Ace844

I agree with "Rid and Dust" on this. It's pretty much akin to giving a FR the "ability" to do a 12 lead...after which they get it and then look and go.."Now what..????" Furthermore, most EMT's/paramedics have little to no exposure/training on the interpretation of X-rays, etc...Thus without the an extensive chnage in training and education...It serves no purpose, as well as serves little change to your management. Even in the ER most of the treatment is on a "clinical" basis. out here, Ace844

Just because you load a pt in your ambulance...this doesn't qualify as "transporting" just because they are in your "vehicle"...nor that you are less likely "to delay their access toi definative care" which BTW, you as an EMS provider are....food for thought, Ace844

"Stephen," Aparently we American EMS professionals aren't the only ones with this problem....seems the Croats are at least as bad...[video width=CROATIA: AMBULANCE VS PD height=350]http://video.google.com/videoplay?docid=6304425630605907409

"NSmedic393," Here's some links to the info you requested as well as a study for you and anyone whose interested. Also, I posted the "full text" of the study instead of just the abstract above, that has some more info for you. Primary Crae management of Cocaine Drug Abuser , Inhaled Heroin-Induced Status Asthmaticus , Pulmonary Pathophysiology and Immune Consequences of , Cocaine cardiac Phys Chest, Vol 110, 904-910, Copyright © 1996 by American College of Chest Physicians Acute effects of inhaled and i.v. cocaine on airway dynamics DP Tashkin, EC Kleerup, SN Koyal, JA Marques and MD Goldman Department of Medicine, UCLA School of Medicine 90024, USA. BACKGROUND: Wheezing has been reported by 32% of habitual smokers of crack cocaine, and several cases of crack-related acute exacerbations of asthma have been reported. STUDY OBJECTIVE: To compare the acute effects of physiologically active doses of smoked cocaine base and, i.v. cocaine hydrochloride (HCl), a subphysiologic dose of cocaine base (smoked "placebo"), and i.v. saline solution placebo on bronchomotor tone, subjective level of intoxication, and cardiovascular responses in healthy habitual crack users. DESIGN: A single-blind crossover study in which the order of route of administration (inhaled vs i.v.) was random but placebo always preceded the active drug. SUBJECTS: Fourteen healthy, nonasthmatic current crack-smoking subjects, 34 to 48 years of age, with a history of previous i.v. cocaine use (1 to 12 times per lifetime). METHODS: Heart rate, BP, self-rated level of intoxication (scale of 0 to 10), and measurements of airway resistance (Raw) and specific airway conductance (SGaw) were recorded during separate sessions before and 3 to 5, 10, 15, and 30 min after administration of smoked cocaine base (38.5 +/- 2.3 [sEM] mg), smoked placebo (2.3 +/- 0.9 mg cocaine base), i.v. cocaine HCl (30.0 +/- 2.0 mg), and i.v placebo (saline solution). RESULTS: Both smoked active cocaine and i.v. cocaine HCl caused comparable, significant (p < 0.05) peak levels of acute intoxication (6.7 +/- 0.7 and 7.3 +/- 0.8, respectively) and increases in heart rate from baseline (29.6 +/- 2.9% and 21.4 +/- 3.7%, respectively, at 5 min). However, only smoked active cocaine caused significant decreases from baseline in SGaw (25.4 +/- 6.3% at 5 min), in contrast to nonsignificant changes after i.v. cocaine HCl (5.6 +/- 7.0% increase) and smoked placebo (10.2 +/- 6.0% decrease). CONCLUSIONS: Smoked cocaine base, but not systemically administered cocaine HCl, causes acute bronchoconstriction that is probably mediated by local airway irritation and could account for reports of crack- induced wheezing and asthma attacks in nonasthmatic and asthmatic individuals, respectively. Hemodynamic basis for cocaine-induced pulmonary edema in dogs S. A. Lang and M. B. Maron Department of Physiology, Northeastern Ohio Universities College of Medicine, Rootstown 44272. Journal of Applied Physiology, Vol 71, Issue 3 1166-1170, Copyright © 1991 by American Physiological Society We tested the hypothesis that cocaine-induced impairment of left ventricular function results in cardiogenic pulmonary edema. Mongrel dogs, anesthetized with alpha-chloralose, were injected with two doses of cocaine (5 mg/kg iv) 27 min apart. Cocaine produced transient decreases in aortic and left ventricular systolic pressures that were followed by increases exceeding control. As aortic pressure recovered, left ventricular end-diastolic, left atrial (Pla), pulmonary arterial (Ppa), and central venous pressures rose. Cardiac output and stroke volume were reduced when measured 4-5 min after cocaine administration. Peak Ppa and Pla were 31 +/- 5 (SE) mmHg (range 17-51 mmHg) and 26 +/- 5 mmHg (range 12-47 mmHg), respectively. Increases in extravascular lung water content (4.10 to 6.24 g H2O/g dry lung wt) developed in four animals in which Pla exceeded 30 mmHg. Analysis of left ventricular function curves revealed that cocaine depressed the inotropic state of the left ventricle. Cocaine-induced changes in hemodynamics spontaneously recovered and could be elicited again by the second dose of the drug. Our results show that cocaine-induced pulmonary hypertension, associated with decreased left ventricular function, produces pulmonary edema if pulmonary vascular pressures rise sufficiently. Hope this helps, ACE844

"NSmedic393," Thanks for the info. The study covered some of the issues you mentioned, and as I said i thought it was interesting as I don't, and haven't ususally made the drug use question as part of my assessment on isolated asthma attack patients. Methods: We conducted a retrospective chart review of adult patients who had been admitted to an inner-city hospital and who subsequently had received a hospital discharge diagnosis of acute asthma exacerbation. Patients were classified as cocaine users if they had admitted to using cocaine within 24 h of symptom onset, or if a positive drug screen result was obtained. A similar classification was employed for heroin. The severity of asthma exacerbations among cocaine and heroin users was compared to severity among nonusers (ie, individuals without evidence of having used either drug within the 24 h preceding symptom onset).

