kohlerrf

I am stumped? We all know that we inspire roughly 79% Nitrogen and 21% oxygen at one atmosphere of 760mm/hg. Leaving water vapor out of the mix for now this brakes down to partial pressures of 600.4 mm/hg of Nitrogen and 159.6 mm/hg Oxygen. In a homeostatic body with a proper pH we normally absorb roughly 5% of that oxygen and none of the nitrogen leaving a "partial pressure" void of 5% which is commonly filled by C02 creating the value we know as End Tidal CO2. In addition our O2 sat has risen to 100% because our pH has become more alkolotic causing a left shift in the oxy-hemoglobin curve resulting in greater affinity for hemoglobin to bind with oxygen The numbers may be a little off here but bear with me. If CO2 diffuses to fill the void in the partial pressure, in a state of hyperventilation where our CO2 levels drop what files the void to maintain a partial pressure of 760 mm/hg in our exhaled air? Do we just absorb less Oxygen because the Hemi sites are full and we have saturated the plasma?

I routinely use Midaz for RSI. Usualy I will give 5mg Midaz fast push IV, the pt usualy goes down enough to intuabte with out a problem. If that does not work next I use Etomidate and because I used midaz first I don't have to worry about myoclonus ( an untoward side effect of Etomidate). if that does not work my next step is Sux. Anecdotally I have seen that the rate at which you administer Midazolam the deeper the sedation (all be it short lived) a fast push of 5 or 10 mg is usually enough to knock the pt down you will be able to tell this because when you initially stick the Blade into the mouth pt pulse rate will remain unchanged. If you notice an increase in rate your pt is not sedated enough. Same with the use of Sux if the pt pulse rate rises under Sux it usually means your pt has awoken but remains paralyzed!

I am stumped? We all know that we inspire roughly 79% Nitrogen and 21% oxygen at one atmosphere of 760mm/hg. Leaving water vapor out of the mix for now this brakes down to partial pressures of 600.4 mm/hg of Nitrogen and 159.6 mm/hg Oxygen. In a homeostatic body with a proper pH we normally absorb roughly 5% of that oxygen and none of the nitrogen leaving a "partial pressure" void of 5% which is commonly filled by C02 creating the value we know as End Tidal CO2. In addition our O2 sat has risen to 100% because our pH has become more alkolotic causing a left shift in the oxy-hemoglobin curve resulting in greater affinity for hemoglobin to bind with oxygen The numbers may be a little off here but bear with me. If CO2 diffuses to fill the void in the partial pressure, in a state of hyperventilation where our CO2 levels drop what files the void to maintain a partial pressure of 760 mm/hg in our exhaled air? Do we just absorb less Oxygen because the Hemi sites are full and we have saturated the plasma?

When using a Bag Valve Mask if you are not using ETCO2 you have no Idea if you are ventilating a patient properly. The body and all its organs and systems only operate properly within a very narrow range of pH. We devote a substantial amount of ATP in our efforts to maintain this narrow pH range weather it be through bicarb release kidney excretion or ventilation, second by second the body struggles to maintain the pH so that all systems are "GO"! There is an indirect but very real relationship between End Tidal CO2 and the pH of the blood. The lower the ETCO2 the more alkalies the blood becomes and visa versa. While we do not generally know what the baseline pH of the blood is when we arrive at a patient in the field we do know the body is mapping too and if necessary trying to correct it. If we come along with a BVM, intubate and start to ventilate without End Tidal CO2 we do know you will create and inconsistent minute volume. This inconsistent Minute volume will be reflected in an inconstant End tidal CO2. Because pH moves with CO2 the already sick body will now have to chase and inconstant pH value you create and may in fact never be able to compensate. For every deviation of the pH so goes the efficiency of all the bodily systems. Ventilating with a BVM and no End Tidal CO2? When does the mantra "DO NO HARM" come into play?

EJ's are tough I agree your best bet is trendelenburg. In the old days we use to put a 3 CC syringe on the back of our IV needle and with our pinky pull back on the plunger to create a suction in the needle. Remember the EJ is at a very low pressure and often times you will be in and get no flash! unfortunately you put a syringe on the back of a needle cath today, but the IO work great instead? ;-)

I use Midazolam (versed) almost exclusively. I generally give 5mg fast IV. That is usually enough to put anyone down. My preference it to keep the patient light even breathing if possible and put them is assist mode on the vent in our ambulance. Although, I did have a case last night I had to use SUX. The order went 5 of versed 15 of Etomidate and 50 of Sux. I always use versed prior to Etomidate to prevent myoclonus and although we carry versed ativan and valium my preference in adults is versed, and I only use sux as a last resort when I have trismus.

