What is the relationship between End-Diastolic Volume (EDV), Stroke Volume (SV), and Cardiac Output (CO) in heart function?

Cardiac Hemodynamic Relationships: EDV, SV, and CO

Cardiac output (CO) equals heart rate (HR) multiplied by stroke volume (SV), while stroke volume is determined by the difference between end-diastolic volume (EDV) and end-systolic volume (ESV). 1

Fundamental Relationships

The core equation is: CO = HR × SV, where SV = EDV - ESV 1

• End-Diastolic Volume (EDV) represents the maximum blood volume in the ventricle at the end of filling (diastole), typically 100-120 mL in healthy adults 1
• Stroke Volume (SV) is the amount of blood ejected per heartbeat, normally around 70-100 mL in healthy individuals at rest 1
• Cardiac Output (CO) is the total volume of blood pumped per minute, calculated as HR × SV, typically 4-8 L/min at rest 1

Physiological Determinants

EDV and Preload

• EDV directly reflects ventricular preload, which represents the initial stretching of cardiac myocytes before contraction through the Frank-Starling mechanism 2
• Larger EDV increases sarcomere length, enhancing contractile force and thereby increasing stroke volume 2
• In trained athletes, augmentation of stroke volume during exercise is attributable primarily to a larger end-diastolic volume 1

Stroke Volume Regulation

SV increases through two mechanisms: increased EDV (preload) and decreased ESV (enhanced contractility) 1

• In healthy individuals during exercise, stroke volume rises from ~70 mL at rest to ~100 mL at peak exercise 1
• Enhanced systolic emptying (reduced ESV) contributes to increased SV, particularly in trained individuals 1
• The relationship between EDV and SV follows the Frank-Starling curve, though this relationship can be weak (r = 0.54) in certain conditions 3

Cardiac Output Optimization

• CO increases initially through both increased SV and HR, then at moderate-to-high intensity exercise almost exclusively through HR increases 1
• In healthy subjects, CO increases linearly with oxygen consumption (V̇O₂) 1
• Maximal cardiac output in healthy individuals can reach 20-25 L/min during peak exercise 1

Pathophysiology in Heart Failure

Patients with heart failure demonstrate fundamentally impaired hemodynamic relationships 1

• Stroke volume remains markedly reduced, rising only modestly to 50-65 mL at peak exercise compared to 100 mL in healthy subjects 1
• The inability to increase CO is related primarily to minimal SV increase coupled with lower maximal HR achieved at lower workload 1
• EDV augmentation is blunted because the already dilated left ventricle operates near maximal volume, exhausting preload reserve 1
• Patients with heart failure may achieve only 50% of the maximal cardiac output attained by healthy individuals 1

Mechanisms of Impaired SV in Heart Failure

• Reduced ability to increase both LV preload and ejection fraction during exercise 1
• Impaired intrinsic contractility and reduced β-adrenergic responsiveness 1
• Elevated systemic vascular resistance due to increased sympathetic and renin-angiotensin system activity 1
• Exercise-induced mitral regurgitation reduces forward stroke volume 1

Clinical Assessment Implications

EDV cannot be reliably estimated from filling pressures alone 3

• Central venous pressure and pulmonary capillary wedge pressure are generally insensitive indicators of preload status 2
• Echocardiographic measurement of EDV provides direct assessment of preload 2
• Changes in EDV may occur independently of changes in filling pressure, particularly with alterations in ventricular shape 3

Dynamic Relationships

• For CO to increase by the Starling mechanism, the ventricle must dilate, increasing ESV 3
• If fluid loading causes right atrial pressure to increase without increasing CO, resuscitation should stop as the patient is developing acute cor pulmonale 3
• The relationship between LVEF and contractility is improved when adjusted for afterload (r² = 0.75 vs r² = 0.43 unadjusted) 4

Key Clinical Pitfalls

• Do not assume elevated filling pressures indicate adequate preload—ventricular compliance and shape changes affect the EDV-pressure relationship 3
• Ejection fraction alone poorly reflects contractility as it is heavily influenced by both preload (EDV) and afterload 4
• In heart failure, the ventricle may be operating at maximal EDV despite "normal" filling pressures due to chamber remodeling 1
• Maximal heart rate achievement does not guarantee maximal effort in patients on β-blockers or with chronotropic incompetence 1