RomeViking09

No pics but... Majority of our units are dodge truck cab boxes, and a few Chevy vans. We also have 2 quad cab dodges 1 is used for BLS NET for Bari unit the other is used by ALS 911/CCT crew. We have a few older Chevy boxes getting phased out and I think the last ford went away around the time I started. Service I was at before flipped almost overnight from a fleet of ford vans & boxes to all Mercedes sprinters (except a limited number of fords kept for CCT & Bari)

Albuterol started (Atrovent not in the drug box), EtCO2 is 28-32 with shark fin w/treatment going. What we did: CPAP w/Neb, 20mg Decadron & 2gm Mag mixed in a 100mL bag given over 10min, PT was transported to the closer facility at his request, on arrival at the ER he was placed on BiPAP and given A&A Neb thru BiPAP and admitted overnight for observation. The fumes from the apartment below his was in fact the cause of his attack.

Real question is why is the patient having a desat... Is it the intubation attempt or the patho of why the patient is getting the tube? Not many stable patients get a pre-hospital tube. (Personal note: on "elective" intubations (i.e. Not in arrest or apnea) I place the patient on a NRB while I set up if there is no need to bag them and then intubate once ready. Has worked well so far (also look for a sat > 90% at all times while attempting to tube)

Sorry been busy... Scene finds an apartment with strong smell of paint fumes, patient only able to speak 1-2 words at a time. Hx- Asthma with 1 prior intubation 3 months ago and ICU admit, HTN. Meds- Albuterol MDI, Unknow name HTN med (and you can't find it on scene), NKDA VS- HR: 120 RR:30+ BP: 142/88 SpO2: 90% on room air BGL: 122 mg/dL ECG: Sinus Tachycardia with ST depression in all leads BLS crew places the patient on 15 L/min by NRB, your Paramedic partner gets an 18G in the Left hand for you Assessment LOC: A/Ox4 GCS 15 Head/Neck: Pupils PERRL, + JVD, Trachea Midline, No notes trauma or other abnormalities Chest: No noted trauma or abnormalities, Lung sounds: Bilateral wheezing in upper lobes, diminished bilater in bases, clear S1 & S2 heart tones, no noted trauma or other abnormalities ABD: Soft and non-tender in all quads, no trauma or abnormalities Extremities: + CSM x4, no trauma or abnormalities Patient unable to walk due to distress, weights 300lbs Treatment Plans?

Our protocols push for NTG in all MI patients with NS & DOPamine as a backup if their BP drops. Our criteria includes chest pain for determining symptomatic bradycardia, DOPamine to improve the rate at the low end of the dosage range (why I said 5 mcg/kg/min and not a 5-20 mcg/kg/min Titrate to a set BP) while the heart is damaged and we need to take that into account we also need to keep everything else perfusing including the heart, if the rate is in the 40s increasing the rate with a goal of 55-60 will help keep in perfusing the rest of the heart (I.e. left vertical that is keeping the BP in a "normal range") also note this patient has a history of hypertension so her body is used to working with a higher BP. I agree with the other treatments and plans and always follow your local protocols first but in the eyes of education let's look beyond the "norm" and look what is going to happen in the ER and if we can start those treatments sooner in a safe manner to benifit the patient. The ER (or cath team if the patient goes right to the cath lab as this patient should) is going to hang a low dose DOPamine or another chronotrophic agent to correct the rate and also hang an NTG drip to open up the arteries to aid on the cath and the perfusion of the damaged area of the heart (based on this 12-lead the RCA and right ventrical) My first critical care job we did a lot of cath lab stand by at a smaller hospital doing PCI that did not have cardiac surgery in house, I was surprised to learn how much the ER and cath lab do that we have the ability to do (assuming we have a dead on STEMI vs a NSTEMI or UA requiring a cath) to expidite care. One more side note: AHA criteria for symptomatic bradycardia Hypotension Acute Altered Mental Status Ischemic Chest Pain (I.e. STEMI) Sings of Shock Acute Heart Failure

