Hello all! Thanks for visiting the RespiratoryReview Channel. This aim with these videos is to provide a bit of a different approach to traditional instruction.
These videos will cover many areas of respiratory care including: Principles of Mechanical Ventilation, Respiratory and Cardiac Physiology, and hopefully many more. I will eventually be making an Anesthesia Fundamentals Playlist.
I started my career as a Respiratory Therapist (RRT), and worked mostly in critical care. I then completed medical school and I'm now a senior resident in the department of Anesthesiology, Pain Management and Perioperative Medicine at Dalhousie University in Halifax. I have interests in critical care and cardiothoracic anesthesia.
I hope you get something from these videos! I will do my best to respond to as many questions/comments as I can.
Have Fun!
Ollie
Пікірлер
Hello Friend, just read your bio, thank you for your time and content but we need more of it please it is great! 🙏🏾
First of all, thank you so much for detailed explanation. There are relatively new guidelines (2021) published by SCCM regarding sepsis. There are two recommendations on "Ventilation" section, regarding recruitment maneuvers. These are as follows : 53. For adults with sepsis-induced moderate-severe ARDS, we suggest using traditional recruitment maneuvers. 54. When using recruitment maneuvers, we recommend against using incremental PEEP titration/strategy. In rationale, there is explanation, that when the incremental PEEP recruitment studies are analyzed separately from studies utilizing traditional recruitment maneuvers, recruitment with incremental PEEP is associated with increased 28-day mortality RR, 1.12; 95% CI, 1.00−1.25), which justifies the strong recommendation against using incremental PEEP titration for recruitment. Taking all above mentioned, what is your opinion regarding recruitment type in sepsis patient?
Hi thanks for the great question. I’ve seen the guidelines and my opinion is that the recommendation against stepwise recruitment is a bit strong. Things I’d encourage you to look at would be the trials that used stepwise methods that were used to support the recommendation. There was no consistency in approach. Some had very large driving pressures while others kept driving pressure fixed while increasing PEEP. I think driving pressure drives mortality and it’s no different in the RM space. Ultimately I don’t think there’s strong enough evidence to prescribe a fixed RM tactic, which makes it hard to put into guidelines.
Thank you
Thank you so much. You clear all my doubts. Please upload more videos on ventilator and ABG correction. Thank you!
🙏Thank you so much...
Have a good day productions
Thank you
Thank you very much ❤
Thank you very much!
Wt about ASV mode
Great format for presenting these videos by layering things in! Lovely diagrams too - clear and simple, thank you
awesome video thanks. A pop filter might help the audio though
Great Video, Great education...I feel you simplified SIMV for me...THANKS!
Bro. How did I even find such a gem of a video at the corner of the KZread! Thank you so much!!!
I'm so grateful to find you for the way you patiently presents these videos ..thnx 👌
Thank you, the volume is very low
Hysteresis is due to the property of surfactants. Their molecules are more apart during inspiration, leading to slight attractions between water molecules the surfactant is in between trying to reduce surface tension. In expiration, surfactant comes closer together and prevents that water-to-water attraction, reducing surface tension. So inspiration and expiration follow the different pressure-volume loops. This property of surfactants is the reason why the lungs don't collapse at the end of expiration. Without surfactants, your lungs collapse like in Neonatal respiratory distress syndrome or ARDS where surfactants are reduced/diluted.
Thank you,this was very helpful.
Good video - nice general overview. I'll share a rare case - CACNA1e (I believe r-type Ca Channel?). Regardless, patient was in status and was administered Verapamil. Appeared to be some immediate effect/impact (6+ hours with no seizures upon administering) but then seizures picked back up. Interesting point about the various Ca channel types and mode of action for those blockers.
“Good question because I asked it. I’m super smart. I have a monotone voice I use for my KZread channel. Are you asleep yet?”
Golden retrievers are supposed to be friendly Cooper. No one forced you to watch anything on KZread.
@@RespiratoryReview do you know how lithium effects the adrenal gland specifically? Can you make a video on that?
you are my hero
Verry ❤nicy from iraq
Thank you so much!! your teaching is extremely amazing and easy to follow!! best ever!
