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I stand corrected.
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Thought there might be a better turn out than ths. Mind you it's not trauma so maybe it's not that exciting.
I'll give the "answer" then (how I worked it anyway)
CPR continued, epi 1mg given with no change. Intubated, size 9 tube, no extensions or so forth to minimize dead space in the circuit. Initial end tidal of 160mmHg, SpO2 of 77%. Ventilated at a rate of about 6/min with a Vt of about 8-10ml/kg. ILS crew continued giving epi and CPR under direction.
Then the kicker: bilateral chest decompression with pneumocaths- immediate release of copious free air from both sides with an almost immediate ROSC, AF rate of 150, BP 170/100. Occassional agonal respiratory effort, increasing with time, and pt starts to not tolerate the tube so well but GCS remains 3.
SpO2 increased to 98% EtCO2 trending down to about 100mmHg on arrival at hospital. Chest is still tight, but now has biphasic wheeze and is significantly more compliant.
So, now we have an output, how would you continue management?
So, now we have got an output
Vt seems a little high even for a normal pt. Were you wanting to increase the Vt in an asthmatic arrest? I would have thought you'd back off on the Vt what with dynamic hyperinflation and so on...focussing more on the expiratory phase. With their functional residual capacity through the roof you don't need to be overloading them.
Intubated, size 9 tube,
CPR continued, epi 1mg given with no change. Intubated, size 9 tube, no extensions or so forth to minimize dead space in the circuit. Initial end tidal of 160mmHg, SpO2 of 77%. Ventilated at a rate of about 6/min with a Vt of about 8-10ml/kg. ILS crew continued giving epi and CPR under direction.
If this patient is hyperinflated with a bronchospasm, the chances of bagging with much to any Vt will be slim to nil without excessive pressure which will of course cause the pneumos.
If the patient has bilateral tension pneumos, the chances of ventilating with PIPs of less than 60 cmH2O would not be likely. Of course, even with the pneumos decompresssed the inflammation and bronchospasm will persist and if it is servere enough to cause the patient to code one still won't be able to bag unless they happen to be carrying heliox on their truck.
Gotcha. That makes sense. What role does gastric insufflation play? Surely you'll be inflating the stomach long before an iatrogenic pneumo.
You mean positive inspiratory pressure (PIP) right? Not P1P (intrapleural pressure). You meant that you will likely need to provide >/= 60cmH2O of pressure to overcome the compression caused by the tension pneumo?
How useful is heliox in this situation? It makes good sense, being a lower density, and it obviously has some mesurable desirable effects, but everything I've read has said that the evidence just isn't there that it improves outcomes (although there does seem to be a distinct lack of evidence in general regarding heliox's use in ventilated pts). Do you use it to aerosolise medications as well?
EDIT: Our guidelines still say to ventilate everyone with Vt of 10ml/kg although we have all been instructed that 6-7 are better numbers. Why such high numbers if the normal Vt is more like 3-5? Any idea why our service keeps pushing this idea of 10mls/kg despite the fact that it seems to be way too much and impossible for us to measure.
Qualifications changed; it's all about the badge and statusHow did you work it like that being an EMT-B, do you mean that you were with a medic who did that, or are you telling little phibs about your level of practice? Student maybe?
Vt seems a little high even for a normal pt. Were you wanting to increase the Vt in an asthmatic arrest? I would have thought you'd back off on the Vt what with dynamic hyperinflation and so on...focussing more on the expiratory phase. With their functional residual capacity through the roof you don't need to be overloading them.
Size 9 tube?
What was the PetCO2 during the cardiac arrest?
Where was the pulse ox placed?
EtCo2 levels as noted, ILS do not have capnography, so numbers unknown until immediately before and after intubation. Spo2 probe placed on an earlobe.
Anyway, ongoing treatment was: Infusion of IV beta-agonists.
12 days in ICU and the patient was discharged to home, neurologically intact and with no ongoing health issues as a result of this episode.
Manthous CA. Heliox for Status Asthmaticus? Chest. 2003 March 2003;123(3):676-7.Finally, one may ask whether there is a role for heliox in mechanically ventilated patients. Studies by Menitove and Goldring10 and Darioli and Perret11 have demonstrated that mortality from mechanical ventilation for asthma can be eliminated using techniques to reduce dynamic hyperinflation. No similar data exist for heliox when it is used in such cases.
Rodrigo Gustavo J, Pollack Charles V, Rodrigo C, Rowe Brian H. Heliox for non-intubated acute asthma patients. Cochrane Database of Systematic Reviews [serial on the Internet]. 2006; (4): Available from: http://www.mrw.interscience.wiley.com/cochrane/clsysrev/articles/CD002884/frame.html.The existing evidence fails to demonstrate a clear benefit from the administration of helium-oxygenmixtures to all ED patients with acute asthma.
Treatment with heliox may improve pulmonary function in the most severe acute asthma patients; however, clinicians must ensure other evidence-based treatments are employed.
Reuben AD, Harris AR. Heliox for asthma in the emergency department: a review of the literature. Emerg Med J. 2004 March 1, 2004;21(2):131-5.Despite the lack of concrete evidence to support its use in asthma, Heliox still forms an integral part of the treatment algorithms for exacerbations of asthma in some centres....There also exists a small population of patients with status asthmaticus who fail to respond to routine therapy but still have respiratory muscle reserve. It is this second group who they may benefit from breathing Heliox until definitive therapies take hold.
How was his voice after a size 9 through his cords?
Do you feel that the evidence that exists is enough to warrant its use in selected situations in a pre-hospital setting?
As dulcet as always. At 300lb and 6'6" he could have had a garden hose down there and not noticed the difference.
Qualifications changed; it's all about the badge and status
Smash,
I ask again, what country are you from so we can get a better idea about your training, available meds and protocols especially since you did mention the IV beta agonists?
At the moment I'm lying on a beach in Thailand. Really, where I am or what level of training I identify myself as has no bearing. The scenario was as stated and I was curious to know what people would do and why. Fashions may vary from country to country, protocols may differ, training may not be standardized, but none of that interferes with the discussion of the case or the science (or lack of) behind such treatments. For example, intravenous beta agonists do not find favor in many places and for sound reasons, however in others they are recommended for refractory bronchospasm, and there are also reasonable grounds for this.
You initiate a scenario but can not answer simple questions when asked and get defensive or embarrassed when someone asks about your country or level. That sounds like you are not comfortable with your title and you probably should continue your education so you will understand why some of these questions are relevant to patient care. Even as an EMT-B, one can be advanced enough in education regardless of level to at least answer what country they are citing protocols from and explain a few things concerning treatment. That is what this thread is about and not your ego or beach time in Thailand.
One more question: Did you use 300# as the ideal body weight for calculating VT or did you use the height?