crazycanuck

Ventmedic linked up a thread with extensive discussion on what others consider "a save". I believe Medic26 is looking for some data and academic discussion of the definitions and guidelines if I read the request correctly. Personal definitions of survival are based on semantics and were discussed in the earlier thread. Survival outcomes and definitions will vary by study design. They will usually be as you mentioned based on time-line from intervention to time of death. Do you count it as a save if the patient has ROSC but no neuro function? Do you count it as a save if the patient goes on to discharge with previous level of function? This is the great debate, but here's what the literature says.... Here's some of what I could dig up and I hope it is of assistance to you 26. 1) http://circ.ahajournals.org/cgi/content/full/114/25/2760 Increasing Use of Cardiopulmonary Resuscitation During Out-of-Hospital Ventricular Fibrillation Arrest **see the section outcomes for their definitions and descriptions of "survival" posted here as well "Outcomes The primary outcome was survival status at hospital discharge. We also assessed discharge destination (home versus nursing or rehabilitation facility) and neurological status at discharge based on hospital record review using Cerebral Performance Category. A Cerebral Performance Category score of 1 or 2 was classified as favorable neurological status.15,18 Using the electronic AED record, we assessed the timing of CPR between the first (stack of) shock(s) and the second (stack of) shock(s) to help determine whether the protocol changes influenced the timing and quantity of CPR. Specifically, we assessed the time interval between the first shock and the start of CPR (hands-off interval 1), the total time spent performing CPR between the first and second shock, the interval between the completion of CPR and the second (stack of) shock(s) (hands-off interval 2), and the total time between the first (stack of) shock(s) and the second (stack of) shock(s) (hands-off interval 1+CPR interval+hands-off interval 2).19 This review used both the real-time electronic ECG and the audio recording information to assess CPR timing. Prior study has indicated good interviewer reliability with regard to the timing of CPR with this approach.11" 2) http://eurheartj.oxfordjournals.org/cgi/co...full/27/23/2840 Predicting survival with good neurological recovery at hospital admission after successful resuscitation of out-of-hospital cardiac arrest: the OHCA score 3) http://content.nejm.org/cgi/content/full/3...2473fbbdcdbfd38 Long-Term Outcomes of Out-of-Hospital Cardiac Arrest after Successful Early Defibrillation **see the results section and it gives definitions for survival and outcomes 4) http://content.onlinejacc.org/cgi/content/abstract/7/4/752 Factors influencing survival after out-of-hospital cardiac arrest *check out the references at the bottom of that link as well for more articles**

*crazycanuck retracts claws and puts them away* Cayer, just making a point. It seems my comments toward you were misdirected. Sorry about that! I hope the links are useful. All the best and stay safe. :wink:

Here are the "new guidelines" from 2005 :shock: Here is a link if you see right next to the white and red icon it links to the full content in Circulation: http://www.americanheart.org/presenter.jht...ntifier=3035517 Here is said link with individual sections for your perusal: http://circ.ahajournals.org/content/vol112/24_suppl/ Adult BLS: http://circ.ahajournals.org/cgi/content/fu.../24_suppl/IV-19 For peds: http://pediatrics.aappublications.org/cgi/...full/117/5/e989 Often you do not need a journal subscription to get these online. Sometimes google will do the trick, and if not try: www.scholar.google.com and this will bring up journals and academic literature. Also, one more thing cayer, don't take this the wrong way. Last I checked it was a duty and responsibility of a person within a profession to know and understand the scope of their practice and all of the guidelines under which they practice. It does not reflect well on any person to not have the materials they need for knowledge and education for the reason you gave of not wanting to pay for it. Go to the library they have services to print articles or at very least have access to fulltext. Better to ask here than not at all, but it is your professional responsibility to have the materials. Don't ever use the answer that you didn't want to buy the book/paper/materials, it looks bad on you and you represent others. I hope you see the point without being completely offended. And if you are offended you'll get over it soon :wink:

