Wall Stress = (Intracavitary Pressure * Radius)
Wall Thickness
As a reminder, Intracavitary Pressure refers to the pressure in a specific chamber of the heart. Radius, similarly, refers to the radius of that specific chamber of the heart. And wall thickness refers to the thickness of that specific chamber of the heart, as well. The four chambers of the heart are the Right Atrium, Right Ventricle, Left Atrium, and Left Ventricle (listed in order of blood progression through the heart).
Utilizing the equation, we can see that if wall thickness were maintained, an increase in either Intracavitary Pressure or Radius (or both) would result in an increase in Wall Stress. To relieve (or diminish) the increased wall stress, hypertrophy of the heart (or an increase in wall thickness within the heart) could help out. If this doesn't make sense to you, please refer to the previous post on 'Wall Stress' for some examples that might help you.
Back to hypertrophy. Hypertrophy in the heart occurs in one of two ways, either are eccentric hypertrophy or as concentric hypertrophy. Let's begin with a diagram to assist in the grasping of this concept:
(In this photo, A depicts a normal, healthy heart; B depicts a heart with concentric hypertrophy, and C depicts a heart with eccentric hypertrophy)
Beginning with heart C: Eccentric Hypertrophy, what changes do you see when you compare that chamber to Heart A or Heart B? Well, in my opinion, one of the easier differences to notice is the increase in chamber size. In cases of eccentric hypertrophy, the increase in cardiac mass occurs when cardiac myocytes are added to a chamber in this fashion. The volume of the chamber has increased in eccentric hypertrophy, but the wall thickness was remained about the same.
Let's contrast that to heart B: Concentric Hypertrophy. What changes do you see in this heart when compared to the others? Excellent! There is a definite increase in the thickness of the LV in this heart. And that helps us to define concentric hypertrophy: an increase in cardiac mass due to an increase in wall thickness, and either no change in chamber size, or even a small change in chamber size.
When does either occur? Well, cases of eccentric hypertrophy (Heart C) normally accompany conditions that cause "volume overloads" in the heart. Things that cause volume overload to occur are associated with increases in preload (remember that preload refers to diastole or the period of time in which the heart is filling). A disorder that commonly cause an increase in preload is Mitral Regurgitation. Mitral regurgitation is a disorder in which the mitral valve (the valve that separates the LA from the LV) is faulty. What I mean by this is, the mitral valve is capable of being a perfect seal in a normal, healthy heart. In the healthy heart, the mitral valve opens and closes in a very defined process (we should be addressing that process in the next post). This is how the heart was designed. In individuals with mitral regurgitation, the valve isn't able to seal closed during the appropriate time. Without being fully sealed at the right time (and, in regards to the mitral valve, it should be fully sealed shut during LV contraction), blood is able to leak back into the LA. That's bad news! Remember that blood flows Body→RA→RV→LA→LV→Body. If blood is able to go backwards, to return to the LA, that means that the body is receiving less blood than it should be following LV contraction. Having discussed many of the compensatory responses of the heart, can you think of a few ways the heart might handle this inappropriate stroke volume? We have already mentioned one above, the increase in preload.
In regards to concentric hypertrophy, diseases of afterload typically trigger this type of growth. Remember that afterload refers to the force that must occur for the heart to eject the blood from the specified chamber. A disorder that commonly causes concentric hypertrophy is stenosis. Stenosis merely describes the narrowing of a vessels. Let's take the aorta as an example. The aorta is the vessel that transports the blood ejected by the left ventricle to the rest of the body. Now, let's imagine what would occur if the aorta had stenosis (or narrowing). As an aside, let's have a practical example. If you were asked to blow air through a drinking straw versus a coffee stirrer, which would be easier (hopefully you have tried this)? That's right! It would be easier to blow air through a drinking straw versus a coffee stirrer. Why is that? Well, the diameter if the drinking straw is much larger. Therefore, the drinking straw offers less resistance than the coffee stirrer. Now, back to the aorta. In cases of aortic stenosis, the blood must flow through a smaller diameter, one that offers greater resistance to the flow of blood through the vessel. This result in an increase in afterload (and therefore an increase in intracavitary pressure within the LV to overcome that afterload). How might the heart compensate for this? Certainly, concentric hypertrophy is a great idea! By increasing the wall thickness (remember our equation), the heart is able to attempt to return the wall stress (increased due to the increase in intracavitary pressure) to a more normal value.
I would be remiss if I didn't not the following: wall thickness is not something that occurs in a day. This is a long-term adaptation to a chronic change in the heart. Suppose an animal has lost a considerable amount of blood, thereby decreasing the amount available for preload. What can occur? Remember, this is an instance in one particular day. How do you suppose the heart compensates? Well, let's start with this: A decrease in preload is likely going to create a decrease in stroke volume due to less blood being in the heart for ejection. That's true! What were the other two factors that affected stroke volume? Contractility and afterload, that's right! So, in regards to contractility, what change would positively affect (or increase) preload? An increase in contractility could increase preload. By the heart pumping harder, it will likely force blood to move further through the cardiovascular system, thereby returning more blood back to the heart to meet the demands of preload. How about afterload? Well, remember, afterload is specifically referring to the force that most be overcome to eject blood from the chamber. So, in this case, a decrease in afterload (or less force to overcome for ejection) would likely increase stoke volume. Unfortunately, a decrease in afterload is really only going to occur with loss of cardiac myocytes. We really don't want to lose cardiac myocytes in this situation (and really, most situations)!
So, that was a lot! There was a lot of really big concepts in the post. But, I think everything is coming along well. Through knowledge gained over successive posts, a bigger picture of the complex relationships within the heart (to maintain those top three priorities has started to emerge). To just provide a nicely bulleted list on the big concepts from the previous paragraph:
- Increased Preload = Increased Stroke Volume
- Increased Contractility = Increased Stroke Volume
- Decreased Afterload = Increased Stroke Volume
Cheers! - JD
ive learned so much from u!
ReplyDeletethank u