Hi All, Whne I read through this study it made me stop and think....How many of us ask our asthmatic patient who are in distress about narcotic or opiate use before their attack???? I must admit it's not really something that popped up at the top of my list...What about you?? out here, Ace844

here's a study with some of the related info. you asked for..... Also, it has some citations and related links for you to check...::: Lime-Yellow Fire Trucks Safer Than Red -- A Conclusion from Four Years of , Emergency Vehicle Safety Initiative , The Wake Effect: Emergency Vehicle-Related Collisions, Now lets see some data from you... Hope this helps, ACE844 Prehospital and Disaster Medicine, 1997, Jeff Clawson Prehospital and Disaster Medicine; Vol. 12, No. 4; October-December 1997 Jeff J. Clawson, MD; Robert L. Martin; Geoff A. Cady, REMT-P; Ronald F. Maio, DO The Wake Effect: Emergency Vehicle-Related Collisions Introduction Emergency medical vehicle collisions (EMVCs) occurring during lights-and-siren (L&S) response, pursuit, or transport are a curse on public safety and often are publicized and criticized in the media (1-3). In addition, many collisions result in significant damages, serious injury, or death and provoke lawsuits and public outrage (4-6). An increased sense of awareness of the problem has resulted in industry-wide introspection regarding the ethics of these dilemmas (7-10). While the number of lights and siren discussions are growing, little has been done by the emergency medical services community (at large) to study this issue (11-12). In 1985, James O. Page, reflecting on what appeared to be an industry-wide attitude regarding emergency medical vehicle collisions (EMVCs), stated that, "For some reason, most of us don't like to talk about ambulance vehicle accidents—even though most of them are preventable (13)." Because EMVC reporting systems in most places are fragmented or non-existent, vehicle collisions involving EMS vehicles responding or transporting lights and siren in the United States or Canada are impossible to quantify (14). However, significant data regarding some types of EMVCs, do exist, and this phenomenon is receiving increased attention in the EMS literature (15-18). In 1994, the National Association of EMS Physicians published its position paper Use of Warning Lights and Siren in Emergency Medical Vehicle Response and Patient Transport. It established a series of positions and recommendations regarding the emergency operation of EMS vehicles. In 1987, Auerbach reported on 102 ambulance collisions that occurred during a three and one-half year period in Tennessee (19). More recently, Elling studied 1,412 EMVCs over four years in New York state (20), and Sharpe described 250 EMVCs for three years in Alberta, Canada (21). The government estimate by the U.S. National Safety Council’s system reported an estimated 2,400 ambulance and 5,400 fire apparatus collisions in 1990 (22). Various EMS and insurance industry experts estimate that the number of EMVCs could approach 12,000 in a given year (23,24). The cost of EMVCs is estimated to be in the millions of dollars and constitute the greatest cause of monetary liability loss in EMS, far eclipsing the loss due to malpractice by emergency medical technicians and paramedics. Their efforts to define the scope of this problem are only quasi-scientific, which for some, raises doubts about the validity of these number or their significance. A few have suggested (without supporting data) that the frequency of EMVCs in traffic is the same as is that for the non-emergency general public. However, Saunders et al reported that ambulance collision involvements per one 100,000,000 miles traveled was 3,548 nationally compared to 24,494 in San Francisco's urban environment. Understanding the potential scope and effects of EMVC occurrences may create a new awareness of this dilemma and, as a result, redefine its relative priority as an EMS-related problem. More than 10 years ago, the authors suggested that, in addition to EMVCs, there is an emergency roadway accident phenomenon that might redefine the actual scope of effects caused by lights and siren responses and transports. Such collisions initially were dubbed "wake-effect" accidents, since they appeared to be caused by the passage of emergency vehicle but did not actually involve the emergency vehicle (25). If this phenomenon does occur, it would add to the potential damage caused by EMVCs during lights and siren responses and transports. Anecdotally, discussions with EMS responders at conferences and via telephone interviews revealed that the wake-effect phenomenon does exist . Most EMS responders could recollect witnessing at least one such incident. The extent of the wake-effect phenomenon forms the hypothesis of this study. In light of the absence of data to quantify the actual numbers of wake-effect collisions and their connection to EMVCs, the objectives of this study were to verify the existence of wake-effect collisions as well as to determine their relative frequency compared to reported numbers of EMVCs. This hypothesis proposes that the impact of EMVCs is understated, since it does not include the wake-effect phenomenon. Methods All paramedics employed by the Salt Lake City and Salt Lake County Fire Departments were surveyed using a written questionnaire. At the time of the survey, there were 30 paramedics employed with the Salt Lake County Fire Department. These paramedics served a population of approximately 650,000 during the study period. Each paramedic was queried regarding his or her number of years as an emergency medical technician or paramedic, as well as the number of EMVCs and wake-effect collisions they recalled. Although the completion of the survey was voluntary, through the assistance of the Utah Paramedic Association, 100% of the surveys were returned. A computer database program and spreadsheet were used to sort and analyze the survey data (Paradox for Windows 5.0, Borland, International, Scotts Valley, CA USA). Results All of the paramedics who received the survey responded (75/75; 100%). Two surveys were eliminated from the study because of incomplete data, leaving a sample size of 73 respondents; 29 from Salt Lake City and 44 from the Salt Lake County. The total number of actual emergency medical vehicle collisions in the sample set was 60, with the Salt Lake City paramedics reporting 25 and Salt Lake County reporting 35 (Table 1). Comparatively, the total number of EMV-related, wake-effect collisions reported was 255: 133 by Salt Lake City and 122 by Salt lake County. These data produce in a ratio of 1:4,25 EMVCs to wake-effect collisions for all of the paramedic in the two service areas. The urban respondents had a ratio of 1:5,3 compared to 1:2,5 for suburban/rural respondents. The paramedics had an average of 8.1 years experience as EMS responders. Salt Lake City respondents had an average of 9.2 years compared to 7.4 years for those employed by Salt Lake County. Experience levels ranged from a minimum of three to a maximum of 12 years. Of the 73 respondents, 78% (57) reported either being involved in an EMVC personally or witnessing at least one wake-effect collision. Of that group, 55% (40) reported wake-effect collisions as occurring more frequently than actual EMVCs: 4% (3) reported that wake-effect collisions occurred in equal numbers to EMVCs; 19% (14) indicated that these collisions occurred less often than did actual EMVCs; and 22% (16) did not report either. The mean value for the number of EMVCs per polled paramedic was 0.82 (0.86 among Salt Lake City personnel, and 0.80 for Salt Lake County personnel). This is compared to the mean value for the number of reported wake-effect collisions per polled paramedic of 3.49, with 4.59 and 2.76 in Salt Lake City and Salt Lake County respectively. Discussion The results validate the occurrence of wake-effect collisions and report their frequency relative to actual EMVCs. The subsequent finding that possibly there occur five times more wake-effect collisions than actual EMVCs is the antithesis of the most basic premise of medical care: "First, do no harm." Although the seriousness of wake-effect collisions was not determined in this study, even small, fender-bender collisions without injuries have other community and economic repercussions that should be considered in evaluated the costs and benefits of a lights and siren policy. The location of the reported EMVCs and the associated wake-effect collisions were not studied nor were the prevailing weather conditions, surface street conditions, or time of the day. Auerbach reported that half of the crashes studied in Tennessee occurred at intersections, while Elling indicated that 70% of EMVCs in New York state happened on the roadway at intersections. The location of wake-effect collisions also may be important to determine. For example, do they occur more frequently at intersections, on the open roadway, or by veering off the road and striking other objects? Do they occur more frequently during response to or transport from an emergency scene? Such data could provide insight as to the causative nature of these collisions. It should be added that no professional avoidance, low-force, or other nationally recognized driver training programs were employed by either department participating in the study during or before the term covered by the survey. Also, no automated system of traffic-light control was in use in the Salt Lake metropolitan area. These facts bring up questions of whether