Heart Failure (Systolic and Diastolic)
≤40%
HFrEF
Systolic heart failure EF cutoff
≥50%
HFpEF
Diastolic heart failure EF cutoff
4
NYHA Classes
Functional classification I through IV
HFrEF vs HFpEF
two very different problems with the same symptomsHFrEF (EF ≤40%)
Systolic Dysfunction
- Weak contractility, dilated ventricle
- S3 gallop (volume overload sound)
- Responds to GDMT (ACEi/ARB/ARNI, BB, MRA, SGLT2i)
- Eccentric hypertrophy pattern
HFpEF (EF ≥50%)
Diastolic Dysfunction
- Stiff ventricle, impaired relaxation
- S4 gallop (stiff ventricle sound)
- Diuretics, BP control, treat comorbidities
- Concentric hypertrophy pattern
Guideline-Directed Medical Therapy
ACEi/ARB/ARNI Reduce afterload, prevent remodeling. ARNI (sacubitril/valsartan) superior to ACEi alone
Beta-Blockers Reduce HR, prevent remodeling. ONLY carvedilol or metoprolol succinate
MRA Block aldosterone, reduce fibrosis. Spironolactone or eplerenone, watch K+
SGLT2 Inhibitors Reduce preload, cardioprotective. Dapagliflozin, empagliflozin, benefit even without diabetes
Cold-wet profile (low CO, high PAOP) is the most dangerous and requires inotropes for contractility support plus diuretics for decongestion.
Key Values to Memorize
HFrEF EF ≤40%
HFpEF EF ≥50%
BNP >400 pg/mL (HF likely)
NYHA I = asymptomatic
NYHA IV = symptoms at rest
Target HR 60-70 on BB
you know the pathophysiology, now prove it under pressure
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Practice CCRN QuestionsExam Traps
ACEi contraindicated in bilateral renal artery stenosis
Both kidneys depend on angiotensin II to maintain GFR when renal arteries are stenosed. Blocking that with an ACEi can cause acute kidney injury. The exam will pair renal artery stenosis with an ACEi order and ask you to intervene.
Monitor K+ closely with ACEi plus MRA combination
Both ACE inhibitors and mineralocorticoid receptor antagonists (spironolactone, eplerenone) raise potassium. Together they create significant hyperkalemia risk. The exam expects you to identify this drug interaction.
Only carvedilol and metoprolol succinate are evidence-based for HF
Not all beta-blockers reduce mortality in heart failure. Atenolol, metoprolol tartrate, and propranolol do NOT have the evidence. The exam will offer a wrong beta-blocker as a distractor.
Cold-wet profile requires inotropes plus diuretics
A patient with low cardiac output AND volume overload (cold and wet) is in the most dangerous hemodynamic profile. They need contractility support AND decongestion simultaneously.
Beta-Blocker Specificity
Not all beta-blockers work for heart failure. Only carvedilol and metoprolol succinate have the evidence. The exam WILL test this.
Four Hemodynamic Profiles
Warm-wet = diuretics. Cold-wet = inotropes + diuretics. Cold-dry = careful fluids. Warm-dry = optimized, no acute intervention.
Imagine a water pump that has lost its strength. It can still fill up with water, but when it squeezes, it barely pushes anything out. The ejection fraction is low because the squeeze is weak. Treatment focuses on helping the pump squeeze better and reducing the workload.
Now imagine a pump that squeezes just fine, but its walls have become thick and stiff. It cannot relax enough to fill properly. The EF looks normal because it ejects a good percentage of what little gets in, but the total output is still reduced.
Think of two axes. Warm vs cold (is the pump pushing enough?). Wet vs dry (is fluid backing up?). Cold-wet is the worst because the pump is weak AND fluid is everywhere. Warm-dry is the goal.
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