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Smaller BVMs?


melclin

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One of the PhD students at uni has been focusing on ventilation during cardiac arrest and the effectiveness of different sized bags.

As I understand it, he is trying to get the ambulance service to ditch the adult size BVM (1600mls) and recommend the paeds BVM (1000mls)for vents during adult cardiac arrest. He's published a number of papers to that affect.

Nehme Z, Boyle M. Smaller self-inflating bags produce greater guideline consistent ventilation in simulated cardiopulmonary resuscitation. BMC Emerg Med. 2009;9(4).

Nehme Z, Boyle M. Accuracy of bag ventilation in simulated resuscitation. Journal of Paramedic Practice. 2009;1(4):167-72.

In the interests of privacy I suppose I should not say which of the two authors is the student in question. I couldn't remove the bold format from Boyle M for some reason, its not necessarily him.

The following values were considered desirable, apparently, as per ILCOR guidelines.

1. a ventilation rate between 8 and 10, inclusive;

2. a tidal volume between 480 ml and 560 ml inclusive (based on 6–7 ml/kg for the 80 kg simulated patient); and

3. a minute volume between 3840 ml and 5600 ml inclusive (based on multiple of lowest and highest acceptable ventilation rate and tidal volume).

I was wondering what everyone here thought about the idea.

As an aside, there was no mention of artificial airway type that I've noticed in the papers. I was wondering if this could be considered a confounding variable. I have used the lung simulator in question and its attachments are probably most similar to ETT pt. Could the airway type make a difference to the outcome?

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Looking at literature used by AHA, airway type does not appear to make any difference. Bag mask versus ETT versus supraglottic are all options. However, advanced airways do not appear to effect outcomes.

Take care,

chbare.

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This is no where new it has been studied extensively for over 12 years its only now through AHA following ILCOR consensus has dribbled it down to the EMS masses:

http://www.google.ca/search?rlz=1C1CHMA_enCA347CA347&sourceid=chrome&ie=UTF-8&q=small+vs+conventional+volume+ventilation

Look under scholarly studies and a plethora studies of small (5 to 7 ml/kg) vs conventional (10 to 15 ml/kg)

The the "flow inflating" bags for EMS requires a very reliable supply of O2 and a far more educated hand, IMHO not for use on every truck out there in EMS world.

cheers

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Yes I realise the 6-7ml/kg is nothing new. He wasn't suggesting it. The suggestion was that the best way to insure that this smaller tidal volume is achieved is to do away with 1600ml bags in favour of 1000ml bags.

We use flow inflating bags in the Victorian service (in addition to BVMs. The choice is left to the individual medic). Something like the Jackson Reese bags (as is my understanding according to previous discussions with Vent) in a closed circuit with a CO2 scrubber and purge valve attached. I very much like them. The are great for assessing patterns of breathing and getting much more intimate with a persons lungs during APPV or IPPV.

My experience with the lung simulators has indicated that it is much easier to cause gastric insufflation with them though, even at a healthy lower esophageal sphincter pressure of ~30 cmH2O.

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I think the whole debate is a wank personally.

What is the main aim in ventilation? Perfusion maintenence in the event of return of spontaneous circulation.

Evidence has shown that perfusion rates decrease by approx 50% at the time of arrest. This means we need to maintain less Oxygen during the arrest.

Will the size of the bag really effect this? No. In the until an ETT is insitu, you cannot gaurentee the amount of oxygen actually entering the lungs. Poor seals, lack of effective jaw thrust, head tilt can lead to air being pumped into the stomach.

Studies that the current guidlines are written from show there should be a primary focus on compression, even before defibrillation in some cases.

To me this makes the who debate mute. What would be more interesting is to see how effective -placing a high concentration mask on a pt & see how much O2 enters the system through partial pressure changes with cardiac compressions.

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We've got two very different applications and theories of thought going here.

Low volume ventilation of 5-7ml/kg, which was included in the google link, is at the low end of the ARDSnet protocol scale. We rarely go below 6 ml/kg in the ICU and probably would not attempt very low VT ventilation if we do not know circuit compliance or the automated system does not do compression compensation as you might be ventilating with <3 ml/kg. (Fatal mistakes made by some CCTs and Flight teams) Of course the standard self inflating bag should not have that problem but monitor VTs might be an issue. Also, for that literature, this protocol takes into effect when lung compliance is very low and the plateau pressure is over 30 cmH2O. Thus, the PIPs will be high and the goal it to spare the lungs that are already damaged which can be sensitive to both volutrauma and barotrauma.

