Preload is a fundamental concept in heart function, representing the degree of stretch experienced by the heart muscle fibers just before they contract. Understanding preload is important because it dictates how powerfully the heart can pump, establishing a direct connection between the amount of blood returning to the heart and the amount of blood the heart ejects into the body.
Defining Preload and End-Diastolic Volume
Preload is the physiological measurement of the tension or stretch on the walls of the cardiac muscle cells, known as myocytes, immediately before the heart begins to contract (systole). This stretching occurs during the heart’s filling or relaxation phase (diastole). Since directly measuring the microscopic stretch of muscle fibers in a beating heart is impractical, clinicians use other metrics to estimate preload.
The most common way to approximate preload is by measuring the End-Diastolic Volume (EDV) or End-Diastolic Pressure (EDP). EDV is the volume of blood contained within the ventricles at the very end of diastole, when filling is complete. A greater volume of blood stretches the ventricular walls more extensively, resulting in a higher preload.
The Primary Determinants
The level of preload is dynamically regulated by several factors that control how much blood returns to and fills the ventricles.
Venous Return
The first major factor is venous return, which is the rate of blood flow back to the heart from the systemic circulation. Venous return is highly dependent on total circulating blood volume. It is also affected by the tone of the veins, which can constrict to push blood toward the heart or dilate to hold more blood.
Ventricular Compliance
Ventricular compliance describes the stiffness or elasticity of the heart muscle walls. A highly compliant ventricle is pliable and can expand easily to accommodate a large volume of blood without a significant rise in pressure. Conditions that make the walls stiff, such as long-standing hypertension or certain heart diseases, reduce compliance. This requires a much higher pressure to achieve the same filling volume, thereby limiting preload.
Time for Filling
The time for filling, which is controlled by heart rate, also plays a significant role in setting preload. When the heart rate increases rapidly (tachycardia), the duration of diastole, or the filling time, is severely shortened. This reduced time means the ventricles may not have enough time to fill completely before the next contraction begins. As a result, the End-Diastolic Volume is reduced, leading to a lower preload.
The Frank-Starling Mechanism
The importance of preload lies in its relationship to the heart’s pumping efficiency, a principle known as the Frank-Starling Law of the Heart. This law dictates that, within physiological limits, the stroke volume—the amount of blood ejected with each beat—is directly proportional to the End-Diastolic Volume.
This mechanism works at the cellular level by adjusting the physical arrangement of the heart muscle fibers. Heart muscle contains contractile units called sarcomeres, made up of overlapping actin and myosin filaments. When the ventricle fills with blood, the sarcomeres are stretched, increasing the distance between the ends of the filaments.
This stretch optimizes the physical overlap between the actin and myosin filaments, which allows for a greater number of cross-bridges to form during contraction. This leads to a more forceful and efficient contraction. This intrinsic ability allows the heart to synchronize the output of the left and right ventricles, preventing blood from backing up in the lungs or the rest of the body.
Clinical Implications of Abnormal Levels
Maintaining an optimal preload is necessary for healthy heart function, and deviations from this range are associated with serious health conditions.
Abnormally low preload occurs when there is insufficient blood volume to stretch the ventricles adequately, such as in cases of severe dehydration or hemorrhage. With less stretch, the Frank-Starling mechanism produces a weak contraction, resulting in a low stroke volume. This leads to inadequate blood flow to the body’s tissues, a state often seen in various forms of shock.
Conversely, excessively high preload often occurs in conditions like congestive heart failure or volume overload. In heart failure, the diseased ventricle is unable to pump effectively, causing blood to back up and increase the End-Diastolic Volume and pressure. This excessive stretch pushes the sarcomeres beyond their optimal length, where the actin and myosin overlap becomes inefficient, and the contraction force begins to decline.
When preload is too high, it leads to a buildup of fluid and pressure. This can result in symptoms like pulmonary congestion, where fluid leaks into the lungs, or peripheral edema, which is swelling in the limbs. Clinicians must carefully manage preload using medications like diuretics to reduce fluid volume or intravenous fluids to increase it, aiming to keep the heart operating at the peak efficiency of the Frank-Starling mechanism.