Explain: Preload vs Afterload

Med-SurgRN311, BSN · Nov 13, 2013

It would not be decreased afterload because that would indicate that it is easier for the heart to move blood out. Decreased afterload equals decreased resistance, meaning it is easier for the heart to pump blood to the systemic circulation. Any medication that causes vasodilation has this effect. An occluded coronary artery and the ischemia that results decreases contractility. Contractility and preload are related, the relationship described in Starling's Law. Increased preload leads to increased contractility to a point, after which contractility decreases, picture a balloon blown up several times until it loses its elasticity. Damage to the heart inherently reduces contractility, decreasing overall Cardiac Output. Blood and fluids backing up into the systemic/pulmonary circulation as in heart failure further increases preload and decreases contractility.

FlyOR · Nov 13, 2013

Bravo! What a generous post Esme! I wish I had seen that when I was in anatomy!

Just a suggestion, if you google "cardiac animations" or really any animations, you can get some good stuff. Sometimes the visual is the trick for certain learners, it helped me during my NCLEX studying.

Hope this helps and I LOVE the backed up toilet analogy!

nurseprnRN, BSN, RN · Nov 14, 2013

It's helpful if you can step back first and think of what the anatomy of the circulatory system is supposed to accomplish. It's supposed to move a fluid around in a bunch of blood vessels, pumped out at high pressure from the left side of the heart, returned to the heart by passive squeezing in the veins and kept from sloshing backwards by valves in the vessels. Then the right side of the heart is supposed to push it through the lungs (at a lower pressure, because it only has to perfuse the lungs right next door, not all the way down to the toes like the arterial system) to do the gas-exchange thing. Then the fluid goes back to the left side of the heart and out to the body again.

Ventricular filling pressure is just the pressure that is in the ventricles at the end of diastole (LVEDP, left ventricular end-diastolic presssure). For a given volume delivered to a ventricle, pressure can be lower if the ventricle is nice and soft and flexible and empty, ready to accept a new load, than if it's hard and scarred up or has leftover blood in it from the last systole because the AV is hard to open OR because its contractility was so lousy that it didn't empty well. Another term that is used could be "preload," pre- meaning "before systole," and load, well, being the load of blood delivered to the ventricle that it is gonna have to move out in systole. You can measure load as weight or volume, but the way we look at it is by measuring the pressure that occurs there. Pressure changes tell us what's going on in there. Think about a soft balloon (low pressure) and a hard one (high pressure). Which has more air in it?

Let's look at the blood flow in a linear fashion. I regret that I cannot give these in color so you can see the blue of venous, the red of arterial. But hey. Draw them on a piece of paper in color. The lungs are pink ?

Body > Veins > Vena Cava > Right Atrium > tricuspid valve > Right Ventricle > pulmonic valve > Pulmonary Artery > LUNGS >Pulmonary Vein > Left Atrium > mitral valve > Left ventricle > aortic valve > Arteries > Body

Think about when the valves between two chambers are OPEN. By definition, each chamber must be at the same pressure, right? So, at the end of diastole, just before systole, the pressure in the LV is the same as LA pressure is the same as the pressure in the pulmonary vein (no valve in the way there) and in the pulmonary capillary bed. And since there are no valves in the pulmonary capillary bed, tracking backwards, you can see that LV end diastolic pressure equals end-diastolic PULMONARY ARTERY PRESSURE, which is, conveniently, what we look at when we are wondering what's going on in the left heart. You can even follow it back all the way to the right atrium, and the vena cava-- central venous pressure! Wow!

OK. Now, why do we care about LV end-diastolic (filling) pressure? It's because that's where the work of supplying the whole body goes. For that, I wish I could draw you a nice little curve here. I can't, so I will describe it and YOU will draw it on a piece of paper to look at while we chat.

Horizontal axis: label this "preload" or any other term you like. Filling pressure, PA diastolic pressure is the same thing (see above) and you can even extrapolate all the way back to central venous pressure, for a rough trend-setting bit of data.

The vertical axis you will call "cardiac output," or "blood pressure," because the line we are going to draw is going to explain something really cool.

Start lowish on the left, near the vertical axis-- low filling pressure means low BP. Think: hemorrhage, hypovolemia, makes your BP low, right?

