- Sep 2023
food intake and vasoconstriction
Is this why eating is causing instant sleepiness? Non-digestive vessels vasoconstrict and shut off too much cerebral blood flow, then nerves instantly have reduced firing/waste and CO2 build up/diminished mitochondria output/oxidative buildup/ &or then resultant inflammatory triggering cytokine increase?
Vessel endothelial enormous surface area, manipulator of blood flow vasoconstrictor system, and cytokine producer/influencer, and high vulnerability sensitivity to viral infection/corruption...and then it's role or adjacent system and the immediate available Google research on COVID affecting> the vascular elastin system and corrupted elevated production of destructive elastases resulting in reduced vascular compliance then resulting too narrow "pulse pressure" band essentially creating arteriosclerosis.
Also, make sure to be thinking of the entire vascular system not as one system, but subsided by dynamic changing gated sections and inspect signaling creating changing locations and amounts of high/low pressure zones. Also, keep in mind 3 things about BP: 1, when taken with a cuff it is only measuring a reading at the elbow. 2, is a reading from the artery and not giving any direct data from vein part of the system. 3, BP is not the same as blood flow. So I conceive that you could read a good BP, but actual flow could be completely inadequate.
Remember analogy, vascular system is just like car AC system, or any pressurized hydraulic system, or even actually electric circuits. Meaning that there is a high pressure side, the load component(s), and a low pressure side. Also remember veins act as the reservoir tank, and when they constrict it is injecting more blood into the system to, if functioning correctly, allow higher performance and meet increase load demand. It also, therefore has less direct effect on whole system BP vs artery constriction because it's downstream of the load. Arterial constriction conversely has immediate direct effect on systolic BP as it is essentially putting a wall directly downstream of the heart. Therefore, regardless if diastolic pressure is zero or high, when the heart contacts, the pressure shoots straight up.
A working theory component: my pulmonary vein is inappropriately constricting too much. That causes high back up pressure at alveoli. Exercise then induces veinous reservoir injection and increased blood volume into the "working system" further increasing pressure. Possibly arterious had already been fully dilated at rest in order to compensate and then when exercise happens, it can't be dilated further to increase blood flow throughout and BP increases further all behind the pulmonary vein "dam". However it doesn't present as right side heart failure like might initially be guessed (with leg and belly edema) because the right side heart is not failing...yet. So it contains any further backflow and the alveoli are the weakest point and taking the most abuse and pressure is relieved as pulmonary edema. And therefore what may be present is if we look for it, we'll find that actual blood throughput output exiting the heart is too low. And this can exist with a normal ejection fraction because the heart is functioning correctly and pumping the right percentage of what is a low starting volume. And also this can support why right ventricle is showing first signs of enlarging because it's being overpressured and stretching out (enlarging). And this can support why normal BP readings are measured at the arm because it can completely handle the abnormally low blood volume being received in the downstream location it's at. And then therefore this further supports why BP is normal but HR is riding the high limit at rest and then instantly jumps on exertion AND why dizziness happens because the artery system was already maxed out dilation at rest and for any amount of exertion, increasing HR because of the immediate too fast rise in tissue hypoxia due to too low blood supply the brain keeps driving up HR to meet demand. Total result upon exercise: supply continues to more and more not meet demand, HR rises faster and faster to try to inadequately compensate, physically become weaker especially after high output anaerobic every supply deleted in 1-3 minutes and there is no aerobic capacity cavalry with it's O2 rushing in to take over and that's when I fall off the cliff> HR spikes even faster, chest pain immediately jumps, lung edema turns on full tilt as the HR spikes and the resulting pressure is forced to "spray out of the gaskets (alveoli), and brain blood O2 supply immediately becomes super inadequate and the dizziness and need to fall over is the instant result effect. And since dysfuntioning cerebral vasoconstriction is likely the cause or highly involved in migraines, this also supports why the headaches come. ... And perhaps this explaining the rest pain and how it increases with dex and exertion because blood flow o2 becomes inadequate. Then causing lactic acid waste and CO2 buildup... (ie pain). And then it, like all body tissues being deprived necessary blood flow trigger cytokine inflammation response. ... And then, fuck it, maybe this IS chronic fatigue syndrome, and IS long covid explaining PEM, explaining why every symptom imaginable in any combination permutation is being shown, is explaining the observed elevated varing soups of cytokinesis, explaining all variety of tissue damage depending on any person's unique amount of total hit and their particular systems vulnerabilities and ultimately how far down they went on the increasing spiralling cascading systems failure towards total shutdown, and explains why measures at addressing the variety of manifestations are all somewhat helpful, but inadequate and varing efficacy from patient to patient because they are all too downstream of the root cause trunk of the symptom tree where the need to relieve vascular over constriction is the root or next to the root of the symptom tree that is common to all patients. If this were all to be accurate, then the seed would be what caused the break in vasoconstrictor system and repairing/killing it, or perhaps it's a PC bootstrap phenomenon where the simple uncomplex virus was just enough bios code to place innocuous wrenches in any of machines of the systems and then those malfunctioning systems took over control in their new malfunctioning patterns and became the new bosses that are infact the disease, you become your disease, and the initial virus seed has long been killed/departed (they're the ultimate down the road end game that is the totally corrupted bcdhhs that will then exist now as a new monstrous organism slowly lingering and depleting itself and eventually all resources at which point it will have finally killed itself after it destroyed the once thriving self sustaining world it lived in. COVID then is the teenage abusive bf or mean drunk father from their past, that put in motion what would become decades and generations of monsters, years and years after they had been long since gone). And maybe this explains the phasing leaving and returning it symptoms. Because when enough if the symptoms start to be reset/repaired, that starts spiraling the spread of the shutdown of the corruption back to health, but if the spiral up isn't strong enough to overcome the consequential reactive spiral down response, the monster returns and the rebellion is quashed. And so explains why the overall, in every system, stronger less vulnerabilities less armor chinks youth are able to quash with ease the spiral down with their incumbent exceptional spiral up response. .... And aside, this explains why dysautonomia has become a top suspect. And explains why POTS has become almost synonymous with long COVID and CFS.
- Jun 2023
D-dimer levels (a fibrin degradation product used to determine the activation of the coagulation cascade), are enhanced in acute COVID-19 cases (Zhou F. et al., 2020; Berger et al., 2020). Different reports have found a correlation between the increase of D-dimer levels and COVID-19 severity with an about 7-fold increase in critically ill patients, associated with an increased mortality risk (Zhou F. et al., 2020; Yao Y. et al., 2020)