Peter, I don't know if you saw my conversation with a patient about blood pressure, but the hospital which sent them back home with no warnings about BP falling under severe covid infection why they waited to see if they should come back to the hospital when "they could no longer breathe" despite the fact that the hospital knows they hav…
Peter, I don't know if you saw my conversation with a patient about blood pressure, but the hospital which sent them back home with no warnings about BP falling under severe covid infection why they waited to see if they should come back to the hospital when "they could no longer breathe" despite the fact that the hospital knows they have to use pressers for certain patients, more than others, depending on the BP meds they were taking.
For instance, calcium channel blockers (CCBs), not much need for Bp increasing drugs.
But Angiotensin-converting enzyme inhibitors (ACE) and particularly ACE II inhibitors are known to be affected by the SARS-CoV-19 virus and require frequent presser use.
From a recent article (7-13-2020):
Conclusions
"The RAS and ACE2/angiotensin-(1–7)/MAS axis play important roles in various physiological and pathophysiological contexts. Both SARS-CoV-2 and SARS-CoV use ACE2 as the receptor for entry into host cells. Because ACE2 is highly expressed in various organs and tissues, SARS-CoV-2 not only invades the lungs but also attacks other organs with high ACE2 expression. The pathogenesis of COVID-19 is highly complex, with multiple factors involved. In addition to the direct viral effects and inflammatory and immune factors, the downregulation of ACE2 and imbalance between the RAS and ACE2/angiotensin-(1–7)/MAS axis may also contribute to the multiple organ injuries in COVID-19. The spike glycoprotein of SARS-CoV-2 is a potential target for the development of specific drugs, antibodies, and vaccines. Restoring the balance between the RAS and ACE2/angiotensin-(1–7)/MAS may help attenuate organ injuries in COVID-19."
Peter, I don't know if you saw my conversation with a patient about blood pressure, but the hospital which sent them back home with no warnings about BP falling under severe covid infection why they waited to see if they should come back to the hospital when "they could no longer breathe" despite the fact that the hospital knows they have to use pressers for certain patients, more than others, depending on the BP meds they were taking.
For instance, calcium channel blockers (CCBs), not much need for Bp increasing drugs.
But Angiotensin-converting enzyme inhibitors (ACE) and particularly ACE II inhibitors are known to be affected by the SARS-CoV-19 virus and require frequent presser use.
From a recent article (7-13-2020):
Conclusions
"The RAS and ACE2/angiotensin-(1–7)/MAS axis play important roles in various physiological and pathophysiological contexts. Both SARS-CoV-2 and SARS-CoV use ACE2 as the receptor for entry into host cells. Because ACE2 is highly expressed in various organs and tissues, SARS-CoV-2 not only invades the lungs but also attacks other organs with high ACE2 expression. The pathogenesis of COVID-19 is highly complex, with multiple factors involved. In addition to the direct viral effects and inflammatory and immune factors, the downregulation of ACE2 and imbalance between the RAS and ACE2/angiotensin-(1–7)/MAS axis may also contribute to the multiple organ injuries in COVID-19. The spike glycoprotein of SARS-CoV-2 is a potential target for the development of specific drugs, antibodies, and vaccines. Restoring the balance between the RAS and ACE2/angiotensin-(1–7)/MAS may help attenuate organ injuries in COVID-19."
https://ccforum.biomedcentral.com/track/pdf/10.1186/s13054-020-03120-0.pdf