What are stroke volume, preload, afterload, and cardiac output?

Fundamental Cardiac Hemodynamic Parameters

Stroke Volume (SV)

Stroke volume is the amount of blood ejected by the ventricle with each heartbeat, calculated as the difference between end-diastolic volume (EDV) and end-systolic volume (ESV), typically 70-100 mL in healthy adults at rest. 1

• SV = EDV - ESV, where this represents the actual volume of blood pumped per contraction 2, 1
• Normal values range from 70-100 mL per beat in healthy individuals 1
• During peak exercise in trained individuals, stroke volume can increase to approximately 100 mL 2, 1
• SV increases through two primary mechanisms: larger EDV (increased preload via Frank-Starling mechanism) and smaller ESV (enhanced contractility) 1

Preload

Preload is the initial stretching of cardiac myocytes before contraction, directly reflected by end-diastolic volume (EDV), which represents the maximum blood volume in the ventricle at the end of diastolic filling. 1

• EDV typically measures 100-120 mL in healthy adults 1
• Larger EDV increases sarcomere length through the Frank-Starling mechanism, enhancing contractile force and thereby increasing stroke volume 1
• In trained athletes, stroke volume augmentation during exercise is attributable primarily to larger end-diastolic volume 2, 1
• Preload assessment using static pressure measurements (central venous pressure, pulmonary capillary wedge pressure) is unreliable; volumetric estimates of preload are more predictive of volume status 2
• Dynamic indicators like stroke volume variation are preferable to static parameters for predicting fluid responsiveness 2

Afterload

Afterload is the resistance the ventricle must overcome to eject blood, determined by systemic vascular resistance and arterial pressure, which creates a pressure load on the left ventricle. 2, 3

• Static exercise primarily causes a pressure load (increased afterload) on the left ventricle, whereas dynamic exercise causes a volume load 2
• Elevated afterload in chronic aortic regurgitation results from enlarged chamber size with associated increase in systolic wall stress 2
• In heart failure, elevated systemic vascular resistance occurs due to increased sympathetic and renin-angiotensin system activity, contributing to blunted peripheral arterial vasodilator response to exercise 2
• Afterload excess in heart failure patients leads to reduced ejection fraction when preload reserve is exhausted and hypertrophic response is inadequate 2

Cardiac Output (CO)

Cardiac output is the total volume of blood pumped per minute, calculated as heart rate multiplied by stroke volume (CO = HR × SV), typically 4-8 L/min at rest in healthy adults. 1, 3

• The fundamental equation is CO = HR × SV, where SV = EDV - ESV 1
• Normal resting cardiac output ranges from 4-8 L/min 1
• Maximal cardiac output in healthy individuals can reach 20-25 L/min during peak exercise 1
• CO increases linearly with oxygen consumption (VO₂) in healthy subjects, with every 1 L/min increase in oxygen uptake requiring a 5-6 L/min increase in cardiac output 2
• Initially during exercise, CO increases through both increased SV and HR, then at moderate-to-high intensity almost exclusively through HR increases 1

Pathophysiology in Heart Failure

In heart failure, stroke volume remains markedly reduced (rising only to 50-65 mL at peak exercise versus 100 mL in healthy subjects), and patients achieve only 50% of the maximal cardiac output attained by healthy individuals. 2, 1

• The inability to increase CO relates primarily to minimal SV increase coupled with lower maximal HR achieved at lower workload 2, 1
• EDV augmentation is blunted because the already dilated left ventricle operates near maximal volume, exhausting preload reserve 2, 1
• Failure to increase left ventricular systolic emptying derives from impaired intrinsic contractility, reduced β-adrenergic responsiveness, and elevated systemic vascular resistance 2
• Exercise-induced mitral regurgitation in heart failure patients reduces forward stroke volume but can be attenuated with vasodilators and diuretics 2
• The primary means to augment cardiac output in heart failure patients is through cardioacceleration, though heart rate reserve is substantially blunted due to elevated resting heart rate 2