For doctors or nurses reading — there’s a call to share this widely
An information event on this online SUNDAY April 12 8pm US Eastern time. (Open, free to anyone who wants to listen). That’s 10am Monday morning EST Australia.
This is not the flu. Most of the time apparently it’s not ARDS either. Coronavirus it turns out — is a vascular disease as much as lung disease. In fact in 70-80% of ICU patients putting them on a ventilator straight away may make the situation worse.
Currently patients in ICUs have about a 50:50 chance of making it out alive. The odds are terrible. Doctors have been reporting how people can degenerate suddenly into a life threatening crisis situation. Now, perhaps this explains it. This kind of hypothesis is one of the reasons we really want to crush the curve, now, because we are so underprepared and there is so much to learn. If this is right it will save many lives.
This could solve several mysteries at once
This virus causes heart damage, it raises clotting factors. People seem fine, then they relapse.
One recent paper found people with high levels of D-dimer, a clotting factor, are the most likely to die. In another mystery, some autopsies show heart damage and inflammation occurred, yet there was no virus present in the heart tissue. It also explains why people with heart disease and high blood pressure could be the most at risk group.
There are two different lung conditions in Covid patients; one is not ARDS
The news from ICU specialists is that Coronavirus patients are presenting with two very different lung conditions. The most common one is the L type (unknown til now) and these people still have an elastic working lung, but they are desperately in need of oxygen. The second type is the H type, which L types may degenerate to, which is worse, a heavy lung, filled with fluid, and is the ARDS-type crisis.
This virus appears to trigger a normal healthy vascular reflex in a diabolical way
In a normal infection if the small parts of the lung called the alveoli are filling up with fluid or pus, the blood circulation around it will squeeze or vasoconstrict. This forces the blood to flow to the other parts of the lung instead, where there isn’t so much damage, and blood can still pick up oxygen. That’s a good way for our vascular system to compensate and route blood around the damaged part of the lung.
The coronavirus is causing something similar to high altitude sickness
This reflexive vasoconstriction gets us into trouble at high altitudes where oxygen levels are low. Because the levels are ubiquitously low throughout the lung, the whole blood supply throughout the lung tries to constrict at once, which is a major problem. The back pressure in the pulmonary artery builds up right back to the heart. The pressure becomes so high it causes fluid to leak, and the thinnest, most delicate membranes are in the lungs. If these collapse, the fluid suddenly fills some alveoli and it’s a crisis. This condition is known as high altitude pulmonary edema (HAPE). In mountain climbers, it’s treatable, we just get the oxygen up (or the person down to where the oxygen is). That isn’t enough with Covid patients.
Something like this HAPE high altitude event seems to be occurring in Coronavirus patients due to the virus. Covid-19 binds to an enzyme involved in controlling the vasoconstriction. It targets and sticks to the ACE2 enzyme, stopping it working. Normally ACE1 raises angiotensin II and ACE2 lowers it. Angiotensin II raises blood pressure (ACE Inhibitors, the very common drugs against hypertension, act against ACE1 to lower blood pressure). So if the virus multiplies to the point it takes out all the ACE2, then there is nothing stopping Angiotensin from creating a vasoconstriction crisis (or a type of cytokine storm).
As the blood pressure builds it will force the fluids into the alveoli, flooding the lungs, dropping the oxygen levels in a vicious cycle. The high pressure may also increase blood clotting which could block flow, clogging up the blood vessels further. But the clotting problem may be due to antibodies against the virus. At this point, the patient (I gather) probably does need a ventilator but the odds are awful and it’s remarkable that doctors can keep many people alive with this kind of damage rapidly spreading through the lungs and back to the heart.
Assuming this pans out, it will make treatment so much better and also help us figure out who is at risk of ending up in ICU. Is it genetic changes to the ACE2 enzyme which allow the virus to bind better? Is it people who produce more ACE2 (or less)? It opens lots of questions about ACE inhibitor drugs.
ABBREVIATIONS
HPV: Hypoxic Pulmonary Vasoconstriction
HAPE: High Altitude Pulmonary Edema
Type L patients: They have good lung elasticity – i.e. A low ventilation to perfusion ratio. Most patients start this way but some in ICU may progress to Type H where fluid may fill the lungs and make them heavy.
REFERENCES and RESOURCES
Free Online Event Dr. Seheult is speaking at on Sunday, April 12: https://awr.org/health
Gattione (2020) Covid-19 Pnumonia different respiratory treatment for different phenotypes?
Marik, Paul (2020) COVID-19 MANAGEMENT PROTOCOL, EVMS Critical Care Management Protocol
Marik, Paul (2020) Covid Protocol
Worldometer – https://www.worldometers.info/coronavirus