49 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 41.1) consists of four distinct phases, each representing a specific event during the cardiac cycle:

1. Isovolumic Contraction (IVC): This phase begins when the mitral valve closes and the aortic valve remains shut. During this phase, ventricular pressure rises rapidly as the myocardium contracts, but no change in volume occurs.
2. Ejection Phase: As ventricular pressure surpasses aortic pressure, the aortic 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 valve opens, blood flows from the atria into the ventricle. Ventricular volume increases, but pressure remains relatively low.

The x-axis represents volume, typically on the left ventricle side, 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

Simply put venous return is the rate at which blood return back to the heart. There are several factors that can affect venous return such as total blood volume, the respiratory and skeletal muscle pumps, venous tone, and torsion of the heart. People that have larger blood volume will likely have a greater venous return. The simple act of breathing will affect venous return, with inspiration increasing venous return and expiration decreasing venous return (this will be discussed in more detail later). Skeletal muscle contractions help propel blood to the heart, which increases venous return. While it might seem counterintuitive, when veins have a smaller radius, or are constricted, venous return increases. This is because venoconstriction limits venous pooling, thus making it easier for blood to return to the heart. Finally, as the heart contracts it actually twists and creates a torsional force. This torsion creates a suction effect that allows the right side of the heart to pull blood into from the systemic venous circulation.

Preload

As discussed earlier, preload is the force exerted on the walls of the ventricles prior to contraction. This force is caused by the amount of blood in the ventricle prior to contraction. Thus preload corresponds with end-diastolic volume. Factors that affect preload include heart rate, venous return, and atrial contraction. Increased heart rate results in a decreased filling time, which will reduce the amount of blood that can get enter the ventricles.

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 41.2). 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 41.3). 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.