Another tidbit for your perusal: www.kardio.ch/pdf/2006/2006-06/2006-06-001.PDF

Intervention set point is going to be different according to the patient but you are correct that most times this minimum rate is usually set around 50-80bpm. There are a few possibilities that come to mind here. 1) It is possible this is a pacemaker-mediated tachycardia (PMT). This can easily be tested by placing a magnet over the pacemaker which will set it into an asynchronous pacing mode (each device has a set rate, somewhere usually around 85bpm). This mode will cease the re-entry circuit that is needed for pacemaker mediated tachycardia to occur. (**I would not suggest placing a magnet over an implanted defibrillator without appropriate defibrillation backup as usually this will place the ICD into a non-sensing mode and will not deliver cardioversion. The magnet is often used in the case of "electrical storms" or multiple possibly inappropriate shocks from a device) http://www.emedicine.com/med/topic2918.htm 2) The intervention rate is sometimes set to 100bpm or a hysteresis rate to prevent rapid rate drops. This newer algorithm called rate drop response (RDR) is often used in patients with severe debilitating vasovagal syncope or cardioinhibitory syncope. Though this may not be the reason for your patient being paced at this rate, it is out there. This intervention pacing is set to detect a specified drop of x bpm then set to intervene and pace at x bpm for x minutes. For eg. If there is a drop of 25bpm in 30 sec, then the pacemaker is set to pace at 100bpm for 2 minutes. One current model of pacemaker with this is the Medtronic EnPulse RDR. http://europace.oxfordjournals.org/cgi/con...bstract/2/3/245 3) It is possible the rate responsiveness on the device has gone out of whack. Devices will vary but often on most newer ones a rate responsive feature can be programmed and activated. The purpose of this is to allow the patient to attain a rate appropriate to their activity level. Older pacemakers were set rates and the patient could be stuck at 60bpm regardless of if they were sleeping or running. With developments many attempts at designing sensors based on minute ventilation or peizo-electric crystals were designed to sense either body movement or activity level and then a program would tell the pacemaker to pace higher because the person is exercising or being active. The problem here sometimes is that this can be triggered by vibrations or electromagnetic interference (now uncommon with shielding of devices). www.ipej.org/0403/greco.pdf 4) Another possibility though unlikely is a pacemaker lead malfunction. This is fairly uncommon and I think would be more likely to result in under-sensing or failure to capture than an inappropriate intervention rate. This problem can be more troublesome in ICDs as it can lead to inappropriate therapy. www.ipej.org/0304/toquero.pdf Pacemakers and cardiac implants have come a very long way. There is a lot that can be customized in programming and though I can't answer why this patient had what appeared to be an inappropriate intervention rate, it is very likely that a device rep would be called to come and interrogate the pacemaker. Th read out would include all of the specific details and likely reprogramming would solve it if it is a problem. A couple of questions: was this patient paced only in the atrium? Could you just see pacer spikes in the p-wave area? Or did this look like a slow wide rhythm? Patients who are A-V paced sequentially can appear to have a very wide complex and it can even be mistaken for a slow VT, especially if it is one of those higher intervention rates or with the case of PMT. You said his paced rate was >100bpm then later went down to 70bpm. When he was at 100bpm was anything going on? Had he just been moving around or was there anything to suggest that vibrations could have activated the rate responsive setting? If the patient has one of those RDR algorithms, this usually only lasts for a minute or two but can happen repeatedly if they satisfy the criteria for pacing intervention. From the information and in retrospect I don't know the answer but those are some of the possibilities. Do you have any follow-up? Was this related to the patient complaint or an incidental finding on exam? Oh and one more thing....you mentioned you thought it would not pace above a set point. Most newer devices have a much higher tracking and pacing rate available than the older fixed ones. Now a patient who wants rate responsiveness can be set at a very high or sensitive activity level and is able to be paced quite fast when needed some up to 150-160bpm. Many will have tracking rates up to 180bpm.

