Rupture of Free-Wall + Heart Attack

While this injury is cool in its own way, a good part of this post explains "Acute MI" [heart attack], as its a leading cause of death in virtually all modernized countries and has been for many years. So if you've ever wanted to know more, let's dive into:

Rupture of Free-Wall of the Ventricle secondary to Acute MI
Short 'n Sweet:
A weakening of the wall of the left ventricle causes the muscle to tear apart, leading to cardiac tamponade and death.

Background Anat&Physio:
The heart is a muscular pump that is supplied blood (and thus, oxygen) by a set of arteries termed the coronary arteries. If this supply of blood is interrupted (ie: by fat buildup, a blood clot, abnormal constriction/tightening of the blood vessel, etc.), the heart muscle in the area it normally supplies will temporarily recieve no oxygen. Depending how long this lasts, this can lead to irreversible muscle cell death! The areas supplied by these coronary arteries include all of the muscle and thus, all the chambers, of the heart: The left ventricle, right ventricle(pumps blood to lungs), left atrium, right atrium, and other associated internal structures. As I mentioned in a previous tidbit, the Left Ventricle is the last chamber of the heart (and typically the largest) - from there, blood is pumped to the entire body and so the pressure generated there is quite high.
When body tissues (most) anywhere in the body actually die from lack of blood(called 'ischemia') - and therefore lack of oxygen - there's a step-by-step process that follows in each cell termed "necrosis". The tissue-wide effect on the group of cells is called "infarction" and it proceeds something like this:
 [1]The tissues first are infiltrated by general cells from the immune system (white blood cells) which begin the process of neutralizing all the noxious cell-contents that have been released from the dead/dying cells.
[2]Next, more specialized immune cells enter/form to continue the cleaning process, dissolving away the underlying dead tissue and start laying down granulation tissue instead.
[3]Finally, a final type of cell lays down collagen and make a firm scar tissue in the place of the dead tissue. This collagenous scar tissue has none of the functioning of the original tissue, but it at least serves as a firm placeholder rather than leaving a gaping hole behind.


What goes wrong?:
In a Myocardial Infarction ('myo' means muscle, 'cardiac' to do with the heart), we get blockage of a coronary vessel (artery). If the blockage persists for 30-60 minutes, some irreversible cell death begins to occur. It's worth noting that time really is of the essence here - in the first hour, <10% of the supplied muscle cells are likely to die . . . by the 3rd hour 80% or more will be beyond saving.
Once the blockage is cleared - say at the 90minute mark - the heart muscle is re-supplied and the repair process can begin. As discussed, the infarct follows a very predictable timing and course in a post-MI patient. Going off the 3 stages (again - this is simplified) I discussed above, the first stage happens over the course of the first 3 days. The second stage happens from days 3-10, the final stage takes a 6months-1year to finish.
Now here's where it gets interesting, the first step to fixing the heart is to remove the offending debris and the useless dead bits right? So during the second stage, we find ourselves removing the original muscle tissue altogether to replace it with the far weaker granulation tissue - the precursor to the very strong scar tissue. It turns out the heart wall is at its weakest in this second stage. . . and thus leaves our patient prone to the extreme pressure forces in the left ventricle (discussed earlier).

When a patient gets ventricular rupture, the wall of the heart muscle literally *bursts* open,

 and blood gushes out! Since the heart is encased in a sac (the pericardial sac), it quickly fills

 it up and compresses the heart from the outside, leaving it unable to pump (and leaking) blood!!

The majority of post-MI deaths in the 3-10 day range are due to rupture of the free wall of the ventricle.


Why it's cool: Apart from the heart *actually* bursting, I must say I found it really interesting that the repair process *itself* leaves you temporarily weaker rather than stronger. Especially because of how delayed (3-10 days AFTER your hospitalization) the effects can be!