different types of vehicles, colors of vehicles, warning devices, or training for drivers may affect the occurrence or frequency of wake-effect collisions or, more interestingly, affect them in a way different from their effects on direct EMVCs. The apparent presence of a wake-effect phenomenon expands understanding of the potential harm that can occur while using lights and siren as warning devices to reduce response times. The National Association of Emergency Medical Services Physician’s position paper states that protocols for lights and siren use "should be based on reasonable identification of situations for which a reduction in response and transport times might improve patient outcome," emphasizes the importance of applying logical medical rationale to this relatively uncharted territory of public safety decision-making. This study establishes a preliminary relationship of EMVCs to wake-effect collisions, but is limited in its ability to quantify these relationships. Definitions of the relationships need to be determined and implemented in police reporting systems as a significant step toward quantifying these incidents. A well-designed, long-term, prospective study should involve law enforcement orientation and consistent reporting of wake-effect incidents. While this study only involved EMS-related collisions, it is reasonable to assume that some form of wake-effect phenomena may occur as the result of fire-suppression response as well as police response or pursuit. To date, no "blame" or responsibility for such collisions has been placed on the EMS system. In discussions with responders, the blame for EMVCs is routinely placed on the public's failure to clear a path or to look for the emergency vehicle. The use of lights and siren only requests right-of-way, but does not grant the right-of-way privilege, and any effort to reduce the number of EMVCs and wake-effect collisions cannot succeed if reeducating the entire population of cities, states, provinces, or nations continues to be entertained as a possible solution to these dilemmas. Limitations This study did not determine if EMVCs or wake-effect collisions actually occur, but rather relied on the respondent’s recollections of these occurrences. Significant recall bias may exist based on the nature or severity of the crash. The authors speculate that respondents would be more likely to remember EMVCs and also more serious crashes. However, there are no data to support this speculation, not can the relative magnitude of bias effect for type of crash compared to severity of crash be determined. The assumption is that recall bias would favor EMVC reporting and could result in underestimation of wake-effect collisions. Misclassification bias is also a concern. No standard definition of wake-effect collisions has been developed or validated, nor have the parameters used to classify a wake-effect collision been developed and validated. It is possible that there exists significant variations between respondents as to defining a wake-effect collision. This could constitute significant limitations to both internal and external validity of this study. However, the similarity of mean values for wake-effect collisions among fire services, combined with overlapping of the 95% confidence intervals suggest that the concept of a wake-effect collision can be determined with some reliability. Further studies are needed to support this interpretation. Also of concern is the difficulty in determining how many of the emergency medical vehicle collisions and wake-effect collisions are unique events. For instance, the 60 emergency medical vehicle collisions reported in this study actually many represent 30 specific crashes due to dual reporting when two (or more) EMS personnel are involved in or co-witness to an accident. The magnitude of this effect could vary between emergency medical vehicle and wake-effect collisions. It is not known if reported wake-effect collisions actually were caused or affected by the responding emergency medical vehicle. It is possible they merely occurred coincidentally. Likewise, it is not known how many wake-effect collisions might have escaped notice. Observational differences may exist between response and transport due to the different positions of the personnel within the vehicle and their relative ability to see around and behind the emergency medical vehicle. Therefore, these data cannot be used to estimate the exact number of wake-effect collisions occurring in the study area or nationwide. It also is not clear whether the reported emergency medical vehicle collisions occurred during lights and siren or non-lights and siren transit mode. However, at the time of this study, it was blanket policy for all Salt Lake City and Salt Lake County fire department vehicles to respond lights and siren to emergency scenes. No accurate statement regarding travel mode can be made for transport-related incidents. Conclusion The results of this study support the hypothesis that a wake-effect collision phenomenon exists and that it has measurable impact. Given the introduction of this information regarding the potential extent of wake-effect collisions, more attention to and study of the cause-and-effect relationships between EMS systems' response policies should be undertaken. Awareness of the wake-effect phenomenon also should be cause for increased focus on the methods of driving emergency medical vehicles through traffic. The implications of this study suggest that further evaluation of lights and siren use as effective warning devices and benefits of their use in comparison to wake-effect costs to society be undertaken. Furthermore, responsibility for and acknowledgment of the potential negative effects of lights and siren EMS response within a community must be addressed more professionally and openly. The presence of the wake-effect, at minimum, should increase an EMS system's responsibility to assure a more measured and professional response and transport role within the community it serves. It also reveals added potential liability to EMS system, especially when considering the unnecessary or inappropriate use of warning lights-and-siren within the context of improving medical care and patient outcome. In acknowledging the existence of wake effect collisions as the apparent result of emergency medical responses, the potential "price" of both initial response and patient transport now must be multiplied by a wake-effect factor to obtain the societal cost of lights and siren responses. Perhaps lyricist Billy Joel, in his appropriately titled hit song, "Don't Ask Me Why," was calling to the EMS community about the wake-effect problem when he sang, "You are still a victim of the accidents you leave (26)." Acknowledgments Special thanks to the Utah Paramedics Association, John Zimmerman, MD, formerly of the Salt Lake City Fire Department and Ron Palmer, MSW, of the Salt Lake County Fire Department. References Safety and Risk Management Information Update, Management Focus 1993;9:4. Chicago-fewer "follow that car" orders expected. USA Today 1984;May 7. Clawson JJ: Running Hot and the case of Sharron Rose. Journal of Emergency Medical Service 1991;16:11-13. Caldwell LH: Hard Lessons. Fire Command 1990;84:20-21. Wallace Nelson, as guardian ad lietem for Amanda Nelson, v. USA, Case. George JE, Quattrone MS: Above all—do no harm. EMT Legal Bulletin 1991;15:2-6. Leonard WH: What a waste when a system fails. Ambulance Industry Journal1991;12:38-40. Wolfberg D: Lights and siren and liability. Journal of Emergency Medical Services 1996;12:38-40. Page JO: Waking primal instinct. Journal of Emergency Medical Services 1993;9:18:7. Meijer JE: About Speed. Journal of Emergency Medical Services 1981;6:9. National Association of Emergency Medical Physicians (NAEMSP): Position Paper: Use of Warning lights and siren in emergency medical vehicle response and patient transport. Prehospital and Disaster Medicine 1994;9:133-135. DeLorenzo RA, Eilers MA: Lights and siren: A review of emergency vehicle warning systems. Ann of Emerg Med 1991;20:13310-13314. Page JO: EMS legal primer. JEMS Publishing Co. Inc., 1985.p 2. Blades K: EMVAs—A tragic but preventable paradox. Canadian Emergency News 1990;13:14-16. Saunders CE: Ambulance collisions in an urban environment. Prehospital and Disaster Medicine 1994;9:133-135. Pirrallo RG, Swor RA: Characteristics of fatal ambulance crashes during emergency and non-emergency operation. Prehospital and Disaster Medicine 1994;9:125-132. Kupas D, Julla D, Pino B: Patient outcome using medical protocol to limit "red lights and siren" transport. Prehospital and Disaster Medicine 1994;9:226-229. Hunt RC, Brown LH, Cabinum ES, Whitley TW, Prasad NH, Owens CF Jr., Mayo CE Jr.,: Is ambulance transport time with lights and siren faster than without? Ann Emerg Med 1995;25:507-511. Auerbach PS, Morris JA, Phillips JB Jr., et al: An analysis of ambulance accidents in Tennessee. JAMA 1987;258:1487-1490. Elling R: Dispelling myths on ambulance accidents. Journal of Emergency Medical Services 1988;11:60-64. Sharp D: Ambulance fatality accidents. Research Paper Presentation—Canadian Interphase 1990 (Research Award Recipient). National Safety Council: Emergency vehicles involved in accidents. Accidents Facts, 1990:79. Forry S: written communication, September 3,1996. Leonard B: written communication. September 10,1996. Clawson JJ: Hit or myth. Journal of Emergency Medical Services 1989;14:8. Joel Billy: Don’t Ask Me Why. Impulsive Music and April Music (ASCAP), 1980.

