need help explaining preload and afterload

The way that I think about it is preload (RAP/PAWP) is the stretch that you need to pump effectively. If there is too little volume, the heart does not have what it needs to work the best that is can. If you have too much, you are "over stretched" and can't "bounce back" the way you need too (kind of like overstretching a rubber band). The right amount of volume however, allows the heart to fill and stretch effectively for the best contraction.

Afterload (PVR/SVR) is what the heart has to work against. If your afterload is too high...it's like trying to push volume against a little tiny opening--like a hose that has a kink in it- it is not effective, the heart has to work hard. If the afterload is too low...it is like water running though a bunch of wet noodles, not enough resistance, also not so good. Optimally is a balance between all of these parts...I don't know if that works for you...it helped me remember when I first learned...it is kind of like a big puzzle...you have all of these pieces and you need to find the best fit for the patient...you may have to use volume, vasodilators, or vasopressors to assist you in obtaining the optimal results. Gotta love that frank starling curve!

Thank you for the explanation on preload and afterload. it was very helpful. I had forgotten the rubberband example. cornxp

The way that I think about it is preload (RAP/PAWP) is the stretch that you need to pump effectively. If there is too little volume, the heart does not have what it needs to work the best that is can. If you have too much, you are "over stretched" and can't "bounce back" the way you need too (kind of like overstretching a rubber band). The right amount of volume however, allows the heart to fill and stretch effectively for the best contraction.

Afterload (PVR/SVR) is what the heart has to work against. If your afterload is too high...it's like trying to push volume against a little tiny opening--like a hose that has a kink in it- it is not effective, the heart has to work hard. If the afterload is too low...it is like water running though a bunch of wet noodles, not enough resistance, also not so good. Optimally is a balance between all of these parts...I don't know if that works for you...it helped me remember when I first learned...it is kind of like a big puzzle...you have all of these pieces and you need to find the best fit for the patient...you may have to use volume, vasodilators, or vasopressors to assist you in obtaining the optimal results. Gotta love that frank starling curve!

Here's how I understand it:

Each ventricle of the heart has a preload and an afterload. The preload is the volume coming in that the ventricle has to work with. The afterload is the resistance that the ventricle has to pump that volume out against. So on the right side, the preload is measured as CVP, and the afterload is how tight the lungs are: pulmonary vascular resistance, or PVR. On the left side, the preload is measured as PCW, and the afterload is how tight the arterial bed is: the systemic vascular resistance - the SVR. High is tight, low is loose.

So - right-side problems:if the patient has chronically stiff lungs, the right side of the heart has a high afterload - a high resistance to pump into. The result is right-sided hypertrophy, chamber stretch, a-fib, cor pulmonale. Likewise if the patient has a big PE, the right-sided afterload suddenly pops up, and the right side gets a strain pattern on EKG, all that. If the PE is big enough, then blood won't get through the lungs over to the left side - the wedge pressure will drop. Not enough left-sided preload - their BP is "preload-dependent", and they get hydrated, waiting for clot lysis.

Left side problems: if the patient has a bad pump, i.e. LV failure, whether acute (MI) or chronic (low EF), then the physiologic response is to tighten up the arterial bed - increasing the left-side afterload, raising the SVR, trying to keep up the BP. This makes more work for the failing LV, as it's harder to pump into a tight arterial bed, but it's the only thing the body knows how to do. That's why there's so much emphasis in heart failure situations on "afterload reduction" - loosening up the arterial bed to make it easier for that LV to pump the blood out into it, as long as there's enough BP to work with. Alpha blockers - just the thing. Wedge rises in that situation, right? Too much preload - these patients get diuretics to get rid of some of it.

Sepsis produces the opposite reflex: the SVR drops because of a dilated, rather than a tightened arterial bed. There's nothing like a little sepsis for afterload reduction! Now the problem is: the volume you had, suddenly isn't enough anymore. Not enough preload: everything is dilated, the blood pools in the extremities, there's not enough volume returning to the right side of the heart (CVP is low), which means there isn't enough to get across the lungs to the left side (PCW is low) - so you have a preload (volume) problem on both sides. So you give volume to increase it, and this time an alpha agonist to increase the left-sided afterload: tighten up the arterial bed. Phenylephrine. Levophed maybe, although that has beta in it as well, and can kick up the heart rate, which already up, trying to compensate: "Where'd all my volume go?"

Hope that's helpful. (Hope I got it right!)

Mark, You explained it so well. I went to your website yesterday and printed off the info on reading EKGs. Thank you for taking the time to respond. The info in preload and afterload helped alot.