Here is the link to fulltext article posted above ^ once again: http://www.aemj.org/cgi/content/full/8/7/758 1: Acad Emerg Med. 2001 Jul;8(7):758-60 Lerner & Moscati

As mentioned in the link Phil posted, the concept of the Golden Hour goes back to R. Adams Cowley, founder of Shock Trauma in Baltimore. Cowley was a 1st Lieutenant of the Medical Corps of the US Army. Ask Croaker if you're interested in this bit of history or check out the classic book Shock Trauma by R. Adams Cowley. It is a piece of EMS history and he was one of the "founding fathers" in the emergency medicine field. He devoted his life to the development of trauma protocols and the intensive study of the effect of shock on the body and outcomes. Opinions aside I will leave the discussion to people here with more direct input but here are some references for your perusal. This is just on the general concept of the golden hour, though this can be applied to specific problems such as outcomes for intervention of CVA or penetrating trauma. Reference #1 below was cited as the article of scientific review of cowley's principles that did not support the golden hour theory. 1) Lerner, EB; Moscati (2001). "The Golden Hour: Scientific Fact or Medical "Urban Legend?"". Academic Emergency Medicine 8 (7): 758-760. http://www.aemj.org/cgi/content/full/8/7/758 2) Bledsoe, Bryan E (2002). "The Golden Hour: Fact or Fiction". Emergency Medical Services 6 (31): 105. 3) DJ Lockey - Resuscitation. 2001 Jan;48(1):5-15. http://www.skyaid.org/Skyaid%20Org/Medical...al%20trauma.pdf

Terri this is an interesting link and brings up a few thoughts. Implanted cardiac technology has come a long way and now it is possible to use these devices in a wide population. Possible but perhaps not indicated. This device is somewhat similar to the Reveal implanted loop recorder. http://wwwp.medtronic.com/Newsroom/LinkedI...&lang=en_US There are specific guidelines in place for indications of implanting devices and I'm sure that ACC/AHA/NASPE would come up with clear indications for this and eventually allow physicians to bill insurance for it. I'm not sure insurance is going to go for a "heart attack warning" implant and I'm sure there will be issues with justifying implantation procedures and possible misuse of these as well but that's a whole separate issue. It seems like if the person has a high enough risk for sudden death that either treatment of the blocked vessels or underlying cause of the problem would be the proper way to go. It can be difficult enough to obtain approval for cardiac devices when there is a clear indication for them. Due to cost of procedure and the number of people who are candidates, insurance companies may often reject the initial request for coverage of these procedures. It will be interesting to see how they come up with the guidelines and justifications for implantation and what tests will be used to quantify risk and what the criterion for implant approval will be. It seems like this device would be targeted toward the middle age patient with not enough risk factors to indicate any other device or intervention, but rather as a CYA policy that may be too often relied on instead of focusing on health and well being in the form of prevention and regular check ups. Furthermore, if this device is aimed at the patient who may not recognize their symptoms or ignores them, then what is the likelihood of that target patient seeing a physician about this device or following through with an implant procedure? I think that as AZ said, if the medical system would focus on prevention we would not have so many people with coronary artery disease and we would not be focusing on damage control. Please understand, I'm all for these device developments and really these types of things can be a blessing to people. I do think too that we need to remove ourselves from the age of invinsibility where we think we can continue to abuse our bodies and our health and that modern medicine will have a quick fix readily available for us. References: Gregoratos, G, Abrams, J, Epstein, AE, et al. ACC/AHA/NASPE 2002 Guideline update for implantation of cardiac pacemakers and antiarrhythmia devices: summary article. A report of the American College of Cardiology/American Heart Association task force on practice guidelines (ACC/AHA/NASPE committee to update the 1998 pacemaker guidelines). Circulation 2002; 106:2145.

OMG :shock: :shock: :shock: :shock: LMAO katie, niiiiice. AK hun, sorry the gig is up, you're busted!!!

Khanek, Here are some references, some of them you may have to use library access for full text or PDF but worth a try: http://circ.ahajournals.org/cgi/content/abstract/37/6/979 http://www.circ.ahajournals.org/cgi/conten...stract/57/1/163 http://131.188.28.126/links/199904030367.pdf http://www.circ.ahajournals.org/cgi/content/full/91/5/1602 http://www.anesthesia-analgesia.org/cgi/co.../full/96/4/1232 Happy reading

http://www.ncbi.nlm.nih.gov/entrez/query.f...p;dopt=Abstract www.blackwell-synergy.com/doi/pdf/10.1111/j.1540-8167.1997.tb01021.x http://circ.ahajournals.org/cgi/content/abstract/58/6/1036 http://www.circ.ahajournals.org/cgi/conten...act/103/25/3092 Had this lady had any PMH of an ablation procedure for arrhythmia?

