Normal Systolic & Diastolic Function

RDCS Adult Echocardiography AE

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1 Introduction & Exam Overview

The RDCS AE Exam, SPI Requirement & Logistics Content Outline, Domain Weights & How to Study

2 Cardiac Anatomy

Chambers, Walls, Myocardial Layers & the 17-Segment Model Cardiac Valves & Subvalvular Apparatus Great Vessels, Pericardium, Coronary & Venous Anatomy

3 Cardiac Physiology & Hemodynamics

Cardiac Cycle, Phases & Pressure-Volume Relationships Normal Systolic & Diastolic Function Hemodynamic Principles & Response to Stress

4 Echo Modalities, Instrumentation & Contrast

2D (B-Mode) and M-Mode Imaging Spectral, Color, and Tissue Doppler Modalities Image Optimization, Artifacts, and Contrast Echocardiography

5 Standard Views, Windows & Protocol

Parasternal Long- & Short-Axis Views Apical Views Subcostal & Suprasternal-Notch Views Exam Protocol, Patient Positioning & Provocative Maneuvers

6 Quantification & Doppler Hemodynamic Calculations

Chamber Quantification: LV, LA, RA, and RV Size, Mass, and Volumes Systolic Function: Ejection Fraction Methods, Fractional Shortening & Strain Diastolic Function Grading (ASE/EACVI 2016) Core Doppler Math: Modified Bernoulli, VTI, Stroke Volume & the Continuity Equation Advanced Hemodynamics: PISA/EROA, Pressure Half-Time, dP/dt, Qp/Qs & RVSP

7 Aortic & Mitral Valve Disease

Aortic Stenosis Aortic Regurgitation Mitral Stenosis Mitral Regurgitation

8 Right-Sided, Prosthetic & Infective Valve Disease

Tricuspid & Pulmonic Valve Disease and Pulmonary Hypertension Assessment Infective Endocarditis and Vegetations Prosthetic Valves and Postoperative Evaluation

9 Ischemic Disease & Cardiomyopathies

Coronary Anatomy, Ischemic Heart Disease & Wall-Motion Abnormalities Stress Echocardiography & Myocardial Viability Mechanical Complications of Myocardial Infarction Dilated & Restrictive Cardiomyopathy Hypertrophic Cardiomyopathy, SAM & LVOT Obstruction

10 Pericardial Disease, Masses & Aorta

Pericardial Effusion & Cardiac Tamponade Constrictive Pericarditis vs. Restrictive Physiology Cardiac Masses, Tumors & Thrombi Aortic Disease: Aneurysm, Dissection & Atheroma

11 Congenital Heart Disease & Shunts

Septal Defects & Shunt Quantification Common Adult Congenital Lesions

12 Clinical Care & Safety

Patient Care, Clinical-Data Integration & Exam Protocols Bioeffects, ALARA, Infection Control & Ergonomics

Normal Systolic & Diastolic Function

Key Takeaways Explain This Topic AI

Normal left ventricular ejection fraction is 52-72% in men and 54-74% in women per the 2015 ASE/EACVI chamber quantification guideline.

Severely abnormal ejection fraction is defined as below 30% in both men and women.

Preload, afterload, and contractility are the three determinants of systolic function; contractility is intrinsic and not directly measured by standard echocardiography.

The 2016 ASE/EACVI algorithm for a patient with normal LVEF uses four variables — septal/lateral e' velocity, average E/e' ratio, LA volume index, and peak TR velocity — to separate normal from abnormal diastolic function.

Diastolic dysfunction is graded I (impaired relaxation), II (pseudonormal filling), or III (restrictive filling), in order of increasing severity.

Last updated: July 2026

Normal Systolic Function

Systolic (pump) function describes how effectively the left ventricle ejects blood, and it is governed by three physiologic determinants:

Preload — the load stretching the ventricle before contraction begins, approximated clinically by LV end-diastolic volume or pressure. Per the Frank-Starling relationship, increased preload increases stroke volume (within limits) by optimizing actin-myosin overlap.

Afterload — the load the ventricle must overcome during ejection, related to arterial pressure, chamber size, and wall thickness through LaPlace's law (wall stress is proportional to pressure times radius, divided by twice the wall thickness). Increased afterload reduces stroke volume for a given contractile state.

Contractility (inotropy) — the intrinsic force-generating capacity of the myocardium, independent of loading conditions. Contractility is not measured directly by standard 2D or Doppler echocardiography; it is inferred indirectly from tools such as strain, dP/dt, or the end-systolic pressure-volume relationship.

