Flashcards in Heart Failure Deck (17):
What class of drugs are 1st line treatment for patients with mild-mod-severe HF?
What is their general mechanism of action?
How do they affect HR and contractility?
Arteriovenous dilation --> decrease SVR + BP --> increase CO + exercise tolerance
*ACE-Is also induce diuresis/natriuresis
No effect on HR/contractility
What are 3 therapeutic advantages of ACE-inhibitors?
1. Inhibit LV remodeling post-MI
2. No neurohormonal activation or reflex tachycardia
3. No tolerance issues
What are two situations when Angiotensin Receptor Blockers can be used?
There were 6 examples of ARBs, and they all have the end in -sartan. Name them.
1) Use in place of ACE-Inh when cough is an issue
2) Can be used in tandem with ACE-Inh
What is the mechanism of action for ARBs?
How do ARBs affect the following?
--cardiac/vascular remodeling (promote or inhibit?)
--renal excretion of Na & H2O (promote or inhibit?)
Block AT1-Rs on vasc endo --> inhibit vasc sm mm contraction
--No effect on bradykinin (so no cough)
--Inhibit CV remodeling
--Promote renal excretion of Na + H2O
Characterize how the following are altered as side effects of ARBs.
What side effect is missing, compared to ACE-Is?
ARB Side Effects
There is no cough.
In the setting of HF, how do diuretics affect the following factors?
--volume & preload
Diuretics in HF:
--decreased volume & preload
--no direct effect on CO, but preload reduction can decrease CO
--improved arterial distensibility
--increased levels of noradrenaline, Ang2
In the setting of HF, what are two side effects and one contraindication to the use of diuretics?
1) volume contraction
2) electrolyte depletion
What are two aldosterone antagonists that are used in treatment of HF?
In what type of HF are they used?
What are their side effects as related to electrolyte levels, sex hormones, and GI?
Used in more serious types of HF (eg, Class3-4 symptoms), sometimes in combo with ACE-Is
--hyperkalemia, metabolic acidosis, gynecomastia, GI disturbances (eg peptic ulcer)
What are the 3 Beta Blockers that are used in HF to inhibit the adverse effects of the sympathetic nervous system?
Bisoprolol, Carvedilol, Metoprolol
What is the name of the cardiac glycoside used to treat HF?
Describe the mechanism of action related to:
1) increasing contractility
2) reducing AV node conduction velocity
Mechanism of Action
1) inhibit Na/K ATPase --> increase [Na]i --> alter activity of NCX --> increase [Ca]i --> increased contractility
2) increase vagal efferent activity to heart --> reduce AV node conduction velocity
How does Digoxin affect the following hemodynamic parameters?
CO, LVEF, exercise tolerance, natriuresis, and LVEDP?
--CO, LVEF, exercise tolerance, natriuresis
How does Digoxin affect the following neurohormonal parameters?
peripheral nervous system activity
--plasma NE levels
--peripheral NS activity
Normalizes arterial baroreceptors
What are some toxic effects associated with Digoxin?
Cardiac arrhythmias (atrial tachycardia, AV block)
How does Dobutamine increased contractility and HR?
In what situation is it used?
Dobutamine = B1-R agonist --> increase contractility & HR
Acutely decompensated HF
What are the side effects of Dobutamine...
at low doses?
at high doses?
Dobutamine Side Effects
@ low dose
--stimulate B2-Rs --> vasodilation
@ high dose
--stimulate alpha-Rs --> vasoconstriction
What is the name of the PDE3a inhbitor and how does it affect cAMP levels?
What two side effects make it not very practical?
Milrinone --> increase cAMP
(--> vasodilation, increased contractility, increased HR)