Hi Skibum, I have never heard of this, though let's wait to see what everybody else has to say. My suspicion is maybe this is her old school perception-- back in the day pacer and ICD pulse generators were large and implanted abdominally. Now this is not frequently the case, unless it's a ped patient who is too small for traditional implant or someone with erosion problems or other anatomical anomalies. Perhaps back in the dark ages when we had much larger pulse generators implanted in the abdomen she was told not to perform abdominal thrusts due to risk of lead dislodgement. Even then, is she going to let someone choke so she doesn't "hurt their pacemaker"?!??!?! Just my 0.02. CC

The first company I know of doing VNS was Cyberonics. There is also more recently a company developing a similar neurostimulatioin devie. Here's some info on VNS: http://www.vnstherapy.com/depression/hcp/ As for the mechanism of action of vagal stimulation, it's not quite clear how it works, but it is known to alter NT release (nor-epi and dopamine primarily I think). As for selective stimulation of one section of the nerve versus another, I'm not familiar with minute vagus nerve anatomy to say for sure how the electrode is implanted. It is a wrap-around type electrode. Now, purely from a thinking point of view, I'm not sure it is anatomically possible to have selective depolarization of one region of the nerve and not another. I know in some neural systems the strength of the response is coded by both firing of different types of neurons and intensity of the response is dictated by the number of neurons firing. If you think of a pacemaker analogy, the leads are implanted in different regions depending on the need, so for example a dual chamber device with an A lead and a V lead. Though the leads stimulate that one area that they are implanted, for eg, the V lead in the right ventricular apex gives electrical stim right in that one area, BUT, it spreads right? The electrical impulses generated by a pacemaker do not just selectively affect that one spot, they act to propagate electrical impulses through the conduction system. So, while I think perhaps there is a particular specific area on the left vagus nerve that the electrode is wrapped, I'm not sure such selective stimulation is possible. I think it has to do more with settings as I mentioned. The pule width, duration of intervention, and voltage setting of the VNS can be altered, and I'm not sure of the physical values, but perhaps they have limited effect on the cardiac system, and they are still able to exert an effect on a neural level in the case of treating refractory depression and refractory epilepsy. If this were a major problem, the device would not have made it through the FDA approval. Interesting discussion.

The VNS is implanted on the left side and connected to the left vagus nerve with the idea that the left vagus does not exert as much control over cardiac function, perhaps someone can elaborate more here. However, there is research on R VNS therapy as well, so right sided-implantation is not contraindicated. I do think though that the way the device is programmed has a lot to do with how much potential there is for side effects, if the pulse is intermittent and at a low voltage setting, it is less likely to exert negative cardiac side effects. Research that I have seen with R-sided Vagal stim appears to have more cardiac effect, though the evidence base has some that also says no difference. http://www.blackwell-synergy.com/doi/abs/10.1113/eph8602146 www.blackwell-synergy.com/doi/pdf/10.1111/j.0013-9580.2005.16404.x

