Heart Failure Flashcards
E/A 1.0 - 1.5
Normal diastolic fx
E/A <1
Grade I diastolic dysfunction
E/A 0.8-1.5
Grade II diastolic dysfunction (Pseudonormal)
E/A >2
Grade III (Reversible restricted)
Grade IV (Fixed restricted)
Drug therapy that precipitate/exacerbate HF
1) Negative inotropes (diltiazem/verapamil)
2) Corticosteroids
3) NSAIDs
4) Thiazolidinediones (T2DM)
5) Chemotherapy agents
> Anthracyclines
> Trastuzumab
Changes to cardiac myocytes during heart failure
- Decreased sarcoplasmic reticulum Ca2+ ATPase activity
- Decreased alpha myosin, increased beta myosin production
HFrEF pharmacological therapy
- ACEi/ARB or ARNI
- Beta blocker
- Mineralocorticoid receptor antagonist (spironolactone or eplerenone)
- SGLT2 inhibitor
Other:
- Ivabradine
- Vericiguat
- Iron infusion (can improve symptoms, not mortality benefit)
Ivabradine indications
LVEF <40%
Sinus rhythm
HR >70bpm despite maximal beta-blocker therapy
Where is BNP produced?
Heart ventricles (majority)
+ brain
Pro-BNP released into bloodstream, cleaved by protein –> NT-proBNP and BNP
What can increase BNP?
Age
Female
ARNIs (measure NT-proBNP)
CAD
Valvular disease
Pulmonary HTN
CKD
Sepsis
Mortality benefit pharmacotherapy in HFpEF
SGLT2 inhibitors
How does GTN improve APO?
Decreases preload