3.2 / 3.3 HFrEF pharm and inotropes Flashcards
What the first line medications for HFrEF?
- How to ACE-I’s benefit patients with HFrEF?
- Are ACE-I’s and ARBs equally effective?
- ACE-I’s affects:
- After-load reduction
- decreases amount of retained fluid volumed
- reverses cardiac remodeling
- ACE-I’s have an advantage over ARBs due to their preservation of bradykinin, which helps reduce or reverse remodeling.
What is prolematic about the inhibition of neprilysin?
What class of anti-hypertensives is a neprilysin inhibitor paired with and why?
Neprilysin breaks down ANP and BNP, so inhibiting it preserves these and helps reduce cardiac load. However, neprolysin plays a larger role than just metabolizing ANP/BNP. It also metabolizes angiotensin-II and bradykinin
Neprilysin inhibition should be paired with an ARB to suppress angiotensin-II. It should not be paired with an ACE-I, because the double-blocking of bradykinin breakdown creates a high risk of angioedema.
What are the outcomes of activating the natriuretic peptide (NP) system?
What is its relationship to RAAS?
What is the concern about giving a beta blocker for heart failure?
What three beta blockers are approved for HFrEF
The part that is dicey is that we don’t want to decrease the beta receptor activity in the heart, since it may be important for raising cardiac output in heart failure. However, the emperical evidence is that beta blockers improve motality and hospitalization in patients with heart failure.
Bisoprolol, carvedilol, and extended release metoprolol are the only ones approved for HFrEF.
What medication do you give to slow a patient’s heart rate (chronotropy) with no effect on inotropy (contractility) or other cardiac systems?
How does it work?
What is a major risk?
What are digoxin and digitoxin?
What is their purpose?
What are the major safety concerns?
Digoxin and digitoxin are cardiac glycosides. They directly increase myocardial contractility.
They have a narrow therapeutic range.
What is the four step process of normal myocardial contraction?
How does digoxin impact the normal myocardial contraction process?
What are the key electrolytes?
What is the outcome?
Where are Na+ and Ca+ increased or decreased with digoxin?
What are the risks here?
(ORANGE) digoxin can increase risk for dysrhythmias
- How is digoxin used to reduce ventricular rate?
- What is the more significant use for digoxin in HF? What is the target dose for this?
- What type of heart failure is this used for (and which is it not used for)?
- The increased membrane potential (retention of Ca2+ inside the cardiomyocyte) caused by digoxin is also useful for slowing AV node conduction, useful in decreasing ventricular rate in AFib.
- But the REAL MAJOR use of digoxin in HF is Inhibiting SNS activation. This occurs at a LOW dose: (ORANGE) goal 0.5-0.8 ng/mL
- (ORANGE) digoxin is not indicated in diastolic or Right HF (unless using for rate control, but ignore for this class)
What are the red flag concerns about digoxin?
What symptoms indicate a problem?
What electrolyte imbalance makes digoxin dangerous and why?
What drugs can create this situation?
What drugs can increase digoxin concentration?
- Adjust dosing in renal failure
Define lusitropy. What cardiac drug is unique for enhancing it?
What is the mechanism of milrinone?
What are the effects of milrinone?
What are its advantages as a medication?
What are risks?
NOTE: Phosphodiesterase III inhibition, by inhibiting the process for pumping Ca2+, increases reuptake of Ca2++ in the sarcoplasmic reticulum (Ca2+ storage area) in addition to inside the cardiomyocytes. This is what actually causes the lusotropy.
NOTE: Because of lusotropy relaxation, this is one of the few drugs for using in diastolic or R side HF.
NOTE: Concerncs/risks include decreased platelets, demands on renal clearance, and short half-life
What are the three classes of ionotropes?
