Posted on 04/07/2020 11:33:16 AM PDT by COBOL2Java
I salute you.
I was making a sarcastic rejoinder to your earlier “resonance frequencies” sarcasm about 5G.
Here, if you have time. People tend to dismiss out-of-hand even the slightest suggestion of any effects on the body, of WiFi.
But when I tracked down a link listed in a YouTube, I found... peer reviewed journals (Elsevier, for example).
https://www.sciencedirect.com/science/article/pii/S0013935118300355#bib11
The links on this page, appear at first blush to be from reputable, peer-review journals.
e.g. https://www.sciencedirect.com/science/article/pii/S000527361500053X?via%3Dihub
Investigation of the effects of distance from sources on apoptosis, oxidative stress and cytosolic calcium accumulation via TRPV1 channels induced by mobile phones and Wi-Fi in breast cancer cells
is from Elsevier.
It considered oxidative stress on certain breast cancer cell cultures as a function of distance and frequency of several WiFi signals.
It did look at distance not from a tower, but from a cell phone, and found that the control group had no statistically significant difference from 20 cm and 25 cm separation. Consistent with “rapidly-diminishing effects beyond trivial distance” so beloved of the 1/R**2 community.
Have read into detail to suss out in vivo vs in vitro, study design, or sample size.
Or of course, regular tissue compared to breast cancer cells.
Yes, I saw that. I read others making the point and didn’t think they were doing so very clearly so I wanted to make sure you knew it, is all.
You said you see people getting off ventilators. Are you using HCQ too, and if so, with either zinc or azithromycin? Just wondering. Also, if you are using HCQ, did it get added to the treatment protocol after a point and did you see an obvious difference before and after it was added?
They showed (what was it?) 7% or 14% increased survival in ICU patients with this Coronavirus in a real-life hospital setting, other things being equal. Theory should FOLLOW data. Mumble harrumph "not well designed" mumble "small sample" mumble "no control group" ...
well, the medics in the thick of this were a bit overwhelmed for that at the moment, IIRC that report came from...Italy.
Getting *way* more real info from these sorts of F/R discussions than anything in the so-called MSM.
“80 or 90% just die in hours”
Where’s the study proving this percentage?
Where’s the study proving anything you say, ever in your life?
Your points are well taken...In the order presented...
1. I can’t explain why viral PNA looks bilateral and bacterial PNA is lobar. That is an exquisite question that we are just not sophisticated enough to answer. My guess is that bacterial PNA infects a lobe but can’t make it across the fissures so you see lobar consolidation. I suspect (but my opinion only) is that viral replication creates a different and more diffuse release of cytokines that are not limited to a specific lobe.
2. I saw the same Youtube, but it just makes no sense. I am sure there is necrotic debris in the alveoli of ARDS, however, it is so deep in the lung circuity that if you stood on your head for a year it wouldn’t drain. Secondly, the ideas of proning has to do with physiological oxygenation called the West Zones (the sentinel work in respiratory physiology). Briefly, West Zone I is dead space, It is where there is ventilation but not a lot of blood flow. In the supine human standing up, the gravitation effect on liquid (blood) creates a gradient that the apices of the long have less blood flow than the bases. So — dead space mismatch. West Zone 2 is optimal, it is where ventilation and perfusion are matched. It is the site of most efficient oxygen an CO2 exchange. West Zone 3 are where hydrostatic pressures (liquid weighs more than gas) exec alveolar ventilation. So there is Shunt (blood flowing past collapsed gas spaces). So, proning someone tends to create more West Zone 2 because there is less hydrostatic forces across the entire lung (biophysics suggest that in the spin position there is more dorsal lung surface area than ventral). So, putting the thorax below neutral axis would actually expand west zone 3 and increase shunt physiology — it just doesn’t make sense from a bedside perspective
3. I think the myocardial injury is demand ischemia from tissue level hypoperfusion. There is always an increase in Troponin I when there is a patient with shock and ARDS. Positive pressure ventilation is inotropic in nature so without a long discussion of Starling curve, there is improved contractility, BUT it beat the hell out of preload, (impedance to venous inflow). Mechanical vent support is a beast to balance fluid resuscitation and pressure forces to maintain optimal cardiac output and reduce tissue level hypoperfusion....add to this the idea that we should run ARDS patients dry to facilitate oxygenation. Its like walking a tight rope across Niagara Falls in an ice storm
4. When I refer to restrictive transfusion practices, blood transfusion is an ORGAN transplant, and stimulates a SIRS response. All comers studied, including ARDS patients have better survivability at 30 days and one year. The studies are impressive enough that it is a standard of care. Truthfully the survive sepsis work tells the story best on this. We should really perhaps draw VBG and only transfuse when there is saturation <65% st the SVC or 60% at the PA if there is a swan Ganz catheter present.