Just to follow-up on the info here about the "brain pacemaker". This device is called the VNS (Vagus Nerve Stimulator). It is not a new device, however it is just more recently becoming more widely implanted in the treatment of both epilepsy as well as refractory depression. I am not sure of the FDA status for the implantation in depression, I believe large scale trails are still underway. As for the indication of implantation in epilepsy, it is mainly implanted for partial seizure disorders that are refractory to multiple medications in both single drug intervention as well as combination drug therapy. I would guess that this VNS was implanted in this patient not for epilepsy, as you did not mention that as a diagnosis, but for depression/neurological involvement. The actual mechanism of action of the VNS is not completely proven, as we know the vagus nerve has so much involvement and control over the body in general. The basic theory behind it, is that by using impulses to stimulate the vagus nerve, it can cause neuronal discharge and interrupt abberant cortical activity as well as affect the production and balance of excitatory neurotransmitters. Just FYI, the VNS is usually compared to a pacemaker because the general idea is very much similar. The programming on these devices can be altered as far as voltage and timing (pulse width) of interventions. The device can be set to intervene at specified intervals, or in the case of seizure disorders can be activated by a remote magnet (that the patient or parent can carry) that will intervene to hopefully lessen a current or oncoming seizure. Also useful to know, as in a "runaway pacemaker or pacemaker-mediated tachycardia", any device like the VNS has potential for programming error or interference. The VNS can be inhibited by a magnet depending on the settings, usually the patient/paretn will know how. (can be set to activate by one pass over the device and inhibit by holding over device, then turned back on- totally depends on programmed settings) Now- with regards to this patient-- has this patient had any dose changes recently? Missed a dose? Added a new med? Taken any OTCs she forgot to mention? My initial thought on this is that this patient is certainly having an issue of polypharmacy. This is perhaps unavoidable, as she may clearly have a need for the plethora of psychiatric and other medications she is currently taking. This could also, as you know, be a result of discontinuity of care and multiple physician interventions with poor patient report of current meds and history. The motor response does possibly sounds that it's a result of meds, but the index of suspicion you had to r/o anything else is of high quality patient care, rather than assuming "it's just the meds" and there is nothing more serious going on such as CVA, etc. Take a look at this if you like on Neuroleptic Malignant Syndrome. Helpful info on meds and s/sx. http://www.emedicine.com/EMERG/topic339.htm Emergency Psychiatry: Extrapyramidal Side Effects in the Psychiatric Emergency Service http://psychservices.psychiatryonline.org/...t/full/51/3/287 A Guide to the Extrapyramidal Side-Effects of Antipsychotic Drugs http://bjp.rcpsych.org/cgi/content/full/176/5/502 Info on VNS: http://www.vnstherapy.com/ Often times, patient on multiple meds are on a balance of meds to reduce the possibility of the extrapyramidal effects they can create. Very interesting case, thanks for sharing.

Interesting link to a drug trial of an oral anticholinergic tested vs. placebo and irpatropium bromide: http://www.erj.ersjournals.com/cgi/content...6.06.00126005v1 Eur Respir J 2006, doi:10.1183/09031936.06.00126005 Also a good article, with plenty of med info at the end: http://www.emedicine.com/EMERG/topic363.htm

If this was neuro and was in fact a seizure, I'd be leaning toward partial seizure, but not necessarily absence. Absence is usually much more transient, unless this initial presentation was a status event. Could be complex partial, but they can look very similar and we need more info about motor behaviour, automatisms etc as well as EEG findings would be a way to distinguish the variant. However, I would want more neuro information to present to the ED that would give them more indicators if they did think it was a seizure from neurological cause. If theyare leaning to neuro they will have a ped neurologist look into it, and they have the specialty knowledge required with the input form the ER Doc to investigate this further. With that low BGL, I'd lean toward that being the cause, but let's not throw this out the window just yet. Just to play the opposite side, what if it was a seizure that brought on the low BGL, possible though I'm not sure this is possible so rapidly, with the s/sx being 20min in duration I would guess it would take longer for a seizure to reduce a BGL so rapidly....anybody have any ideas on that end?

OK, I think I got it, thanks! Follow-up vitals and BGL on the way. I think it would still be advisable to work this child up metabolically as well as possibly neurologically, as this is a pretty severe episode of hypoglycemia in a child this age. Also, if I am correct- hypoglycemia will more often result in tonic-clonic seizures, as opposed to the deficits shown here. Though it's possible this is simple occurrence of hypoglycemia, I'd still like to err on the side of caution and be sure this child is transported appropriately and worked up. ED intervention will R/o anything severely wrong metabolic wise, check ketones, CO2, BGL, basic CBC, continue fluids and dextrose. Often times I think these episodes in children can be overlooked when the immediate cause is not apparent and then take a wait and see approach or wait for a repeat occurrence. Any insight into the underlying cause of it? No illness as you stated, so no n/v, recent viral infx-, but any change in meal patterns, reduced intake? OK now that we have a BGL, what was the response to treatment and follow-up BGL. Fluids and dextrose. Repeat vitals, any change in LOC, any more info for us.