More videos plz
More videos
Hi, do you mind telling us what kind of equipment and app did you use for making the video? I would like to do similar thing but in my own language. thx u
kzread.info/dash/bejne/ea140LZuYpfQZ7w.html Pulmonary Compliance Alexandr Balan M.D
kzread.info/dash/bejne/ea140LZuYpfQZ7w.html Pulmonary Compliance Alexandr Balan M.D
kzread.info/dash/bejne/ea140LZuYpfQZ7w.html Pulmonary Compliance Alexandr Balan M.D
Ok this standard equation is clearly an approximation. There can be easily 30% difference in volume of blood depending on weight and height of an adult, which means corresponding change in dissolved oxygen at equal pressures. I mean on the one side you are accounting for blood volume by multiplying by total grams of hemoglobin, but on the dissolved side the 0.003 factor can only translate pressure to oxygen amount assuming some standardized amount of blood, like 5L. But since dissolved o2 only accounts for very little of the total (like 2%), the error isn't that significant. Just helps to understand what's going on, because you can't translate a pressure into amount with a constant multiplier if you don't have a fixed volume. But thanks for the explanation with what units we're talking about here otherwise the constants could mean anything.
I don't get why the respiratory factor is in the equation. This is only a pressure equilibrium equation, no other quantitative factors. The alveoli don't need to know where the co2 is coming from.
So only question I still have no answer for, is how does 2000ppm CO2 stuffy room air, which amounts to about 1.5mmHg, cause strong, measurable reduction in cognitive abilities, when this would barely move the gas exchange equation, ie should be easily be compensated for by increase in breathing?
Reasons for intubation: CHF: makes no sense. If you don't pump enough blood how is breathing going to make a difference? I don't see lung issues coming up as causes for CHF . Pulmonary embolism: seriously? There is very specific treatment for that and it involves dissolving a clot the body was too slow to dissolve. Again upping oxygenation makes no difference if blood doesn't move, and stopping to breathe doesn't seem to be a symptom of pulmonary embolism. VQ mismatch: again if it has nothing to do with mechanical movement of the lung, which in almost all cases it won't, why replace very cool negative pressure breathing with stupid, much less effective positive pressure? Just give the patient pure oxygen, that will both improve oxygenation and CO2 clearance vs the probably super high room CO2 of 2000pm in hospitals. It seems the ventilator gas is a mixture of room air with oxygen. ARDS: please explain how a ventilator helps when there is water in the lungs. If anything I read ventilators cause water in the lungs The only ones in the hypercapnic case that make sense is drugs and neuromuscular problems, which is what I thought from the beginning: obviously if you can't move your muscles or your breathing center is knocked out that's your one shot. Airway protection from swelling: how about making the swelling aka inflammation go down? You are going to intubate someone having an asthma attack or something?
How does ventilating normalize blood gas? If anything I'd say it throws it off? For proper pH you need exactly the right amount of breathing, not too much not too little. That's why the body has CO2 sensors. I assume the 'sedation' is to turn those off? I swear I'm not surprised if you have everything backwards. Checking gas once a day cannot possibly be enough, your pH cannot be off for any length of time. To unload breathing: if they were able or willing to properly regulate breathing at least, but so far it seems this is done at the risk of dangerous blood pH, damaging the lungs with positive pressure much higher than required negative pressure, and I can't imagine anything more uncomfortable than intubation with a repetitive fixed breathing rate. Never mind that breathing muscles don't need rest they work 24/7 just fine.
why no word about pCO2 continuous measurement? If anything, that is the number one relevant outcome of this whole ventilator operation. Together with (one time measure of) bicarb, that gives the blood pH, which is what this damn thing should be managing, nothing else.
I mean definition of COPD is a joke, just to start with. It can be chronic Bronchitis, or a condition where lung loses surface area, which have absolutely nothing in common with each other except they affect the lung's function. Per definition, if you have 3 months of productive cough each year for two years, you have COPD. Charlatans.
Thank you very much for providing a basis for the consequences of the positive pressure mechanics. Now that makes sense. So you need 3x more pressure for the same air volume with a ventilator than when breathing normally because of positive vs negative pressure. The lungs were built for the latter obviously. Like we know what high blood pressure does to blood vessels. 69% of over 65 year olds intubated die on the ventilator. The ones sent home have now twice the mortality rate than unintubated. It seems this procedure should be applied only to prevent impending death, forget sedation, and take them off the ventilator after a few hours if what caused the breathing issue can be stabilized enough. Why the hell don't they have iron lungs anymore (maybe a more sexy version), using negative pressure? That wouldn't cause any damage. The whole theory about recruiting bla bla seems to be not feasible anyway with the high pleural pressure. So if the patient can still mechanically move their lungs to effect negative pressure, then that would appear to be much better at oxygenating them than positive pressure ventilators. Why not focus on opening airways without ballooning the lungs? How are the collapsed alveoli supposed to heal if they are being stretched like balloons, just to overcome the surface tension (due to lacking surfectant? Figure out how to replace surfectant then. Or clear pathogens that can interfere with surfectants like candida. I just bought a dirt cheap 10g Ozone generator on Amazon. Works great. Ozone kills candida. As this is not doctor approved (though ozone therapy is very much a real thing, at the same time they say it's a pollutant and bad for the lungs..), I will test this out on myself for the next few days.
