How do we measure afterload

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.

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 volume , which 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 beats , the decrease in EDV is less than the decrease in ESV so that the difference between the two, the stroke volume, is increased i. It is important to note that the changes brought about by altered afterload are modified acutely by baroreceptor reflexes that alter heart rate and inotropy, both of which will modify the changes in EDV, ESV and stroke volume initiated by the change in afterload.

For example, suddenly reducing afterload by decreasing arterial pressure will lead to a reflex increase in heart rate and inotropy. Increased heart rate, by reducing filling time, will further decrease in EDV and tend to attenuate the stroke volume increase produced by reducing the afterload. The final steady-state response will be determined by the sum of the individual, yet interdependent , responses. Cardiovascular Physiology Concepts Richard E. Klabunde, PhD. Klabunde, all rights reserved Web Design by Jimp Studio.

NursingCenter Blog. Continuing Education More. Preload and Afterload — What's the Difference? Share this on. A recent Quick Quiz on our Facebook page resulted in a mix of responses. Do you know what word is used to describe the amount of stretch on the myocardium at the end of diastole? The responses were split between preload and afterload.

Tags :. Log in to leave a comment Login or Register. One does not normally think about this variable or the role it plays in determining cardiac workload, but it is clearly there in the background. Blood has mass and therefore inertia - i.

Several important points can be made regarding this determinant of afterload, without going into excessive detail. And if excessive detail is for some reason required, it can be found in Sugawara et al , from where most of this information was derived.

As has already been mentioned elsewhere, the modulus of arterial impedance is maximal at a frequency of 0 Hz, i. That is thought to be due to the fact that the smallest arterioles are responsible for a lot of the impedance, and by the time it reaches these small vessels, blood flow has probably had most of the pulsatility windkessled out of it. Where flow is constant, "resistance" is the term we use to describe the force acting in opposition to forward flow. Resistance to the flow of fluids through tubes is described by the Poiseuille equation:.

As will be discussed here, of all these parameters, the one which has the greatest clinical significance is the vessel radius, but for completeness let's discuss the others.

The length of the vessel is important: the longer the vessel, the greater the resistance. This is obviously somewhat difficult to discuss in the circulatory system, which is a tree of many branches; various scaling models would need to be applied in order for it to make sense vis.

The ICU being a dark weird place, plausible scenarios where arterial length changes dramatically can be generated by a restless imagination, but these are thankfully quite rare eg. In these scenarios, effective vessel length decreases - but at the same time the compliance of the system and the total radius take a massive dive. In short, in virtually every practical situation, the resistance-improving effects of reducing the length of the vascular tree will be massively overshadowed by the other effects.

Fortunately, under normal circumstances, the length of the arterial tree of critically ill patients does not tend to vary overmuch during their ICU stay, and so this parameter can be safely ignored as something stable and boring.

The viscosity of the blood is a much more variable parameter. Blood is a non-Newtonian fluid, and its apparent viscosity depends on things like shear forces, haematocrit, plasma protein interactions, and the deformability of RBCs particularly where it comes to the small peripheral vessels.

In general, it exhibits "shear-thinning" behaviour, where its viscosity decreases markedly with increasing shear stress. Viscosity is affected by haematocrit Clivati et al, and the unnatural excess of anything unusual eg. LDL, in the study by Pop et al. As one might expect, increasing viscosity has the effect of increasing afterload, but it is probably a relatively minor player, and is often not amenable to direct control by the intensivist. Arterial vessel radius is the most important determinant of arterial resistance because resistance is inversely proportional to the fourth power of the vessel radius.

Miniscule changes in vessel radius, therefore, have massive effects on total peripheral resistance. This is amplified by the fact that the total radius of these small vessels is truly vast.

Imagine all of those vessels simultaneously constricting even slightly. As if defining something that defies definition was insufficiently cruel, in Question 19 from the second paper of CICM examiners also asked the trainees to separate the determinants into right and left ventricular territories as well as factors which affect both. From five lines of examiner comments, it is difficult to reconstruct the sort of answer they were looking for, only that to " describe and not merely list factors" was desirable.

With no guidance beyond this, the following tabulated answer was cobbled together from the contents abovementioned disucssion, more as an expression of the author's anger and frustration. Question 13 from the first paper of asked, "what might happen if the afterload were to abruptly increase?

Probably, some sort of table is in order. For lack of imagination, the following breakdown is offered, which is basically a paraphrased and referenced version of the answer offered by cicmwrecks:. Norton, James M. Vest, Amanda R. Humana, Cham, Milnor, William R.

McDonald's blood flow in arteries: theoretical, experimental and clinical principles. CRC press, Specifically, Chapter 12 is gold.

Moriarty, Thomas F. Its limitations as a relation for diastolic pressure, volume, or wall stress of the left ventricle. Covell, J. Pouleur, and Jr J. Sonnenblick, Edmund H. Evans Downing. Mills, C. Chirinos, Julio A. Nichols, Wilmer W. Hayashida, Wataru, et al. Ross, Jr J. Franklin, and S. Sasayama, Shigetake, et al. Luecke, Thomas, and Paolo Pelosi. Geske, Jeffrey B. Shah, Sachin, et al. Mitchell, Gary F. Sugawara, Motoaki, et al.

Peterson, Lysle H. Huo, Yunlong, and Ghassan S. Baskurt, Oguz K. Possible mechanism for occurrence of anemia in chronic heart failure patients?. Attinger, E. Clivati, Alberto, et al. Chakravarty, S. Seymour, Roger S. Suga, H. Martin, Ronald R. Pao, Y. Ritman, and E. Gsell, Matthias AF, et al. Time-varying myocardial stress and systolic pressure-stress relationship: role in myocardial-arterial coupling in hypertension.