At the end of the day —
1. I will not transfuse CoVID patients liberally because what I do know is that it will promote SIRS which is what we are trying to avoid
2. I will keep looking though the labs and literature to refine my knowledge of the ferritin and hub deficiencies, but I agree with MOM MD that if this were a primary Hgb problem, we would see a different clinical picture (and then hyperbaric may work).
3. Its the daily dilemma to treat critically ill patients because the above is balancing just one of the eight systems that we worry about...
Thanks for the reply. I don’t have medical knowledge so a bit of it was Greek, but I got most of it, ABG PaO@ being the biggest mystery (to me). Also, not sure what you meant by “routing issue.” (Hopefully, not meaning that the paperwork to obtain it is too challenging...*s*)
the 80 - 90 % die in hours is BS
Sorry PaO2 —
ABGs measure three variables:
1. pH of blood (metabolic state)
2. PaO2 arterial tension of oxygen — does the patient have good oxygen exchange
3. PaCO2 — partial pressure of carbon dioxide — which gives us an idea of how the patient is ventilating
The single greatest medical challenge for *any* physician, is not medical. It is
a) paperwork
b) billing / collections
;-)
interesting but imaging (CT and regular x-ray) tend to lag behind the clinical presentation so some nl studies in sick people is not surprising. In my experience most covid pts are pretty short of breath even if oxygen level is OK
we are using hydroxychloroquine and zmax sometimes vitamin c as well. Its not a magic bullet some get sicker and die on it. Its a reality of our supply issues that unless you are in ICU or headed there quickly you dont get it. We simply do not have the supply to give it to everyone
You are using Vitamin C? IV? How much? 3 Grams or so? I read about this the other day...there were some studies from DUKE about 4 years ago...I am just waiting for someone to try a real transplant to stop the inflammatory response.
FYI:
some are getting it Id have to look uo the dose. I think 1500 TID but not sure
Possible confounding variable.
The damage caused by this virus is *diffuse*. I don't think we have enough data, to have defined if there are any regular patterns in the damage, in a majority or even just a plurality, of the patients.
This leaves open the possibility, that there are compromised alveoli (see the WebMD link, which has language contradicting your assertion of inflammation being the sole cause of inhibited O2/CO2 exchange), throughout each of the West Zones. God only knows, what that would do, to either pressure gradients (no longer a monotonic function of distance along the lung), blood flow (necrotic debris probably doesn't have the same rate of flow through the capillaries as intact tissue), or the ratio of the two...
A second issue, in the YouTube you saw, is it necessarily true that all of the fluids being drained, are necrotic debris rather than surfactant-mixed-with-mucus (I read elsewhere, one of the first spots hit by this virus is the cilia in the bronchial tubes, so that mucus doesn't get swept out of the lungs, thereby somewhat mimicking Cystic Fibrosis)...So if you loosen *that*, it doesn't "run downhill" and further clog up the works, just when you have all the inflammation / necrosis / body-trying-to-clean-up going on. Or, as Calvin and Hobbes might put it:
Thank you, Doctor. I do understand the science. It is also ‘the science’ that the ionophore action of BCQ qyickly reduces the vural load when there is not a zinc insufficiency. Thank you for adding to the discussion of ‘the science’.
These are all great questions, but clinically its the risk benefit analysis. I would be hard pressed to give up west zone 2 for 3 in oder to drain.
But anyone who quote Calvin and Hobbes is Ok in my book, even if we disagree...
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