“The pre– and after– in preload and afterload refer to before and after(really during) the contraction of the heart muscle.” KTA
Preload
“Preload is the degree of myocardial distension prior to shortening (i.e. shortening during contraction). As initially demonstrated by Otto Frank and Ernest Starling, an intrinsic property of myocardial cells is that the force of their contraction depends on the length to which they are stretched: the greater the stretch (within certain limits), the greater the force of contraction. An increase in the distension of the ventricle will, therefore, result in an increase in the force of contraction, which will increase cardiac output…Preload largely depends on the amount of ventricular filling. It should not, however, be confused with the venous return. The amount of blood returning to the heart in any period of time must be equal to the amount of blood pumped by the heart in the same period, as there is no place for storage of blood in the heart. Venous return, therefore, equals cardiac output, whereas preload is only one component of cardiac output” (Vincent, 2008).
Clinical Examples
1. IVFs. “Fluid administration takes advantage of the Frank-Starling relationship to increase stroke volume and cardiac output. Although an excessive increase in the end-diastolic volume may increase myocardial oxygen requirements, this intervention is associated with relatively limited consequences, as compared with catecholamines.”
Afterload
“Afterload is the force against which the ventricles must act in order to eject blood, and is largely dependent on the arterial blood pressure and vascular tone. Reducing afterload can increase cardiac output, especially in conditions where contractility is impaired” (Vincent, 2008).
1. Arterial vasodilators. “Arterial vasodilator therapy results in significant improvements in cardiac output in patients with heart failure by reducing afterload.” Arterial vasodilators open up the pipes that carry blood outside of the heart, reduces the arterial resistance against which the heart has to pump, and so increase cardiac output. “Interestingly, this therapeutic approach has been more successful than inotropic stimulation, and has been shown to reduce mortality rates in this patient population. An obvious limitation is the decrease in arterial pressure, which may compromise organ perfusion.” Vincent, 2008.
“In general, you want to increase preload and decrease afterload in a heart that needs help”. KTA
This link explains preload and afterload better than the videos: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2575587/
Another author in the Khan Academy video defines preload and afterload as follows:
- Preload = “LV wall stress at end diastole”. Note that during diastole, the heart muscle is relaxed and the LVs are filling up with blood. The preload is the force per unit area (i.e. pressure) that is exerted on the LV wall prior to contraction (at the end of diastole). Above, Vincent defined preload as “the degree of myocardial distension prior to shortening”. This wall stress is what causes the distention in the cardiac myocyte. Another definition of preload is that “preload is the pressure on the ventricular wall prior to contraction(i.e. at the end of diastole).
- Afterload = “LV wall stress during ejection”. Unlike preload which is the wall stress at a specific point in time, the afterload is the LV wall stress during a period of time (ejection). Vincent defined afterload as “the force against which the ventricles must act in order to eject blood, and is largely dependent on the arterial blood pressure and vascular tone.” Another way to define afterload is that afterload is “the pressure on the ventricular wall during contraction/systole.” Note that LV stress is the force per unit area on the wall which is essentially the pressure on the wall since pressure = Force/area.
References
Vincent, Jean-Louis. “Understanding cardiac output.” Critical care (London, England) vol. 12,4 (2008): 174. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2575587/