"Dust," Is there a study anywhere in medicine in which you could find that it was a flawless, study? One which was able to control all of the variables and other things that effect outcome data?? If so please post it so we can all see. Next, is there a study out there which meets your personal acceptance criteria as valid? Have you been sucessful in those endeavors when and if you were involved in any part of an "evidence based medical study"? If so please share. As far as what I pay and which ones I subscribe to...well thats my business. As I mentioned in another post on this thread I post studies for a variety of reasons and I have yet to say that I necessarily agree with the outcome of this particular one. This very remeniscent of the back and forth you had with "ERDoc", over NEXUS. Yes, I agree that you need to be critical and aware of the bias and other influences in a study, but nonetheless there are soem that are quite useful. Also I'm curious, if all of these studies are "useless", then why are they being conducted and used at the National level by some of our peers to make "The National Scope of Practice?" Also, why would a body of physicians such as the NAEMSP and ACEP use them and accept them to guide their policies on Medical direction, etc...if they weren't in the least valid in some way. Perhaps I am missing something, could you help us all see what we are missing? How would you fix the problem then? out here, Ace844

Hi All, I agree with the comments that "Rid, Dust, and PRPG," et.al. have posted and echo their setiment. I guess in addition to the concerns listed I have a few more. "Statistical analysis and research on patient safety, scope of practice, and EMS personnel competency must become a priority among the leadership of national associations, Federal agencies, and research institutions. When EMS data collection, subsequent analysis, and scientific conclusions are published and replicated, later versions of the National EMS Scope of Practice Model should be driven by those findings." HMMMM...I understand their desire to want to move more towards "evidence based" medical practice in EMS. Yet, it seems to me that to disregard "our current collective pracitice experiences" would be foolhearty at best. Based on this model, (if adopted) progressive EMS systems (Seattle, Richmond, and others) would actually be forced to take a few steps backwards. I had hoped that we as a profession had learned alittle something form the AHA blunder that occurred when it changed its guidelines in 2000 (i.e.:Amiodarone, hypothermic cardiac arrest management, etc..), and that we would not follow a similar path. Now some of the contradictions that were mentioned.."Each State has the statutory authority and responsibility to regulate EMS within its borders, and to determine the scope of practice of State licensed EMS personnel. The National EMS Scope of Practice Model is a consensus-based document that was developed to improve the consistency of EMS personnel levels and nomenclature among States: it does not have any regulatory authority." BUT later they say.. "The adoption of skills and roles beyond those proposed in this model will diminish national consistency, interstate mobility, and legal recognition for EMS personnel. Additionally, content in future national EMS education standards, national certification examinations, and curriculum-focused aspects of national accreditation standards will not include those additional skills. States opting to exceed the skills identified in this model at any given level should do so with caution and purpose. Those States choosing to do so should only add skills from the next higher level (i.e., they should not “skip levelsâ€) and are discouraged from exceeding those skills identified in the National EMS Core Content. “Skipping levels†represents a large increase in cognitive complexity and patient risk and should therefore be avoided. Some States permit licensed EMS personnel to perform skills and roles beyond the minimum skill set as they gain knowledge, additional education, experience, and (possibly) additional certification. Care must be taken to consider the level of cognition necessary to perform a skill safely. Particularly problematic skills are those that appear simple to perform, but require considerable clinical judgment for an individual to know when they should, and should not, be performed." So if I am reading this correctly they are basically saying that this is the basis to bring states in line with our policy, and if you don't do so, we will eventually force you to comply. Next they say that in the implementation of additional skills the states shouldn't "skip levels", yet they themselves do do with the addition of some of their newly proposed "BLS" and "advanced EMT" skills.....such as: Manually Triggered Ventilator (MTV)<<seems to me they took "Demand valves off the trucks for a reason>>, Automatic Transport Ventilator (ATV)<<<What without being able to "Intubate, or even understand the phys and mechanisims behind the what/why/how of this>>Later they state that the "understanding of the 'basic-AEMT' should be "EMT and AEMT-Critical component areas i.e.:critical illness:understanding of principles and phys of these patients should only be::'Fundamental'. Then for 'Emergent Patients':'SIMPLE' ...:scratch: The whole document goes on and on with such contradictions, etc... and in general a "decrease" in our professional abilities and standing....So the question is, WHAT ARE WE GOING TO DO ABOUT IT!?!??!?!?!?! out here, ACE844

You assume I thought my arguement out......or that I was even arguing with someone?!?!? :munky2: :bom: But thats fine if you need me to clarify and present my point for you I will...

Hi Everyone, Just FYI, the MAP and Cardiac Phys teaching posts, have been moved to here:::Training - Other out here, Ace844

You are correct, I did cite the study, for reasons other than to compare what MVC rates are between Emergency Services providers. My point was if you want to know, educate yourself, and if you'd like share the info here...As I have, and regularly do. I'm not going to nor should I be doing your research, and fact finding for you. In addition, I wasn't bashing you, merely suggesting that if you want to know, ASK, and if you don't get an answer than LOOK IT UP!! If you'd like to make a point or make the group aware of this info. go right ahead as thats the purpose of "this discussion board," and for the most part there is freedom of speech here... out here, Ace

"Dust," the point behind posting the study was to make a point and provide a little something more concrete to the discussion. I originally thought our "professional racing colleage" et.al. may try to post it, yet alas he didn't. Also, there were a number of us who "challenged" him to come up with the data to show what/how EMS collisions, compared to regular everyday civillian MVC's. That was the point. The numbers are there you just need to look at the info. So thus it supports certain points that were made during this discussion..... As far as what/how much I do or don't pay for any of the articles/data I submit here....FRANKLY, Thats none of your business and irrellevant to the discussion at hand. Furthermore, as a proponent of EMS education and research which you claim yourself to be, one would hope that you'd be happy that soem of us are trying to promote further education/advocacy in our profession..... out here, Ace844

Seems to me we recently had a "spirited" discussion about this not to long ago as well..!?!?!?

