End systolic pressure volume relationship contractility and afterload

End systolic pressure-volume relationship (ESPVR) (video) | Khan Academy

end systolic pressure volume relationship contractility and afterload

Contractility was measured by three different indexes: end-systolic pressure- volume relations (slope and volume position); preload-corrected first derivative of . Comparison between end-systolic pressure-volume and end-systolic wall stress in determining left ventricular contractility with increased afterload. Ben-Sira. Like contractility, changes in afterload will raise or lower the Starling curve relating the heart will be able to contract to a smaller volume at the end of systole.

end systolic pressure volume relationship contractility and afterload

Vena cava occlusion decreases venous return to the heart, thereby causing a progressive fall in end-diastolic volume preload over several beats. As preload progressively decreases, the PV loop moves to the left and gets smaller. If a line is then drawn through the upper left corner of each loop as shown for the three PV loops in the figurethe line represents the ESPVR, and both the slope and the x-intercept can be determined. It is important to construct the ESPVR relationship within a few seconds of occluding the vena cava usually over several heart beats to prevent sympathetic reflexes from increasing ventricular inotropy, which would increase the ESPVR slope.

This is a valid experimental way to determine ESPVR because this relationship is relatively load independent. Interdependent Effects of Changes in Afterload If afterload is increased e.

end systolic pressure volume relationship contractility and afterload

The increased end-systolic volume, however, leads to a secondary increase in end-diastolic volume because more blood is left inside the ventricle following ejection and this extra blood is added to the venous return, thereby increasing ventricular filling. This secondary increase in preload enables the ventricle to contract with greater force Frank-Starling mechanismwhich partially offsets the reduction in stroke volume caused by the initial increase in afterload.

Consequently, in a normal heart, changes in aortic pressure have relatively little affect on stroke volume. However, in heart failure patients in which the end-diastolic volume is already maximal, an increase in aortic pressure may lead to a significant reduction in stroke volume.

If afterload aortic pressure is reduced green loop in figurethe opposite changes occur - stroke volume increases due to the decrease in end-systolic volume, accompanied by a smaller reduction in end-diastolic volume.

Cardiology - Cardiac Output

This is the basis for giving an arterial dilator to enhance cardiac output in heart failure patients. Interdependent Effects of Changes in Inotropy Increased inotropy red loop in figure increases the slope and shifts the end-systolic pressure-volume relationship ESPVR to the left, which permits the ventricle to generate more pressure at a given LV volume. Increased inotropy also increases the rate of pressure development and ejection velocity, which increases stroke volume and ejection fraction, and decreases end-systolic volume as shown in the figure.

With less blood remaining in the ventricle after ejection, the ventricle fills to a smaller end-diastolic volume during diastole, but this only partially offsets the reduction in end-systolic volume.

end systolic pressure volume relationship contractility and afterload

Increased stroke volume increases cardiac output and arterial pressure. A patient in acute heart failure due to a loss of inotropy may be given a positive inotropic drug to increase stroke volume and to reduce ventricular preload, both of with are beneficial CLICK HERE for more information.

Interdependent Effects of Preload, Afterload and Inotropy on Ventricular Pressure-Volume Loops

Decreasing inotropy has the opposite effects green loop in figure ; namely, it increases end-systolic volume and decreases stroke volume and ejection fraction, accompanied by a small secondary increase in end-diastolic volume. Therefore, ejection begins at a higher aortic diastolic pressure.

If preload end-diastolic volume and inotropy are held constant, this will result in a smaller stroke volume and an increase in end-systolic volume red loop in figure.

Stroke volume is reduced because increased afterload reduces the velocity of muscle fiber shortening and the velocity at which the blood is ejected see force-velocity relationship. A reduced stroke volume at the same end-diastolic volume results in reduced ejection fraction.

CV Physiology | Effects of Preload, Afterload and Inotropy on Ventricular Pressure-Volume Loops

If afterload is reduced by decreasing aortic pressure, the opposite occurs - stroke volume and ejection fraction increase, and end-systolic volume decreases green loop in figure. Independent Effects of Inotropy Increasing inotropy increases the velocity of muscle fiber shortening at any given preload and afterload see force-velocity relationship.

This enables the ventricle to increase the rate of pressure development and ejection velocity, which leads to an increase in stroke volume and ejection fraction, and a decrease in end-systolic volume red loop in figure. Decreasing inotropy has the opposite effects; namely, increased end-systolic volume and decreased stroke volume and ejection fraction green loop in figure.

Interdependent Effects of Preload, Afterload and Inotropy In the intact heart, preload, afterload and inotropy do not remain constant.

To further complicate matters, changing any one of these variables usually changes the other two variables. Therefore, the above PV loops, although they illustrate the independent effects of these three variables, they do not represent what happens when the heart is in the body. However, if one understands the independent effects of these variables, then it is relatively easy combine the loops to illustrate what occurs when multiple variables change.