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!
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