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Heart failure question

Discussion in 'Medical Students - MD' started by equilibr8, Aug 3, 2011.

  1. equilibr8

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    I'm trying to understand the mechanism behind heart failure.

    If there is ischemia in the L ventricle (LV), that means that preload will be higher in the LV.

    Question 1: This means that LVEDV is higher, right? And if the LV is not pumping as much blood out, LVESV should also be higher. If both LVEDV and LVESV are higher, shouldn't the stroke volume remain relatively the same? So why does stroke volume decrease in a patient with heart failure? Or does heart failure cause a huge increase in LVEDV but not as great of an increase in LVEDV?

    Question 2: Also, I know that in a patient with heart failure, an increase in LVEDP will increase L atrial pressure. But why does L atrial pressure increase? And why does L atrial pressure increase pulmonary vein pressure and pulmonary artery pressure? Is it because an increase in L atrial pressure will increase the pressure in the aorta, which will increase CVP, which will then increase pulm. artery pressure and thus pulm. vein pressure (since everything is in series)?

    Question 3: Why do all of the above cause an increase in afterload? Is it because there is more blood in both the L and R ventricles and you need more pressure to pump the blood through?

    Thank you.
     
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  3. isoquin

    isoquin Allopathetic
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    I think you have some of your assumptions and order a little wrong.
    LV Ischemia > dysfunctional pump > lower contractility > lower EF = lower SV.
    lower EF > increased end systolic volume > increased LVEDV (not the other way around)
    In essence, the heart can only pump out so much blood. The overfill by adding the increased remaining blood with the incoming bolus makes EDV higher, but the heart still can only push so hard at that point.
    [​IMG]
    Stroke volume is the width of these circuits. In this case, the width of the red circuit is less than the width of the yellow.

    Question 2: increased volume > increased pressure. Because the heart isn't able to output as well as it should, but blood is still coming in, it backs up a little, increasing preload and atrial pressure. Think of it like a partially clogged tub. Everything that comes before the clog gets backed up a little. Ventricle = clog > backs atria > pulm system > right heart. This is why the #1 cause of right heart failure is.... left heart failure. :)
     
  4. aSagacious

    Moderator Emeritus 7+ Year Member

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    I think Isoquin did a good job with the rest, so I'll just answer the above question. The basic concept that dictates contractility (and indirectly stroke volume) is the Frank-Starling law... which is just a special case of the length-tension relationship. This states that there is an optimal pre-stimulus length of a myocyte and any significant deviation in length (whether taught or flaccid) will yield a decrease in contractility and stroke volume.

    [​IMG]

    This decrease in stroke volume then continues in a positive feedback mechanism and eventually further exacerbates volume overload (as described by Isoquin).
     
  5. Medicine4Bruhs

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    Hypoxia caused by ischemia of the heart causes many things including metabolic changes that cause a decrease in ATP availability (no O2 as last electron acceptor) and essentially leads to a decrease in the contractility of the heart. This means it is not as efficient in contracting and ejecting blood from the LV (decrease in dP/dt). If the LV cannot eject blood as well, then more blood remains in the LV, and as more blood remains in the LV, it increases the pressure of the LV. This increase in pressure is what is meant by an increase in preload. In fact, it is called a "pre-load" because this increase in pressure is what helps propel blood out of the LV and into the aorta. Now, the aorta has blood in it as well, so the new blood injected from the LV must displace the blood already present in the aorta (the "afterload"). As afterload increases, it takes more force for the LV to contract (increase in pressure or basically a larger preload) to displace the pre-existing blood in the aorta. In heart failure, the ability of the heart to overcome afterload is decreased.

    On the other side of the coin is that since the LV is pumping out less blood, more remains in the ventricle each contraction cycle, incrementally increasing pressure. At a certain point (such as during left heart failure), this increase in LVEDV causes enough of an increase in pressure that the LA has to contract even harder to pump blood from the LA to the LV. In essence, the roles have switched for this upstream pump such that the blood in the left ventricle now becomes the afterload and the blood in the left atrium now becomes the preload. As this is a series, this increases pressure throughout upstream vascular beds, with relatively smaller increases in the capacitance (venous) vessels.

    Stroke volume decreases partly because initially, the same amount of blood is entering the LV from the atrium but less is getting pumped out due to failure of the LV. Since there is an increase in LVEDV, there is a decrease in the amount blood pumped out (a smaller SV), resulting in a decrease in the ejection fraction. This is one reason why patients with heart failure get prescribed beta adrenergic receptor blockers in hopes of decreasing heart RATE, leading to more (ventricular) filling time, leading to more of a preload that is able to be push out of the LV and into the aorta. As we want to increase preload in HF patients, we can also decrease afterload with diuretics to decrease fluid volume in the body (and thus blood volume in the vasculature with which the heart must pump against).
     
