Chapter 19 - Section 19.6 - Cardiac Output - Building Your Medical Vocabulary - Page 737: 26

Preload, contractility, and afterload are three important factors that influence stroke volume and cardiac output, which in turn affect how effectively the heart pumps blood to meet the body's needs. 1. **Preload**: Preload refers to the amount of stretch that the ventricles of the heart experience just before they contract. It is primarily determined by the volume of blood returning to the heart (venous return). An increase in preload leads to an increase in the length of the cardiac muscle fibers, resulting in a stronger contraction due to the Frank-Starling mechanism. This phenomenon states that the more the cardiac muscle fibers are stretched during diastole, the more forcefully they contract during systole. **Effect on Stroke Volume and Cardiac Output**: An increase in preload typically leads to an increase in stroke volume, as the heart contracts more forcefully due to the increased stretch of the ventricular walls. This, in turn, contributes to an increase in cardiac output. 2. **Contractility**: Contractility refers to the inherent strength of the heart's contraction, regardless of preload or afterload. It represents how effectively the heart muscle contracts in response to a given stimulus. Positive inotropic agents, like certain hormones or medications, can increase contractility, while negative inotropic agents decrease it. **Effect on Stroke Volume and Cardiac Output**: An increase in contractility results in a stronger contraction of the heart, which increases stroke volume. As a result, cardiac output increases as well. Conversely, a decrease in contractility would lead to a decrease in stroke volume and cardiac output. 3. **Afterload**: Afterload is the resistance that the heart has to overcome to eject blood into the systemic circulation. It is largely determined by the systemic vascular resistance, which is the resistance encountered by the blood as it flows through the arteries. Higher afterload means the heart has to work harder to pump blood out. **Effect on Stroke Volume and Cardiac Output**: An increase in afterload makes it more difficult for the heart to eject blood from the ventricles, resulting in a decrease in stroke volume. This, in turn, can lead to a decrease in cardiac output. On the other hand, a decrease in afterload allows the heart to eject blood more easily, leading to an increase in stroke volume and potentially an increase in cardiac output. In summary: - Preload: Increasing preload generally increases stroke volume and cardiac output due to the Frank-Starling mechanism. - Contractility: Increasing contractility increases stroke volume and cardiac output, while decreasing contractility has the opposite effect. - Afterload: Increasing afterload decreases stroke volume and cardiac output, whereas decreasing afterload can increase them. These factors are interrelated and collectively determine how effectively the heart pumps blood and maintains the overall cardiovascular function.

Preload, contractility, and afterload are three important factors that influence stroke volume and cardiac output, which in turn affect how effectively the heart pumps blood to meet the body's needs. 1. **Preload**: Preload refers to the amount of stretch that the ventricles of the heart experience just before they contract. It is primarily determined by the volume of blood returning to the heart (venous return). An increase in preload leads to an increase in the length of the cardiac muscle fibers, resulting in a stronger contraction due to the Frank-Starling mechanism. This phenomenon states that the more the cardiac muscle fibers are stretched during diastole, the more forcefully they contract during systole. **Effect on Stroke Volume and Cardiac Output**: An increase in preload typically leads to an increase in stroke volume, as the heart contracts more forcefully due to the increased stretch of the ventricular walls. This, in turn, contributes to an increase in cardiac output. 2. **Contractility**: Contractility refers to the inherent strength of the heart's contraction, regardless of preload or afterload. It represents how effectively the heart muscle contracts in response to a given stimulus. Positive inotropic agents, like certain hormones or medications, can increase contractility, while negative inotropic agents decrease it. **Effect on Stroke Volume and Cardiac Output**: An increase in contractility results in a stronger contraction of the heart, which increases stroke volume. As a result, cardiac output increases as well. Conversely, a decrease in contractility would lead to a decrease in stroke volume and cardiac output. 3. **Afterload**: Afterload is the resistance that the heart has to overcome to eject blood into the systemic circulation. It is largely determined by the systemic vascular resistance, which is the resistance encountered by the blood as it flows through the arteries. Higher afterload means the heart has to work harder to pump blood out. **Effect on Stroke Volume and Cardiac Output**: An increase in afterload makes it more difficult for the heart to eject blood from the ventricles, resulting in a decrease in stroke volume. This, in turn, can lead to a decrease in cardiac output. On the other hand, a decrease in afterload allows the heart to eject blood more easily, leading to an increase in stroke volume and potentially an increase in cardiac output. In summary: - Preload: Increasing preload generally increases stroke volume and cardiac output due to the Frank-Starling mechanism. - Contractility: Increasing contractility increases stroke volume and cardiac output, while decreasing contractility has the opposite effect. - Afterload: Increasing afterload decreases stroke volume and cardiac output, whereas decreasing afterload can increase them. These factors are interrelated and collectively determine how effectively the heart pumps blood and maintains the overall cardiovascular function.