What is heart failure (definition)?
A progressive clinical syndrome where the heart cannot supply sufficient oxygen-rich blood due to structural/functional impairment of ventricular filling or ejection.
Most common cause of HF etiology?
Ischemic heart disease (chronic CAD, prior MI).
Key non-ischemic HF risk factors?
HTN, obesity, DM, dilated cardiomyopathy (familial/cardiotoxins/viral), thyroid disease, stress (Takotsubo), valvular disease.
Cardiac output (CO) formula?
CO = SV × HR.
Mean arterial pressure (MAP) relationship?
MAP = CO × SVR.
Define preload.
Volume in ventricle just prior to contraction (stretch).
Define afterload.
Resistance/tension LV must overcome to eject stroke volume.
Normal LVEF range?
~55–70%.
HFpEF EF cutoff?
> 50%.
HFmrEF EF range?
41–49%.
HFrEF EF cutoff?
≤40%.
Diastolic HF equals what EF category?
HFpEF.
Systolic HF equals what EF category?
HFrEF.
Common HF signs/symptoms?
Dyspnea, fatigue, fluid overload, peripheral edema, pulmonary congestion, orthopnea.
Physical exam HF findings (3 classic)?
Rales, S3 gallop, JVD (plus peripheral edema).
What neurohormones drive compensatory responses in HF?
Angiotensin II, norepinephrine, aldosterone, vasopressin (ADH).
Compensatory mechanism #1 in HF?
Tachycardia + increased contractility via norepinephrine.
Why can tachycardia worsen CO at high HR?
Very high HR reduces diastolic filling time → SV drops.
Chronic sympathetic activation leads to what receptor change?
Downregulation/decreased sensitivity of β1 receptors.
Compensatory mechanism #2 in HF?
Fluid retention + increased preload via RAAS activation (reduced renal perfusion).
Downside of excess preload on Frank-Starling curve?
After the flat portion, more preload causes congestion (pulmonary/systemic) without CO benefit.
Compensatory mechanism #3 in HF?
Vasoconstriction → increased SVR → increased afterload (mediated by NE and angiotensin II).
Why does increased afterload worsen HF?
Makes ejection harder → further reduces CO.
BNP: normal cutoff?
<100 pg/mL.