The TOF explained clearly and actually got a hang of the same for the first time today, inspite of reading it a couple of times before. Thanks a ton and God bless! BTW I am an Anesthesia trainee. RIK
You explain it beautifully. I am not an anesthesiologist nor anesthetist. I have been employed as a psychiatric physician assistant. I was doing some research on anesthetics and neuromuscular blockade agents, this evening, and came across Train Of Four ratios. Your video explained it very succinctly and clearly. Thank you for the few-minute education lecture.
helpful only if you only wanna know how to distuingish between depol and non-depol;NOT helpful if you want to understand the underlying mechanism behind the ratios.
I am kind of confused on the last point Can u please explain how phase two succinylcholine appear to fade starting from 100%, isn't it like phase two is paralysis where the receptor of the end plate are resistant to stimulation from Ach. As I understood paralysis will yield no twitch so it's weird that we have 4 twitches and even a 100% twitch Last Q: what train of four count ? Thank you very much very informative explanation
How does this translate to a clinical setting? I understand the concept behind TOF, fade, and TOF ratio. However, how would you be able to assign an actual percentage to your twitches? I feel like this would be very subjective and not necessarily reliable. Is this correct?
You're correct! TOF ratio is an objective measurement with specialized equipment. This is called quantitative assessment of the NMB, whereas twitch count is qualitative and subjective
with succinylcholine - you get depolarization/activation at a bunch of neuromuscular receptors. These receptors then remain "blocked"/unresponsive to acetylcholine for a certain amount of time. When you then do a TOF - what happens is that you stimulate release of acetylcholine into the NMJ and the receptors that aren't "blocked" will respond. They will respond every time. And so there is no FADE but the overall amplitude is lower because not all of the receptors are available to respond. Now with Rocuronium for instance - you have a non-depolarizing agent which acts like a competitive inhibitor at the acetylcholine receptor. So when you start your TOF - what happens is that first you get a release of acetylcholine into the NMJ and this release is strong enough to stimulate all receptors (or most), but with each subsequent stimulation, you get less and less acetylcholine released into the NMJ and because of the competitive inhibitor by rocuronium, less receptors get "activated" because now the competition is starting to "win more". Note: with Succynilcholine you also get less and less acetylcholine released into the NMJ, but there is no competition to the free receptors so they all still get stimulated (i.e there is enough acetylcholine still to activate them all). Hope this made sense.
Anu Priya Follows commands Swallowing reflex present Able to lift head for more than 5 sec -> BEST CLINICAL SIGN Tidal vol > 6ml/kg Vital capacity > 10ml/kg TOF ratio of T4/T1 is > 0.9 -> BEST SIGN OVERALL Dead space/tidal vol < 0.6
