Volume and its relationship to cardiac output and venous return

Abstract

Volume infusions are one of the commonest clinical interventions in critically ill patients yet the relationship of volume to cardiac output is not well understood. Blood volume has a stressed and unstressed component but only the stressed component determines flow. It is usually about 30 % of total volume. Stressed volume is relatively constant under steady state conditions. It creates an elastic recoil pressure that is an important factor in the generation of blood flow. The heart creates circulatory flow by lowering the right atrial pressure and allowing the recoil pressure in veins and venules to drain blood back to the heart. The heart then puts the volume back into the systemic circulation so that stroke return equals stroke volume. The heart cannot pump out more volume than comes back. Changes in cardiac output without changes in stressed volume occur because of changes in arterial and venous resistances which redistribute blood volume and change pressure gradients throughout the vasculature. Stressed volume also can be increased by decreasing vascular capacitance, which means recruiting unstressed volume into stressed volume. This is the equivalent of an auto-transfusion. It is worth noting that during exercise in normal young males, cardiac output can increase five-fold with only small changes in stressed blood volume. The mechanical characteristics of the cardiac chambers and the circulation thus ultimately determine the relationship between volume and cardiac output and are the subject of this review.

Role of Volume Redistribution in the Congestion of Heart Failure

“…In a human case study, the stimulation of the nerves resulted in an increase in preload (50%) and cardiac output (200%) within 2 minutes . Exercise, orthostasis, and hemorrhage are 3 classic examples of an increased demand or a sudden reduction in effective circulatory volume/preload that require rapid recruitment of the unstressed volume via splanchnic bed vasoconstriction …”

“…26 Exercise, orthostasis, and hemorrhage are 3 classic examples of an increased demand or a sudden reduction in effective circulatory volume/preload that require rapid recruitment of the unstressed volume via splanchnic bed vasoconstriction. 12,27 Splanchnic Capacitance in HF In HF, a state of neurohormonal activation, the splanchnic vascular compartment is at the center of volume dysregulation in acute and chronic HF. Current strategies of ADHF management and prevention have focused on the classical paradigm that salt and fluid retention is the culprit of intravascular fluid expansion and cardiac decompensation.…”

Right atrial pressure and venous return during cardiopulmonary bypass

“…is directly measureable after pressure equilibration at zero flow and represents the stressed vascular volume at a given vascular compliance (32). According to Guyton, venous return (VR) is driven by the pressure difference between MSFP and right atrial (RA) pressure (RAP) (20).…”

“…According to Guyton, venous return (VR) is driven by the pressure difference between MSFP and right atrial (RA) pressure (RAP) (20). The heart decreases RAP and maintains the stressed volume in the systemic vessels by left ventricular stroke work (32). This model of circulation was originally formulated for steady states, but it has subsequently been used to interpret dynamic changes in VR and cardiac output (16,47).…”

Fluid therapy in the emergency department: an expert practice review

“…For example, in exercise cardiac output can increase fivefold with minimal change in preload 19. In Guytonian physiology, cardiac output is driven by local tissue requirements, for example, to supply oxygen to skeletal muscles in response to increased demand.…”