The pressure that the ventricle generates during systolic ejection is very close to aortic pressure unless aortic stenosis is present, in which case the left ventricular pressure during ejection can be much greater than aortic pressure.
At a given intraventricular pressure, wall stress and therefore afterload are increased by an increase in ventricular inside radius ventricular dilation. A hypertrophied ventricle , which has a thickened wall, has less wall stress and reduced afterload.
Hypertrophy, therefore can be thought of as a mechanism that permits more parallel muscle fibers actually, sarcomere units to share in the wall tension that is determined at a give pressure and radius. The thicker the wall, the less tension experienced by each sarcomere unit. Afterload is increased when aortic pressure and systemic vascular resistance are increased, by aortic valve stenosis , and by ventricular dilation.
When afterload increases, there is an increase in end-systolic volume and a decrease in stroke volume. As shown in the figure, an increase in afterload shifts the Frank-Starling curve down and to the right from point A to B , which decreases stroke volume SV and at the same time increases left ventricular end-diastolic pressure LVEDP.
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. 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. Log in to leave a comment Login or Register. Arnold Sibanda Quite informative and good for sharpening critical thinking skills!
Anita This was very helpful, thank you. I really like it! Paige Thank you! This helped a lot! Krishna gopal Me a nurse in a conmunity as a community nurse. Evonne Smith Thank you, I like these quizzes to help me remember facts. Very helpful and easy to understand, love the concept, thanks a lot. This combined "aortoventricular" pressure is a major determinant of ventricular wall stress, and is in turn determined by the factors which govern aortic input impedance.
Thus, the hydraulic definition of afterload can be turned into one of the components of the Laplace definition, provided we avert our gaze from certain elements which do not fit this narrative eg. On top of that, it seems that wall stress rather than input impedance is the dominant afterload-determining factor, if you had to pick one. Covell et al , by looking at original and historic data, concluded that. Moreover, changes in input impedance do not, in themselves, appear to influence the force-velocity-length framework for examining ventricular function.
Following from this, the determinants of afterload, arranged into some hierarchical order, must be as follows:. They will be discussed in that order, mainly because to leave arterial resistance to last seemed like a suitable way to emphasise its importance. Of all the aforementioned determinants, most survive only in the minds of physiology professors, trapped there by bushy grey eyebrows. Consider: ventricular radius and wall thickness do not vary excessively.
Intrathoracic pressure is usually within a range of around mm Hg, unless you are really trying to kill your patient with the ventilator.
Arterial compliance varies, but usually only over decades, as does the influence of the reflected waves. The inertia of the blood column is going to be the same for most mildly anaemic ICU patients, as will the viscosity of the blood, and for most people the length of the arterial tree is fairly fixed. This basically leaves the arterial vessel radius as the main determinant of "real" afterload, which varies over clinically relevant timeframes with pathology and therapy.
End-diastolic volume is the volume you would afterload from, if "to afterload" were a verb. It represents the degree of ventricular sarcomere stretch just before the beginning of systole, which is basically the definition of preload. This volume has dimensions, one of which could be described as a "radius", even though the cross-section is very irregular and certainly not circular.
This "radius", in turn, can sort-of plug into the Laplace equation, if we ignore the fact that neither ventricle has anything like spherical geometry. Those caveats politely ignored, we find that plugging a changing radius into the Laplace equation while keeping all the other variables the same basically gives a linear increase in wall tension.
This means that the bigger the ventricle dilates, the larger the amount of wall stress it experiences in the course of generating the same systolic pressure. Is this for real? Turns out, yes. Hayashida et al compared seventeen patients with dilated cardiomyopathy and compared them to eleven normal controls, using clever maths to calculate regional wall stress from ventriculography data.
As you can see from the stolen images below, the patients with dilated ventricles had a markedly increased wall stress. In most parameters, it was at least two to three times greater than controls, even with the lower systolic LV chamber pressures being generated by the DCM group.
When a change in the thickness of the LV wall is substituted into the Laplace equation, a linear decrease in wall tension is observed. This is a purely mathematical thing the thickness happens to be the denominator of the equation. That said, the effect of increased thickness also makes logical sense because a that's what a smart ventricle would do in reaction to increased wall stress, and b because more sarcomeres pulling the same yoke means the wall stress is shared and each individual sarcomere ends up under less stress.
Experimental evidence for this does exist, at least in terms of modelling what happens to wall stress when the thickness changes. Sayasama et al controllably constricted the proximal aortas of dogs and measured LV performance immediately and after enough time has passed for LV hypertrophy to develop. This is discussed in greater detail in the chapter on the effects of positive pressure ventilation on cardiovascular physiology.
In summary:. Anybody who asks for a discussion of ventricular cavity pressure and how it contrasts aortic pressure must surely be asking for a Wiggers diagram. The most prominent visually appealing part of that diagram is the top section where the ventricular cavity pressure triumphantly overcomes aortic pressure in systole. Obviously, there are several barriers in the way of it doing so, and the first of these can be the heart itself.
Specifically, the meaty outflow tract in HOCM or the crusty valve in aortic stenosis can give rise to an increased ventricular outflow impedance. Again, to reduce this concept to an interaction of pressures is an oversimplification, but it certainly helps to explain it.
In the diagram above, the normal waveforms from Curtiss et al on the left are compared to abnormal ones recorded by Geske et al on the right. The colourised region represents an overlap of the graphs where the left ventricle pressure exceeds the aortic; the difference in pressures is produced by the mechanical resistance to ventricular outflow. Of course, this is by no means common. With a competent aortic valve and a normal LVOT, the normal source of input impedance is the arterial circulation.
Arterial compliance is a complicated topic. The compliance the opposite of stiffness is a property of large arterial vessels mainly owed to their tunica media which permits them to expand in systole, store elastic energy, and then return it in diastole as the aortic valve closes thereby maintaining flow - the Windkessel effect.
It is usualy measured or calculated as a change in volume or diameter per change in pressure, over a fixed vessel length. From this, it follows logically that cardiac workload should increase if the arteries become less compliant.
One can imagine a nice elastic artery expanding readily to accommodate the stroke volume, and then contracting elastically to help it along into the capillary circulation - a process which smoothes the pulsatile flow from the ventricle and transforms it into the stable constant flow required by tissues.
Conversely, one can imagine a stiff artery doing the opposite of those things, i. Experimentally, this is difficult to demonstrate, because it is practically challenging to alter the compliance of blood vessels without altering their diameter or other characteristics. Moreover, in a real life model, arterial compliance cannot be measured reliably because the blood volume keeps escaping into the venous circulation. However, it is possible to summarise things crudely for exam purposes, borrowing from Chirinos :.
You could probably represent that in the form of a diagram, at a risk of giving the appearance that it was generated using some real experimental data it wasn't. Increased stiffness is not only a phenomenon which affects the aorta. Distal peripheral arteries can also become stiffened and contribute to afterload, but they do so by a different mechanism.
Decreased peripheral arterial compliance causes an increase in the pulse wave velocity, which means that the reflected wave from the distal circulation arrives too early - during systole - and contributes to the afterload. 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.
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