I suppose pneumothorax would be an exception, where a lung is detached from the chest cavity so to speak and negative pressure won't transmit. Since it's always only one lung affected at a time, and I doubt under positive pressure ventilation that the thorax pressure can heal/normalize, it might be better for survivability to have the functioning lung do double duty until the body restores negative intrapleural pressure to the other lung?
Doing great with the ozone. Slight irritation but I'm pretty much overdoing it. 5-10 minute timer a few times a day for a 10g generator inside a small apartment would probably be sufficient. I've cranked it up to 30min intervals every couple of hours or so yeah.
Please don't experiment on yourself especially with O³. There were reasons why we shifted from iron lungs to positive pressure ventilation. Read and study the basics in detail. You have a good out box thinking, but use it rationally.
@@tubeysr I stopped using ozone since it was hard to make out any benefit. It's still good to clear your place of mold if you step out for an hour.
So if you're not using SIMV often, what are you using? IMV sounds like extra torture, you have to work really hard to adjust your blood acidity.
I hope these vents when backstopping at say 14 breaths a minute stop that automatic cycle if the patient breathes on their own, rather than superimposing assisted breaths with the backstop breaths.
Nope, they don't. Only when there is overlap of assisted breath with automatic breath
8:57 I disagree that this was potentially lost lung volume. Flow is already minimal by this time, so it's more like you're wasting time, not air, if you waited until lungs were at capacity. If you want to get a proper answer you need to formulate this as a gas flow maximization problem and mathematically optimize it. Though the optimal solution probably won't make a big difference.
At least I felt better when I knew that I'm not the only one who doesnt fully understand this mode.😅 Thanks for your effort of explaining.
I thought boyles law was inversely related? If you increase pressure the volume decreases… ?
Very informative and educative.. But the lip smacking and mouth noises were nails on a chalk board.
This was freaking awesome. Seriously as soon as it finally clicked I stood up and yelled I’m the smartest person alive!!! Thank you
Really glad it helped!
I thought SIMV was pressure supported only if its "SIMV+PS" is SIMV always with PS?
SIMV as it’s classically described will have PS breaths. How ventilator companies label it will vary a lot but the principles will be the same. I’ve never heard of an SIMV mode that doesn’t allow PS breaths. Perhaps you can share an example with everyone?
@@RespiratoryReview yea its on my school notes. SIMV is described on its own , and then PS is described on its own. and the next slide is SIMV+P/S, and both waveforms are drawn which is why I get confused what's accurate and not. THANK YOU
5:54- u said pressure controlled which is pressure limited time cyceld. isn't pressure control also FLOW LIMITED PRESSURE CYCELD ? there's two types of pressure controls right ? so why did you choose to say its only pressure limited time cyceld when there's another form
Please share with everyone the specifics (reference) for a pressure control breath type that’s flow limited, pressure cycled. I’ve never seen or heard of such a thing.
@@RespiratoryReview im just looking at my class notes and it has a picture of two types of pressure control waveforms. one of them is described as flow limited pressure cycled; which is why I ask. so im not sure . so is pressure control only time cycled flow limited? and wouldn't pressure control be pressure limited since its controlling pressure?
Thanks for this great video. What is the indicator that detects CO2 in colorimetric capnography?
FANTASTIC - THE WHOLE SERIES
Amazing 🎖
Love the lecture thank you. My question is this when placing a patient on High Flow and they have COVID-19 is it more dangers for the staff as the patients don’t normally keep their mouth closed. Does the High Flow become a a water cannon filled with particalized droplets that can travel a farther distance. Or is the water particle to small to carry the virus with it.
This is an interesting question. The question really is “is High Flow Nasal Prongs an aerosol generating procedure?” At most centres I know people at they are considering it an aerosol generating procedure given the high flows. So patients with covid on it would be ideally in negative pressure rooms and have staff in full PPE. This is hugely variable however, and many centres are managing high flow prongs differently. It is also changing rapidly. At my centre I believe the current policy is that COVID patients on high flow NP are airborne precautions so full PPE with N95s. I’d encourage you to look up what your local institutions are recommending, and if in doubt wear full PPE. We had a lot of success keeping people out of ICU and off ventilators using HFNP during our covid waves.