Sounds similar to the recurring debate we have been having here for awhile....One can only hope that "the advocacy" will take effect and we won't allow ourselves to be "steamrolled" by other professions with differing goals..

ummmm...do a search..look it up....:roll:

Hi All, In case you haven't seen it here's the The National EMS Scope of Practice Final draft version 4....Does anyone else think it's lacking???? Also to be more active in the advocacy here's a link...:::EMS workforce for the 21st Century Out here, Ace844

Comparison of Crashes Involving Ambulances with Those of Similar-Sized Vehicles Adam F. Ray A1 and Douglas F. Kupas A1 A1 Department of Emergency Medicine, Geisinger Health System, Danville, Pennsylvania Abstract: Objective. To describe the characteristics and associated occupant injuries of motor vehicle collisions (MVCs) involving ambulances as compared with MVCs involving similar-sized vehicles. Methods. Motor vehicle crash data in Pennsylvania from 1997–2001 were analyzed to compare the characteristics of crashes involving ambulances with those involving vehicles of a similar size. Crash demographics (e.g., location of crash, roadway conditions, intersection type) and associated injuries were examined and compared using chi-square tests and Fisher's exact test. Results. 2,038 ambulance MVCs and 23,155 crashes involving similar-sized vehicles were identified. Weather and road surface conditions were similar, but ambulance MVCs occurred with increased frequency on evenings and weekends. Ambulances were more likely to be involved in four-way intersection crashes (43% vs. 23%, p = 0.001), angled collisions (45% vs. 29%, p = 0.001), and collisions at traffic signals (37% vs. 18%, p = 0.001). More people were involved in ambulance MVCs (p = 0.001), with 84% of ambulance MVCs involving three or more people and 33% involving five or more people. Injuries were reported in more ambulance MVCs (76% vs. 61%, p = 0.001). Pedestrian involvement was rare (< 5% in both groups). Conclusion. Ambulance crashes occur more frequently at intersections and traffic signals and involve more people and more injuries than those of similar-sized vehicles.

