Posts by Scott Allen10

Honestly, if you're doing transfusions or heavy fluids, you really want a larger gauge needle—something bigger than a standard 20G will move way faster, which is huge when things get intense. I bet the guy was yelling because if you need to run two IV lines at once, toss in some meds, and maybe even blood later on, you’ve got to use those multi-port connectors... trying to push all that through a tiny 20G is a total nightmare, it's painfully slow. Plus, those 20Gs are pretty short, maybe an inch or so, so if you're dealing with a bigger patient, it's way too easy to miss the vein entirely.
But look, if we're just talking about basic saline and maybe a couple of quick meds while the patient is stable and not heading into surgery or anything crazy... then that doctor was definitely being a bit of a smart-ass.

Choosing which IV catheter to use is really down to the individual; you have to look at the patient's overall stability—basically, what kind of fluids or meds they need, how much, and how fast they need them... plus, of course, you have to judge the actual quality of their veins.
The general rule of thumb I follow is to go with the largest gauge possible if the vein looks solid. Honestly, once someone is already getting poked, they usually stop caring about the specific needle size; whether it’s a 20G or a 16G, it’s all pretty much the same level of discomfort to them.

The green ones (18G) aren't actually the thickest out there, and while they get the job done most of the time, surgeons and anesthesiologists usually consider them right on the edge of being acceptable. They can also make blood transfusions a bit of a struggle. That's why we usually aim for the gray ones (16G) as our go-to. They’re sturdy enough that they won't kink or collapse in the vein, and the lumen is wide enough to handle high flow rates for both infusions and blood products. Every once in a while, if we can find a good spot, we might grab an orange one (14G) or even a white one (12G)... but those are basically heavy-duty tools we don't need unless things get intense.

As for the pink (20G) and blue (22G) catheters, they aren't necessarily "bad," but they should really only be used if the patient's veins just aren't big or strong enough to handle anything larger. You'll see these sizes used routinely in pediatrics, whereas in the NICU, they almost always have to stick with the yellow ones (24G).

You might still see a pink catheter (20G) being used for intra-arterial lines—usually in the radial artery when we need to monitor arterial blood pressure—but that’s a whole different conversation...

Just get them to a trauma center or an ER... honestly, any hospital will do, doesn't even matter if it's not in NYC...
Looks like they might have cracked a couple of ribs or something...

It might just be some weirdly twisted blood vessel or something... honestly, I don't think there's any reason to freak out over it. Hang in there, you'll be fine.

cosmicmaker30 said:sooo... one more thing... which vein is actually the easiest to hit? Like, where's the least risk or whatever...

There isn't really a set rule for this since everyone's anatomy is just so different. Honestly, before you even think about sticking a needle in, you should get your Esmarch tourniquet ready and really, really feel around for the veins... I mean, don't just look at them, you have to palpate them. Don't trust your eyes too much when judging a vein. Over half the time, you won't even see the vein, but you can totally find it if you feel under the skin—you can sense the direction, how firm it is, how flexible it feels... you know, that little "springy" feeling under your fingertip. Just make sure the vein is straight for at least 2 or 3 cm so you aren't dealing with some bumpy spot that’s just going to pop the second you pierce the wall. It’s way better to spend ten minutes scouting the right spot than to poke blindly and then end up hunting for the vein with the needle afterward...
Usually, for drawing blood, the veins in the antecubital area (like the v. basilica or v. cubitalis) are the most convenient, but if you're doing a line, you'd ideally want to check the veins on the back of the hand first before moving up toward the elbow. Veins in the legs can work for both blood draws and lines too, though obviously not for patients who are up and walking around—but for someone bedridden, it's definitely an option. You're mostly looking at the veins on the foot or around the ankle...
In those really extreme situations, you might have to go with the jugular in the neck or the femoral vein in the groin area..

cosmicmaker30 said:Sure, epinephrine is used for asystole, VF, pulseless VT, and PEA. But listen to this: when treating VF and pulseless VT, amiodarone is administered as a slow 300 mg bolus, followed by a second dose that's half that size—150 mg IV. At least, that's what one ICU doctor told me. I know because I saw them prescribe that exact regimen for a female patient in VF over in the ICU.

I completely agree—BLS (basic life support) always comes before ALS (advanced life support). What I find really interesting, though, is that according to the latest CPR guidelines, the ratio for compressions to breaths is 30:2. So, 30 chest compressions followed by two breaths...

