What is the difference in SE btw an ACE-inhibitor and an ARB?
all the same except with ARBs, no cough and less angioedema
What are the ACE inhibitors' side effects?
1. cough (dry, nonproductive) 2. hyperkalemia 3. angioedema 4. renal problems 5. neutropenia 6. hypotension
ACE is an enzyme produced in the ____.
How is the RAAS stimulated?
1. hypovolemia 2. low NaCL
Hydralazine is a _____.
ACE inhibitors end in -_____.
Name the 2 vasodilators that are most commonly used.
1. hydralazine 2. isosorbide
What is stage B HFrEF?
heart structure problem w/o symptoms
ACE inhibitors block both ____ and ____.
angiotensin conversion to angiotensin-II AND bradykinin conversion to its inactive fragments
What does angiotensin II do?
1. vasoconstriction 2. increased sympathetic output 3. increased aldosterone production and Na+ reab 4. increased ADH release 5. increased thirst
The ARBs end in -_____.
What is stage C HFrEF?
structural disease w/ symptoms
ARBs mainly have an effect on the ____ receptor.
What is your target creatinine clearance level?
What does digoxin do?
increases CO and SV
Angiotensinogen is a zymogen produced in the ____.
High bradykinin causes?
a cough, remodeling of the LV, and vasodilates
If your pt is stage C HFrEF and is black, add ____ in addition to the beta blocker and ACEI/ARB.
hydralazine and isosorbide
Bradykininogen is a zymogen produced in the ____.
What is stage D HFrEF?
refractory - hospitalized pts
Why do African Americans need a vasodilator, too?
1. they get HFrEF at an earlier age 2. their HFrEF is more advanced 3. they have a higher rate of mortality and hospitalizations 4. they have more TGF-beta (increased fibrosis) 5. they have increased vasothelin 6. sometimes they're NO synthetase deficient 7. the RAAS is decreased