Cardiac Ventricles: Anatomy, Function, and Clinical Significance

The ventricles are the heart's primary pumping chambers, generating pressure to eject blood into pulmonary and systemic circulations.

Anatomy

Feature	Right Ventricle	Left Ventricle
Wall thickness	3-5 mm	10-15 mm (3× thicker)
Shape	Crescentic, wraps around LV	Conical, bullet-shaped
Pressure (systolic)	15-30 mmHg	100-140 mmHg
Inflow	RA → TV → RV	LA → MV → LV
Outflow	RV → PV → PA → lungs	LV → AV → aorta → body
Key structures	Tricuspid valve, pulmonary valve, moderator band, trabeculae	Mitral valve, aortic valve, papillary muscles, chordae

Physiology

• Systole: Isovolumetric contraction → ejection (rapid then reduced) → isovolumetric relaxation.
• Diastole: Isovolumetric relaxation → early rapid filling → diastasis → atrial kick (20-30% of filling).
• Frank-Starling: Preload ↑ → stroke volume ↑ (up to optimal sarcomere length).
• RV-LV interdependence: Shared septum; RV volume overload shifts septum → impairs LV filling.

Clinical Relevance

• RV failure: Cor pulmonale (PE, COPD, PH), RV MI, tricuspid regurgitation → JVD, hepatomegaly, edema, ascites.
• LV failure: Ischemic, hypertensive, valvular, cardiomyopathy → pulmonary edema, low output, cardiogenic shock.
• Imaging: Echo (chamber size, EF, wall motion), MRI (gold standard volumes/mass), cath (pressures).
• Biomarkers: BNP/NT-proBNP (wall stress), troponin (injury).

Key Concept

The LV's thick wall generates systemic pressure; the RV's thin wall is volume-adapted. Pressure overload (AS, HTN) → concentric hypertrophy. Volume overload (AR, MR, VSD) → eccentric hypertrophy. Both progress to failure if uncorrected.