Preload and the Pressure–Volume Loop

Preload is a fundamental determinant of ventricular performance and an essential concept for interpreting the pressure–volume (PV) loop. Operationally, it is the end-diastolic volume (EDV)—a surrogate for end-diastolic fiber stretch—which, via the Frank–Starling mechanism, modulates stroke volume by altering the force of contraction [1].

Effect of Increased Preload

When preload rises, EDV increases and the PV loop shifts rightward; if contractility and afterload are unchanged, the loop widens (↑ stroke volume) consistent with Frank–Starling behavior [2, 3]. At the bedside, however, “preload” is often inferred from pressures (e.g., PCWP), which may poorly reflect volume under altered compliance—caution is warranted when using pressure surrogates to guide fluids [4]. Classic human data also show that Frank–Starling gains are finite: beyond a range, more filling yields little additional forward output and may raise filling pressures disproportionately [5].

Preload in Reduced Ventricular Compliance

With concentric hypertrophy, restrictive physiology, or ischemic remodeling, the EDPVR steepens: small increases in EDV produce large rises in LVEDP, blunting preload reserve and predisposing to pulmonary congestion (dyspnea, exercise intolerance) [6]. In such stiff ventricles, adding preload is typically maladaptive—filling pressures climb without meaningful augmentation of stroke volume [4, 6].

Clinical Perspective

• In healthy physiology, preload is a key reserve: during exercise or hypovolemia, increased venous return raises stroke volume efficiently.
• In diseased or noncompliant ventricles, preload responsiveness is blunted; volume loading drives congestion rather than output [6].
• Practical assessment should integrate volume-sensitive and load-adjusted metrics. ESPVR characterizes contractility independent of preload/afterload [7], and preload-recruitable stroke work (PRSW) provides a near-linear index of pump performance across changing fills [8].
• Clinically, interpret PCWP/RAP in context (compliance, RV function, intrathoracic pressure), and prioritize outcomes (stroke volume/VTI, perfusion) over pressure targets alone [4, 5].

Summary

Preload (EDV) sets the PV loop’s starting point and governs stroke volume through Frank–Starling physiology. In compliant ventricles, greater filling right-shifts and widens the loop with efficient output gains. In stiff ventricles, the steeper EDPVR converts small volume increments into large pressure rises—fueling congestion without benefit. Understanding where a patient lies on the EDPVR and complementing pressure surrogates with volume/flow and load-adjusted indices is essential for sound fluid and hemodynamic management [1–6, 8].

References

[1] Peverill R. Understanding preload and preload reserve within the concept of a limited range of possible left ventricular end-diastolic volumes. Advances in Physiology Education. 2020. doi:10.1152/advan.00043.2020.

[2] Burkhoff D. Pressure–volume loops in clinical research: a contemporary view. Journal of the American College of Cardiology. 2013. doi:10.1016/j.jacc.2013.05.049.

[3] Burkhoff D, Mirsky I, Suga H. Assessment of systolic and diastolic ventricular properties via pressure–volume analysis: a guide for clinical, translational, and basic researchers. Am J Physiol Heart Circ Physiol. 2005. doi:10.1152/AJPHEART.00138.2005.

[4] Van Aken H, Vandermeersch E. Reliability of PCWP as an index for left ventricular preload. British Journal of Anaesthesia. 1988. doi:10.1093/BJA/60.SUPPL_1.85S.

[5] Mangano D, Van Dyke DV, Ellis R. The Effect of Increasing Preload on Ventricular Output and Ejection in Man: Limitations of the Frank-Starling Mechanism. Circulation. 1980. doi:10.1161/01.CIR.62.3.535.

[6] Glantz S, Parmley W. Factors which affect the diastolic pressure–volume curve. Circulation Research. 1978. doi:10.1161/01.RES.42.2.171.

[7] Sagawa K. Editorial: The end-systolic pressure–volume relation of the ventricle—definition, modifications and clinical use. 1981.

[8] Glower D, Spratt JA, Snow ND, et al. Linearity of the Frank–Starling relationship in the intact heart: the concept of preload-recruitable stroke work. Circulation. 1985. doi:10.1161/01.CIR.71.5.994.