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The reasoning we got here in the UK is that by doing 30:2 you build up coronary artery pressure and therefore made the heart more able to sustain a return of rhythm.

When you come off of the chest it only takes 18 seconds to completely lose the pressure so single quick shocks are more effective.

Also as stated, the build up of ATP makes the heart more receptive to a successful shock.

Hope this helps

Andy

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We were informed of this. I don't like it. We are going to wear ourselves out! But if it works... then one more saved!!!!!!

As for getting tired, If your doing two person CPR you can switch; If your doing one person CPR your going to get tired anyway. Unfortunately (because I like my pts. alive) I have had the duty of performing CPR over 10 times in the past 8 months. With the proper mechanics it reduces the stress on your body and increases efficiency.

My point is either way 15x2 or 30x2 your going to get tired eventually.

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Probably that and the need for ATP for muscle contraction (ATP replacing ADP following a contraction is what releases the myosin head from the actin filaments. No ATP, muscle stays contracted and this is why you have rigor mortis).

[physio analness coming] You don't need ATP at the receptor for the heart. Remember, the heart uses gap junctions (literal gaps in the cell membrane where two cells are directly connected to each other) to transmit the action potential throughout the heart. You will need ATP at all of the Na/K pumps to reset after the action potential opens up the ion gates that maintains the action potential, though.

http://americanheart.org/presenter.jhtml?i...ier=3037720#ems

We are esentially saying the same thing but I thought I would extrapolate the thought for the sake of discussion. ATP and ADP are the same molecule. ATP is an ADP that has picked up a phosphate ion. No electron transport chain, no phosphate, and ADP just sits there. I think the extra 02 is for the oxidation-phosphorylation reaction in the Kreb's cycle since that produces alot more ATP than fermentation.

The cardiac muscle uses calcium/sodium channels, not sodium/potassium pump.

Gap junctions are the transverse intercalated discs that have 1/400 the resistance that the impulse across them than the sarcomeres have. Very efficient conduction, but not across the entire organ.

The electrical impulse for cardiac muscle originates through the A-V bundle, not the gap junctions. I think you are thinking of autonomic properties of cardiac muscle. There is a separation of atrial and ventricular muscle of syncytium as well as fibrous tissues between atria and ventricles, otherwise the contractions would be all willy-nilly. The gap junctions conduct impulses across cells sharing the same syncytium only.

I'm not dogging on you. I just love to discuss A&P. I love it when you post and I think we should all think this deeply and discuss both macro and micro concepts to be leaders in our field.

I will not be offended if someone wants to attempt to correct me from the above. This is how we learn to evolve and "stand erect" as more than ambulance drivers.

My reference is Guyton's physiology 10th edition pp96

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We are esentially saying the same thing but I thought I would extrapolate the thought for the sake of discussion. ATP and ADP are the same molecule. ATP is an ADP that has picked up a phosphate ion. No electron transport chain, no phosphate, and ADP just sits there. I think the extra 02 is for the oxidation-phosphorylation reaction in the Kreb's cycle since that produces alot more ATP than fermentation.

The cardiac muscle uses calcium/sodium channels, not sodium/potassium pump.

Gap junctions are the transverse intercalated discs that have 1/400 the resistance that the impulse across them than the sarcomeres have. Very efficient conduction, but not across the entire organ.

The electrical impulse for cardiac muscle originates through the A-V bundle, not the gap junctions. I think you are thinking of autonomic properties of cardiac muscle. There is a separation of atrial and ventricular muscle of syncytium as well as fibrous tissues between atria and ventricles, otherwise the contractions would be all willy-nilly. The gap junctions conduct impulses across cells sharing the same syncytium only.

I'm not dogging on you. I just love to discuss A&P. I love it when you post and I think we should all think this deeply and discuss both macro and micro concepts to be leaders in our field.

I will not be offended if someone wants to attempt to correct me from the above. This is how we learn to evolve and "stand erect" as more than ambulance drivers.

My reference is Guyton's physiology 10th edition pp96

Sorry about that, I wasn't trying to imply that the entire heart was connected by gap junctions or that the gap junctions functioned as a pacemaker. My point was that, unlike muscle cells where each motor unit is connected to a nerve and is activated by neuro transmitters, the heart uses gap junctions to coordinate muscle contractions. Hence you don't need to worry about creating more transmitters, transporting the transmitter to the end plate, or pumping out the Ca++ used to release them. Also the cardiac muscles primarily use Ca++ to extend the AP. The primary rise is still produced through Na+.

I would argue that ATP and ADP are similar, but different molecules by virtue of a phosphate, but that's getting a little too nit-picky. Similarly, most of the ATP is produced in the electron transport chain. Krebs does produce ATP, but the FADH2 and NADH is much more useful.

Discussing A&P is always good. You aren't always going to remember everything and its a good way to review.

Ohh, source=Silverthorn's Human Physiology Third Edition.

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30:2 is all about raising the blood pressure as much as possible. When ever we stop our compressions for ventilation's our patient’s blood pressure will plummet. Our objective is to raise and keep our patients blood pressure as high as possible. Also, experiments have shown that the first 5 compressions are ineffective. Also to many ventilation's (HV) raises thoratic pressure, which in return reduces venous return.

Another important change to remember is that defibrillation if on an non witnessed arrest (down time more then 4 minutes) that 2 minutes of CPR is done before defibrillation.

After shocking (only once at 360j ) we do 2minutes of CPR, and then check vital signs. And if need be shock again.

This is because with out the oxygen our body can not successfully convert VF into a normal rhythm (remember VF consumes a lot of oxygen).

Aaron

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As for getting tired, If your doing two person CPR you can switch; If your doing one person CPR your going to get tired anyway. Unfortunately (because I like my pts. alive) I have had the duty of performing CPR over 10 times in the past 8 months. With the proper mechanics it reduces the stress on your body and increases efficiency.

My point is either way 15x2 or 30x2 your going to get tired eventually.

This is why the new AHA protocols state that if two people CPR is done , that every two minutes the two swap positions.

Aaron

P.S. I had not noticed some of the recent above posts when i wrote my earlier post, a lot of them are very good.

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It will be interesting to see in about 2 years, how much revision(s) will have to re-occur. Like many others, this is my 30't year of CPR education and how many times I have seen the "oh, this is it!".. Technically CPR hardly works a very poor procedure..with very poor resuscitation results on any method that has tried and used. Alas, there is no other procedure that we can implement at this time...and thus we have no choice.

R/r 911

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As we all are aware, without early defibrillation CPR alone survival rate is dismal to say the least. The lay public can do compressions 100:2 if they desire, but the fact remains cardiac arrests require early defibrillation.

The AHA states that if defibrillation is not received within 4 to 6 minutes, brain death starts to occur and as excellent providers, you all were aware of this. According to the AHA, survival rates drop to 10% with CPR alone. I'll do my compressions as required, after all, that's what we're there for.

Come to think of it, can we reprogram our Geezer Squeezer? :wink:

In all seriousness, I'm all for change. And I'd like to see some statistics on the new standards, but alas, I feel they would be hard to come by as by the AHA's own admission, they don't keep them due mostly to the fact they aren't provided with them

http://www.americanheart.org/presenter.jht...ntifier=3034352

http://www.americanheart.org/presenter.jhtml?identifier=4483

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