The heart works continuously to circulate blood throughout the body, delivering oxygen and nutrients. Stroke volume is the precise amount of blood the left ventricle ejects into the aorta in a single, powerful contraction. This measurement provides a direct assessment of the heart’s pumping efficiency. The body’s demand for oxygen and nutrients dictates the required blood flow, making stroke volume a dynamic figure that adjusts constantly. Since stroke volume is a key component in calculating cardiac output—the total volume of blood pumped per minute—it offers immediate insight into the health of the circulatory system.
Defining Stroke Volume and Its Measurement
Stroke volume is a calculated value derived from the volumes of blood within the left ventricle at different points in the cardiac cycle. This relationship is expressed as \(\text{SV} = \text{EDV} – \text{ESV}\).
The End-Diastolic Volume (\(\text{EDV}\)) represents the maximum volume of blood the ventricle holds just as the heart muscle completes its relaxation phase, or diastole. A typical \(\text{EDV}\) in a healthy adult is approximately \(120\text{ to }140\text{ milliliters}\).
Conversely, the End-Systolic Volume (\(\text{ESV}\)) is the blood volume left inside the ventricle immediately after the heart has contracted and ejected blood, which is known as systole. Even a healthy heart does not expel all the blood it contains, and the \(\text{ESV}\) commonly ranges from \(40\text{ to }50\text{ milliliters}\).
Establishing the Normal Range
For a healthy adult at rest, the normal range for stroke volume typically falls between \(60\text{ and }120\text{ milliliters}\) per beat. The average stroke volume for a \(70\text{ kilogram}\) male is often cited as \(70\text{ to }90\text{ milliliters}\). These figures serve as a guideline, as the normal value is highly dependent on an individual’s specific physiological context.
Body size is a significant factor, which is why healthcare professionals sometimes look at the stroke volume index. This index adjusts the volume based on the body surface area to allow for a standardized comparison between individuals. Gender also plays a role, with men generally having a higher stroke volume than women due to differences in heart size.
Activity level causes the most dramatic shift, as the heart adapts to meet increased metabolic demands. During intense physical exertion, the stroke volume will rise substantially, sometimes reaching values as high as \(120\text{ to }200\text{ milliliters}\) in well-trained athletes.
The Three Physiological Determinants
Stroke volume is regulated by three primary physiological factors that govern the heart’s mechanical performance: preload, afterload, and contractility. An alteration in any of these three elements directly changes the volume of blood ejected with each beat.
Preload
Preload is the degree of muscle fiber stretch within the ventricle just before it contracts, which is directly related to the \(\text{EDV}\). It is determined by venous return, the volume of blood returning to the heart from the veins. The Frank-Starling mechanism describes this relationship, asserting that a greater stretch, up to an optimal point, leads to a more forceful contraction and a higher stroke volume. A higher venous return, such as the temporary increase experienced during pregnancy, stretches the cardiac muscle more and results in a greater stroke volume. Conversely, a decrease in the overall blood volume, like from dehydration, reduces the stretch and subsequently lowers the stroke volume.
Afterload
Afterload is the resistance the ventricle must overcome to eject blood into the aorta. This force is primarily determined by the pressure in the systemic circulation and the overall stiffness of the arteries. When afterload increases, such as in individuals with long-standing high blood pressure, the heart must work harder to push the blood out. A high afterload increases the workload on the heart muscle, leading to a reduced stroke volume because the heart cannot empty as completely. Managing conditions that elevate systemic vascular resistance is important for preserving a healthy stroke volume and preventing excessive strain on the heart.
Contractility
Contractility, also called inotropy, is the inherent strength of the heart muscle contraction, independent of the initial stretch or the resistance it faces. This factor is largely modulated by the nervous system and circulating hormones. For instance, sympathetic nervous system activation, which occurs during exercise or stress, releases signals that significantly increase contractility. A stronger contraction reduces the \(\text{ESV}\) by ejecting a greater proportion of the blood held within the ventricle, resulting in an increased stroke volume.
Clinical Implications of Abnormal Stroke Volume
Monitoring stroke volume is an aspect of cardiovascular assessment because deviations from the normal range often indicate underlying health issues. A low stroke volume suggests the heart is not pumping a sufficient amount of blood with each beat, potentially compromising the oxygen supply to the body’s tissues.
One consequence of a persistently low stroke volume is reduced cardiac output, which can lead to symptoms like fatigue and weakness. In severe cases, a drastically low stroke volume is a hallmark of various forms of shock, where the circulatory system fails to perfuse the organs adequately. Cardiogenic shock, for example, is characterized by the heart’s inability to pump effectively despite having enough blood to fill its chambers.
Low stroke volume is also closely associated with heart failure, even in patients who have a preserved ejection fraction (the percentage of blood ejected).
An abnormally high stroke volume is less common but can also signify problems, often related to excessive volume or specific flow dynamics. Conditions that cause blood to flow backward, such as severe regurgitation of a heart valve, can lead to a state where the ventricle is overfilled, resulting in an unnaturally large stroke volume. While a high stroke volume may also be seen in conditions like severe anemia, it is often a compensatory mechanism rather than a sign of optimal heart function.