Scoop & go vs doing a real assessment that mets the complaint. Last week I was double medic, went to a guy for 45 y/o male Chest Pain with no prior history, it was my turn to tech I did my normal and held on scene longer than my partner that day seemed to want to at first.... Inferior MI with HR in the 40s. I had the time to transmit a 12 lead get ASA, NTG, and have a line before transport, our total time from PT contact to cath table was 25 min (including transport and the elevator ride to the cath lab). Had we just scooped and run I would not have done the 12-lead until we where at the door had not time to transmit and guy would have been delayed in the ER because another crew had just arrived with ROSC on a code 3mon before us. After the call my partner noted that my "longer" on scene times benefit the patient because I have a real idea what I am working with (note: many times I have also got to the patient and had an oh shit he needs the ER not me and scoop and run and do what I can in route) don't let scene time goals or policies prevent you from doing a good assessment and any needed treatment (side note I have very short hospital times on patients I stay on scene with so if your worried about times for pay raises it all balances out in the end if you do your job)

I had a 97 TJ SE Soft top but it started to died on me in December of 2012 (right as I was trying to finish up Critical Care school) had to go finish the trade in on a lunch break one day

2011 2 Door Sport Soft Top

D5 can be D5W or D5NS.... (Our hospital won't let you use D5 as an abbreviation it has to be D5W or D5NS to identify what the Dextrose is diluted in) Side note I did not know anyone still used D5LR (if someone can tell me what type patient would be getting D5LR in a interfacility transport ?) BLS (EMT-Intermediate/85): Albuterol, Aspirin, Dextrose 50%, Oral Glucose, EpiPen, EpiPen Jr, NS, D5W BLS (AEMT): Albuterol, Aspirin, Dextrose 50%, Oral Glucose, EpiPen, EpiPen Jr, Narcan, NTG SL, Glucagon, NS, D5W ALS (Paramedic): Albuterol, Aspirin, Dexamethasone, Haldol, Mag Sulfate, NTG SL, NTG Transdermal, Zofran, Acetaminophen, Adenosine, Amiodarone, Atropine, Ca Chloride, D50, Benadryl, Epi 1:1,000, Epi 1:10,000, Glucagon, Oral Glucose, Lidocaine, Ketorolac, Narcan, Na Bicarb, Versed, Fentanyl, NS, D5W Critical Care (In addition to ALS Drugs): Morphine, Ativan, Extra Fentanyl (We get any other transport drugs from the hospital when we pick up the patient)

This is the one I have, I don't have it on the roll cage b/c I don't want it getting stole in the city but fits in the glove box just fine http://www.smittybilt.com/product/index/217.htm

Your a paramedic on a transporting ALS unit in an urban EMS system with a paramedic partner and are dispatched at 1600 on a friday afternoon to a call for a 50 y/o male with chest pain trouble speaking between breaths. Responding with you is a BLS Engine. Your closest hospital is a STEMI Receiving facility with no trauma services 10 min from the scene and your 25 min from a Level I trauma center both in normal traffic. Weather is clear and 62ºF, traffic is congested citywide. You arrive to find a 50 y/o male in a 2nd floor apartment in a tripod position, the engine arrived to the scene at the same time as you. What do you do?

Dx: Inferior MI (ST Elevation in II,III, aVF w/ Depression in V2, V3, I, & aVL) with Symptomatic Bradycardia (3º AV Block) Tx: O2 (3 L/min), NS @ 30 mL/hr IV, 324mg ASA PO (4x 81mg), 75mg Plavix PO, 4mg Morphine IV, 1/2" Transdermal NTG, EtCO2 by Cannula Request Orders from STEMI Facility: Either DOPamine @ 5mcg/kg/min OR 2.5-5mg Versed for sedation and then pace Pt is having symptomatic bradycardia (chest pain, AMS even with the other meds on board) with 3º block and inferior wall MI if untreated for the 40+ min transport patient is at risk for arrest. EtCO2 is because the BP is elevated given the type of STEMI and prior treatment. DOPamine would be preferred over pacer, but if we need to pace then don't worry about hypotension from the Versed to sedate the pacer will take care of that. Don't withhold NTG to any STEMI (unless prohibited by local protocol) that has a good BP (we have DOPamine and fluids to fix hypotension, you can remove the NTG paste PRN vs SL that your can't take back)... also start a 2nd large bore IV for the cath lab team (they will be happy with you)