Chest. 2005;128:1951-1957.) © 2005 American College of Chest Physicians The Effects of Cocaine and Heroin Use on Intubation Rates and Hospital Utilization in Patients With Acute Asthma Exacerbations* By Levine, Michael; Iliescu, Maria Elena; Margellos-Anast, Helen; Estarziau, Melanie; Ansell, David A Background: The use of both heroin and cocaine has been associated with asthma exacerbations. However, the magnitude of this effect has not been adequately described. The purpose of this study was to examine the association between cocaine or heroin use and asthma severity. Methods: We conducted a retrospective chart review of adult patients who had been admitted to an inner-city hospital and who subsequently had received a hospital discharge diagnosis of acute asthma exacerbation. Patients were classified as cocaine users if they had admitted to using cocaine within 24 h of symptom onset, or if a positive drug screen result was obtained. A similar classification was employed for heroin. The severity of asthma exacerbations among cocaine and heroin users was compared to severity among nonusers (ie, individuals without evidence of having used either drug within the 24 h preceding symptom onset). Results: One hundred sixty-six unique patient encounters were identified, and 152 patient records were analyzed. Of these, 27.6% (42 of 152 patients) used cocaine with or without heroin and were classified as cocaine users, while 30.9% (47 of 152 patients) used heroin with or without cocaine and were classified as heroin users. Cocaine users had longer mean lengths of hospital stay than nonusers (3.4 days vs 2.5 days; p < 0.049). Intubation and ICU admission were more common among cocaine users than nonusers (21.4% vs 2.3%, respectively [p = 0.0006]; 31.0% vs 11.5%, respectively [p = 0.0068]). Heroin users were also intubated more frequently than nonusers (17.0% vs 2.3%, respectively; p = 0.0036). Neither the length of hospital stay nor the percentage of ICU admissions was significantly different between heroin users and nonusers. Conclusion: Heroin and cocaine use are common among adult asthmatic patients admitted to an inner-city hospital. Both cocaine and heroin are significantly associated with the need for intubation. Based on these findings, it may be prudent to screen adults with asthma presenting to an urban emergency department for cocaine and heroin use. (CHEST 2005; 128:1951-1957) Key words: asthma; cocaine; drug abuse; heroin; intubation; status asthmaticus Abbreviations: AMA = against medical advice; CI = confidence interval; OR = odds ratio Asthma is a chronic, inflammatory disease, primarily involving the lower airways. It has been estimated that 14 to 15 million Americans currently have asthma,1 and the prevalence is increasing. While individuals of all ages and races are affected, children and African Americans have some of the highest hospitalization rates for acute asthma exacerbations.2,3 In addition, some Hispanic individuals and individuals of lower socioeconomic status have a higher prevalence and severity of asthma.4 Leikauf and colleagues5 cite environmental factors as one of the causes for the increasing prevalence of asthma. Some specific reasons cited for the increasing prevalence of asthma in lower socioeconomic regions include poor access to health care, crowded living conditions, and the use of illicit drugs.6 Substance abuse, a common problem in many inner-city environments, has substantial social, economic, and medical ramifications. Cocaine was first temporally associated with the development of an acute asthma exacerbation in 1932.7 Since that time, numerous other reports8-25 have associated both cocaine and heroin use with asthma exacerbations. Other pulmonary complications of cocaine use have been described elsewhere.8,9,23 While cocaine and heroin use have been associated with asthma exacerbations, the magnitude of this effect has not clearly been established. Therefore, we conducted this study in order to quantify the magnitude of this association. Specifically, we assessed whether patients who had been admitted to the hospital for an asthma exacerbation who used these drugs experienced more severe exacerbations than patients not using these drugs. MATERIALS AND METHODS This study was conducted at an inner-city, university-affiliated teaching hospital in Chicago. We conducted a retrospective medical record review of all adult patients (age ≥ 16 years) who had been admitted to the hospital during the calendar year of 2003 and who ultimately received a hospital discharge diagnosis of acute asthma exacerbation. If a person had multiple hospital admissions for asthma exacerbations during the calendar year, only the first hospitalization was included in the analysis. Study Subjects Patients were classified as cocaine users if they either had admitted to using cocaine within the 24 h preceding the onset of dyspnea or if they had a urine drug screen finding that was positive for cocaine metabolites. A similar classification was used for heroin. The comparison group (nonusers) consisted of individuals with no evidence of having used either drug within the 24 h preceding the onset of dyspnea. Patients with a positive urine drug screen finding, who reported using cocaine or heroin within the week but > 24 h before the onset of dyspnea, were also classified as nonusers. Patients were excluded from analysis if there was no documentation of drug use or a urine drug screen had not been performed. Data Collection Data abstracted from medical records included patient age, sex, date of visit, smoking history, history of prior intubations, initial vital signs in the emergency department, and disposition from the emergency department (ie, admission to a hospital floor vs ICU admission). In addition, information was collected pertaining to the use of cocaine or heroin (by patient admission), the results of a urine drug screen (if performed), intubation during the hospitalization, and length of time receiving ventilation for those patients who had been intubated. Last, information on length of stay, including the number of days spent in the ICU and the total number of days spent in the hospital were obtained. The data were collected on a preprinted data abstraction form and then were entered into a standard spreadsheet (Excel 2000, version 9.0.2720; Microsoft; Redmond, WA) by one author (M.L.). Following data entry, the data were independently checked for accuracy by another investigator (M.E.I.). The urine drug screen for both cocaine and heroin is performed via a homogenous immunoassay method. The urine drug screen for cocaine detects the primary inactive metabolite of cocaine, benzoylecgonine, rather than the cocaine itself. A cutoff of 300 ng/ mL is considered to be a positive result for a cocaine metabolite assay by our hospital laboratory. The detection of benzoylecgonine in concentrations of > 300 ng/mL generally implies use within 1 to 2 days.10 For opiates, the urine drug screen detects morphine and 6- acetylmorphine in the urine; a positive result indicates exposure to morphine, diacetylmorphine (heroin), codeine, hydromorphone, levorphanol, meperidine, or oxycodone/morphine. A cutoff of 2,000 ng/ mL is considered to be a positive result by our hospital laboratory. Using the cutoff value of 2,000 ng/mL, a positive result generally indicates use within the previous 12 h.26 The need for mechanical ventilation or ICU admission, along with the total length of stay were used as markers for asthma severity. Patients who left the hospital against medical advice (AMA) were included in all data analyses except for length of stay. Data Analysis Independent associations were assessed via χ^sup 2^ test and Fisher Exact Test (as appropriate) for categorie variables, and t tests were used for assessing continuous variables. Logistic regression analysis was utilized to identify variables that were independently associated with endotracheal intubation and ICU admission. Logistic regression models were also used to obtain odds ratios (ORs) and 95% confidence intervals (CIs) for the association between risk factors (cocaine or heroin) and outcome variables (endotracheal intubation and ICU admission), after adjustment for identified confounders. All statistical analyses were performed using a statistical software package (SAS, version 8.2; SAS Institute; Cary, NC). The study received approval from the institutional review board. RESULTS Between January 1, 2003, and December 31, 2003, a total of 166 unique patient encounters were identified. Of the 166 patients, 3 were excluded because neither had a urine drug screen been performed nor was there any documentation of drug use in the chart. Of the remaining 163 charts, 152 (93.3%) were located and included in the study analysis. Eighteen patients (11.8%) had exclusively used cocaine, and 23 patients (15.1%) had exclusively used heroin. An additional 24 patients (15.8%) had used both cocaine and heroin. Thus, a total of 42 patients (27.6%) used cocaine, and 47 patients (30.9%) used heroin. The overall prevalence of either illicit drug in our study population was 42.8% (65 of 152 patients). More than half of all subjects were women (62.5%), and the mean age of subjects was 43.2 years. African-Americans accounted for 88.1% of the sample, with the remainder being Hispanic (11.3%) or white (0.7%). Fifty-four percent of the patients were current tobacco smokers, and 33.6% of the patients had been intubated at least once in the past. The characteristics of cocaine users compared to nonnsers are presented in Table 1, and the characteristics of heroin users compared to nonusers are presented in Table 2. Cocaine users were more likely to be tobacco smokers than were nonusers (69.2% vs 41.9%, respectively; p = 0.0046) [Table 1]. Similarly, heroin users were more likely to be tobacco smokers than were non-drug users (75.0% vs 41.9%, respectively; p = 0.0003) [Table 2]. Patients who used either cocaine or heroin were significantly more likely to be intubated during the