From hammerpcp's post: "When you take over you notice that the child is still looking to the left and is not responding to you or even acknowledging your presence." >Deviated eyes and ALOC. Makes me think neuro involvement.... Can we have some more specific info such as GCS, any response to noxious stimuli or any motor response? From hammerpcp: "The teachers say that this child was reading in another room in the library when one of them tried to talk to him and he would not respond. The teacher then led the child into the adjoining room- he walked on his own but needed to be guided in the direction the teacher wanted him to go." >Non-responsive, still able to perform actions but not purposefully, would lead me to question whether or not this child was having a complex-partial seizure, definitiely still thinking neuro involvement (but still need to R/o hypoglycemia, trauma, infection, PMH, etc. Give us some more info please). Do we have any other info about actions during this time? Did the child display overt automatisms such as lip-smacking behaviour, or repetitive hand gestures, or any repeated facial movements/grimaces? from hammerpcp: "He was still verbally unresponsive and did not seem to be making movements with any particular purpose. For example, he would walk a few steps in one direction as if with intent, but would then stand there "looking off into space". " >Well on initial thought I was thinking, was the kid messing around, but that being said, (correct me if I'm wrong) kids aren't great at victim sims or faking symptoms. So- this type of behaviour, though it could have a non-organic basis such as attention-seeking or psychosomatic, does suggest this needs to be pursued and many many things need to be ruled out in an otherwise healthy child who is displaying sx of transient deficits and ALOC. from hammerpcp: "After approximately ten minutes with this teacher, the boy apparently took several steps and then collapsed to the ground. At this point 911 was activated. The boy's eyes remained open while on the floor and he still appeared to be looking off to the left." >Can we get a more specific description of this "collapse"? Was it a fall direct to the ground, with no hands put out for protection, how did the child drop, was it stiff or was he limp and slumped to the ground? Was there any motion during that time, any tonic/clonic activity, any coordinated or uncoordinated muscle movement? Was there any alteration in respiration? Any report of gurgling noises or any utterance at all from the child? Was there any deviation of eyes or did they remain fixed to the left the entire time. The pt has no medical history, no allergies and nothing like this has ever happened before according to staff and parents who were notified by phone. Your next move? > I want vitals first off. I want a complete H&P and as much info as possible from bystanders on the questions above. Now that you have arrived- you say the child is standing but still unresponsive and looking to the left? Current LOC? Current vitals? Describe his behavior now with him standing, is he responsive to verbal, motor, withdraw form painful stim? Describe his eyes, are they still fixed left or does he have any nystagmus? Any loss of bowel or bladder control? Any bleeding on lateral tongue or cheeks? I also want to know- you said the child is standing but still unresponsive? Did he get up right after he fell? Get some info about this transition from on the floor to back standing up. Did he just get up and then was altered again, or was he out of it the whole time? Hase he been responsive at all? So start with the basics: - Give us current vitals and answer some qns on HPI. BGL, get kid on monitor, O2 if you think you need it (he's been altered for awhile, it probably can't hurt), transport. As far as further assessment goes, it appears this child clearly needs some further investigation. I say look for the basic stuff first- prev trauma, possible ingestion, fam hx of seizures, psychological status, any info you get. Then, depending on the answers- I say eventually this kid will get a complete neuro workup and if that is clean w/o any physiological basis we go from there. Initial thought in the back of my head is neuro- seizure, some type of syndrome (Panayiotopoulos among many other seizure disorders), or non-organic seizure, BUT before I jump the ship on the complicated d/dx I want to know if we have ruled out the basics. Interesting case hammerpcp, thanks for sharing. Let's see where we're going with this. PS. One day I will learn how to quote, I hope this is legible enough. Edited to add that I had not seen your last post yet hammerpcp. Before I make any more comments I'm leaving this to stew awhile. Thanks.