Because contractility itself cannot be measured directly by echocardiography, ejection fraction is often used as its clinical proxy — but EF is a load-dependent index, not a pure measure of intrinsic contractility. A ventricle with normal or even reduced contractility can show a deceptively preserved EF if afterload is acutely low, while a normally contracting ventricle can show a reduced EF if afterload is acutely and severely elevated. Separating loading conditions from the intrinsic muscle state — rather than reading EF alone — is the physiologic reasoning tested at this level.

Ejection fraction: the primary systolic metric

Ejection fraction (EF) — the fraction of end-diastolic volume ejected each beat, EF = (EDV − ESV) ÷ EDV — is the single most-used global systolic index, with sex-specific normal ranges defined by the 2015 ASE/EACVI chamber quantification guideline:

• EF category Men Women
• Normal 52–72% 54–74%
• Mildly abnormal 41–51% 41–53%
• Moderately abnormal 30–40% 30–40%
• Severely abnormal <30% <30%

Because EF is a ratio rather than an absolute volume, it can appear falsely preserved in a concentrically hypertrophied or underfilled ventricle — one reason quantification pairs EF with volumetric and strain data (covered in Chapter 6).

Two additional systolic indices are commonly taught alongside EF: fractional shortening , the percent change in LV minor-axis diameter between diastole and systole (a one-dimensional M-mode surrogate that assumes normal chamber geometry), and stroke volume itself, calculated from the left ventricular outflow tract diameter and the Doppler velocity-time integral (full calculation covered in Chapter 6). Both connect directly to the pressure-volume relationships from Section 3.1: stroke volume is the horizontal width of the PV loop, and EF simply expresses that width as a fraction of end-diastolic volume.

Normal Diastolic Function

Diastolic function describes the ventricle's ability to fill at normal pressures and depends on two separate properties:

Relaxation — an active, energy-dependent process (calcium re-uptake into the sarcoplasmic reticulum) that determines how quickly LV pressure falls after systole and how early filling begins; impaired relaxation is the earliest and mildest form of diastolic dysfunction.

Compliance — the passive stiffness of the ventricular wall, determining how much LA pressure is needed to fill the ventricle to a given volume; reduced compliance (a stiff, non-compliant chamber) requires higher filling pressures to achieve normal volumes.

The 2016 ASE/EACVI four-variable algorithm

For a patient with normal LVEF , current guidelines recommend evaluating four variables and counting how many are abnormal:

• Variable Abnormal cutoff
• Septal e′ velocity <7 cm/s
• Lateral e′ velocity <10 cm/s
• Average E/e′ ratio >14
• LA volume index (LAVI) >34 mL/m²
• Peak TR velocity >2.8 m/s

If more than half of the available parameters are abnormal, diastolic dysfunction is present; if half or fewer are abnormal, diastolic function is normal; and if exactly half are abnormal, the study is classified indeterminate. The normal transmitral E/A ratio in a young healthy adult is roughly 1–2, but E/A declines physiologically with age as relaxation slows, so age-adjusted interpretation matters.

Age and the normal filling pattern

Diastolic filling parameters are strongly age-dependent even in structurally normal hearts. In young, healthy adults, early rapid filling dominates, so the E/A ratio is typically greater than 1 (the E wave is taller than the A wave). With normal aging, myocardial relaxation slows gradually: early filling velocity (E) tends to decline while the atrial contribution (A) increases to compensate, and E/A can fall below 1 by later adulthood without representing true pathology. This is exactly why diastolic assessment always interprets E/A, e′, and E/e′ together with age-appropriate expectations rather than applying one fixed cutoff to every patient.

Grading diastolic dysfunction

Once dysfunction is confirmed — typically in a patient with reduced EF, structural heart disease, or an abnormal normal-EF algorithm result — severity is graded:

Grade I — impaired relaxation : E/A ratio <0.8 with normal filling pressure at rest; the mitral inflow pattern shows a dominant A wave.

Grade II — pseudonormal filling : E/A ratio appears "normal" (0.8–2) but filling pressures are actually elevated; distinguished from a truly normal pattern using e′, E/e′, and a Valsalva maneuver, which unmasks the underlying abnormal relaxation.

Grade III — restrictive filling : E/A ratio ≥2 with short deceleration time and markedly elevated filling pressures; represents the most advanced, least compliant physiology.

Both systolic and diastolic assessment ultimately answer the same clinical question from opposite directions — systolic evaluation asks how much blood the ventricle ejects, diastolic evaluation asks at what pressure cost the ventricle fills — and a complete functional assessment always reports both.