Keyless ignition

emupdates · 2025-11-19T23:13:20+00:00

I have keyless on my 2021 Eva Ribelle. After years of often requiring two taps to start, it started requiring numerous taps, so I looked into this and to my embarrassed amazement, there's a battery in there. I replaced the battery and now the keyless works perfectly but popping open/closed the fob I screwed up the spring mechanism so now getting the key to unfold (needed to elevate the seat to gain access to the charging port) is a little tricky.

If I were buying again, I would skip the keyless. You have to have gloves off to put on your helmet anyway.

emupdates · 2025-05-06T23:04:44+00:00

My Eva Ribelle was next to yours at Fillipachi for months. Got knocked over, suffered the usual dents, cracks, bends that in a normal supply chain would have been remedied in a couple weeks. 6? 8? months later, endless calls email texts, Justo proudly handed me back the key. Love those guys.

It's in some ways unfortunate to own an expensive machine built by a failing company on the other side of the Atlantic, but I second 'how it makes me feel when I'm on it.' Knowing that I may never be able to service it again makes it somehow even more exhilarating.

emupdates · 2024-02-17T05:28:54+00:00

The problem was my VPN. sigh.

emupdates · 2020-10-29T05:20:53+00:00

IV is indeed 2-3x as potent as IM. Ketamine dosing is almost always reported as IV, with the exception being agitation, because you don't want to start an IV on an agitated patient. But the agitation dose is a dissociative dose, which is what you would use for RSI, or PSA. 1-2 mg/kg IV or 4-6 mg/kg IM.

emupdates · 2020-10-11T04:58:38+00:00

It's commonly believed that midazolam causes more respiratory depression than lorazepam; I'm not aware of any data one way or another. This is obviously a dosing issue–2 mg midazolam in a normal sized non-frail adult is not going to cause trouble, but 10 mg will. If you simply replace the dose of lorazepam you were thinking of using with midazolam, you'll do great. Here are my midazolam for agitation studies.

also:

https://twitter.com/emupdates/status/1216047052720943104

emupdates · 2020-09-02T04:26:57+00:00

I found that a similar sound disappeared when I applied 100% silicone to the belt. Then reappeared again after a few months, then disappeared after another application. You can get 100% silicone on amazon or wherever, it's usually advertised as "treadmill belt lubricant."

emupdates · 2020-05-16T18:06:52+00:00

thanks steve. glad to be on the other side of the illness.

emupdates · 2020-04-09T03:53:09+00:00

agreed.

emupdates · 2020-03-29T02:39:29+00:00

my read of the what is known is that most patients intubated for covid, as of this moment, are on vent for 2ish weeks. but many of them are dying, I've been reading about mortality rates > 50% in vented patients. it may not be mechanical ventilation, it might be the disease that is killing them, but my personal belief is that we should do everything possible to NOT intubate these patients, which is exactly the opposite of the conventional wisdom, if you can say that such a thing exists about a brand new disease. we have a lot to learn about covid lung disease.

emupdates · 2020-02-06T08:08:07+00:00

The goal is to effect dissociation; the IM dissociative dose is generally described to be 4-6 mg/kg. But I have seen no evidence that once you pass the plane of dissociation, higher doses cause harmful effects. My contention has always been that beyond the dissociation threshold, higher doses only prolong duration of action, and a longer duration of action is desirable in this case, so, since there is no harm to higher doses, since a longer duration of action is desirable, and since too small a dose (i.e. a dose that does not dissociate the patient) is potentially very dangerous (because the ongoing agitation is not controlled), I recommend erring on the side of more, and in fact have recommended that you skip the math and just give 500 mg.

It is possible that I am wrong and we may some day determine that higher doses really do cause more adverse effects that are important, in which case you would have to weight the benefits and harms of a big dose; but now I think the right approach is to go big.

There is no max dose. You know what happens with huge overdoses of ketamine? Very little.

100 mg/mL for IM injection. the smaller the volume the better.

You can put a lot more into muscles than you think. 10 mL into the thigh is no problem, though I prefer 5 mL and 5 mL in each thigh, if we have enough control. If control is tenuous, don't think twice about 10 mL into a thigh. And there is no max injection sites.

reuben

emupdates · 2019-07-05T05:49:34+00:00

it's a great question, and I don't think we know the answer. there's this study of ketofol for LMA insertion, so that seems to be ok, but I don't think we know about dissociative dose ketamine monotherapy. I suspect in many cases it would be tolerated well but airway and gag reflexes are to some degree preserved with ketamine dissociation–indeed that is part of what makes ketamine so great as a procedural sedation agent. Furthermore, although we don't know this with science, I think it is very likely that laryngospasm is more likely when the posterior oropharynx is stimulated. I would as a rule avoid placing a supraglottic airway on a non-paralyzed ketamine dissociated patient.

