ventricle is relaxing and filling.

Pulmonary Regurgitation

Pulmonary valve incompetence permits backward flow from the pulmonary trunk into the right ventricle during diastole.

The hemodynamic effect depends on the severity and chronicity of the regurgitation.

Pericardial Constriction

A rigid or constricting pericardium can limit normal expansion of the cardiac chambers during diastolic filling.

This may produce elevated systemic venous pressures and abnormal ventricular filling patterns.

Cardiac Tamponade

In cardiac tamponade, increased pressure within the pericardial space restricts diastolic expansion of the cardiac chambers.

Impaired filling reduces ventricular preload and can decrease cardiac output.

Key Features of Diastole

Feature	Key Point
Primary mechanical event	Myocardial relaxation and chamber filling
Initial ventricular phase	Isovolumetric relaxation
AV valves during filling	Open
Semilunar valves during filling	Closed
Major filling phases	Rapid filling, diastasis and atrial systole
Final ventricular volume	End-diastolic volume
Electrical event near onset	Ventricular repolarization represented by the T wave
Coronary significance	Left ventricular coronary perfusion occurs predominantly during diastole

Anatomical and Physiological Importance

Diastole is an active and highly coordinated component of cardiac function. The ventricles must relax rapidly enough to lower intracavitary pressure, the atrioventricular valves must open normally, and the ventricular walls must remain sufficiently compliant to accept incoming blood without excessive increases in filling pressure.

Diastole also has an important relationship with coronary circulation. Relaxation of the ventricular myocardium reduces compression of intramyocardial coronary vessels, allowing particularly strong perfusion of the left ventricular myocardium during this phase.

Normal cardiac output therefore depends not only on the ability of the heart to contract during systole but also on efficient relaxation and filling during diastole. Abnormalities of relaxation, compliance, valve function, rhythm, pericardial constraint, or filling pressure can significantly impair cardiovascular performance even when systolic ejection remains relatively preserved.