*this info is only my personal opinion and does not represent any external agencies* (end of infomercial intro ) There are a lot of options in buying an amplified or electronic stethoscope. First, I have had a chance to demo one specifically that I personally was not sold on the Cardionics E-Scope. It is expensive and didn't have that great of sound quality as far as I was concerned. Also, the scope has a fast turn off time, around 2 seconds and must be touched to reactivate, which could end up being a pain. The battery contacts were also quite loose in the unit making it intermittent. I have not personally had a chance to demo many other amplified stethoscopes so I can't offer specific brand advice but there are also a few modifications you may wish to also try. First, a custom set of earmolds, (generally made in an ear,nose, throat clinic- or by an audiologist) can go a long way in helping to get a higher intensity of the scope's sound delivered directly to your ear canals as well as the snug fit helping to keep external stimuli out of the external auditory canals. It may also be of benefit to be sure you buy a scope with a thicker covering on the outside, serving to help protect from sound leakage and interference with the signal from outside sources. Here is a link to an excellent resource with some tips for purchasing a new amplified stethoscope: http://www.amphl.org/forums/viewtopic.php?t=81 Not knowing the type, severity, and configuration of your hearing loss it is hard to recommend an appropriate product. You may also want to look at the scope's specs and determine where the amplification is in the frequency range, as it would be useless for you to have an amplified stethoscope that amplified in only regions of normal hearing, and not in the places you need. I also wonder- do you have a severe enough degree of loss to warrant the use of amplification at all times, or are you just needing the additional assistance with using the stethoscope in a noisy environment? The reason I ask is that often in hearing loss, it is not only an issue of lack of auditory sensitivity (not enough intensity/volume) but also an issue of CLARITY- which may or may not be addressed by amplifying the sound. For some people, amplification will result in a louder, still muffled signal in which case the device is useless to you. In general, for a mild loss it may be enough to opt for the custom molds. Moving to a more moderate to severe loss, you may erceive more benefit from an amplified stethoscope. As for the external noise reduction, often these terms are a marketing strategy rather than the actual process of active noise cancellation or feedback suppression. Unless you sink a petty penny into a digital stethoscope programmed with noise reduction algorithms, the stethoscope does not really have the ability to actively cancel external noise. This being said, the extra money may be better spent on custom tips, and a good high quality amplified scope versus the more expensive and cumbersome stethoscopes with separate receiver attachments and external adjuncts. Also, with a pre-existing hearing loss as well as tinnitus I am certain you understand the need to safeguard your intact hair cells within the cochlea- which will mean diligent use of noise protection when necessary. I would say that any reputable company will allow you to return the product if you aren't satisfied. These amplified devices can be expensive so it is within your best interest to take the time up front and try out a few, versus regretting the purchase later. Good luck!!! CC

{"It says if there is brain stem damage, then the eyes will move with the head. I tried this in a mirror and turned my head, my eyes maintained an opposite angle to the tilt of my head. To my knowledge I have no brainstem injury (boy did I leave myself open with that)"NREMT-Basic } The vestibulo-ocular reflex in normals is affected by the response of the semi-circular canals in response to head movement. As you found in your own test of looking in the mirror, if you move your head to the left, the eyes move to the right. In normals, without vestibular dysfunction or brain injury the eye gaze will be in the opposite direction of the head movement. An abnormal response indicating brain injury or some related problem with the VOR occurs when the eyes move in the same direction as the head movement. The doll's eye test of the oculocephalic reflex should also be performed with the head elevated by 30 degrees. This is because of the interaction of the fluids in the three planes (anterior, posterior, and horizontal)of the semicircular canals, the horizontal canal is actually in the neutral position with this 30 degrees of elevation. The other point worthy of mention is that the vestibular system is so dynamic that when we're performing these types of provocative such as head turning and caloric testing, as tests in conscious patients to do as a neuro check-often times we are able to suppress nystagmus or abnormal movements, this is why the oculucephalic reflex is only able to be demonstrated in unconscious patients. To avoid suppression of response in clinical vestibular testing, we often perform "alerting tasks" which simply means you distract the patient with mental tasks in order to elicit a true response.

