Preload and Afterload??????

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im confused abt preload and afterload, can anyone give me a hand and list what is the factors increase and decrease of preload and afterload?

i am trying to review the cardiac physiology for my med-surg and stuck here, any good web site recommend for cardiovascular, or EKG webs, it drives me crazy:(:(:(:(:banghead::banghead::banghead:

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im confused abt preload and afterload, can anyone give me a hand and list what is the factors increase and decrease of preload and afterload?

i am trying to review the cardiac physiology for my med-surg and stuck here, any good web site recommend for cardiovascular, or EKG webs, it drives me crazy:(:(:(:(:banghead::banghead::banghead:

https://allnurses.com/forums/f15/cardiac-preload-afterload-31705.html

:heartbeat

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I don't know if that link will really help but I hope it'll somewhat help. Good luck!

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Specializes in med/surg, telemetry, IV therapy, mgmt.

these are difficult concepts to understand. i recommend that you read this information over a number of times until you begin to feel that you understand it.

preload is the initial stretching of the cardiac myocytes prior to contraction, and it is dependent on ventricular filling (or end diastolic volume.) it is related to right atrial pressure. the most important determining factor for preload is venous return. a general relationship called the frank-starling mechanism (frank-starling relationship: increasing preload leads to increased cardiac output) is at play here. several factors influence end diastolic volumes and lead to increased or decreased preload:

  • blood volume depletion
  • blood volume distribution in the body
    • in the upright individual, blood will pool to extrathoracic compartments, especially the legs
    • in the recumbent individual, blood will redistribute into the thorax, which increases preload

    [*]venous tone

    • is under sympathetic neural and humoral control
    • responds to blood volume during exercise and movement by vasoconstriction

    [*]skeletal muscle action

    • during exercise, blood is displaced from the periphery to the thorax and trunk due to the squeezing action of contracting muscle on the venous bed causing an increase in preload as well as cardiac output because blood volume to the heart increases.

afterload is the stress developed in the wall of the ventricle during ejection of the blood out of the ventricles, or it is the "load" that the heart must eject blood against. it depends on aortic pressure and ventricular dimensions (size and amount of blood the ventricles can hold). afterload increases with ventricular dilation. it is ventricular wall stress. afterload is the tension (or the arterial pressure) against which the ventricle must contract. if arterial pressure increases, afterload also increases. afterload for the left ventricle is determined by aortic pressure, afterload for the right ventricle is determined by pulmonary artery pressure.

factors that impair ventricular contraction include: hypertrophy, ischemia, hypertension, collagen deposition & fibrosis, regional asynchrony, increase preload & afterload, intrinsic abnormalities in calcium movement, and tachycardia.

http://cvphysiology.com/heart%20failure/hf006.htm

a couple of other websites where afterload was discussed are:

websites for ekgs are listed on this thread:

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Specializes in DNAP Student.
im confused abt preload and afterload, can anyone give me a hand and list what is the factors increase and decrease of preload and afterload?

i am trying to review the cardiac physiology for my med-surg and stuck here, any good web site recommend for cardiovascular, or EKG webs, it drives me crazy:(:(:(:(:banghead::banghead::banghead:

Just think of preload as volume and afterload as resistance.

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im confused abt preload and afterload, can anyone give me a hand and list what is the factors increase and decrease of preload and afterload?

i am trying to review the cardiac physiology for my med-surg and stuck here, any good web site recommend for cardiovascular, or EKG webs, it drives me crazy:(:(:(:(:banghead::banghead::banghead:

XIGRIS- Simple but PERFECT advice!! Thank you so much. I have had issues with preload/afterload too but your advice is simple and EASY to remember!!

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Preload is venous return/ventricular filling...so anything that would increase those increases your preload, for instance fluid volume overload or dilated ventricles.

Afterload is systemic vascular resistance...so anything that increases that increases you afterload, for instance hypertension or SNS stimulation (vasoconstriciton).

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Specializes in Critical Care, ED, Cath lab, CTPAC,Trauma.

Even though this thread is 4 years old it is always good to revist some subjects.

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here's a little back story about preload/afterload, how it's measured, and why we care.

filling pressure is just the pressure that is in the ventricles at the end of diastole. 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.

first, let's look at the blood flow in a linear fashion.

body > veins > vena cava > right atrium > tricuspid valve > right ventricle > pulmonic valve > pulmonary artery > [color=#ee82ee]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, when that happens 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.

ok. now, why do we care about lv end-diastolic (filling) pressure (preload)? 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-- the place at which 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, preload is too high, 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 cardiac muscle's 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-- 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.

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