CV Physiology | Cardiac Afterload
Given greater pre-load and thus end-diastolic volume is it expected that diastolic BP would be Stroke volume (SV) refers to the quantity of blood pumped out of the left ventricle with every heart beat. The equation for cardiac output is. Stroke volume is determined by the difference between left ventricular end diastolic volume (LVEDV) and left ventricular end systolic volume (LVESV): Since SV is rather hard to measure, we use the FICK equation to estimate Q. This relationship is similar to the Law of LaPlace, which states that wall tension (T ) The exact equation depends on the cardiac chamber shape, which changes there is an increase in end-systolic volume and a decrease in stroke volume.
However, recent experimental investigations suggest that arterial pulse pressure is not linearly proportional to stroke volume. However, mechanisms underlying the relation between the two have not been clearly understood. The goal of this study was to elucidate how arterial pulse pressure and stroke volume respond to a perturbation in the left ventricular blood volume based on a systematic mathematical analysis.
- 1. Introduction
- What is Afterload?
- How Afterload Affects Stroke Volume and Preload
Both our mathematical analysis and experimental data showed that the relative change in arterial pulse pressure due to a left ventricular blood volume perturbation was consistently smaller than the corresponding relative change in stroke volume, due to the nonlinear left ventricular pressure-volume relation during diastole that reduces the sensitivity of arterial pulse pressure to perturbations in the left ventricular blood volume.
Therefore, arterial pulse pressure must be used with care when used as surrogate of stroke volume in guiding fluid therapy.
Introduction Stroke volume SV is the volume of blood pumped out by the heart to the arterial tree. It is known to be highly correlated with cardiac function in that it typically decreases in the presence of diseases such as cardiogenic shock [ 1 ], hemorrhage [ 2 ], sepsis [ 3 ], spinal cord injury [ 4 ], and hypothyroid [ 5 ].
It is also an important determinant of cardiac output, which is modulated by the demand for oxygen delivery to the tissues in the body [ 6 ] and the capacitance of the arteriovenous system [ 7 ]. Regarding its clinical applications, the interpretation of SV or correspondingly cardiac output can help caregivers to better understand the complex pathophysiological alterations in the critical illness, thereby helping to avoid deleterious effects of inotropic therapy [ 8 ], potentially harmful effects of vasopressor agents [ 9 ], and the detrimental edema in fluid administration [ 10 ].
Despite its clinical significance, SV has not been widely utilized for routine diagnostic and therapeutic purposes due to the difficulty in its measurement [ 11 ]. In fact, most state-of-the-art methods to directly measure SV e. To exploit SV in clinical applications without encountering the problems listed above, there have been numerous efforts to indirectly estimate SV from minimally invasive or noninvasive arterial circulatory measurements, which are collectively called the pulse wave analysis PWA methods [ 16 — 19 ].
In one of its simplest form, PWA is based on the assumption that SV is proportional to arterial pulse pressure hereafter called pulse pressure PP [ 16 — 19 ]. The basis for this is found in the force-velocity relationship for cardiac myocytes. Briefly, an increase in afterload decreases the velocity of fiber shortening. Afterload per se does not alter preload; however, preload changes secondarily to changes in afterload.
Stroke volume - Wikipedia
Increasing afterload not only reduces stroke volume, but it also increases left ventricular end-diastolic pressure LVEDP i. This occurs because the increase in end-systolic volume residual volume remaining in ventricle after ejection is added to the venous return into the ventricle and this increases end-diastolic volume.
This increase in preload activates the Frank-Starling mechanism to partially compensate for the reduction in stroke volume caused by the increase in afterload.
The interaction between afterload and preload is utilized in the treatment of heart failurein which vasodilator drugs are used to augment stroke volume by decreasing arterial pressure afterloadand at the same time reduce ventricular preload. This can be illustrated by seeing how ventricular volume changes in response to a decrease in arterial pressure over several heart beats see figure. When arterial pressure is reduced, the ventricle can eject blood more rapidly, which increases the stroke volume difference between EDV and ESV and thereby decreases the ESV.
Because less blood remains in the ventricle after systole, the ventricle does not fill to the same EDV found before the afterload reduction. If afterload is decreased by decreasing arterial pressure as in the example discussed above, the ventricle needs to generate less pressure before the aortic valve opens.
Stroke Volume and Cardiac Output
The ejection velocity after the valve opens is increased because decreased afterload increases the velocity of cardiac fiber shortening as described by the force-velocity relationship. More blood is ejected increased stroke volumewhich decreases the ventricular ESV as shown in the pressure-volume loop. Because end-systolic volume is decreased, there is less blood within the ventricle to be added to the venous return, which decreases EDV. Ordinarily, in the final steady-state after several beatsthe decrease in EDV is less than the decrease in ESV so that the difference between the two, the stroke volume, is increased i.