Overview
This lecture covers pressure-volume (PV) loops of the left ventricle, how they relate to cardiac cycle phases, and how preload, afterload, and contractility affect cardiac output and stroke volume.
Pressure-Volume Loop Basics
- PV loops plot left ventricular pressure (y-axis) vs. volume (x-axis) through one cardiac cycle.
- The loop’s right side represents diastole (filling); the left side represents systole (contraction/ejection).
- Point A: End-systolic volume (ESV)—lowest ventricular volume, low pressure (2–3 mmHg).
- Between A and B: Ventricular filling (rapid inflow, diastasis, atrial systole).
- Point B: End-diastolic volume (EDV)—maximum ventricular volume before contraction (about 120 ml, 5–7 mmHg).
- Systole begins after B, with rising pressure and mitral valve closure (S1 heart sound).
- Isovolumetric contraction: Pressure rises, volume constant, until aortic valve opens (~80 mmHg).
- Between C and D: Ejection phase—volume decreases as blood leaves the ventricle.
- Point D: Aortic valve closure (S2 heart sound), followed by isovolumetric relaxation.
- ESV typically ~50 ml; stroke volume = EDV - ESV.
Determinants of Stroke Volume & Cardiac Output
- Stroke volume increases if ESV decreases or EDV increases.
- Cardiac output = Stroke volume × Heart rate.
- Larger stroke volume and higher heart rate both raise cardiac output.
Frank-Starling Mechanism and Myocardial Relationships
- Frank-Starling law: Increased EDV (preload) stretches cardiac muscle, boosting contraction force and output.
- Length-tension relationship: Cardiac muscle generates optimal force at intermediate sarcomere length, similar to skeletal muscle.
- Diastolic PV relationship: Compliant ventricle yields a flatter curve; systolic curve is steeper due to higher pressure for a given volume.
Force-Velocity Relationship
- At greater preload (higher EDV), the heart produces more tension and contracts faster at a given afterload.
- Increased preload = higher stroke volume and contractility.
Influences on Cardiac Performance
- Preload: Higher filling pressure or EDV increases stroke volume and cardiac output.
- Afterload: Higher afterload (e.g., high blood pressure) increases ESV, reduces stroke volume.
- Contractility: Increased contractility decreases ESV, increases stroke volume and output.
- Heart rate: Excessively high rates reduce ventricular filling time, lowering EDV and stroke volume.
Factors Affecting Heart Rate and Cardiac Output
- Intrinsic factors: SA/AV node properties, cardiac muscle stretch.
- Extrinsic factors: Autonomic nervous system, circulating hormones (e.g., catecholamines).
PV Loop Changes in Physiologic States
- Increased contractility shifts PV loop left (lower ESV), boosts stroke volume.
- Increased preload shifts loop right (higher EDV), also boosts stroke volume without changing contractility (ESPVR unchanged).
- Increased afterload lifts PV loop upwards (higher pressure), reduces stroke volume and increases ESV.
Key Terms & Definitions
- Pressure-volume (PV) loop — Graph showing LV pressure vs. volume during the cardiac cycle.
- End-diastolic volume (EDV) — Blood volume in LV at cycle’s end of filling (~120 ml).
- End-systolic volume (ESV) — Blood volume in LV after contraction (~50 ml).
- Stroke volume — The blood ejected per beat (EDV - ESV).
- Preload — Initial stretch of the ventricle (approximated by EDV).
- Afterload — Resistance/pressure heart works against to eject blood.
- Contractility — Inherent strength of cardiac contraction.
- ESPVR — End-systolic pressure-volume relationship; index of ventricular contractility.
- Frank-Starling mechanism — Principle that increased preload increases force of contraction.
Action Items / Next Steps
- Answer the PV loop scenario question and discuss it on the class discussion board.
- Review the mechanisms by which preload, afterload, and contractility affect PV loops and cardiac output.