  6. equilibr8

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    MAN YOU ARE ALL TOTALLY AWESOME! THANKS A MiLlION!
     
  7. ElCapone

    ElCapone Don't Lawyer Me
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    Dang. That was beautifully explained. I don't mean to imply that aSagacious and isoquin didn't do as good of a job, but the way you explained it makes sense to a layman like me.
     
  8. danieldrews092

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  9. equilibr8

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    My professor explained a situation where a vasodilator was infused into a patient. He said that if you infuse a vasodilator, Pdiastolic decreases, which causes SVR to decrease, which decreases MAP and increases afterload. This logic does NOT make sense to me AT ALL and I don't understand why afterload increases.

    Can I instead think of it in the following way? Infuse a vasodilator > the blood vessels in the body will dilate > SVR decreases > MAP decreases (since MAP = CO x SVR)?

    But if MAP decreases, the pressure in the aorta (or pulmonary artery) is decreased. Doesn't this mean that afterload decreases (since the pressure that the heart must generate in order to open the aortic valve or pulmonic valve is decreased) and, consequently, stroke volume increases?

    Then I become confused all over again because if stroke volume increases, shouldn't MAP increase as well (according to MAP = CO x SVR)? MAN I feel like I go in circles when it comes to cardiology...
     
  10. Subaru

    Subaru ASA Member
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    You are correct in that MAP will also decrease. MAP and afterload, as far as I understand, are essentially synonymous. Also, this decrease in MAP would increase preload/CVP unless of course the vasodilator is an equal amount venodilator.
     
  11. Medicine4Bruhs

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    These questions entail the crux of cardiovascular physiology and this blurb will do it no justice. Arterial pressure, as its name entails, is the pressure inside the arterial vessels (rather than venous or other vessel types). Arterial pressure changes with respect to the heart's contractions, meaning that arterial pressure changes depending on whether the heart is in contraction (systole) or when the heart is relaxed (diastole). Mean arterial pressure (MAP) is the average of this rise and fall in pressure over time and can be calculated by integrating pressure tracings and dividing them over time. Graphically, if we instead assume that a diastole->systole->diastole contraction cycle causes a rise and drop in pressure tracings such that it looks similarly in shape to a triangle, MAP is half of the area of this triangle, and thus about the pressure 1/3 of the way up the height of the triangle. Pretty cool.

    Anyway, arterial pressure is a pressure directly dependent upon two physical factors: arterial blood volume and arterial compliance (a measure of vessel distensibility defined as the change in arterial blood volume over the change in arterial pressure, dV/dP). How these two elements directly affect arterial pressure (ie MAP) is by thinking that the heart injects a certain amount of blood volume into the arterial vessels, which then works to increase the pressure inside the arteries. This increase in pressure is offset if the arteries can expand in luminal size and accommodate this increase in blood volume, and is a characteristic of healthy (high compliance) patients. Another way to think about this is by trying to stuff water in plastic tubing of varying rigidity: it is much easier to stuff water in a more elastic tube filled with water than to stuff water in a more rigid tube also partially filled with water. This exact pressure with which you must overcome to stuff more water into is called "afterload" and is why, after all of the water injected by the heart is emptied into the aorta and the heart begins to relax, afterload=MAP. The relationship also helps explain why high compliance individuals are healthier than low compliance individuals, because if certain vessels are less distensible, they can therefore accommodate less blood volume inside them before there is a sharp increase in arterial pressure. If there is now an increase in arterial pressure, the heart has to pump harder against this greater vasculature pressure (again, since MAP=afterload). The heart overcomes this afterload by increasing its contractility through a number of certain ways, one of which is by increasing cardiac muscle, explaining why patients with low compliance can present with "enlarged hearts".

    Now, remember how I said that MAP is a function of two physical factors (arterial blood volume and arterial compliance)? Well, these two physical factors are an effect of earlier physiological factors: cardiac output (essentially the volume of blood pumped by the heart per contraction, CO=heart rate times stroke volume) and peripheral resistance (ie total peripheral resistance, TPR or also systemic vascular resistance, SVR). The physiological factors influence the physical factors which directly influence arterial pressure. Since CO is a measure of the volume of blood pumped by the heart, increasing the heart's CO increases arterial volume, which then increases arterial blood pressure, demonstrating how CO affects MAP. Regarding TPR, one way to overcome this increase in blood pressure/volume is ensuring more blood leaves the arterial system and passes into the venous or lymphatic system, decreasing arterial pressure. This is done by decreasing peripheral resistance and allowing more flow from the arteries into the veins (where increases in blood volume have less of an effect on blood pressure because they can expand more). This also explains why veins are also termed "capacitance" vessels because they can "hold" blood volume similar to how capacitors can hold charge in physics. Remember the equations for series and parallel circuits? I hope you do since they are the exact equations used in cardio phys (electrical current is blood flow and voltage is pressure difference).