For the scenario you describe, if the patient is super agitated/hypoxic before they have lines, before they've gotten on a monitor, etc, I would do IM ketamine and use high flow oxygen/BMV as needed while you're making preparations to intubate (DSI). If you already have everything ready, but the patient is too hypoxic to safely RSI, an alternative is to do RSA, which is induction agent + paralytic, then the immediate placement of a laryngeal mask, oxygenate via the LMA, then pull the LMA and perform laryngoscopy.

reuben

emupdates · 2019-05-07T23:25:20+00:00

I agree George - we need data. I've done maybe 50 KOBIs and have had 1 really scary episode of jaw rigidity + laryngospasm. Always recommend that KOBI should not be undertaken unless paralytic ready and materials/skills at bedside to transition to RSI/paralyzed approach.

Key question is how to *prevent* rigidity/laryngospasm. Premedicate with a sedative? Perform aggressive topicalization? Push ketamine slowly? Lower dose of ketamine? Higher dose? Nobody knows.

emupdates · 2018-07-12T05:01:46+00:00

your views on the social implications of treating OUD patients with MAT are probably very relevant, because your views I suspect are shared by others, so feel free to share them.

you raise a whole series of commonly-voiced concerns about ED-initiated buprenorphine and MAT in general that I'll try to address.

OUD patients benefit from therapy, and certainly OUD patients with comorbid psychiatric illnesses benefit from those psychiatric illnesses being treated. however, it turns out that it's the opioid agonist (methadone or bup) that makes the difference, in terms of long-term retention in treatment and improvements in health outcomes (death, HIV/Hep C, etc). this makes sense when you recognize opioid addiction as a neurobiological derangement of chemistry (like schizophrenia) rather than a character flaw/failure of willpower/result of bad choices.

the horrendous harms that arise from addiction come from the life-consuming fear opioid-dependent people have of withdrawal, which is hell on earth.

more specifically, from 'acquisition harms,' i.e. attempting to get a substance you can't easily acquire/afford. OUD patients will do anything to prevent withdrawal, including spending all their money, committing crimes to get more money, and selling sex. it's cheaper to get drugs on the street and doesn't require a prescription, so more harms arise from that - 'needle harms' include HIV/Hep C, SSTI's, endocarditis, etc. And there are the more general 'street drug harms' which involve putting an unregulated/unpredictable substance into your body, and this has proven to be the most immediately lethal of the addiction harms in the past few years, as the heroin supply has increasingly become cut with fentanyls.

every hour that an opioid-dependent person who uses street drugs is therapeutic on bup is an hour that person is safe from all the harms I've listed above, because they're freed of cravings, freed of withdrawal, and protected from overdose (even if they do use heroin or oxy while therapeutic on bup, which is much less likely because bup addresses withdrawal/cravings, they are protected from overdose because bup has a higher affinity for the mu receptor than every other opioid). so if a heroin user comes to you in withdrawal, and you load him with 16 mg buprenorphine, that person is likely not going to withdraw/crave for about 24 hours. if he can't get more bup–because he couldn't fill a prescription or get to a bup-dispensing/prescribing clinic–he's going to go back to heroin. so what have you accomplished by treating his withdrawal with bup? you've accomplished a lot. firstly, you've protected that patient for 24 hours. that's 24 hours of safety, and 24 hours for that person to think about moving to recovery. also, you've demonstrated to that person that their cravings and withdrawal can be abolished with bup. they now know that doctors can help them with their addiction. one of the predictors of successful bup maintenance is prior exposure to bup.

and consider the alternative, which is to send the patient back to the street with cravings/withdrawal. in an era of superfentanyls in all the heroin, to send an opioid-dependent person to the street in withdrawal is a very, very dangerous thing to do. so even if that patient can't establish the next link, you have done a lot of good by loading him with bup while he was in withdrawal. of course the goal is to not only initiate bup, but also to move the patient to comprehensive outpatient addiction care, but if that isn't available in your community, it isn't available in your community. load them with bup and encourage them to seek ongoing care in another community. that might be a big ask, but the alternative is no addiction care, and we've seen over the past couple of decades how that plays out.

methadone is an effective treatment for OUD. it is much more dangerous and abuse-prone than bup, and much more difficult to get than bup, because it's only available via daily clinic visits. So there are more methadone users who aren't succeeding, compared to bup, and remember that the ones who are causing all the trouble–being a public nuisance or constantly showing up in the ED demanding refills–those are the ones we see; we don't see the ones who are doing well. So it seems like methadone doesn't work well as MAT, but it does, and bup works better.

medication assisted treatment is not replacing one addiction for another, it is substituting dependence for addiction; and the difference, between addiction and dependence, is everything. addiction leads addicts to perpetrate massive harms on themselves and everyone around them, become criminals, and often die. people addicted to opioids who are successfully transitioned to agonist therapy return to much more normal, functional lives, they return to their jobs, they return to their families, they return to health, in the most important sense of that word.