In resuscitation medicine, the idea of giving a drug "slowly as a bolus" doesn't even exist... which makes me pretty skeptical about whether that specific case you mentioned was actually handled correctly. Also, we have to ask—which ICU are we talking about? Honestly, almost every hospital ward has some little corner or room they call "the ICU." But most of the time, it's just a tiny nook with an oxygen tank and maybe a pulse oximeter, if you're lucky...
The term "ICU" gets thrown around so loosely in American hospitals that basically any little storage closet or side room gets slapped with the label, even if there isn't a shred of intense medical activity happening in there...
Sure, maybe that specific example was actually a perfectly handled amiodarone case, but you’d still need DC cardioversion and continuous chest compressions along with proper ventilation and oxygenation... It's just hard to judge a single individual case or the flow of a crisis like that based on one anecdote...
You're spot on regarding those new compression-to-ventilation ratios... It turns out that during resuscitation, the absolute priority is maintaining blood flow through the vessels, and you achieve that through compressions. Doing just one or two breaths for every 30 compressions is plenty to ensure the body gets enough oxygen as that blood is pumped through the system, especially to the brain....
Still, I think those breaths have to be high quality, with a full volume of well-oxygenated air... which brings us right back to the "A" and "B" of the airway and breathing alphabet. You have to secure a safe airway and make sure lung ventilation is sufficient.
And honestly, in the middle of all that chaos during a code, the best way to do that is via endotracheal intubation, which needs to happen ASAP—right in the thick of compressions, DC shocks, and trying to find a vein. Using a mask with an Ambu bag is pretty questionable... Not because it's useless, but because people do it so poorly! You wouldn't believe how incredibly hard it is to ventilate someone using an Ambu bag. If you haven't tried it, you probably can't imagine it, but trying to get a good seal between the mask and the face while performing compressions and dealing with the madness around the bed—all while tilting the head back to keep the airway open so the tongue doesn't block it, and squeezing the Ambu bag at the same time—you have to be seriously skilled. Sometimes it feels like you need an extra hand just to keep up...

cosmicmaker30 said:take adrenaline, for example—I know 1ml equals 1mg... so if someone asks for 1mg, I’d just hand them the whole vial, but if they want 0.5, I’d give them half... unless there’s already a 0.5mg vial out there? It’s honestly such a mess when we're doing our clinical rotations... the doctor yells, "give me 0.5mg of atropine," and then I just pass the task off to my colleague because I can't wrap my head around it...

but honestly, it's not even that deep once you get the hang of it. If you need to dose 0.5mg of Atropine, you just grab a vial that's pre-measured at 0.5mg, pop it open, and use the whole thing... or, if you've got a 1mg vial, you just draw up the full amount into the syringe and then pull back until you have exactly 0.5mg left to give... it's simple enough....

With epinephrine, it’s always 1ml = 1mg... but you really have to watch your step because you're often diluting it to a 1:10 or 1:100 ratio... sometimes even 1:1000... So, when the doctor tells you, "administer 1 ml of 1:10 epinephrine," here's what you do:
- grab the vial and open it up
- take a 10 ml syringe and draw up the entire dose of epinephrine. That's our 1 ml, as we established.
- grab a bag of saline and draw another 9 ml of saline into that same syringe with the epinephrine.
- now you've got a 1:10 epinephrine solution, and you administer 1 ml from that syringe intravenously.

If you need to give 1 ml of 1:100 epinephrine, the process changes slightly:
- grab a fresh, empty 10 ml syringe and attach a needle to it
- hold that pre-prepared 1:10 epinephrine syringe in your other hand
- use the empty syringe and needle in one hand to aspirate 1 ml of the 1:10 epinephrine from the first syringe held in your other hand....
- then, add 9 ml of saline to bring the total volume back up to 10 ml... and boom, you've got 1:100 epinephrine ready to go.
- from that syringe containing the 1:100 dilution, you administer 1 ml of the medication.

The absolute golden rule when you're messing around with all these meds is to label your syringes immediately. Seriously, write exactly what it is on the side right away, because later on, heaven help you, you won't have any clue which syringe is which...

Honestly, there’s really no need to get caught up in those kinds of calculations. Every finished medication is already diluted in its own specific volume... for instance, you'll find atropine in 0.5 mg or 1 mg ampules... nobody ever tells you to grab "xx ml" of atropine, they just tell you to give 0.5 or 1 mg.

Andrew Jones12 said:Heh, lol. Must be nice to understand everything so clearly. Looking at this, you're either a doctor, a med student, or just a dedicated researcher like me. Yeah, what you're saying is probably spot on—all the knowledge I'm gathering comes straight from medical encyclopedias, so it's far from exhaustive. I actually enjoy posts like this, Scott Allen10, because I always end up learning something significant. Please, write more often. I'm still waiting to enroll in my program, but once I finish med school, we'll have plenty to debate. Sorry if my post was off; I'm just going by what the textbooks say.🙂🙂

Seriously though, please keep posting about this topic... I live for these resuscitation stories, so there's nothing wrong with having a little discussion now and then.