Slant the line upwards to the right, showing that blood pressure (cardiac output) increases the more blood you put into the heart. (Tank up that hypovolemic guy, and BP improves.) But at some point, that upward-going curve peaks, flattens out...and then it DROPS as the preload keeps increasing. This is because cardiac muscle is like a rubber band-- the more you stretch it, the harder it contracts...to a point, at which point it gets too stretched out and actually contracts less well. Draw a little asterisk at the top of that curve, where it starts to fall, then let it fall a little bit. That asterisk marks the best cardiac output you can get-- preload and output are optimal for that heart. Beyond that point, where the line slopes downwards, lies congestive heart failure- the heart is too full, has more than it can handle, and it fails. (This is, BTW, called the Frank-Starling Law of the heart, and you just drew the Frank-Starling curve) Pressure backs up into the pulmonary capillary bed making the lungs get wet and heavy. This is when people get diuretics (to decrease that excessive preload) AND drugs to improve their contractility.

Of course, if contractility is lousy because of coronary artery disease, previous MI, or whatever, this whole curvy line thing will kinda slide over to the left-- the myocardium will fail with lower pressures than it would if it had better contractility. Better contractility (a right shift) means it will handle more preload (higher filling pressures) and make better BP out of it. Draw a second curve to the right of the first one, parallel to it, to see that. With me so far?

I think you can see how CAD will give you higher filling pressures (preload)-- when the heart is failing a bit, it goes past the top of its curve more easily because its contractility is diminished.

Mitral STENOSIS will, in fact, decrease your LV preload, but it will increase pressures back into the lungs and, eventually, the right heart, because of the resistance to flow from the right side to the LV. Mitral REGURGITATION, on the other hand, will result in higher filling pressures because when the ventricle contracts in systole, some of the blood goes backwards, leaving excess sloshing around between the atrium and ventricle; the ventricle will have to accept a higher reload at diastole, and it doesn't like it. Over the top of the curve again.

Well, I hope this hasn't confused you. I used to tell my students they had to know this because we saw lots of people with all sorts of deficits, but if they didn't have hearts and lungs, they were dead and we didn't have to take care of them anymore. Works in every possible area you could work, except pathology. Please ask me if I've confused you anywhere.

fah33mkamboh · Nov 25, 2015

sorry i couldnt understand you very well, preload is end diastolic volume or its the presuure that is generated in the ventricle from end diastolic volume thus we say it end diastolic pressure, what does it do if this pressure increase or decrease kindly can you explain it to me,

sharifi9879 · Dec 3, 2015

Preload is defined as the actual stretch or tension on the ventricular myocardium prior to contraction (Totora & Gabowski 2002). The greater the preload on the myocardium (the larger the amount of blood that has filled the heart during diastole), the greater the contraction will be. A simple analogy to explain this concept is that the further you stretch an elastic band prior to releasing it, the further it will recoil. The same principle applies here: the greater the stretch or tension on the myocardium, the greater the force of contraction. When venous return to the heart increases, ventricular filling and preload also increase. The Frank Starling Law of the Heart (Starling's Law) asserts that the more the ventricle is filled with blood during diastole (EDV), the greater the volume of blood that will be ejected (stroke volume) during the ensuing systolic contraction.

sharifi9879 · Dec 3, 2015

Afterload is defined as the force or pressure against which the ventricular myocardium must push prior to contraction (Totora & Grabowski 2003). This force or pressure is constantly present in the arteries as arterial blood pressure. Therefore, any increase in systemic blood pressure will result in the left ventricular myocardium having to contract more forcefully to eject its volume of blood. Any increase in the pressure of the pulmonary circulation, such as pulmonary oedema, or the presence of any physical obstruction to the pulmonary circulation, such as lung scar tissue, will result in the right ventricular myocardium having to contract more forcefully. In the long term, this increased workload for the myocardium will eventually result in the abnormal enlargement of the myocardium (hypertrophy), which may in turn lead to heart failure.

sharifi9879 · Dec 3, 2015

Pheebz777, BSN, RN · Jan 21, 2016

You tube has a low of wonderful animated videos that explain this. Once you watch one, you'll never forget it.

armyicurn · Jan 29, 2016

Great topic! Thanks for taking the time to explain it in basic terms.