FA 2012; pg. 280: Cardiovascular System
CO= SV X HR
This formula stipulates the different variables that affect the CO: Stroke volume and heart rate. Of these two variables, the CO is more dependent on the Stroke Volume which is intern dependant on 3 different variables: 1) Contractility
Of the three mentioned above, contractility is the most important determinant of SV. Therefore, we can say that CO is very much dependent on contractility. If you increase contractility, you increase CO and vise versa.
Now the heart rate is one of the variables but it doesn’t really impact CO as much under normal circumstances. If, however, our HR increases or decreases dramatically, then the CO will change accordingly.
For ex: FA talks about what happens in exercise: At first, the increase in CO is attributed to both SV and HR. Why does SV increase? Well, SV is proprotional to contractility as I said earlier, so if contractility increases—> SV increases as well. Why would contractility increase?
Exercise—> Increase in ATP demand as the muscles now are actively working (need ATP for those actin myosin filaments)—> Glycogenolysis tens to maintain this ATP by breaking down glycogen into glucose (what’s the enzyme? Glycogen phosphorylase and debranching enzyme). This only maintains the energy supply for a short period of time afterwhich, the muscle resorts to using ANAEROBIC glycolysis (so substrate level phosphyrlation). In the process of creating ATP anaerobically, we make LACTIC ACID (LA). LA is a potent vasodialator—> decreases TPR in the ARTERIES—> which means that we are now sending more blood to the veins. NOTE: The veins are NOT changing their diameters, it is only the ARTERIES that vasodialate so therefore, the veins are just going to send all of that blood that they received from the arteries back up into the heart. Therefore, our venous return/preload INCREASES during exercise.
The more you increase your preload, the more you increase your contractility. I struggled with this concept until I finally came up with a simple analogy. You agree that for every ACTION, there’s a REACTION. That’s just a simple concept in life. Same thing applies here. Imagine picking up a heavy grocery bag. That’s an action, you have put weight on those filaments and stretched them passively (why passive? because the weight of the bag exerted this effect on your muscle, not you). As a reaction, you try to maintain that weight (so that the bag doesn’t fall) and you CONTRACT your bicep muscle for example. This contraction in your muscle is an action process. The heavier the grocery bag, the more you’ll have to contract and work that muscle so that you don’t drop the bag. Easy right? Now the grocery bag is your PRELOAD and the bicep muscle is your HEART. Same thing. The more you increase your preload, the harder the heart contracts. BUT only up to a certain point. There’s an optimal point at which you have “optimal” overlaping btw the myosin and actin heads and it is at that point that our contractility matches our preload (the heart works at a point lower than that optimal point under resting conditions). Now what would happen if you INCREASED the preload (say for example you administered a venoconstrictor)—-> You would naturally increase your contractility. But what happens if that increase is so dramatic that the heart cannot handle it? That’s right, the heart would fail. And that’s what happens with CHF. Your contractility decreases (myocytes get lazy or tired) and it can no longer maintain that preload that it receives from the venous circulation….so we put that patient on drugs like venodialators…why? because we want to decrease their venous return or preload so that the poor failing heart won’t have to work so hard to pump all that blood that it just received.
If you’re wondering why venous dialation would decrease the preload you would have to understand another concept: Compliance.
The veins happen to be very compliant, which means if we tell them to venodialate, they do just that. They expand and hold the blood there for as long as needed. Contrast that to what would happen if you tell an artery to dialate. Arteries are not as compliant as veins (becuase they are very elastic). So dialating an artery would in fact PUSH the blood out of the arterial system into the venous system which would eventually send the blood back up into the heart. So in summary:
Dialating a vein= DECREASES venous return to the heart
Constricting a vein= INCREASES venous return to the heart
Dialating an artery= INCREASES venous return to the heart
Constricting an artery= DECREASES venous return to the heart
This below is from page 281. I struggled with this image a lot but I think I finally understand it. First it is important to understand what the x-axis and y-axis refer to so lets begin:
So on the x-axis we have our PRELOAD which is essentially the venous return.
on the y-axis we have CO which we said was mainly determined by SV
Before I begin describing this image, I should stop to remind you and myself that this curve can be very confusing because what it essentially tries to demonstrate is that ALL of these variables are inter-related. As I previously mentioned, CO ∞ (proportional) SV ∞ Contractility ∞ Preload. So really, they’re all connected. So What’s the point? We’re trying to see how each one of those variables behaves when it inc/dec by itself or when faced with an increase/decrease of a dependent variable? Still confused? follow me:
The black line that says “normal” demonstrates what would happen under resting conditions. The black curve that intersects the “Normal curve” is the curve that resembles “Contractility”. So this isn’t exactly a normal graph. Anything ABOVE that normal point of intersection is going to have a higher contractility. So for ex: the GREEN curve has higher contractility at ALL points, not just the point that is directly above the black point of intersection. All points on the green curve have an increased contractility when compared to the black curve. Similarly, all points on the red and yellow curve have a decreased contractility when compared to the black curve. Now, we already talked about what would happen during exercise: You increase your CO! If you notice though, the CO increases even when the preload stays the same. What do you think explains this increase if preload has not changed? Contractility!
I read somewhere that even BEFORE you start working out, just the thought of exercising can actually trigger a powerful increase in your catecholamines level (epi and Nepi). These two will go to the heart, bind to their Beta 1 receptor and INCREASE contractility by increasing the amount of Ca+ inside the myocytes. So now although we previous stated that preload is a determinant of contractility, we now know that contractility can be increased without an increase in preload.
The yellow graph shows what would happen if the heart fails (CHF). The heart can fail for many reasons but the bottom line is that when it fails, the myocytes can no longer contract and hence the curve is below the normal operating point of the heart. But you’ll notice that preload INCREASED. Why would preload increase in a CHF patient? Well lets think about it: The heart isn’t pumping blood adequately so therefore we have a general decrease in our blood volume in the circulation. A reflex response is triggered when this hypotension is sensed by the baroreceptors and the medulla in turn increases our sympathetic response. So we end up with a general VASOCONSTRICTION. What does that mean? We are sending more blood from the arteries to the veins and from the veins to the heart. So we’ve increased our preload. It’s a way for the body to compensate, it’s trying to “fix” the situation but instead, its making it worse. So preload increases but as you seen on the graph, contractility DECREASES. So there again we prove that contractility can work by itself, independent of preload’s influence.