The cardiac arrest will usually not have lung issues that will decrease compliance to where the PIPs and Plateau pressures will be as high. Thus, we are not thinking low VTs for the sake of ARDS. Instead, the AHA is, and quite possibly the theory behind the low tidal volume BVM, is to lower the pressure by limiting flow and VT in hopes of giving a more laminar flow and effective ventilation. This is also why the AHA is now support devices such as the Oxylator which are like tricked out Elder valves.

In summary, the low tidal volume theories (or implimented protocols) for ARDS or ALI (acute lung injury) must not be confused with the low volume/low pressure/flow limited objectives of the AHA which is to lower pressures to prevent over inflation and increase coronary artery perfusion. These low VTs will work until the patient is spontaneously breathing and demands more VT and overall minute volume. For the OP, it sounds like that researcher is trying to build a better mouse trap with the BVM to achieve lower VTs, limited flow and lower pressures when some of the automated devices like the Oxylator are not available.

Here is one decent article and of course it is from Toronto. It is the theory using pigs.

The results of the human trials should be presented in early 2010 when the new AHA guidelines will be discussed.

Abstract 34: The Effects of an Automatic Low Pressure Ventilation Device versus Manual Ventilation During Cardiopulmonary Resuscitation in a Porcine Model of Cardiac Arrest

http://circ.ahajournals.org/cgi/content/meeting_abstract/114/18_MeetingAbstracts/II_1195

Xudong Hu1; Gabriel Laurent1; Petsy P So2; Suzan Cvitkovic3; Paul Dorian3

1 St. Michael’s Hosp, Toronto, Canada

2 Univ of Toronto, Toronto, Canada

3 St. Michael’s Hosp, Toronto, Canada

Background: The Oxylator® is an automatic, pressure powered, flow triggered ventilation device which delivers pressure and flow limited gas when expiratory flow falls to < 2 L/min (approximately 2 cmH2O of airway PEEP). The effects of this device on hemodynamics and gas exchange during CPR have not been evaluated.

Methods: Twelve Yorkshire pigs (35–45 kg) each underwent 3 episodes of 30 second untreated VF followed by 5 minutes of CPR: 90 piston driven mechanical chest compressions/min and three different ventilation types in balanced random order:

manual ventilation with an Ambu® bag (12 breaths/min),

OxylatorP15F20 (max. pressure 15 cmH2O, constant flow 20 L/min) and

OxylatorP20F30 (max. pressure 20 cmH2O, constant flow 30 L/min).

Aortic, right atrial, esophageal (to estimate pleural pressure) and airway pressures were continuously recorded. ETCO2 and O2 saturation were measured every minute. Arterial blood gases were collected before induction of VF (baseline) and at the end of each 5 minute CPR episode. The animals were then defibrillated with 200J, 250J, 300J or 360J x 3 times, as needed. VF episodes were repeated at 20–30 minute intervals. There were no other therapeutic interventions before, during or after CPR.

Results: Coronary perfusion pressure (CPP, diastolic; aortic minus right atrial pressure), end-tidal CO2 (ETCO2), the partial pressure of CO2 (pCO2), the partial pressure of O2 (pO2), trough of esophageal pressure (EsoP-t), trough of airway pressure (AirwayP-t) and peak airway pressure (AirwayP-p) are presented in the table. The threshold for defibrillation and peak esophageal pressure (EsoP-p) are not different among the groups.

Conclusion: Automated pressure and flow limited ventilation during CPR results in higher coronary perfusion pressure and ETCO2 than manual ventilation, despite continuously positive airway pressure.

Table of their results is at the site...not able to paste.

note 1 mm Hg = 1 Torr = 1.36 cm H20

The Oxylator

http://www.lifesavingsystemsinc.com/em100.htm

Here's another one from CareVent.

http://www.securityprousa.com/careventemt.html

Below is just a little extra rambling about ARDS which again this ventilation protocol is not to be confused with low VT ventilation of the cardiac arrest. Those discussing ventilation on this thread have demonstrated a higher knowledge so I am taking it to that level and making that clear before someone accuses me of using medical terms that aren't appropriate for EMS providers.