Not a fan of vasopressors, they have a habit of constricting all the blood vessels in the body including the ones that supply the brain, in addition we all overdose our patients at one time or another because we lose track of time! I have heard, and am very interested, that they are experimenting on swine now using "vasodilators" in cardiac arrest and have had some promising results!

The bougie is the most elegant way to intubate. once you have mastered this brilliantly simple device you will never go back and you can get rid of your secondary airways because you will get the tube every time! Bougie dont leave home without it!

We are a Non-Profit private ambulance service with the contract to provide all the 911 ambulances to our city. we are not funded from the tax base. I would like to speak with any similar organization that currently has in place a "Community Paramedic" or "Advanced Practice Paramedic" program in place. if you could pleas send me a "PM" (Private Message) Ill contact you and we can talk off line. Thanks.

No there is not. But this is off topic although it sounds like the start of a great thread;-) I agree it just seems frustrating when we are the give the task and required to gain the knowledge and held accountable they don't give us the best tool to do the job even though it is readily available and only a stroke of a pen stopping it from happening?#@$$%

My service does not figure in transport time to the ER if the pt needs it you are suppose to do it regardless of where you are. We qualify patients the same way that Croaker260 does My concern is that we use the low dose Albuterol(for bronchial spasm) and subsequently we cant physically get the 10-15 mg into the before and there is resistance of the doctors to giv us the high dose Albuterol for what reason I don't know. In addition being that Calcium is the lynch pin in this protocol we only carry Calcium Chloride on the truck and they wont give us Gluconate either, why again I don't know but the problem here is that the Doc's only rarely give us the order for drip in Calcium because, it is Chloride and not Gluconate. I understand to dnagers of "Rock Heart", although remote, but why not just give us Gluconate which is relatively speaking much safer?

I never palpate the abdomen. no new information will be gained that would ever change your treatment and the possibility (although remote) exists that you may exacerbate what is acutely a minor problem and make it a major problem.

Does anyone else treat for Hyperkalemia in a living breathing patient and not just as one of the 5 H's. We use Albuterol, Bicarb, Calcium and sometimes Lasix.

DigDugDude, Let me speak to you as a "Brother in Arms" and welcome you to the world of critical pre-hospital care. I would submit that your frustration with the current staff you work with is your inability to realize how much you can learn from a medical doctor. Correct this short falling, add a dash of humility and you just might have a future in this business. Every day I go to work I learn how much more I don't know, and I have only been a Medic since 1980. Step back, look listen and feel then slowly move forward. Good Luck Sir!

I agree! You should never palpate the abdomen in spinal trauma or ever for that matter. Information gleaned from abdominal palpation is highly subjective, example; what if the patient is ticklish and tenses up when they have their abdomen prodded? Remember we are not in a warm doctors office with a decades long patient/doctor relationship. More over, there is a possibility (although very remote) that your poking around may exacerbate an existing condition like a fractured L3. Your course of treatment should be based on information that is more objective. I teach my students the technique of abdominal palpation for testing purposes, but I discourage its practical use in the pre-hospital setting.

Nothing beats a open airway and early defibrillator and or proper continuous chest compression! My last 2 saves I did not even intubate. You don't need an ACLS course to teach you that.

Nope ;-)

ERdoc said it all. Most of all remember that intubation is a very simple skill. The problem and the bad press about it come from poor education and quality control. Although we have versed, Ativan, Valium, Etomidate,morphine and Sux all at our disposal I rarely need anything more than Lidocane spray 10 of versed and a boogie to get the job done. and then an Etomidate chaser to keep them comfortably numb but breathing on their own. Practice the skill and do this skill and you will need the drugs less and less and that is good. Lastly we use to use low and high dose Vec but Rock is a better substitute but frankly I would drop the Vec from your protocol in the first place and replace it with Sux.

Thank you systemet. this topic is generally dealing in uncharted waters of which I feel need to be addressed. With regard to respiratory acidosis as paramagic said this is generally better tolerated than alkalosis partially because we can increase the partial pressure of oxygen which will compensate somewhat for the hemoglobin loss of affinity for oxygen in an acidotic state. However although this occurs we cant lose sight of the fact that the body lives in a very narrow range of pH and the big picture still needs to be corrected. Regarding your scenario, I would ventilate to what ever was needed to maintain and oxygen saturation of 95%. If his ETCO2 remained at 65mm/mg with a pulsox in the high 90's and not 100% that would be fine with me.

This is the exact reason why I gave up all of my AHA instructor certs. The AHA is dumming down the curriculum in order to appeal to the masses to generate more income form more and easier classes instead of requiring the masses to put in the time to learn and practice so you get it right!