hospitalization than were those who used neither drug. Among cocaine users, 21.4% were intubated compared to only 2.3% of non-drug users (p = 0.0006) [Table 1]. In the heroin group, similar results were obtained (17% vs 2.3%, respectively; p = 0.0036) [Table 2]. Even after adjusting for tobacco smoking, patients who used cocaine were still more likely to be intubated than those who had not used either cocaine or heroin (adjusted OR, 15.3; 95% CI, 2.7 to 86.7). A similar phenomenon was observed in the heroin group (adjusted OR, 16.5; 95% CI, 2.8 to 97.2). Patients who used cocaine were more likely to be admitted to the ICU than those who had not used drugs (31.0% vs 11.5%, respectively; p = 0.0068) [Table 1]. Even after adjusting for tobacco smoking, patients who used cocaine were more likely to be admitted to the ICU (adjusted OR, 4.7; 95% CI, 1.6 to 13.8). When comparing the patients who used heroin to those who had not used drugs, there was no statistical difference with regard to ICU admission (Table 2). Table 1-Characteristics of Cocaine Users and Non-Drug Users* Among cocaine users, 14% (9 of 42 patients) left the hospital AMA compared to 25% of heroin users (12 of 47 patients). Only 3% of patients (3 of 87 patients) who had used neither drug left the hospital AMA. Patients leaving the hospital AMA were not included in the analysis of length of stay. Patients who used cocaine had significantly longer total mean ( SD) lengths of stay in the hospital than did the non-drug users (3.4 2.3 days vs 2.5 1.8 days, respectively; p = 0.049) [Table 1]. Among patients who had been admitted to the ICU, cocaine users received an average of 4.2 2.2 days of critical care compared to 1.8 1.5 days among non-drug users (p = 0.0268) [Table 1]. There was no statistical difference noted when comparing the total length of hospital stay for heroin users compared to non-drug users. However, heroin users admitted to the ICU did spend significantly more days in the ICU than did non-drug users (3.9 days vs 1.8 days, respectively; p = 0.0420) [Table 2]. DISCUSSION Our results found a 42.8% prevalence of cocaine or heroin use among adult patients who had been admitted for acute asthma exacerbations to an innercity Chicago hospital. We also found that both cocaine and heroin use were associated with higher intubation rates. Cocaine use, but not heroin use, was also associated with longer lengths of stay and a higher likelihood of being admitted to the ICU. To our knowledge, this study is the first to place numerical values on the extent to which both cocaine and heroin affect acute asthma exacerbations. Table 2-Characteristics of Heroin Users and Non-Drug Users* We used the length of stay as well as the need for ICU admission or intubation as markers for asthma severity. We chose these parameters because they are readily quantifiable, and subject to little interobserver variability. In our hospital, patients < 16 years of age are admitted to the pediatric service, while patients ≥ 16 years of age are admitted to the medicine service. However, neither asthma nor illicit drug use is uncommon among teenagers. Nonetheless, in order to further minimize the confounding variables, we opted to include only those patients who were ≥ 16 years of age, in order to ensure that the same group of physicians had been responsible for the care of all patients in the study. Pathophysiologically, there are several reasons why both cocaine and heroin might induce an acute asthma exacerbation. Direct thermal injury can occur following the inhalation of either cocaine or heroin. The bronchoconstrictive effects of morphine, which is a metabolite of heroin, have been known since the early 1900s.27 It is now known that bronchoconstriction after heroin use is likely because of the ability of heroin to directly cause the degranulation of the mast cells, with the subsequent release of preformed inflammatory mediators such as histamines.28 Furthermore, under normal circumstances, asthmatic patients will increase their respiratory rate in an effort to compensate for the relative hypoxemia caused by bronchoconstriction. Since opioids cause respiratory depression, it is possible that the heroin-induced respiratory depression at least partly thwarts the ability of the body to adequately compensate, thus exacerbating the severity of an asthma attack. Heroin users were clearly intubated more frequently than patients who had used neither cocaine nor heroin. However, unlike cocaine users, heroin users did not have any longer lengths of hospital stay or more days spent receiving mechanical ventilation when compared to non-drug users. Thus, it is certainly possible that heroin induced some degree of respiratory depression, and this respiratory depression contributed to a worsening initial presentation. Nonetheless, all patients were thought to be experiencing an asthma exacerbation, and not simply respiratory depression, by at least two board-certified attending physicians (ie, an emergency medicine physician, who saw the patient in the emergency department, and an internist or pulmonary/critical care specialist, who treated the patient once they had been admitted to the hospital). Regardless of the etiology, the use of heroin was associated with a more severe acute asthma exacerbation than was observed in non-drug users. This initial presentation has significant implications for the early management and disposition of heroin-using patients experiencing an acute asthma exacerbation. Cocaine and its adulterants can cause inflammation of the respiratory epithelium.6,9 It is most likely that inhaled cocaine serves as a topical irritant on the airways.9 In addition, some cases of cocaine-induced asthma exacerbations may occur through an IgE-mediated sensitivity.15 There have been several case reports8,20 of life-threatening or fatal status asthmaticus following heroin insufflation in the same geographic region as ours. Krantz and colleagues20 examined the prevalence of drug use in asthmatic patients who had been admitted to the ICU and compared the pattern of drug use in these patients to patients in the ICU who had been admitted for diabetic ketoacidosis. The authors observed that asthmatic patients in the ICU were more likely to have used heroin than were the diabetic ketoacidosis patients in the ICU. They did not observe any difference between the two groups regarding cocaine use. The reasons for the discrepancies observed in our study compared with the study by Krantz and colleagues20 are not entirely clear. It is possible, however, that the small number of patients who used only cocaine in their study merely did not permit Krantz and colleagues20 to appreciate the effect of cocaine. In our study, there were no fatalities. Levenson and colleagues13 examined asthma deaths in Cook County, IL, where our hospital is located. They reported that 31.5% of asthma deaths were confounded by substance abuse or alcohol ingestion. Cocaine was the most frequently identified drug found on toxicologic analysis in their study. Weitzman and colleagues29 examined asthma deaths in the state of Maryland. They reported that 17.5% of asthma patients who died had a history of drug abuse, and that 12.7% of them had toxicology screens that were positive for drugs that are normally abused. While our study revealed a much higher rate of drug use, the study by Weitzman and colleagues29 included young children. Therefore, it is likely that among adults, the percentage of patients with toxicologie screens that were positive for drugs of abuse would be higher. The study by Weitzman et al29 also demonstrated that the majority of fatal asthma attacks are likely to begin at home. Thus, it is possible that many patients who die from an acute asthma exacerbation would do so either prior to arriving in the emergency department or while in the emergency department. Therefore, they would not have been admitted to the hospital. If this scenario is correct, we might have missed patients with the most severe cases of asthma, as we included only those patients who had been admitted to the hospital. Given the high prevalence rate of both cocaine and heroin use in our population, it is unlikely that patient underreporting of their drug usage contributed significantly to our findings. However, even if underreporting were to occur, one would expect our observed differences to be even larger. Thus, if any drug-using patients were incorrectly categorized into a nonuser group rather than a user group, we would expect the true differences between the two groups to be even greater. Our study was limited by its retrospective nature. As a result, we were limited to the data that were recorded in the medical chart, and our conclusions are limited by the quality and completeness of those data. Gilbert and colleagues30 have noted that retrospective reviews can further be limited by the specific variables that are chosen for examination. For example, parameters such as medication histories, ECG results, or "appropriateness of care" are subject to much interrater variability during retrospective reviews.30 However, in our study, most of the data abstracted included continuous variables (ie, days in the hospital) and dichotomous variables (ie, intubated or not). This fact likely reduced any bias on behalf of the abstracter and, thus, reduced some of the limitations of a retrospective study. The routes of drug consumption were too inconsistently documented to permit any meaningful analysis. In our experience, however, most of our patients smoke these drugs, rather than inject or insufflate them. It is likely that drug-induced asthma will primarily be observed in patients who smoke the drug, as this route is associated with the most direct damage and inflammation of the bronchial epithelium.15 Support for this theory has come from a study by Tashkin and colleagues,31 who examined airway dynamics in patients who consumed cocaine via various routes. They observed that smoking cocaine, but not injecting cocaine, produced acute