Heart Failure – Study Notes
Definition
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Systolic HF: heart unable to pump effectively → reduced ejection fraction.
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Diastolic HF: heart unable to fill properly → ejection fraction preserved.
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Both result in reduced cardiac output.
Pathophysiology
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↓ Cardiac output → compensatory activation of:
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RAAS → vasoconstriction, ↑ BP, ↑ HR, ventricular remodeling.
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Sympathetic system → worsens cardiac workload.
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Aldosterone → ventricular scarring, vascular injury.
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Natriuretic peptides (protective) → vasodilation, natriuresis, ↓ remodeling.
Drug Therapy (Targets: inhibit RAAS/sympathetic, enhance natriuretic system, ↑ contractility, ↓ fluid retention)
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ACE Inhibitors
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Block angiotensin I → II.
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Effects: ↓ RAAS activation.
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SE: dry cough, headache, hypotension, rare angioedema.
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ARBs
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Block angiotensin II receptor.
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Similar to ACEi, but no cough.
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Less effective; used if ACEi not tolerated.
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Beta-blockers
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Block β1-receptors → ↓ HR, ↓ sympathetic effects.
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SE: hypotension, bradycardia, AV block (rare).
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Vasodilators
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↓ BP; alternative for ACEi/ARB intolerance.
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SE: nausea, palpitations, rash, joint pain.
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Diuretics
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Relieve fluid retention.
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Loop diuretics = most potent.
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Thiazides = mild effect + vasodilation (good for HTN + mild fluid retention).
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SE: electrolyte imbalance, hypovolemia, metabolic alkalosis.
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Aldosterone Antagonists
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Block aldosterone → K⁺-sparing diuretic + protective cardiac effect.
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SE: hyperkalemia, renal impairment.
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Digoxin
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↑ Contractility via Na⁺/K⁺ pump inhibition → ↑ intracellular Ca²⁺.
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↓ Sympathetic activity → slows HR.
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Used if no response to first-line drugs.
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SE: numerous, potentially toxic.
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Ivabradine
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Blocks “funny” channel (SA node) → ↓ HR.
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SE: bradycardia, AFib, visual disturbances.
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Avoid in: low HR, low BP, certain heart conditions.
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ARNIs (Angiotensin receptor–neprilysin inhibitor)
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Combo: neprilysin inhibitor + ARB.
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Mechanism: ↑ natriuretic peptides, prevents RAAS activation.
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SE: hypotension, hyperkalemia, renal failure.
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Used when ACEi + beta-blockers inadequate.
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