Explain: Preload and afterload

  1. 1
    Can someone please break it down really simple, elementary my dear: what is cardiac preload, afterload? Feel free to give specific examples with drugs that affect each to make it crystal clear, thanks.
    Joe V likes this.
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  3. 7 Comments so far...

  4. 4
    Per Professor Carl Rothe of IU, the definitions are as follows:

    Preload is the end-diastolic volume (EDV) at the beginning of systole. The EDV is directly related to the degree of stretch of the myocardial sarcomeres. This is the basis of the Frank-Starling Law of the Heart.

    Afterload is the ventricular pressure at the end of systole (ESP). Ejection stops because the ventricular pressure developed by the myocardial contraction is less than the arterial pressure. This determines the end-systolic volume (ESV). Because the EDV equals the presystolic volume for a given beat of a ventricle, then the pre- and postsystolic volumes define the stroke volume (if the valves are fully functioning and there are no ventricular-septal leaks). The product of stroke volume and heart rate determines the cardiac output—the primary function of the heart.
  5. 19
    Quote from cfsleo812
    Can someone please break it down really simple, elementary my dear: what is cardiac preload, afterload? Feel free to give specific examples with drugs that affect each to make it crystal clear, thanks.
    Hey cfsleo812,
    So: really simple, elementary preload and afterload, huh? Good question.
    Basically, preload is stretch. The amount of volume being returned to the right side of the heart from systemic circulation. Afterload is squeeze. The amount of resistance the left side of the heart has to overcome in order to eject blood.
    Just look at the mechanism of action with different drugs to see what they do. e.g. a dilator will decrease, so the pressure comes down and the heart has less resistance to overcome, the catch is that it can also lead to less venous return, hypotension, ischemia. A pressor will increase, hopefully leading to better return to the heart. But it can also create too much resistance, which also can lead to problems.
    This is a very simplified definition, hope it helps. Sometimes the simplest things are the most useful.
    Trinibabe, blueberry13, Revan, and 16 others like this.
  6. 3
    Pre load of the right side of the heart is measured by the central venous pressure or CVP

    Preload of the left side of the heart is measured by the pulmonary cappilary wedge pressure or PCWP (wedge)

    Preload refers to the heart's "filling pressures".
    Trinibabe, Revan, and Dmp24 like this.
  7. 0
    This is an simple, but excellently simple explanation! Thanks!
  8. 2
    Preload enhancers: fluid! Preload = stretch, so think volume.

    Preload reducers: nitrates (both preload and afterload, but more so venous than arteriole), diuretics.

    Afterload enhancers: vasoconstrictors.

    Afterload reducers: vasodilators. Many have mixed venous/arteriole action. Hydralazine is an example of a highly-selective arteriole vasodilator.

    It's important to know about preload, afterload & contractility and how they relate to your patient. For example, for an RV infarct, you do NOT want to give preload reducers because these patients are preload dependent. If you lessen the "stretch" (volume) that can lead to decreased left ventricular filling = decreased CO.

    If you have a patient with a low BP, are they volume depleted? You don't want to "squeeze a dry tank"
    Dmp24 and LPN2RN2013 like this.
  9. 1
    preload-volume ( i think of it as the amt of blood getting in the Right atria)

    afterload-force of contraction (blood coming out of the aorta)

    in and out!
    LPN2RN2013 likes this.
  10. 4
    Preload = volume of blood received by the heart.

    Afterload = pressure or resistance the heart has to overcome to eject blood.

    Drugs that dilate the vasculature thus reducing blood return to the heart effect pre-load... for example nitroglycerin by making the venous side bigger. There is some effect on arterial side which reduces afterload not not as much as venous / preload. Fluid boluses increase preload.

    Drugs that increase afterload are sympathomimetics like epinephrine, dopamine, levophed, etc. They increase systemic vascular resistance and clamp down on the arterial side which increases the pressure making it harder for the heart to overcome and be able to eject its blood volume. ACE inhibitors and CPAP offer afterload reduction.

    That is as simple as it gets
    Trinibabe, Anoetos, LPN2RN2013, and 1 other like this.


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