The answer to this question depends on a whole lot of variables. The short answer in general is that it may take more albuterol to relieve SOB in a person who is also receiving beta blockers. As you know there are Beta 1, 2, and 3 receptors. You're most concerned with beta 1 (heart) and beta 2 (lung) mechanisms. A beta blocker (antagonist) comes in two basic categories: beta 1 selective (cardioselective) or non-cardioselective. Some examples of cardioselective beta antagonists are bisoprolol, atenolol, metoprolol. Some non-cardioselective are: nadolol, labetolol, sotalol(also class3 antiarrhythmic properties). Non-cardioselective beta antagonists are contraindicated in patients with prior hx of mod-severe asthma or other resp problems. The amount of affinity for the beta receptors, or cardioselectivity is proportional to the dose. So even if a patient is taking a cardioselective beta antagonist, if they get to a high enough dosage, there will be spillover to the beta 2 lung receptors. Now, getting to albuterol, it is an inhaled B2 agonist. If a patient is taking a beta blocker that is already blocking the receptor then the intuitive answer is that the response to the inhaled B2agonist will be reduced. Getting into non-competitive and competitive antagonism- I'm not sure if the B2 agonist albuterol will override the blockade, I don't think it does but that discussion is over my pharmacology knowledge. So- the answer is kind of beating around the bush but it really depends on a lot of things- the dose and type of the beta blocker, the severity of the SOB, the amount of albuterol administered, etc. I'm sure someone else will give you some more hands on knowledge of this and their experiences in use of both meds concurrently. Hope that helps. *Edited to replace "the obvious answer is" to "the intuitive answer is" :wink:

My dear squint, I normally am a definite metric person, however sometimes I choose to just go with the flow :wink: ___ CC lover of the metric system since 1963

As you know, there are several different types of SVT within the umbrella of atrial, or supraventricular tachycardias. There are atrial ectopic tachycardias, which originate from one or more irritable focus/foci in the atria. There are also AV re-entry tachycardias (AVRT) and AV-nodal re-entry tachycardias (AVNRT) and these can all be classified from specific EKG classification of intervals and origin of p-waves, etc. which is well above my capability in this discussion. The reason I bring this up, is that the type/origin, and rate of the SVT may dictate whether or not you will have success with Vagal maneuvers such as Valsalva or carotid sinus massage. Also as previously mentioned, CSM is contraindicated in the presence of carotid bruits, as well as in individuals with carotid-sinus hypersensitivity w/o a pacer implanted, and in persons with hx of atherosclerotic disease. The success for vagal maneuvers may also have to due with the individual sensitivity to the carotid sinus reflex, and the presenting rate of the rhythm. As for whether or not this is indicated in your protocols, I suspect it is possible in some areas and not in many others. ____ CC And for reference just in case you're interested: eurheartj.oxfordjournals.org/cgi/reprint/25/15/1310.pdf (pdf is available in entirety online, worth a look) These others you may be able to get abstract, but I think you need fulltext access: Lim SH, Anantharaman V, Teo WS, Goh PP, Tan AT. Comparison of treatment of supraventricular tachycardia by Valsalva maneuver and carotid sinus massage. Ann Emerg Med. 1998 Jan;31(1):30-5. Journal Watch Emergency Medicine, Vagal maneuvers for SVT:Should we bother? Vol. 1998, Issue 301, 10 March 1, 1998

Most new pacemakers and ICDs are getting very discreet. The current models are just 1.5-2 inches square and < 1/4" thick. Many times, they are implanted in a pocket subdurally, however it is becoming increasingly popular, especially in younger people to implant them subpectorally for extra protection and cosmetic purposes. It is also possible to have them implanted not only as aforementioned abdominally or right-sided, but also rather than directly under the clavicle to have them placed more laterally toward the midaxillary line, or even within the breast tissue in females. Incisions as well are becoming much smaller and unless you look specifically, you may overlook some of the more discreet insertions. Unless I point it out, nobody would find my device. Often you can feel a ridge on the lateral edge where the interface of the leads connects with the battery/processor unit, but again it is not usually a glaring finding. Also most current models are demand pacers, and often times may have a low pace rate of 50bpm. If your patient is in NSR and their intrinsic rate is capable of exceeding 50bpm, they will not be paced and therefore only the sensing by the internal leads is detected. Unless you have a new model of monitor capable of direct telemetry you may have no idea unless they are being overtly paced. That being said, hopefully in most cases your patient will have informed you or you will have access to PMH or their implant ID. Hope this helps, crazycanuck