Hypertrophy

So, an increase in wall thickness of the heart is better known as concentric hypertrophy.  The term hypertrophy (in regards to the heart) refers to an increase in cardiac mass, which can occur in one of two fashions (which we'll discuss below).  So, why does the wall thickness of the heart ever change by means of concentric hypertrophy?  Well, let's think back to the previous post.  Wall thickness has a close relationship with wall stress.  In fact, here it is displayed by the following equation:

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

Cardiac Loads

Previously, we talked about 'loads' of the heart.  In particular, preload and afterload (remember, that preload and afterload are two major determinants of stroke volume).

We likened preload to the resistance (or stress) we'd have to overcome to fill a latex balloon with air.  Afterload was likened to the resistance that would have to be overcome to squirt water out of a rubber duck, or even the force that retracts the latex of the balloon back to normal size once popped.

So, in cardiac terms, Preload is the resistance that must be overcome to fill the heart with blood.  If you'll remember, filling of the heart occurs during diastole.  Now, 'filling' in the heart is not as simple as, say, placing a gas nozzle in the heart and 'filling her up' with blood.  It's more than that.  In order for the heart to fill, the myocardial (or heart) cells are stretched to accommodate the amount of blood that is needed for the body to properly function.  As you can imagine, this causes a stress (or resistance) which we've termed Preload.

Afterload, in a way, is the stress or resistance that has to be overcome to eject blood from the heart.  It's as if the myocardial cells become accustomed to their 'stretched' state.  Just like stretch in a pair of pants too big for you, the pants just don't decide to "fit."  No.  You are going to have to pull a drawstring to shrink them up.  While there is no liquid in this example, the concept holds true.  The heart has to overcome the force that results from the myocardial cells being stretched, which results in ejection of the blood from the heart.  This is what we've termed afterload, which occurs during the period of systole (or contraction) in the heart.

"I know all of this," you say.  Very well!  Let's talk more in-depth about Cardiac Stress/Loads:

Here is the equation for determination of cardiac load:

Wall Stress = intracavitary pressure * radius

                wall thickness  

Wall Thickness is as simple as it sounds, how 'thick or thin' the wall of the heart is.  In the perfect individual, this remains a constant thickness throughout life.  Unfortunately, this isn't really the case.  In many cases, disease in particular, the thickness of the wall is altered to adjust the above equation to remain at an acceptable level of wall stress.  Confused?  Don't be!  Let's talk about the other terms first, then we'll revisit the subject of wall thickness. 

Intracavitary pressure is the pressure that exists in the cavity of the chamber of interest (in the heart).  There are four chambers in the heart:  Right Atrium, Right Ventricle, Left Atrium, Left Ventricle.  This is true of all mammalian (as well as avian) hearts (I'll have a discussion on comparative, across species, anatomy of the heart at a different time).  For now, think about yourself, or your cat, dog, horse, chinchilla, etc.  The order that I have listed the above (RA, RV, LA, LV) is the precise way in which blood travels through the heart (meaning Body→RA→RV→LA→LV→Body) .  Here is a diagram of the heart:

Currently, I have removed the lungs from the picture.  But, that's alright.  We will visit the lungs in the future (in regards to the heart).  What's important to understand is that intracavitary pressure is particular to each one of those chambers, alone. 

The other factor yet to be mentioned is radius.  Radius refers to the diameter of any one of those chambers (meaning, the radius of the RA, the radius of the RV, the radius of the LA, etc.).  The radius can change alongside disease in the heart (and for the very same reason the wall thickness might change).  A change in chamber radius often coincides with the heart being modified to normalize the amount of wall stress in the heart (and really, this is a change that one really doesn't want to see in the heart). 

So, how do we use this equation?  Let's have an example!  Suppose you (or a patient) is suffering from hypertension (or blood pressure that is extremely high).  Well, in cases of hypertension, there is an increase in intracavitary pressure of the heart chambers (in particular, the pressure of the left ventricle, as the blood is ejected from this chamber out into the body for circulation).  Let's place some pretend numbers into the equation to see what would happen: 

The equation (for ease of calculation):

Wall Stress = intracavitary pressure * radius

                wall thickness  

Let's say in a normal, healthy individual, the numbers are as follows: 

• Intracavitary Pressure of the LV = 25
• Radius of the LV = 10
• Wall Thickness of the LV = 5

So, wall stress = (25 * 10) = 50

                    5

Now, Let's say that our individual now suffers from hypertension, which has increased intracavitary pressure of the LV: 

• Intracavitary Pressure of the LV = 40
• Radius of the LV = 10
• Wall Thickness of the LV = 5

So, wall stress = (40 * 10) = 80

                     5

Hooooooooly cow!!!  Wall Stress is dramatically increased!  Just imagine that, now, the heart (and really the brain) is thinking.... "Mayday, mayday, mayday!"  And, rightfully so!  The heart was just not created to deal with this type of stress, particularly if this stress persists.  So what can the body do about this?  Well, it can cause change in either of the two remaining factors (either radius or wall thickness). 

Without getting too in depth, it is unlikely that the body wants to decrease chamber radius.  Why is that?  Well, though not part of this equation, a decrease in chamber radius comes with some consequences that aren't good.  In particular, a decrease in chamber radius is going to lead to a decrease in the amount of blood that the heart can hold.  This will lead to a decrease in stroke volume.  Remember, that Priority #2 is to Maintain Cardiac Output.  Oh no, a stroke volume decrease would cause a decrease in cardiac output!  Can you guess (maybe using one of our three important equations) what happens when cardiac output falls?  Yep!  Heart Rate increases to maintain cardiac output (the equation being: CO = HR * SV).  And, before we walk away from this subject, remember that cardiac output is a factor in our equation for arterial blood pressure (ArtBP = TPR * CO).  So, the heart has no choice but to remedy CO by increasing heart rate, as Arterial Blood Pressure must be maintained (Priority #1).  

Okay, that was a LOT more than I initially meant to explain.  So be it!  So that leaves the other factor, in regards to wall stress: Wall Thickness.  So, let's go ahead an increase wall thickness in our example and see what happens!

• Intracavitary Pressure of the LV = 40
• Radius of the LV = 10
• Wall Thickness of the LV = 8

So, wall stress = (40 * 10) = 50

                     8

And just like that, the wall stress is back to its original value of 50.  This is why hypertension is bad news!  It's not merely a number that's too high.  It's really a high number that will eventually cause the walls in your heart to thicken!  As the walls thicken, the heart begins to enlarge.  Unfortunately, this often times exacerbates heart disease or even creates arrhythmias.  

Something you may be thinking is that, "Well, an increase in wall thickness?  That has to come with it's own bad side effects."  It does!  See, as the thickness of the wall increases, the load that must be overcome to either fill or eject blood from the heart increases.  This means that the heart will have to work harder during preload, afterload, or even alter contractility to compensate.  This will just propogate this vicious cycle of heart disease, oftentimes until it's unmanageable.  

So, typically I would end with a cheer, but I'm feeling a bit too macabre to even attempt it!  See ya!