Pathophysiology of Heart Failure and Drug Targets
Start with the big picture
A central concept in heart failure is the shift from short-term compensation to chronic harm. Neurohormonal activation can increase heart rate and vascular resistance, retain sodium and water, and promote hypertrophy and fibrosis. Hemodynamic changes also affect preload, afterload, and cardiac contractility. Pharmacologic strategies target these mechanisms: examples include β-blockers for sympathetic effects, ACE inhibitors or ARBs for the renin–angiotensin pathway, and mineralocorticoid receptor antagonists for aldosterone effects. Other targets introduced in the lesson include neprilysin, renal sodium transport, heart-rate regulation, vasopressin, and contractility. Together, these mechanisms provide a framework for understanding why heart failure treatment addresses more than cardiac output alone.
What you'll learn
- Explain how reduced cardiac output activates compensatory neurohormonal pathways.
- Describe how chronic SNS and RAAS activity contributes to heart failure progression.
- Relate preload, afterload, and contractility to relevant pharmacologic targets.
- Identify major drug classes that act on neurohormonal pathways and hemodynamics.
Continue your study
Work through the complete notes and reinforce the topic with the study tools available in the full lesson.
