Heart failure pathophysiology

HF Fundamentals - It's All Pumping

• Core Equation: $CO = HR \times SV$. Heart failure occurs when CO is inadequate for the body's metabolic demands.
• Stroke Volume (SV) Determinants:
  • Preload: Ventricular stretch at end-diastole. Initially compensatory (Frank-Starling mechanism), but excessive preload causes congestion.
  • Afterload: Resistance the ventricle pumps against (e.g., SVR). Chronically ↑ reduces SV.
  • Contractility: Inherent myocardial pump strength. Primarily impaired in HFrEF.

• Primary Types based on Ejection Fraction (EF):
  • HFrEF (Systolic): EF < 40%. Impaired contractility.
  • HFpEF (Diastolic): EF ≥ 50%. Impaired ventricular relaxation and filling.

⭐ Long-standing hypertension is the most common cause of HFpEF, leading to left ventricular hypertrophy and diastolic dysfunction.

Initial Insult - Body's First Responders

• Primary Trigger: An index event damages the heart muscle or disrupts its function (e.g., MI, uncontrolled HTN, valvular disease).
• Core Defect: ↓ Cardiac Output (CO) and ↓ mean arterial pressure (MAP).
• Immediate Compensation (Maladaptive Over Time): The body activates neurohormonal systems to restore perfusion.
  • Sympathetic Nervous System (SNS): Releases norepinephrine → ↑ Heart rate, ↑ contractility, and peripheral vasoconstriction.
  • RAAS Activation: ↓ Renal perfusion triggers renin release → Angiotensin II & Aldosterone production.
    • Angiotensin II: Potent vasoconstrictor; stimulates aldosterone release.
    • Aldosterone: Promotes renal Na⁺ and H₂O retention → ↑ intravascular volume.

⭐ The neurohormonal activation, while initially life-saving, drives the long-term progression of heart failure through cardiac remodeling, fibrosis, and myocyte death.

The Vicious Cycle - Remodeling Gone Wrong

• An initial cardiac insult (e.g., MI, HTN) leads to ↓ cardiac output, triggering compensatory neurohormonal systems.
• Key Systems Activated:
  • RAAS (Renin-Angiotensin-Aldosterone): Angiotensin II & aldosterone cause vasoconstriction and volume retention (↑ preload/afterload).
  • SNS (Sympathetic Nervous System): Norepinephrine increases heart rate, contractility, and vasoconstriction.
• This chronic activation, though initially helpful, becomes maladaptive, driving the disease forward.

⭐ The cornerstones of HFrEF therapy (ACEi/ARBs, β-blockers, MRAs) are effective precisely because they interrupt this neurohormonal vicious cycle, improving survival.

High‑Yield Points - ⚡ Biggest Takeaways

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