If the patient presented with ARDS and not as a cardiac arrest patient we would be running pressors, serious sedation and possibly a paralytic. We also wouldn't be using a little Elder Valve or ATV to ventilate. If you didn't have the technology like the LTV ventilator, you would be leaning into the BV/ETT. Manually ventilating them is a hefty task. Prepping for ETI, we may run the patient on a HFNC (high flow NC) at 40 l/m with a NRBM or Oxymask at 15 l/m. The HFNC may definitely be needed or at least an additional 6 L/m NC since the NRBM is not a high flow device and won't meet patient demand if the patient is in ARDS like what is now associated with the H1N1 flu. This is also when I like the flow inflating bags to give the patient the flow they need. Then, as soon as the RSI meds are in, intubate. Using a self inflating BVM is difficult at best with very high PIPs and the flow wanting to follow the path of least resistance which definitely is not in the lungs. Hopefully these patients will be in the ED before they fully crash although I've had a few that just made it. Intubation was initiated within 15 minutes of arrival or as soon as the CXR confirmed how the patient looked which nixed messing too long with CPAP/BIPAP even with the capabilities of the hospital machines.

Edited by VentMedic
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'melclin'

One of the PhD students at uni has been focusing on ventilation during cardiac arrest and the effectiveness of different sized bags. As I understand it, he is trying to get the ambulance service to ditch the adult size BVM (1600mls) and recommend the paeds BVM (1000mls)for vents during adult cardiac arrest. He's published a number of papers to that affect.

Nehme Z, Boyle M. Smaller self-inflating bags produce greater guideline consistent ventilation in simulated cardiopulmonary resuscitation. BMC Emerg Med. 2009;9(4).

Nehme Z, Boyle M. Accuracy of bag ventilation in simulated resuscitation. Journal of Paramedic Practice. 2009;1(4):167-72.

Perhaps it is my lack of skills with a plastic brain but searches to these studies is sub optimal, if you could be so kind as provide a link.

1- PC = Presser Control (type) Ventilation with a flow inflating "bagger" and VT is subject to R= Resistance and C= Compliance)If a Paramedic is to use this mode of ventilation best get further training as a member of this website for quite some time the group as a whole (well in this Ventilation subject area) seriously lacking education (I hope that most using PC will recognize that one can ventilate a brick !)and without monitoring devices/ watching chest rise, or belly rise (in the non intubated) and the addition of pulse oximetry and ETCO2 well. if you think this is far from the truth ? It does happen far more frequently than you can fathom and unrecognized besides I have the court cases to prove it.

2 VC = Volume Control Ventilation ... well I have a little scenario on a little course I developed for Paramedics: Called Transport Ventilation in the Flight Environment ... would you guess that based on the 5 to 7 ml per kg that 90 % of Paramedic students FAIL ... when presented with a Patient that is 200 kgs .. HUGE FAIL!

This is where I start then titrate PIP > 40 to achieve Plateau pressures less than 32 cmH20 "in the fresh Intubated" and non complicated pulmonary patient.

Point to be made this is based on IDEAL Body wieght something seriously lacking in ALL the posts.

To the OP could you please explain APPV or IPPV (is that intermittent positive pressure ventilation?)

I understand PRCV, APRV, PC, VC, Control, PS, CPAP, and SIMV (a few more oldies too)... but APPV has got me scratching my balding head?

Comparing 1 PC and 2 VC is like comparing apples to oranges in the first place unless one has volume measuring devices in line as well as pressure ...

http://www.lifesavingsystemsinc.com/em100.htm well IMHO is a toy and also should hit file "G" the Carevent ATV has nice colours on the twisty knobs again belong in file "G" for anything more than a transport across the street (I call them the Educated Fire Fighter) as far less extubations enroute.

In the interests of privacy I suppose I should not say which of the two authors is the student in question. I couldn't remove the bold format from Boyle M for some reason, its not necessarily him.

Honestly I have no idea why if these are published studies why one would wish to remain "private" just the drift of the convo suggests that yet just another capitalized approach, inventing another gimmick as in the Smart Bag IMHO should recycled into gargbage bags ! http://www.otwo.com/prod_bmv.htm

The following values were considered desirable, apparently, as per ILCOR guidelines.

I was wondering what everyone here thought about the idea.

ILCOR are standards set for those that rely purely on the dummied down for the Paramedic Masses AND so that every RN can get a card for their wallet. Its not a gospel,and its a consensus and vast majority of those with input a cardiologists or ER Mds ... hint: the footnotes are an indicator.

As an aside, there was no mention of artificial airway type that I've noticed in the papers. I was wondering if this could be considered a confounding variable. I have used the lung simulator in question and its attachments are probably most similar to ETT pt. Could the airway type make a difference to the outcome?

