Cardiac Preload and Afterload

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    Hi Everyone!!!

    I hope everyone's weekend has been full of fun, excitement, and in my case STUDYING

    I was wondering if anyone could give me sdome info on Preload and Afterload. I am a bit confused and being tested on it tomorrow.

    Thanks

    Lisa
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  3. 11 Comments so far...

  4. 6
    What exactly are you looking for? This is what I know....

    Preload- it's the pressure at the end of diastole (filling of ventricles)...aka left ventricular end diastolic pressure. It's primarily a reflection of volume and is influenced by venous return. Increased preload (to a point) = increased cardiac output

    Afterload- (in aorta) resistance to ejection during systole (the force opposing ventricular ejection). The ventricle must overcome aortic pressure in order to eject blood. Increased afterload = increased workload and decreased cardiac output and slower contraction.

    Basically, preload is how much blood are you giving your heart to pump. Along with this is the Frank-Starling Law (see below).

    With afterload, the left vent pressure has to be more than the aorta so the blood can get out. There is no benefit to increased afterload.

    Contractility goes hand in hand with this also. It's the degree of myocardial shortening. It depends on ATP and other factors including hypoxemia. Moderate hypoxemia (O2 = 50-80) = increased contractility. Sever hypoxemia (O2 = <50) = decreased contractility. When it's severe, your heart works less efficiently.

    Frank-Starling Law- the bigger the stretch (to a point), the stronger the contraction.
    *stretch of the myocardium is increased by increased filling.
    *increase or decrease in the volume of blood = an increase or decrease in the force of contraction (like a rubber band flying)
    *this can max out...your actin and myosin can disengage and your force of contraction will drop to zero (like a rubber band breaking)

    Hope this helps!!!

    Kristy
    McKinneyMom, ldyjstce, hikingcole, and 3 others like this.
  5. 0
    Well...no need for me to post now! Good job Em's M!
  6. 0
    Originally posted by emily_mom
    What exactly are you looking for? This is what I know....

    Preload- it's the pressure at the end of diastole (filling of ventricles)...aka left ventricular end diastolic pressure. It's primarily a reflection of volume and is influenced by venous return. Increased preload (to a point) = increased cardiac output

    Afterload- (in aorta) resistance to ejection during systole (the force opposing ventricular ejection). The ventricle must overcome aortic pressure in order to eject blood. Increased afterload = increased workload and decreased cardiac output and slower contraction.

    Basically, preload is how much blood are you giving your heart to pump. Along with this is the Frank-Starling Law (see below).

    With afterload, the left vent pressure has to be more than the aorta so the blood can get out. There is no benefit to increased afterload.

    Contractility goes hand in hand with this also. It's the degree of myocardial shortening. It depends on ATP and other factors including hypoxemia. Moderate hypoxemia (O2 = 50-80) = increased contractility. Sever hypoxemia (O2 = <50) = decreased contractility. When it's severe, your heart works less efficiently.

    Frank-Starling Law- the bigger the stretch (to a point), the stronger the contraction.
    *stretch of the myocardium is increased by increased filling.
    *increase or decrease in the volume of blood = an increase or decrease in the force of contraction (like a rubber band flying)
    *this can max out...your actin and myosin can disengage and your force of contraction will drop to zero (like a rubber band breaking)

    Hope this helps!!!

    Kristy



    WOW! You Go Girl! I wish I had those brains!
  7. 0
    Oh my gosh!!! I wish I could think like that. I am printing your response as I write and will be memorizing it for tomorrow.

    Thanks
    Lisa
  8. 0
    Hi .I just wanted to say thanks for the info.I am testing on this info on Tuesday and you make alot of sense.
  9. 0
    It's easier to remember with arrows, but I couldn't do that with this BB.

    You're welcome! Glad to help (nice to know I retained something!!). Let me know if you have any other problems. I can try!

    One thing I forgot to mention.

    The L side of the heart is usually bigger due to the intense amount of work needed to pump that blood out against aortic pressure. The R side is smaller b/c the pressure is smaller as it really wants to be oxygenated by the lungs.

    Good luck on your tests all!

    Kristy
  10. 0
    I don't this you would need to know this for your test, it's one of those "nice to know, but not need to know for a student, but....

    Just a note to add on afterload. Resistance can occur at any point in the heart, not just the aorta, ex mitral valve stenosis can cause inc afterload to the left atrium, pulmonary Hypertension can create inc afterload to the right side of the heart, etc... Pulm HTN would be treated much differently than ordinary HTN, that is why I threw that in.
  11. 0
    Pulm HTN will cause the R side of the heart to enlarge, as it's doing way more work than it did before.
  12. 0


    Thanks Kristy!!!!! I to have this on a Midterm Monday!!!! Almost 1/2 way thru my second and hardest semester!!!


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