Thank you "Usalsfyre" for stepping up! You can treat my family members any day. Intubation is just a mechanical act to protect and allow us to take control of the airway it does not give us licence to fool with mother nature. in the absence of any other information the default "AHA Rescue Breathing" might be adequate but in this scenario this is not the case. Further more just as important as what we know about this patient is to realize what we don't know about this patient in determining the best course of treatment given our limited tools in the field. I am not entirely sure that ETCO2 is the panacea either but so far barring specifically a traumatic head injury head injury I think maintenance of pre intubation numbers is key here with one caveat, 02 Saturation should not be ignored. With all the pitfalls of pulsoximitry accepted through at least clinical observation or other means we must maintain an confirm a saturation of at least 95% at all cost. We can now see that respiratory rate is a tertiary concern here and it should be driven to what ever will maintain the pre-intubation numbers. And along with what "DwayneEMTP" said Im not sure i would of hooked up oxygen to the BVM either, and had the patient woke from the paralytics and began to breath on his own again I may have made the patient comfortably numb and just draped a 1 ply 4x4 over the opening to the tube to filter particulates and let him continue to breath on his own as long as he maintained his numbers and not used a BVM. There are real dangers of positive pressure ventilation and I always prefer the patient to have a negative intra thoracic pressure on inspiration.

Frankly I agree with DwayneEMTP but this is not the question not the question every one? Does everyone with an ET tube in their throat pre-hospital get vetilated at 10-12 breaths per minute regardless of their condition and must we maintian an ETCO2 of 40 +/-. What if you cant maintain an ETCO2 of 40 +/- with a rate or 10-12? Please don't tell me that there is someone out there that thinks they can accurately control the tidal volume with a manual BVM! Should pre intubation ETCO2 reading be the ventilation target?

All good input. and your right "tcripp" you never learned to maintain a respiratory rate of 30 nor did I, however every day I learn how much more I don't know.While I am not trying to pick a fight with the AHA I think they have pounded into our heads that "Rescue Breathing" is the panacea! Conversely we as Paramedics are told we must "think first" and not just "blindly do"? The thinking part here should tell us that essentially this patient is not in respiratory distress and does not have a problem with his airway as he is obviously moving air in quantity and able to exchange gas efficiently in the lungs as evident by the ETCO2 and Pulsox. Our intent behind intubation here is not to improve gas exchange or ventilation but merely to protect the airway in route to the hospital this, I feel is not "Rescue Breathing" the patient was breathing just fine before I intubated. As I said this is not a discussion on why intubate! We have to accept the fact that we do not know! Primarily, why this patient is hyperventilating. if one did not intubate this patient would you use the BVM to retard his intrinsic respiratory rate to the standard 10-12 breaths per min? Just because we put a plastic tube into the trachea to prevent aspiration doesn't mean we are rescuing a patient in respiratory distress! Remembering this, if in the process if I temporarily inhibit his respiratory effort it is incumbent on me to restore or maintain it until the intrinsic drive is restored. This problem is well documented http://www.anaesthesiamcq.com/AcidBaseBook/ab5_5.php As Paramedics we have to make a distinction between "Rescue Breathing" and maintaining the pt own breathing while we are just protecting his airway.

Thank you "tcripp". what if your patient was unc and unr from any number of conditions that cause a metabolic acidosis and has a low pH. Currently he is breathing on his own at 30 with an ETCO2 of 25 clearly hyperventilating. However, this hyperventilation is a compensatory mechanism due to his acidosis and is blowing off CO2 in an effort to raise the pH. If we take away his ability to breath and slow his respiration to 10-12 with an ETCO2 of 35 as the AHA suggests we will in fact be lowering his pH even more making the situation worse. Would it not be better to use the information we have regarding respiratory rate ETCO2 and Pulsox and maintain those numbers in route to the hospital were definitive blood work can be done? This is a common situation of which I think the term "Rescue Breathing" and the AHA guidelines DO NOT APPLY. I think, in this scenario we are are mechanically protecting the airway and should just maintain its intrinsic respiratory rate, ETCO2 and Pulsox. I don't feel we have enough information in the field to determine the cause or to alter the bodies natural response. Remember the patient was not apnec pre-intubation and if he was then certainly i would agree 10-12 breaths with an ETCO2 of 35-45 and pulsox of greater than 95% is appropriate.

You arrive on the scene of a 60yo male who is unconscious and unresponsive GCS 3 with an unknown etiology. You are unable to obtain any patent history. The patients skin is warm pink and dry he is normotensive with good cap refill and he is breathing 30 breaths per minute his 02 saturation is 100% and he has an end tidal CO2 of 25mm/hg, you, for what ever reason decide to intubate and protect airway. ( the discussion here is not weather or not to intubate). After RSI you have knocked out the respiratory drive and know you must ventilate the patient. You have only a BVM , Oxygen, Capnography and Pulsoximetry, how would you properly ventilate this patient and what values would you seek?