Commotio-cordis

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Re: Commotio-cordis

Postby Bill Glasheen » Thu Mar 07, 2013 4:24 am

Here's a nice picture that shows the "window of risk" for commotio cordis on a single cardiac cycle of an EKG. I'm leaving it as a url rather than posting it because the picture is so large.

Commotio Cordis Risk Window

For the lay folk:

  • The "P" wave is when the atrium contracts. The atrium contains the heart "pace maker" (SA node) which can be modulated by vagal input. The two atriums are the chambers where the blood first comes in from the body after being used (right atrium) or back from the lung after being oxygenated (left atrium).
    ...
  • The "QRS" wave is when the ventricles contract. The ventricles are the main pumping chambers.
    ...
  • The "T" wave is when the heart is repolarizing. Note how it's in the middle of that phase with part of the cardiac muscle in latency phase and part repolarized where things can go wrong.

- Bill
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Re: Commotio-cordis

Postby Van Canna » Thu Mar 07, 2013 3:46 pm

Muscle, fat, and skin provide a better low pass filter to an impulse function than does bone. In other words... yes!

It's also difficult to "condition" bone this way.


Thanks Bill, my feelings as well.

Another problem,as you well know, is the 'pre-existing' condition that can be there unknown to the person who is receiving chest blows, thinking he is conditioned to take them.
The possibility that young, well-trained athletes at the high school, college, or professional level could die suddenly seems incomprehensible. It is a dramatic and tragic event that devastates families and the community. Sports, per se, are not a cause of enhanced mortality, but they can trigger sudden death in athletes with heart or blood vessel abnormalities by predisposing them to life-threatening heart irregularities.

In the rest of the world, soccer is the sport most commonly associated with sudden death. Sudden death occurs in 1 to 2 in 200,000 athletes annually and predominately strikes male athletes.


The CC danger is well known to soccer coaches. When I was playing soccer, our coach always advised to either blade the body, if possible, while blocking an incoming power ball...and or as seen in pro games today, to place the right forearm across the chest when standing in the 'wall' 10 yards from a striker against a free/penalty kick, plus the left hand covering the groin for obvious reasons.

What is strange to me, Bill, is that given the real danger of CC in all athletes, young or mature, so many Uechi teachers in Okinawa have and still continue in the practice of striking students in the ‘heart zone’[some teachers call it the ‘heart punch’] for whatever 'immunity reason' Uechi people might have to CC not ever explained medically.

And they never address the possibility of underlying conditions.
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Re: Commotio-cordis

Postby Van Canna » Thu Mar 07, 2013 4:43 pm

Bill,

As you know, in addition to Commotio-cordis, blows to the chest can also cause Contusio-Cordis. Here is a report of a 30 year old professional soccer player hit in the chest by a 'power soccer ball'
Considering the clinical presentation of the patient, the normal coronary angiography, and the findings of the CMR examination, we made the diagnosis of contusio cordis.

The patient was advised to refrain from strenuous physical activity for a month. At the 6-week follow-up, the patient was symptom free, and his ECG changes normalized with complete resolution of the ST- and T-wave abnormalities.

On the follow-up CMR examination, both the regional wall motion abnormality and edema were no longer present.

On the late gadolinium-enhancement images, the focal region with hyperenhancement persisted, still involving 6% of the left ventricular myocardial mass, reflecting permanent myocardial structural damage.


The heart muscle is nothing to 'toy' with.
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Re: Commotio-cordis

Postby Van Canna » Thu Mar 07, 2013 4:52 pm

The 'killer kick' soccer players and goal keepers fear the most is the one that comes in with no spin...

'dead weight' flying at you like a musket ball.

Image
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Re: Commotio-cordis

Postby Van Canna » Wed Mar 20, 2013 3:47 pm

I was discussing the 'chest beating' for conditioning and testing, we see in Uechi Ryu, the other night with Jim Maloney and Art Rabesa, and we reminisced about this 'practice' we were submitted to years back. Maloney reported a case where someone hit in the chest by a punch in a fight died from the CC condition.

Now I am informed that in Uechi, this particular aspect of conditioning goes under the name of:

MUNEKAN-KITAE
Pounding of the chest area


And it reminds me of monkeys/gorillas pounding their chest.

Maybe this so called 'conditioning' has a sexual root... known as 'red chesting'
'Red Chested' _ The sexual act where the partner on top repeatedly slaps or punches the bottom partner's chest...

Guy 1:aw man my chest is still throbbing from last night
Guy 2: what for?
Guy 1:because my girl red chested me so hard last night


Damn…I suspected the old Okinawan masters knew the real reason behind chest pounding. :mrgreen:

Bill
For the lay folk:
•The "P" wave is when the atrium contracts. The atrium contains the heart "pace maker" (SA node) which can be modulated by vagal input. The two atriums are the chambers where the blood first comes in from the body after being used (right atrium) or back from the lung after being oxygenated (left atrium).
...
•The "QRS" wave is when the ventricles contract. The ventricles are the main pumping chambers.
...
•The "T" wave is when the heart is repolarizing. Note how it's in the middle of that phase with part of the cardiac muscle in latency phase and part repolarized where things can go wrong.


Being 'red chested' by your sexual partner…well...what a way to go.
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Re: Commotio-cordis

Postby Van Canna » Wed Mar 20, 2013 7:43 pm

Then there is 'contusio cordis' worth taking another look at:
Here's one case:
Considering the clinical presentation of the patient, the normal coronary angiography, and the findings of the CMR examination, we made the diagnosis of contusio cordis.

The patient was advised to refrain from strenuous physical activity for a month. At the 6-week follow-up, the patient was symptom free, and his ECG changes normalized with complete resolution of the ST- and T-wave abnormalities.

On the follow-up CMR examination, both the regional wall motion abnormality and edema were no longer present.

On the late gadolinium-enhancement images, the focal region with hyperenhancement persisted, still involving 6% of the left ventricular myocardial mass, reflecting permanent myocardial structural damage.
Van
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