Stroke volume is the measured amount of blood expelled from the left ventricle of the heart with a single contraction. This measurement provides a window into the heart’s pumping efficiency. For an average 154-pound (70 kg) male, this volume is about 70 milliliters per beat. This metric is a direct indicator of cardiovascular health and is calculated by subtracting the blood volume left after contraction (end-systolic volume) from the volume when the ventricle is full (end-diastolic volume). The resulting number shows how effectively the heart is meeting the body’s demands.
Preload and the Frank-Starling Mechanism
Preload refers to the stretching of the heart’s muscle cells, or cardiac myocytes, right before they contract. This stretch is determined by the amount of blood that has filled the ventricle at the end of its relaxation phase, a value known as the end-diastolic volume. An increase in the volume of blood returning to the heart leads to a greater end-diastolic volume, which stretches the muscle fibers more.
This relationship between the stretch and the force of contraction is described by the Frank-Starling mechanism. This principle functions much like a rubber band; the more it is stretched, the more forcefully it snaps back. When the ventricular muscle fibers are stretched by a higher volume of blood, they contract with greater force, pushing more blood out and increasing stroke volume.
Several factors can influence preload. An increase in the return of blood to the heart, such as during physical exercise, will increase preload. A slower heart rate also elevates preload by allowing more time for the ventricles to fill.
Conversely, conditions that reduce the amount of blood returning to the heart will decrease preload and stroke volume. Dehydration leads to a lower overall blood volume, while hemorrhage has a similar effect. Standing up quickly can also cause a temporary drop in preload as blood pools in the lower extremities.
The Role of Myocardial Contractility
Myocardial contractility, also known as inotropy, is the inherent strength of the heart muscle’s contraction. This property is independent of the degree of stretch from preload and describes how forcefully the heart squeezes for any given starting volume of blood. It is determined by chemical and neurological signals rather than mechanical stretching.
The primary driver of contractility is the autonomic nervous system. During a “fight or flight” response, the sympathetic nervous system releases hormones like epinephrine. These hormones increase the concentration of calcium ions within the heart muscle cells, leading to a stronger contraction. This means that for the same amount of blood filling the ventricle, the heart will eject a larger stroke volume.
Exercise is a prime example where contractility increases, as sympathetic stimulation ensures the heart pumps more forcefully to meet the body’s rising demand for oxygenated blood. Stress and excitement can trigger a similar hormonal response. Certain medications, like digoxin, are also designed to strengthen the heart’s contractions.
Some conditions and substances can decrease myocardial contractility. In cases of heart failure, the muscle itself is weakened and cannot pump as effectively. A lack of oxygen, known as hypoxia, can impair the muscle’s ability to contract, and some medications like beta-blockers are prescribed to reduce contractility.
Afterload as an Opposing Force
Afterload is the pressure or resistance the heart must overcome to eject blood from the ventricle into the aorta. Imagine trying to push open a heavy, spring-loaded door; the resistance from the door is analogous to afterload. The heart’s left ventricle must generate enough force to push open the aortic valve and propel blood into circulation against this pressure.
This factor has an inverse relationship with stroke volume. When afterload increases, the heart has to work harder to push blood out, which means it cannot eject as much with each beat. A higher afterload results in a lower stroke volume, leaving more blood in the ventricle after contraction.
The most common condition that increases afterload is high blood pressure (hypertension), where the heart perpetually works against greater resistance. Aortic valve stenosis, a narrowing of the aortic valve opening, also physically obstructs the outflow of blood. The constriction of blood vessels, called vasoconstriction, also raises arterial pressure and afterload.
A decrease in afterload allows the heart to pump blood more easily, increasing stroke volume. This can be achieved through vasodilation, the widening of blood vessels, which lowers overall arterial pressure. Certain blood pressure medications function by inducing vasodilation to reduce afterload.
Analyzing Common Scenarios
The interplay of preload, contractility, and afterload determines the net effect on stroke volume in various situations.
During aerobic exercise, stroke volume increases significantly. This is because both preload and contractility are enhanced. Venous return is boosted by muscle activity, and sympathetic nervous system stimulation increases the force of contraction.
In chronic high blood pressure, the primary factor is a sustained increase in afterload. This persistent resistance makes it more difficult for the ventricle to eject blood, leading to a gradual decrease in stroke volume over time.
When a person stands up suddenly, they may experience a momentary drop in stroke volume. This is an issue of preload, as gravity causes blood to pool in the legs, temporarily reducing the volume of blood returning to the heart.
Dehydration directly impacts blood volume, causing it to decrease. This reduction means less blood is available to return to the heart. The resulting drop in venous return leads to a lower preload and a correspondingly lower stroke volume.