.....When I asked for the reasoning behind it, basically I've been told that it's more of the "book vs. the real world", and "this is how things are really done"...... ......... I just want to know WHY.
Sounds oddly familiar.... lets see if I can shove my hallucinations into words.
About 8 or so years ago, there was a study using new ultrasound technology showing that each time CPR was stopped, there was a forward blood flow that continued because of a pressure gradient between aortic pressure and central venous pressure that lasted for a short time ( like a minute or so ).
The kicker.... it took about a minute of high quality compressions to get that forward flow going again after a pause ( 5 sec or more ).
As published now, 30:2... of you stop compressions for 2 sec, 5 times in a 2 minute cycle - you have 5 pauses which potentially keeps you from reaching an optimum forward blood flow and keeping any action potential stimulated.
I am convinced that the more you keep the heart stimulated, the better chance of creating a more viable situation. You push drugs.... do you give enough time for the drugs to take effect? - or do you push them every 2 minutes knowing that you only have 1 minute or less of forward blood flow for them to reach therapuetic levels? ( then you get that ROSC whos HR goes tachy and BP is 240/160 when thay all take effect at the same time, etc etc... sound familiar? ). Why send them on that roller coaster?
It seems to be more effective to do continuous compressions with little to no pausing to keep the forward blood flow continuous and allow the meds to reach thier full potential in the time AHA allots. That is where I tend to see the medications full actions, and end up giving less meds during a code - with great results.
This has been tried on down times for up to 20-30 minutes, we know we can get mechanical activity going again - but those cases are neurologically shot with anoxic damage. For us, 10 minutes or less ( where the etiology is reversable - e.i. not a disecting aneurysm, etc ) will mean the difference. And its the numbers that I have been seeing that is becoming the proof. The only thing different that we are doing is CCC.
With a well trained crew, your ventilator person should not be so over-zealous to cause any additional gastric distention. You will have some passive air movement anyway with good head positioning during compressions. And with Waveform EtCO2, you should be able to titrate those resps perfectly. According to the WF EtCO2 feedback that I have been receiving, once we have established a good couple minutes of CPR, the values have been optimum with very little ventilatory assistance.
I just don't speak out my rear on this, I have numerous ROSC cases that have been discharged without any neurological deficits, and I talk with them. There us so much that contributes to this ( good post care, therapeutic hypothermia, chemistry homeostasis ) - but it all starts with us in the field getting the ball rolling with efficient results.
Maybe this gives you a little insight.... not being a "John Wayne", but its the evidence based outcomes that is driving this.
AHA and other publications are at least 5 years behind. Sad....