Patsy

Here's how I understand it:

Each ventricle of the heart has a preload and an afterload. The preload is the volume coming in that the ventricle has to work with. The afterload is the resistance that the ventricle has to pump that volume out against. So on the right side, the preload is measured as CVP, and the afterload is how tight the lungs are: pulmonary vascular resistance, or PVR. On the left side, the preload is measured as PCW, and the afterload is how tight the arterial bed is: the systemic vascular resistance - the SVR. High is tight, low is loose.

So - right-side problems:if the patient has chronically stiff lungs, the right side of the heart has a high afterload - a high resistance to pump into. The result is right-sided hypertrophy, chamber stretch, a-fib, cor pulmonale. Likewise if the patient has a big PE, the right-sided afterload suddenly pops up, and the right side gets a strain pattern on EKG, all that. If the PE is big enough, then blood won't get through the lungs over to the left side - the wedge pressure will drop. Not enough left-sided preload - their BP is "preload-dependent", and they get hydrated, waiting for clot lysis.

Left side problems: if the patient has a bad pump, i.e. LV failure, whether acute (MI) or chronic (low EF), then the physiologic response is to tighten up the arterial bed - increasing the left-side afterload, raising the SVR, trying to keep up the BP. This makes more work for the failing LV, as it's harder to pump into a tight arterial bed, but it's the only thing the body knows how to do. That's why there's so much emphasis in heart failure situations on "afterload reduction" - loosening up the arterial bed to make it easier for that LV to pump the blood out into it, as long as there's enough BP to work with. Alpha blockers - just the thing. Wedge rises in that situation, right? Too much preload - these patients get diuretics to get rid of some of it.

Sepsis produces the opposite reflex: the SVR drops because of a dilated, rather than a tightened arterial bed. There's nothing like a little sepsis for afterload reduction! Now the problem is: the volume you had, suddenly isn't enough anymore. Not enough preload: everything is dilated, the blood pools in the extremities, there's not enough volume returning to the right side of the heart (CVP is low), which means there isn't enough to get across the lungs to the left side (PCW is low) - so you have a preload (volume) problem on both sides. So you give volume to increase it, and this time an alpha agonist to increase the left-sided afterload: tighten up the arterial bed. Phenylephrine. Levophed maybe, although that has beta in it as well, and can kick up the heart rate, which already up, trying to compensate: "Where'd all my volume go?"

Hope that's helpful. (Hope I got it right!)

Mark is the greatest !!!

The #1 all time best resource person on this BB !!!!

What an EXCELLENT web site!!!! Thanks for sharing!!!!!

Here's how I understand it:

Each ventricle of the heart has a preload and an afterload. The preload is the volume coming in that the ventricle has to work with. The afterload is the resistance that the ventricle has to pump that volume out against. So on the right side, the preload is measured as CVP, and the afterload is how tight the lungs are: pulmonary vascular resistance, or PVR. On the left side, the preload is measured as PCW, and the afterload is how tight the arterial bed is: the systemic vascular resistance - the SVR. High is tight, low is loose.

So - right-side problems:if the patient has chronically stiff lungs, the right side of the heart has a high afterload - a high resistance to pump into. The result is right-sided hypertrophy, chamber stretch, a-fib, cor pulmonale. Likewise if the patient has a big PE, the right-sided afterload suddenly pops up, and the right side gets a strain pattern on EKG, all that. If the PE is big enough, then blood won't get through the lungs over to the left side - the wedge pressure will drop. Not enough left-sided preload - their BP is "preload-dependent", and they get hydrated, waiting for clot lysis.

Left side problems: if the patient has a bad pump, i.e. LV failure, whether acute (MI) or chronic (low EF), then the physiologic response is to tighten up the arterial bed - increasing the left-side afterload, raising the SVR, trying to keep up the BP. This makes more work for the failing LV, as it's harder to pump into a tight arterial bed, but it's the only thing the body knows how to do. That's why there's so much emphasis in heart failure situations on "afterload reduction" - loosening up the arterial bed to make it easier for that LV to pump the blood out into it, as long as there's enough BP to work with. Alpha blockers - just the thing. Wedge rises in that situation, right? Too much preload - these patients get diuretics to get rid of some of it.

Sepsis produces the opposite reflex: the SVR drops because of a dilated, rather than a tightened arterial bed. There's nothing like a little sepsis for afterload reduction! Now the problem is: the volume you had, suddenly isn't enough anymore. Not enough preload: everything is dilated, the blood pools in the extremities, there's not enough volume returning to the right side of the heart (CVP is low), which means there isn't enough to get across the lungs to the left side (PCW is low) - so you have a preload (volume) problem on both sides. So you give volume to increase it, and this time an alpha agonist to increase the left-sided afterload: tighten up the arterial bed. Phenylephrine. Levophed maybe, although that has beta in it as well, and can kick up the heart rate, which already up, trying to compensate: "Where'd all my volume go?"

Hope that's helpful. (Hope I got it right!)