Explain: Preload vs Afterload

  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.
    Last edit by Joe V on Nov 15, '16
  2. 13 Comments

  3. by   soccerbsn
    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.
  4. by   getoverit
    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.
  5. by   pghfoxfan
    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".
  6. by   3TimesACharm
    This is an simple, but excellently simple explanation! Thanks!
  7. by   turnforthenurse
    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"
  8. by   iwillbecomenurse
    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!
  9. by   Medic7714
    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
  10. by   fah33mkamboh
    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,
  11. by   sharifi9879
    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.
  12. by   sharifi9879
    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.
  13. by   sharifi9879
  14. by   Pheebz777
    You tube has a low of wonderful animated videos that explain this. Once you watch one, you'll never forget it.