Especially since I feel like every single healthcare worker, whether they're a doctor or a nurse, needs to have a full grasp on this... rather than having someone like this one anesthesiologist I know who actually tries to shock a flatline during asystole...😲...if I hadn't seen it with my own eyes, I wouldn't have believed it...

cosmicmaker30 said:My bad... I really messed that one up. It’s all still a bit too fresh in my mind for me to be making silly mistakes like this... I managed to mix up Rytmonorm (propafenone), which you'd typically use for rapid atrial fibrillation, paroxysmal supraventricular tachycardia, or even paroxysmal ventricular tachycardia, with Cordarone (amiodarone), which is what we look toward for ventricular fibrillation or rhythm issues tied to WPW syndrome, atrial fibrillation, and flutter...

I know, I know—even though epinephrine is the go-to during CPR, when you're actually dealing with ventricular fibrillation or pulseless tachycardia, amiodarone is the move.

That last part isn't quite right. Epinephrine is the first line of defense in CPR regardless of what the rhythm looks like—whether it's asystole or VF. The only difference is that with VF, you need to hit them with a DC shock first. You keep doing chest compressions for both types of arrest, but with VF, you only pause the compressions long enough to deliver the DC shock... take a quick look at the ECG, and if the fibrillation is still there, get back to compressions, give the epinephrine, and then hit them with another DC shock...
What I'm trying to say is that while ventricular tachycardia is definitely life-threatening and often leads to VF, it’s technically not the same thing as ventricular fibrillation. With VT, if the patient is stable, you can primarily treat them with amiodarone without jumping straight to a DC shock... but VF is a true cardiac arrest situation. There's no time to mess around with amiodarone there, especially not at the start when there isn't even a recognizable rhythm on the ECG.
Lately, vasopressin has been popping up more in resuscitation protocols. Over here, we have it available as Pitressin. In CPR, whether it's asystole or VF, you can start with it by giving a bolus of two ampules of vasopressin (40 units). We've seen some really solid results from it, but it hasn't really become the standard practice in our hospitals yet. Mostly because epinephrine is still considered the "gold standard" and that's what everyone is trained on... but honestly, a huge reason is just that Pitressin is incredibly expensive. Depending on which supplier you use, an ampule can cost hundreds of dollars!
Just a side note: all this talk about "C" (circulation) and "D" (drugs) only matters if you've already handled "A" (airway) and "B" (breathing) right at the start of resuscitation... which, if I'm being honest, doesn't always happen perfectly in our hospital settings... hm... sometimes things get a bit messy...

Harold Ramirez49 said:I wanted to make one more quick correction regarding VT or V-fib. Using amiodarone combined with DC is definitely the preferred way to go. You could technically use Xylocaine for VT, though that’s becoming a bit old-school. As for epinephrine, it really isn't the first choice for this, though I suppose in an environment filled with bystanders, that distinction doesn't matter much as much as just getting something done

Just so we're on the same page... I was talking about VF (ventricular fibrillation), but looking at what you wrote, it seems like you're referring to VT (ventricular tachycardia), where there’s usually—though not always—some kind of peripheral pulse... which is a totally different ballgame. Obviously, with VT, you wouldn't lead with epinephrine; you'd go for an antiarrhythmic and maybe some DC, but once you hit VF... man, that's full-on arrest territory. You go straight to epinephrine and DC as your primary move, and then if you manage to get any kind of rhythm back, you can start thinking about other meds...🙂
I'm with you on the Lidocaine.

Harold Ramirez49 said:Where did this idea come from that Propafenone shouldn't be used for FA ????

I was just talking about using that med for V-fib the other day.

Andrew Jones12 said:A quick rundown on atrial fibrillation

AFib is essentially a fast, irregular heartbeat. The most dangerous complication you’re looking at here is a stroke, and honestly, that risk just climbs as the years go by. Sometimes AFib shows up out of nowhere without an obvious trigger, but more often than not, it's driven by underlying issues that cause the atrium to enlarge—think things like coronary insufficiency or high blood pressure. Smoking and a sedentary lifestyle don't help matters either, and you'll see it pop up frequently in patients dealing with hyperthyroidism or chronic alcohol use.
Common symptoms include shortness of breath, chest pain, and dizziness.