bronchoconstriction. However, it should be noted that the insufflation of cocaine has also been linked to near-fatal status asthmaticus.18 Another limitation of the study is that the limited sample size made it difficult to distinguish between individuals who had used one drug vs both drugs in the analysis. In other words, when assessing the association between cocaine use and the severity of asthma exacerbations, cocaine users, whether they had used only cocaine or both cocaine and heroin, were compared to non-drug users. Similarly, when assessing the relationship with heroin use, heroin users, whether they had used only heroin or both heroin and cocaine, were compared to non-drug users. It would have been ideal to have examined individuals who had used only cocaine (n = 18), individuals who had used only heroin (n = 23), and individuals who had used both (n = 24) separately, but the small numbers of patients would have made the adjusted logistic regression models unstable. It could, however, be argued that this detail is irrelevant. For example, if a clinician knows that a patient has used cocaine, then the clinician knows that the patient is at risk for a more severe exacerbation, regardless of whether or not other drugs were consumed simultaneously. We only examined cocaine and heroin. While we did correct for tobacco smoking, we neither investigated nor corrected the data for other potentially confounding variables such as exposure to marijuana smoke or second-hand tobacco smoke, as well as for the concurrent use of alcohol. Other potential confounding variables such as a history of allergies, current medications being used, and access to medical care were also not measured. The consideration of marijuana might have been important, as marijuana smoking has several pulmonary effects. While marijuana is associated with increased airway injury and hyperresponsiveness,32,33 it is also associated with bronchodilation.34 The combination of cocaine and ethanol produces the metabolite cocaethylene, which is believed to be more toxic to the brain and heart than either parent compound alone.35 It is not known whether cocaethylene produces specific pulmonary complications beyond that produced by cocaine alone. The high prevalence of both tobacco use and drug use in our population may reduce the generalizability of our study to regions where drug use is less prevalent. While there is clearly an association between cocaine use and asthma, and possibly between heroin use and asthma, the limited sample size makes it difficult for us to conclude anything about the strength of the association. Also, our study design does not permit us to evaluate a dose- response relationship. A prospective study is needed to evaluate whether the route of administration affects the degree of bronchoconstriction. In addition, a prospective study would allow us to further correct for some additional confounding variables. It is interesting to note that there is a higher prevalence of male patients in the drug-abusing groups. This finding likely reflects the overall patterns of drug abuse, as men use drugs more frequently than women.36 In addition, patients who used these illicit drugs left the hospital AMA much more frequently than did patients who did not use drugs. The exact reasons are not entirely clear, but could be further investigated in a prospective study. In addition, this observation would imply that clinicians should commence patient education early in the course of a hospital stay. CONCLUSION We have reported a surprisingly high prevalence of cocaine and heroin use among adults who were admitted to an inner-city hospital for asthma exacerbation. The use of cocaine is a risk factor for triggering severe acute asthma exacerbations. Heroin also appears to be a risk factor for intubation. It is probable that the high prevalence of drug use in inner-city populations contributes to the high rates of asthma exacerbations in patients in inner-city settings. Patients who have been admitted to the hospital with acute asthma exacerbations in areas where illicit drug use is prevalent should be screened for the use of cocaine or heroin. * From the Harvard-Affiliated Emergency Medicine Residency Program (Dr. Levine), Brigham and Women's and Massachusetts General Hospital, Boston, MA; the Rosalind Franklin University of Medicine and Science/The Chicago Medical School, Chicago, IL; and the Department of Medicine (Drs. Iliescu and Ansell) and the Sinai Urban Health Institute (Ms. Margellos-Anast and Ms. Estarziau), Mount Sinai Hospital, Chicago, IL. REFERENCES 1 Mannino DM, Homa DM, Akinbami LF, et al. Surveillance for asthma: United States, 1980-1999. MMWR Surveill Summ 2002; 51:1-13 2 National Asthma Education and Prevention Program. Expert panel report 2: guidelines for the diagnosis and management of asthma. Bethesda, MD: National Institutes of Health, 1997; NIH Publication No. 97-4051 3 Thomas SD, Whitman S. Asthma hospitalizations and mortality in Chicago: an epidemiologic overview. Chest 1999; 116:135S-141S 4 Coultas DB, Gong HHR, Grand R, et al. Respiratory diseases in minorities of the United States. Am J Respir Crit Care Med 1994; 149(suppl):S93-S131 5 Leikauf GD, Kline S, Albert RE, et al. Evaluation of a possible association of urban air toxics and asthma. Environ Health Perspect 1995; 103:253-271 6 Rome LA, Lippmann ML, Dalsey WC, et al. Provalence of cocaine use and its impact on asthma exacerbations in an urban population. Chest 2000; 117:1324-1329 7 Waklbott GL. Asthma due to a local anesthetic. JAMA 1932; 99:1942 8 Gygan J, Trunsky M, Corbridge T. 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Crack abuse and asthma: a fatal combination. N Y State J Med 1990; 90:511-512 18 Averbach M, Casey KK, Frank E. Near-fatal status asthmaticus induced by nasal insufflation of cocaine. South Med J 1996; 89:340- 341 19 Gaeta TJ, Hammock R, Spevack TA, et al. Association between substance abuse and acute exacerbation of bronchial asthma. Acad Emerg Med 1996; 3:1170-1171 20 Krantz AJ, Hershow RC, Praehand N, et al. Heroin insufflation as a trigger for patients with life-threatening asthma. Chest 2003; 123:510-517 21 Osborn HH, Tang M, Bradley K, et al. New-onset bronchospasm or recrudescence of asthma associated with cocaine abuse. Acad Emerg Med 1997; 4:689-692 22 Hughes S, Calverley PMA. Heroin inhalation and asthma. BMJ 1997; 297:1151-1152 23 Albertson TE, Walby WF, Derlet RW. Stimulant-induced pulmonary toxicity. Chest 1995; 108:1140-1149 24 de los Bueis AB, Vega AF, Ramos JLS, et al. Bronchial hyperreactivity in patients who inhale heroin mixed with cocaine vaporized on aluminum foil. Chest 2002; 121:1223-1230 25 Oliver RM. Bronchospasm and heroin inhalation [letter]. Lancet 1986; 1:915 26 Cone EJ, Jufer R, Darwin WD, et al. Forensic drug testing for opiates: VII. Urinary excretion profile for intranasal (snorted) heroin. J Anal Toxicol 1995; 20:379-392 27 Dixon WE, Brodie TB. Contributions to the physiology of the lungs: Part 1. The bronchial muscles, their innervation, and the action of the drugs upon them. J Physiol 1903; 29:171 28 Withington DE, Patrick JA, Reynolds F. Histamine release by morphine and diamorphine in man. Anaesthesia 1993; 48: 26-29 29 Weitzman JB, Kanarek NF, Smialek JE. Medical examiner asthma death autopsies: a distinct subgroup of asthma deaths with implications for public health preventative strategies. Arch Pathol Lab Med 1998; 122:091-699 30 Gilbert EH, Lowenstein SR. Koziol-McLain J. et al. Chart reviews in emergency medicine research: what are the methods? Ann Emerg Med 1990; 27:305-308 31 Tashkin DP, Kleerup EC, Koyal SN, et al. Acute effects of inhaled and IV cocaine on airway dynamics. Chest 1996; 110:904-910 32 Tashkin DP, Simmons MS, Chang P, et al. Effects of smoked substance abuse on nonspecific airway hyperresponsiveness. Am Rev Respir Dis 1993; 147:97-103 33 Tashkin DP. Airway effects of marijuana, cocaine, and other inhaled illicit agents. Opin Pulm Med 2001; 7:43-61 34 Grotenhermen F. Pharmacokinetics and pharmacodynamics of cannabinoids. Clin Pharmacokinet 2003; 42:327-360 35 Rose JS. Cocaethylene: a current understanding of the active metabolite of cocaine and ethanol. Am J Emerg Med 1994; 12:489-490 36 US Department of Health and Human Services. Health, United States, 2004: with Chartbook on Trends in the Health of Americans. Atlanta, GA: Centers for Disease Control and Prevention, National Center for Health Statistics, September 2004; Department of Health and Human Services Publication No. 2004-1232 Michael Levine, MD; Maria Elena Iliescu, MD; Helen Margellos- Anast, MPH; Melanie Estarziau, MPH; and David A. Ansell, MD, MPH Manuscript received August 10, 2004; revision accepted February 28, 2005. Reproduction of this article is prohibited without written permission from the American College or Chest Physicians (www.chestjournal. org/misc/reprints.shtml). Correspondence to: Michael Levine, MD, Harvard Affiliated Emergency Medicine Residency, Brigham and Women's Hospital, 75 Francis St, Neville House, second floor, Boston, MA 02115; e-mail: mdlevine@partners.org Copyright American College of Chest Physicians Oct 2005

In relation::; Some people say that guns kill people....:?::arrow::volient3:..yet IMHO more than likely it is the husbands and lovers who come home early that more often than not do this...:iroc::violent2::walk: ACE844

No problem..."Richard B" I will do so in the future. Thanks Ace

the poster didn't imply they would do anything different...???? :?:

To continue your line of thinking "Dust, etal.," There is going to come a time when you don't bring your gear into a call or all of the appropriate gear, and then your gonna hang because you didn't have it....food for thought...Not a Lesson to be Learned firsthand..:blob6::boxing::ky::sign3::blackeye: out here, Ace844

Read my original post..it covers this... Ace844

Also, it should be noted that in my original post I covered the phys and principles of this D/O, and management, so that those who don't know can learn about it.... Ace844