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Stroke volume vs cardiac output: two key parameters of cardiac function in direct comparison

The distinction between Stroke Volume vs Cardiac Output is fundamental to understanding cardiac physiology and clinical diagnostics. While both parameters are closely linked, they provide different information about cardiac function. This precise differentiation enables cardiologists to identify specific pathologies and make targeted treatment decisions. Modern measurement systems such as the evolution series from Schwarzer Cardiotek record both parameters simultaneously and enable a comprehensive hemodynamic assessment.

Basic definitions and their meaning

Stroke Volume (SV) – The stroke volume

Stroke volume is the volume of blood ejected from the left ventricle during each individual heartbeat. It is calculated using:

SV = EDV – ESV

  • EDV: End-diastolic volume (diastolic volume)
  • ESV: End systolic volume (systolic volume)

Normal values are between 60 and 100 ml per heartbeat. The stroke volume represents the immediate pumping power of the heart and is significantly influenced by

  • Preload: Ventricular filling at the end of diastole
  • Afterload: Resistance against which the heart pumps
  • Contractility: Intrinsic muscle strength

Cardiac output (CO) – The cardiac output

Cardiac output describes the total blood that the heart pumps per unit of time, usually per minute:

CO = SV × HR

With normal values of 4-8 L/min in adults, cardiac output quantifies the global cardiac output. It directly determines organ perfusion and oxygenation of the entire body.

Understanding the mathematical relationship

The formula CO = heart rate (HR) multiplied by stroke volume (SV) shows the direct relationship:

Practical example:

  • Stroke Volume: 70 ml
  • Heart rate: 75 bpm
  • Cardiac output: 70 ml × 75 = 5,250 ml/min = 5.25 L/min

This relationship illustrates that cardiac output (the volume that the heart pumps in one minute) is the product of single stroke volume and heart rate.

Compensation mechanisms:

  • With reduced SV, an increased HR can maintain the CO
  • In the case of bradycardia, an increased SV often compensates
  • However, these adaptations have physiological limits

Factors that influence the stroke volume

Preload and the Frank-Starling mechanism

The preload determines the end-diastolic filling volume. According to the Frank-Starling law, increased pre-dilation leads to

  • Increased contraction
  • Increased stroke volume (SV)
  • Optimal overlap of the myofilaments

Clinical situations:

  • Volume loading increases preload and SV
  • Dehydration reduces preload and SV
  • Atrial fibrillation disturbs atrial filling

Afterload and ejection resistance

The resistance against which the heart works directly influences SV:

  • Hypertension increases afterload → reduced SV
  • Vasodilation lowers afterload → increased SV
  • Aortic stenosis mechanically increases the afterload

Contractility and myocardial function

Intrinsic pumping force determines the amount of ejected blood

  • Sympathetic activation increases contractility
  • Inotropic drugs increase contractility
  • Ischemia reduces contractility regionally or globally

Clinical significance of differentiation

The SV provides information about

  • Single beat performance: Direct pump force assessment
  • Ejection fraction: SV/EDV × 100 = ejection fraction
  • Valve function: Regurgitations reduce effective SV
  • Ventricular function: wall motion abnormalities influence SV

In heart failure, SV is often primarily reduced, while HR increases as compensation.

Cardiac output as a global parameter

The CO reflects:

  • Systemic perfusion: blood volume for all organs
  • Metabolic requirements: Adaptation to stress
  • Forms of shock: Differentiation cardiogenic vs. distributive
  • Therapeutic success: monitoring during treatment

In sepsis, CO can be elevated due to tachycardia despite reduced SV.

Modern measurement methods in direct comparison

Echocardiography:

  • 2D volumetry: EDV and ESV measured directly
  • Doppler: SV = VTI × LVOT area
  • 3D echo: most accurate non-invasive method

Impedance cardiography:

  • Continuous SV measurement
  • Based on thoracic impedance change
  • Limited for arrhythmias

Measurement of cardiac output

Thermodilution:

  • Gold standard of invasive CO measurement
  • Intermittent or continuous
  • Measures the total cardiac output directly

Pulse contour analysis:

  • Calculates CO from arterial pressure curve
  • Requires calibration
  • Continuous monitoring possible

Precision measurement with Schwarzer Cardiotek technology

The evolution series records stroke volume vs cardiac output simultaneously:

evolution system:

  • Automatic SV calculation from pressure curves
  • HR acquisition in real time
  • CO calculation with continuous display
  • Smart keyboard for intuitive operation

evolution ProCart:

  • Mobile complete solution
  • Flexible use in different clinical areas
  • Transportable between hybrid ORs

evolution duo – Integrated diagnostics:

  • Combines hemodynamics with electrophysiology
  • Simultaneous SV and HR analysis
  • Advanced arrhythmia detection
  • Precise CO determination even with irregular rhythms

Automatic logging continuously records both parameters, enabling the detection of trends and acute changes.

Optimize your haemodynamic diagnostics

Live demonstration: Experience simultaneous SV/CO measurement with evolution duo in your cath lab. Our specialists will demonstrate the seamless integration of both parameters.

Expert advice: Do you have specific questions about the differentiation of SV- and CO-based pathologies? Our medical-technical team will support you with the optimal system configuration.

With over 80 years of experience in cardiology, Schwarzer Cardiotek offers precise solutions for the comprehensive assessment of stroke volume vs cardiac output – for better diagnostic certainty and optimal therapy decisions.

Frequently asked questions about clinical application

Which varies more physiologically – SV or HR?

Heart rate shows greater short-term variability (sinus arrhythmia, exercise). The stroke volume remains relatively constant in healthy individuals, except in the case of changes in position or volume shifts.

When is the SV primarily pathological?

In structural heart diseases such as cardiomyopathies, valvular disease or regional wall motion abnormalities, the SV is primarily affected. The stroke volume divided by the end-diastolic volume (EDV) results in the ejection fraction as an important prognostic parameter.

Can SV and HR compensate for each other?

Yes, up to certain limits. In the case of chronic SV reduction, an increased HR initially compensates. However, this compensation is energetically unfavorable and harmful in the long term.

When are invasive measurements necessary?

In haemodynamically unstable patients, complex vitals or when non-invasive methods are unreliable (obesity, COPD, arrhythmias).

 

Note: This article is for information purposes only and does not replace scientific or medical advice. For specific questions about cardiac output vs. cardiac output, please consult appropriate experts or scientific literature.