Treatment for AFib typically involves beta-blockers.🙂

I missed jumping in on this earlier... it feels a bit "all or nothing" to me. Honestly, the most dangerous complication of FA is actually V-fib. A stroke falls more into a different category; it isn't always directly linked to atrial fibrillation, so I don't think we should label it as the "most dangerous" thing.
The idea that "enlarging the atrium" is directly tied to the onset of AFib isn't quite right either—not sure where that came from. Also, things like shortness of breath or chest pain aren't really hallmarks of AFib itself; those are much more likely signs of myocardial ischemia. A patient with AFib can actually have totally stable hemodynamics with decent blood pressure and good ventricular filling during the cardiac cycle.
With AFib, the real deal is that the atrium doesn't contract; instead, blood just passively flows from the atrium into the ventricle during diastole. Since such a huge chunk of blood moves passively like that anyway, you don't usually run into major hemodynamic issues. Normally, the electrical impulse starts at the SA node and travels through the AV node to trigger the atrial contraction. In AFib, that signal gets hijacked—it fires off in multiple spots all over the atrium randomly, which means the atrium never actually gets that coordinated squeeze.
On an ECG, you'll notice that patients with AFib pretty much lack a P-wave.
It's only if a patient happens to have something else going on, like mitral stenosis that messes with passive filling, that you start seeing real problems with how the pump is working.
The goal with AFib is to try and convert it back to a normal sinus rhythm. Cardioversion can be done with meds, like giving a bolus of amiodarone via IV.
If that doesn't do the trick, you can go the route of electrical cardioversion, or basically defibrillation. We'd put the patient under briefly with something like propofol or ketamine... and you absolutely have to use the synchronized mode on the defibrillator. If you're using a biphasic machine, you wouldn't want to go over 50 - 100 J... you just try a few rounds of cardioversion.
This method works great, but it's definitely most effective if you catch it early.
At the end of the day, every case is different. What works perfectly for one person might not work for another, so the doctor has to make the call on what's best for the situation.

When you’re looking at pharmacological ways to handle heart rhythm issues, you really can't go wrong with IV amiodarone—which we usually just call Cordarone here in the States. Of course, if someone hits V-fib, you're skipping straight to cardioversion and adrenaline, but for most other stuff, this is pretty much the gold standard.

Not a chance. We're talking about V-fib here, which is a total emergency that needs immediate resuscitation—you’ve got to prioritize cardioversion, and while you're waiting for the defibrillator to charge, you better be cranking through chest compressions and pushing IV adrenaline.

hm....

So, are you actually heading over to the States? I’m still trying to wrap my head around this "Level 3 hospital" thing you mentioned. Plus, I’m totally lost on how a group like the Maltese Knights—or honestly, any religious order—could even train medical staff who have already finished nursing school or some kind of vocational program, let alone be authorized to go around giving people injections... could you walk me through how that all works?

"Chronic diarrhea caused by psychological issues"?...😕....

Have you actually done any kind of medical testing to back that up? Because honestly, just like any other medication, an unknown shouldn't be taken without a good reason.

coastaljackal8 said:My son is finally bouncing back from mono he caught back in February
He’s been getting blood work done every month, and his liver numbers and lymphocyte counts actually looked totally normal about two months ago.
But looking at today's results, I see his LDH is up to 352 U/L (it was at 432 when he first got sick, then dropped down to 119 two months ago),
and his alkaline phosphatase hit 164 U/L today.
Why would the LDH spike again—is that something to worry about—and is that alkaline phosphatase level within the normal range?

The alkaline phosphatase is just a tiny bit over the limit, but yeah, that LDH is definitely high.
Of course, nothing means anything without a doctor actually looking at him... You didn't mention if he's feeling any symptoms lately? Like a fever, a sore throat, any bloating under the right side of his ribs, or maybe just feeling super wiped out? I'm not an expert, but I think once you fight this thing off, it really messes with your immune system for a bit... Usually, it's EBV that causes it, though sometimes it's CMV, and I honestly can't remember if catching one makes you immune to the other too...😕...
Also, sometimes after mono, you can deal with a type of hemolytic anemia—where red blood cells break down—which ends up driving those LDH levels way up... Man, I'm really just guessing here... I truly hope you guys got a full panel done, but otherwise, you should probably just get him in to see the pediatrician first thing Monday morning... I don't want to freak anyone out with internet guesswork, but I'm pretty sure it's nothing to lose sleep over.🙂

I wouldn't sweat it too much... honestly, it really just depends on which lab you're using for your bloodwork, because sometimes those numbers can be totally fine. Every single lab out there seems to have its own specific reference range they go by...

So, what kind of internship are you even doing where you're learning how to give IV injections? Honestly, your intro was a little bit all over the place... obviously medications come in ampules, I mean, what else would they be in?
Every single method tells you exactly how to handle the injection. You go IM straight into the muscle at a 90° angle, SC under the skin at about 45°, ID just under the surface at maybe 15 to 20°, and then there's IV right into the vein, which totally depends on which vein you're hitting, what needle you're using, and what the actual goal is...

And seriously, did nobody teaching you this stuff actually explain it? Or are you just out here playing "wannabe" nurse or something? Hmm... weird, really weird... 🙂