53 Pressure-volume loops

Cardiovascular pressure-volume loops are graphical representations that provide valuable insights into the functioning of the heart and vasculature. They help visualize the dynamic changes in pressure and volume within the heart throughout the cardiac cycle. These loops are crucial for understanding the relationships between preload, afterload, and cardiac performance.

A typical cardiovascular pressure-volume loop (Figure 53.1) consists of four distinct phases, each representing a specific event during the cardiac cycle:

1. Isovolumic Contraction (IVC): This phase begins when the mitral AV valve closes, and the aortic SL valve remains shut (thus, both the AV and SL valves are closed). During this phase, ventricular pressure rises rapidly as the myocardium contracts, but no change in volume occurs because all valves are closed.
2. Ejection Phase: As ventricular pressure surpasses aortic pressure, the aortic SL valve opens, allowing blood to be ejected into the aorta. This phase is characterized by an increase in ventricular pressure and a decrease in ventricular volume.
3. Isovolumic Relaxation (IVR): With the closure of the aortic valve and the onset of ventricular relaxation, ventricular pressure rapidly declines while volume remains constant.
4. Filling Phase: During diastole, when the mitral AV valve opens, blood flows from the atria into the ventricle. Ventricular volume increases, but pressure remains relatively low.

The x-axis represents volume, typically in the left ventricle, while the y-axis represents pressure. A normal cardiac cycle begins in the bottom right corner, which represents end-diastole, when the ventricles are fully relaxed and filled with blood. As the ventricles contract during systole, pressure rapidly rises (from the bottom right to the top right corner) while volume remains relatively constant. This phase is called isovolumetric contraction.

As the pressure in the left ventricle exceeds that in the aorta (afterload), the aortic valve opens, and blood is ejected into the aorta, causing a sharp increase in pressure and a decrease in volume (from the top right corner to the top left corner). This phase is called ejection.

After the ejection phase, the ventricles relax (from the top left corner to the bottom left corner), causing a rapid decrease in pressure as the aortic valve closes. The ventricles continue to relax until they reach end-diastolic volume, and the cycle repeats.

Venous return

Venous return is the rate at which blood returns to the heart. Factors influencing venous return include total blood volume, the respiratory pump (where inspiration increases and expiration decreases venous return), the skeletal muscle pump (where muscle contractions help propel blood to the heart), venous tone (where constricted veins increase venous return), and heart torsion (where heart contractions create a suction effect enhancing venous return).

Preload

Preload is the force exerted on the ventricular walls at the end of diastole, corresponds to the end-diastolic volume (EDV). Factors affecting preload include heart rate (higher heart rates reduce filling time, thus decreasing preload), venous return (increased venous return enhances preload), and atrial contraction (stronger atrial contractions increase preload).

An increase in preload, often due to increased venous return or enhanced ventricular filling, results in a shift of the entire loop to the right (Figure 53.2). This means that at any given point in time, the heart is operating at a higher volume. This increased preload generally leads to greater stroke volume and cardiac output as the heart pumps out more blood.

Conversely, a decrease in preload, which can occur due to decreased venous return or reduced ventricular filling, shifts the loop to the left. In this case, the heart operates at a lower volume, leading to decreased stroke volume and cardiac output.

Afterload

Afterload represents the resistance against which the heart must pump blood during systole. An increase in afterload, often due to conditions like hypertension or aortic stenosis, shifts the loop upwards and to the left (Figure 53.3). This indicates that more pressure is required for the ventricles to overcome the increased resistance and eject blood into the aorta. Consequently, stroke volume decreases, and the heart has to work harder to maintain cardiac output. Conversely, a decrease in afterload, such as during vasodilation or with certain medications, shifts the loop downwards and to the right. Lower afterload allows the ventricles to eject blood more easily, leading to increased stroke volume and reduced cardiac workload.

Cardiovascular pressure-volume loops are essential tools for understanding the dynamic interactions between preload, afterload, and cardiac function. Changes in preload and afterload can significantly impact the shape and position of these loops.