Small first aid pouch in my glove box with 4x4s, 1 ABD pad, roll gauze, gloves, & CPR mask. Keep a traffic vest and an MRE in the jack compartment. I do carry a stocked BLS bag if I am camping or climbing in more remote areas. I used to live in a more remote area (now live in a major metro area) and kept my bag in the back all the time (I also was doing S&R at the time so my BLS bag and my 72 hour pack lived in my jeep in case of a call out when I was not at home to save the trip to the house then to report to the search/incident). All for the Be Prepared attitude just not to the extreme of having an ambulance worth of gear in my jeep at all times (also had a jump bag stolen before and it is a pain in the ass to replace everything.)

Jason Strickland was an EMT with Grady EMS driving home from work on his motorcycle when he was hit from behind by a drunk driver and killed. The Atlanta Journal-Constitution A motorcyclist died early Sunday morning after a collision with a passenger vehicle on I-20 Westbound in Douglas County, authorities said. About 5 a.m. Jason Dale Strickland, 37, of Bremen was driving his Harley Davidson west on I-20 near Lee Road. Authorities said a Honda Element driven by Francisco Ferrer, 33, of Dallas, struck Strickland from behind. The impact threw Strickland from the motorcycle into the center travel lane where he was hit by a truck. Strickland was killed in the crash. There were no other injuries. There are no charges pending against the driver of the truck, Joseph Edward Marrett, 66, of Conyers. Ferrer has been charged with driving under the influence and possibly other charges once the police investigation is complete.

1 - Under what case would you need MORE than 3 NTGs in a pre-hospital setting without starting a nitro drip (in ACS if 3x NTG does not work go to morphine, in PE same thing) 2 - Continuous A/A is not of benefit (think about the effect the atrovent has on the body), 1 A/A followed by continuous Albuterol can be of benefit also long as you watch the HR & BP. 3 - Unless you want your patient to stop breathing continuous benzos are not a good thing if you can protect the airway and get them to the ER. 4 - Thiamine in AMS is 6 to 1/ half dozen to be given with D50 or other dextrose/glucose drugs. Not a bad thing to have but not something major your missing. I think people get worked up over protocols sometime and forget we are not doctors and there are time when we should call for orders (not saying we need to go back to the days of Emergency and calling for IVs or Oxygen), basic immediate and lifesaving care needs to be standing orders, continued treatment with possible long term side effects needs to be run by a doc. Lets play the what if game, say I have a patient who is having chest pain, I give them 4x 81MG ASA, 3x NTG SL (5 min apart), and they still have pain and a BP of around 105/palp. Now say we have your continued SL NTG in protocol and I give 1 more NTG they vasodilate again (remember they have had 3 NTG before this) and the BP bottoms out, they have poor cerebral perfusion to the point of stroke and I have just made my patient worse. NTG is a bit (not much) stronger vasodilator than morphine when used as most EMS protocols call for (3x NTG 0.4mg SL, 2-4MG Morphine then titrate to effect). By giving the morphine I can slowly vasodilate (and reverse it with narcan & benadryl if I do not get the desired effect) Before talking up a strom about wanting change look at the change you want and if your in the right to start with. Just my 2cents.

Has anyone had any success with use of Atropine in a bradycardic PEA, I was wondering why remove a drug that speeds up the heart that is too slow (to the point of no pulse). I am not talking about asystolic arrest but those with electrical activity but no pulse. My view is that Epi may not work is cases of beta blockers (as Epi speeds up the heart with Beta-1) and the possibility of arrest that can be reversed by improving the rate to gain perfusion in non-trauma arrest.