The Stroke Volume Index (SVI) is a measurement used in medicine to assess how effectively the heart is pumping blood throughout the body. Calculating this value allows clinicians to determine the volume of blood the heart ejects with each beat relative to the individual’s physical size. This normalization is useful for comparing heart function across different patients, regardless of their height, weight, or gender. Evaluating the SVI helps determine if the circulatory system is delivering an adequate blood supply to meet the body’s metabolic demands.
Defining the Stroke Volume Index
The Stroke Volume Index (SVI) is derived from the basic concept of Stroke Volume (SV), which is the absolute volume of blood the heart ejects with each contraction. Standard SV is a poor measure of efficiency because larger individuals naturally require more blood volume to perfuse their tissues. To account for this, SVI indexes the stroke volume to the patient’s Body Surface Area (BSA).
The BSA is the calculated total surface area of a person’s body, usually measured in square meters (m²). This indexation transforms the absolute volume into a measure of volume per square meter of body surface. The formula is the Stroke Volume (in milliliters) divided by the Body Surface Area (in square meters).
This standardization is necessary because physiological variables like heart size and circulating blood volume scale with the individual’s overall size. By normalizing the measurement, SVI provides a more accurate and comparable gauge of cardiac performance. SVI is directly proportional to the Cardiac Index (CI), the indexed version of Cardiac Output (the total volume of blood pumped per minute). The SVI measures the heart’s pumping efficiency per beat relative to body size.
The Clinical Measurement of SVI
SVI is calculated from stroke volume (SV), which is obtained through several invasive and non-invasive methods. Historically, detailed measurements came from invasive techniques, such as the use of a pulmonary artery catheter (PAC), also known as a Swan-Ganz catheter. This method uses thermodilution, injecting cold fluid and measuring temperature changes to calculate cardiac output, from which SV is derived.
Non-invasive methods are increasingly preferred due to reduced patient risk and include advanced imaging techniques. Echocardiography uses Doppler technology to measure the velocity of blood flow through the left ventricular outflow tract (LVOT). This measurement, the velocity-time integral (VTI), allows for a precise calculation of the volume of blood passing through the heart with each beat.
Minimally invasive approaches are common in intensive care settings and include arterial pulse contour analysis. Devices like the FloTrac or LiDCO analyze the arterial pressure waveform to continuously estimate stroke volume. Other non-invasive technologies, such as bioimpedance or bioreactance, apply electrical currents across the chest to estimate blood flow changes. The resulting stroke volume is then divided by the patient’s BSA to yield the SVI.
Interpreting SVI Values
The interpretation of SVI values provides important information about the patient’s circulatory state. A normal resting range typically falls between 33 and 65 milliliters per square meter (mL/m²). Deviations from this range help clinicians identify the underlying cause of a patient’s hemodynamic instability. A low SVI suggests the heart is failing to eject an adequate volume of blood to meet the body’s needs.
A severely low SVI (less than 30 mL/m²) is a sign of compromised cardiac function and is associated with a poor prognosis. This may indicate conditions characterized by low blood volume, such as hypovolemic shock following severe bleeding or dehydration.
Causes of Low SVI
Low SVI can also point to a mechanical issue, such as severe left-sided heart failure or cardiogenic shock, where the heart muscle is too weak to contract effectively. It is also a significant factor in risk stratification for patients with specific heart conditions, such as low-flow, low-gradient aortic stenosis.
Conversely, an elevated SVI suggests a hyperdynamic circulatory state, meaning the heart is pumping a significantly larger volume of blood than normal relative to the patient’s size. This is frequently seen in distributive shock, such as early-stage septic shock, where widespread inflammation causes peripheral blood vessels to dilate excessively.
Causes of Elevated SVI
The body compensates for the sudden drop in peripheral resistance by dramatically increasing the heart’s output, resulting in a high SVI. Other non-shock causes of an elevated SVI include severe anemia, thyrotoxicosis, or the presence of arteriovenous fistulas.
Factors Affecting Cardiac Output and SVI
The Stroke Volume Index is a direct reflection of the three primary physiological factors that determine stroke volume: preload, afterload, and contractility. Changes in these three determinants will directly alter the stroke volume, leading to predictable changes in the calculated SVI.
Preload
Preload refers to the degree of stretch on the heart muscle fibers at the end of diastole, just before contraction. Clinically, this correlates with the volume of blood filling the ventricles. A lower preload, such as from dehydration, will reduce stroke volume and, consequently, the SVI.
Afterload
Afterload is the resistance the heart must overcome to eject blood into the major arteries (systemic circulation pressure). Conditions that increase afterload, like severe hypertension or aortic stenosis, make it harder for the heart to pump blood, thus decreasing the stroke volume and SVI. Decreasing the afterload, as occurs during systemic vasodilation in septic shock, allows the heart to eject more blood easily, contributing to a high SVI.
Contractility
Contractility is the inherent strength and force of the heart muscle contraction, independent of preload and afterload. A healthy heart muscle increases contractility during exercise to boost SVI. Conversely, a diseased heart, such as one affected by a heart attack or chronic heart failure, will have reduced contractility.