    Vasodilators, the most important endogenous mediator being nitric oxide (NO), function by increasing blood vessel lumen size in the peripherals, decreasing the resistance that prevents the blood in the arteries from passing into the veins. Since blood is leaving the arterial system more readily, there is less blood in the arteries with which the heart must pump against, decreasing systolic pressure (and MAP) and thus decreasing afterload. At a certain point, decreased resistance allows more blood to enter the venous system, which results in more blood returning to the heart. If more blood returns to the heart, this increase in preload causes more blood to be ejected per contraction, resulting in an increase in stroke volume. Increases in stroke volume would eventually cause an increase in afterload when enough blood has been transferred into the aorta such that there is now a substantial amount in the arterial system. This is the only way you can experience an increase in afterload with vasodilator administration, I believe. I would be interested in your professor's explanation.
     
    #10 Medicine4Bruhs, Aug 9, 2011
    Last edited: Aug 9, 2011
  12. equilibr8

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    Thanks a bunch for all of your responses! I'm slowly getting the hang of the patterns of cardiology.

    Unfortunately, I still have another cardiology question...

    I'm trying to understand how compliance of the venous circulation changes when a patient hemorrhages. I understand that, upon hemorrhage, CVP decreases and the body senses the change in CVP by increasing venous tone. This venous tone will then decrease the compliance of the veins so that, at a lower volume, CVP will increase to maintain cardiac output. (I tend to think of this last statement as increasing the stiffness of the veins so that they are not that 'squishy' and properly return blood to the heart. Is this correct?)

    If, at a lower volume, CVP is brought back up to sustain cardiac output, does this mean that a) less volume is ejected from the heart with each beat (hence lowering SV), and b) HR increases as a result?
     
  13. Medicine4Bruhs

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    The vessels are hemorrhaging blood, so there is already a decrease in total blood volume. The capacitance vessels (veins) undergo veno-constriction to ensure that more blood volume returns to the heart. Veno-constriction is one of the primary methods the body uses to compensate for low blood volumes (such as during types of shock). When they constrict, yes, venous compliance decreases as well, but it's ok.

    To answer your question, without veno-constriction, less blood would return to the heart, which would mean less blood is available for the heart to pump and would result in a decrease in stroke volume (because less of a preload). To overcome this decrease in blood returning to the heart, veins constrict in order to try to maintain the amount of blood entering the RA (and thus SV, and thus CO).

    We can plot a cardiac and vascular function curve on a graph with CVP on the x-axis and CO on the y-axis. The CFC is the line with an increasing slope, and the VFC is the one with a decreasing slope (I'm sure it's in your phys book). During hemorrhaging, VFC shifts to the left, and the point that these two lines cross is shifted such that there is now decreased CVP as well as decreased CO. UVa has a good quick review about this stuff on their school's website. Blood transfusions, for instance, have the opposite effect, transiently increasing CVP and CO.

    Your body responds to this drop in BV through many mechanisms including increasing sympathetic stimulation. In smooth muscle, sympathetic stimulation increases norepinephrine release, constricting vessels through a G-protein dependent mechanism that affects Ca2+ influx. Anyway, the catecholamine adrenaline binds to adrenergic (alpha and beta) receptors located on various tissues in the body. Activation of alpha receptors generally increases constriction in smooth muscle (think of the greek alpha symbol as a knot that is tying something) and beta activation in cardiac tissue generally causes an increase in heart rate (among other things). Increasing beta receptor activation is the reason for the increase in HR.
     
    #12 Medicine4Bruhs, Aug 12, 2011
    Last edited: Aug 12, 2011
  14. Instatewaiter

    Instatewaiter But... there's a troponin
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    Oh my god you're verbose.

    Short answer to the question about vasodilators: Vasodilators that act on the aterial side (Nitroprusside, ACEi as well) decrease afterload. Your professor is wrong.
     
  15. Cardiol

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    It is my hypothesis that beta blockers are favourablein heart failure because they reduce afterload by slowing the rate of LVejection, i.e. slower acceleration of contraction and flow. The aortic andarterial wall consists of viscoelastic material, with less resistance to slowthan to rapid stretching. Slow stretching corresponds to a functional increasein arterial compliance. In other words, more blood/stroke volume can be ejectedwith less work when the rate of ejection is slow. More details can be found in:Soma et al, J Am Soc Echocardiogr 2000;13(12):1000-8

     
  16. mjl1717

    mjl1717 Senior Member
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    Ok, but if someone has mild heart failure...Lets say they are on Isosorbide, Triamterene, and Crestor.. Doesnt it make sense for them not to over exert themself?
    :xf:
     

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