Energy, flow and pressure in the cardiovascular system: a narrative review of how the circulation works.

introductionUnderstanding what determines blood flow in the circulation is central to haemodynamic management in anaesthesia and critical care. Traditional teaching emphasises pressure-based concepts, such as preload; afterload; central venous pressure; and venous return curves. However, these frameworks generate confusion about causality and control. Interpreting pressure variables as drivers of flow has contributed to inconsistent physiological reasoning and potentially harmful treatment. This narrative review re-examines how blood flow is generated and regulated, integrating classical physiology with contemporary mechanisms and provides a coherent clinical framework.

methodsWe performed a search of MEDLINE and Embase with key terms, supplemented by citation tracking. We also included seminal physiological studies.

resultsThe reviewed literature showed that blood flow is constrained by energy supply from the heart and pressure established by vascular volume, elastance and the impedance of the inflow pathway to the heart. Mean systemic pressure reflects potential energy stored within the compliant venous system but does not drive flow. Right atrial pressure and preload are dependent variables that report the equilibrium between venous return and cardiac function, but do not control flow. Starling's mechanism provides passive mechanical matching of inflow to outflow but does not regulate cardiac output actively. Resistance-based interpretations alone fail to account for the influence of compliance, impedance and pulsatility. Misinterpretation of graphical and algebraic representations, particularly venous return curves, has obscured these relationships. DISCUSSION: We describe a unified physiological framework in which the heart supplies energy, vascular properties define what flow is possible, and pressures reflect system state rather than driving forces. This model reconciles historically opposing paradigms and clarifies the limits of pressure-targeted resuscitation. Clinically, it promotes assessing flow responsiveness and cardiac reserve over static pressure targets, and provides a mechanistic basis for contemporary shock management, thus avoiding interventions that increase congestion without improving perfusion.