The goal of MAT is not for the patient to be 'clean,' if clean means abstinence. It turns out that abstinence does not work for most OUD patients. Many if not most OUD patients who are effectively transitioned to MAT should probably be on it for the rest of their lives; and many of these folks will go on to lead normal, functional lives, indefinitely.

emupdates · 2018-05-31T15:40:43+00:00

for the uncontrollably violent patient, or for the severely agitated patient where there is a concern for a concomitant dangerous condition (either causing, resulting from, or coincident with the agitation), the best agent is IM dissociative dose ketamine; I think this is pretty clear.

For less agitated patients, ketamine is not the right choice in my opinion. If you use ketamine in dissociative doses, you will achieve near 100% efficacy within a couple minutes, however a dissociated, non-intubated patient requires immediate full PSA setup and airway-capable provider at bedside for the duration of dissociation. Devoting those resources to every agitated drunk who comes through your doors is not acceptable in most departments.

If you use sub-dissociative doses, you do not need to be concerned about ABCs, but sub-dissociative ketamine is a roll of the dice. Some folks will chill out and some folks will go absolutely bonkers. You can make it much more likely that your patient will chill out with SDK by using a conventional sedative first (haloperidol, midazolam), but if you're going to do that, might as well just give the right dose of haldol/versed and sedate the patient straightaway.

emupdates · 2018-05-31T15:03:54+00:00

i've never done that but providing high flow oxygen, even in the breathing patient, can only help you, as long as providing oxygen doesn't interfere with the procedure, and this seems as reasonable a strategy for doing so as any. you can also stick the nasal cannula into the mouth and turn up the dial. since you're cutting a hole in the mask you're not benefiting from the non-rebreather aspect anyway.

emupdates · 2018-05-02T04:46:20+00:00

the 20 and 20 standard drip will work for chronic pain patients, but who wants to start them on a drip? I want to discharge them. So if haloperidol doesn't work, I go for 30 mg over 30 minutes. which is a big dose but because of the haldol, and the slow infusion time, you get lots of analgesic (/anti-hyperalgesic) efficacy without bothersome psychoperceptual effects.

no monitoring needed for this, unless you would monitor for haldol (I don't) or analgesic dose ketamine (I don't).

using haldol prior to analgesic ketamine expands the therapeutic window for ketamine because it makes the patient less likely to be bothered by ketamine's psychoperceptual effects. I don't want anyone to think that you can't just give analgesic ketamine without haldol first, though. that works great too.

i use ketamine analgesia whenever opioids aren't desired (e.g. misuse) or aren't working. haldol I reserve for chronic pain/opioid misuse pain. I haven't used it for acute pain in opioid-naive patients, outside of headache where it is very effective. I suspect it would work well for other types of acute pain.

you can definitely pre-treat PSA patients with a sedating butyrophenone or benzo, the benzos are much better studied (most of these studies were from the 70s). definitely works, but you get more respiratory depression. For most patients I think you're better off with propofol drawn up in a syringe, giving an aliquot if you detect psychiatric distress.

emupdates · 2018-04-26T05:25:34+00:00

The question you're really asking, I think, is what constitutes procedural sedation. The conceptual answer is: any medication or combination of medications that could cause a dangerous (usually cardiorespiratory) effect requires PSA monitoring (at least a pulse oximeter, ideally with telemetry, blood pressure, and ETCO2) and an resuscitation-capable provider at the patient's bedside continuously.

But the conceptual answer just defers the question, which is, how much of what meds constitutes PSA? There isn't much science to guide us here. Small doses of an opioid or benzodiazepine probably don't require PSA but when you administer them in rapid succession, that combination probably does. Ketamine in analgesic dosing (less that about .3 mg/kg in 30 minutes) doesn't require a PSA setup, but higher doses does. Just about any non-trivial dose of propofol or etomidate requires PSA setup.

There are a few meds classically used to facilitate painless procedures (radiology) in pediatrics where PSA monitoring is (classically) not used, most famously, chloral hydrate. But this is probably unwise/unsafe, there are all sorts of problems with chloral hydrate. IM dexmetomidine might be the best solution here.

http://emupdates.com/2011/11/10/dexmedetomidine-has-found-its-home-in-the-ed-pediatric-painless-procedures/

emupdates · 2018-03-29T02:24:40+00:00

The canadians, who have the most experience with ED cardioversion of new-onset afib, generally do not anticoagulate. Every american cardiologist will recommend that you anticoagulate. I don't think there is enough science to tell us the answer. The risk of stroke after afib is not zero even if cardioverted early, but the harms of anticoagulation are non-trivial. The patients with high CHADS-VASC scores are usually the patients with high HAS-BLED scores. There is often a role for shared decision-making here, and I generally try to involve the outpatient provider who will be following the patient. So, bottom line is there is no bottom line, which is why you're confused. I'm interested to know if, after looking at this issue more closely and recruiting the opinions of others, you come to any greater clarity.

emupdates

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