Really a rhetorical question, short answer of course the type of airway is a variable and what type of lung simulator are we talking here computer sim or one with mechanical springs, just a query is all.

1- I believe chbare is referring to Vd/Vt ie deadspace ventilation with the use of variable airways, I will not put words in his mouth persay.

2- Quote Ventmedic: "For the OP, it sounds like that researcher is trying to build a better mouse trap with the BVM to achieve lower VTs, limited flow and lower pressures" Agreed Fully, education is the long term answer not another I am too stupid to use my brain and the sense of touch and need another plastic invention.

3- Vent goes into great depth to explain compliance compensation, deadspace ventilation and different strategies in the ARDS patient errors in the CCT situation this is why Respiratory Therapy is now a 3 year degree program and a 2 week course for a CCT patch ... is a band aid fix at best, s if one cannot run an LTV like a piano ... get off the bird !

<snip>

What is the main aim in ventilation? Perfusion maintenence in the event of return of spontaneous circulation.

Evidence has shown that perfusion rates decrease by approx 50% at the time of arrest. This means we need to maintain less Oxygen during the arrest.

Will the size of the bag really effect this? No. In the until an ETT is insitu, you cannot gaurentee the amount of oxygen actually entering the lungs. Poor seals, lack of effective jaw thrust, head tilt can lead to air being pumped into the stomach.

Studies that the current guidlines are written from show there should be a primary focus on compression, even before defibrillation in some cases.

To me this makes the who debate mute. What would be more interesting is to see how effective -placing a high concentration mask on a pt & see how much O2 enters the system through partial pressure changes with cardiac compressions.

Phil: Firstly in a full arrest situation there is no spontaneous circulation/ perfusion ! and if one looks back to the Krebs Cycle and production of Lactic acid there is an INCREASE need for O2, and at the cellular level the production of CO2 is still a dynamic process even during DEAD (to a point) and quote ILCOR guidelines all you wish in that regard but one still has to be returned to homeostasis if one HAS a return to spontaneous circulation, there is research to suggest that acidosis is a protective mechanism at the cellular level ... note research, IMHO the increase in stats we are observing is directly related to the focus on education of compressions ONLY in the out-of-hospital ... to door discharge this is a misnomer.

This is not mute at all, the multiple topics here ie during arrest or transporting or the ventilated patient during transport, the concepts for example DHI a "relative hypotension" resulting in PEA and generally is unrecognized by majority of EMS providers, but further compounding this with Oxygenation, Ventilation, and Perfusion with a smattering of Mask Seal and ramblings.

Last point you make Phil we actually place a O2 cath down the ETT tube at a flow 0f 6 lpm and do serial ABGs watching CO2 rise and PH drop ... in fact this is used a criteria to establish Brain Death, therefore are you resuscitating a heart or a brain ?

<end rant>

Edited by tniuqs
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Yes you can put the cart before the horse, but why do we need to change the tools instead of changing how we 'educate' staff and students, new and old. (I purposely did not use the word 'train').

Educate people to use the right tool for the right job. If it happens to be a smaller volume BVM, then so be it. How many people (EMT's, Paramedics) have a good grasp of tidal volume, I/E ratios/pressures, PEEP, etc.

It is a great pet peeve of mine to see an intubated patient transported with the least trained person ventilating with a BVM (firefighter, first responder, etc).

Having a focus of "ventilation during cardiac arrest and the effectiveness of different sized bags" is nice in theory, but what happens if you have a ROSC? Do you change BVM size?

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Having a focus of "ventilation during cardiac arrest and the effectiveness of different sized bags" is nice in theory, but what happens if you have a ROSC? Do you change BVM size?

Exactly. It is like those who freak out when they have a pedi patient but realize all they have is an adult BVM. Learning the basics of how your equipment works should enable you to adjust for many different situations. This is something I have tried many times to stress with even simple things like the NC. I can not give someone the standard blanket recipe since every patient will be different.

I will elaborate a little more on the low VT ventilation. For the cardiac, the theory is not to hyperinflate and do smooth even flows with low pressure. For ARDS, we may do a very rapid flow to hold similar to a square wave pattern to increase airway MAP and thus, hopefully increase oxygenation. However, that may require much pharmacological support to accomplish this as a high PEEP is also used in conjunction with the low VT to improve oxygenation and reduce atelectasis.

Edited by VentMedic
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