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Review
. 2017 Aug 17;6(8):e006817.
doi: 10.1161/JAHA.117.006817.

Role of Volume Redistribution in the Congestion of Heart Failure

Marat Fudim  1 , Adrian F Hernandez  2   3 , G Michael Felker  2   3
Affiliations
Review

Role of Volume Redistribution in the Congestion of Heart Failure

Marat Fudim et al. J Am Heart Assoc. .
No abstract available

Keywords: heart failure; splanchnic compartment; stress and unstressed volume; vascular capacitance.

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Figures

Figure 1
Figure 1
A simplified understanding of heart failure pathophysiology that includes changes in filling pressures using hemodynamic monitoring devices, autonomic adaptation measuring heart rate variability, and alterations in intrathoracic fluid content using thoracic impedance. Reproduced with permission from Adamson.7
Figure 2
Figure 2
(Central Illustration): Illustrated is the 2‐compartment model of the human blood pool. The splanchnic compartment (left) serves as the venous reservoir/unstressed volume. To the right is the central compartment that contributes to the effective circulation/stressed volume and regulates volume content via the kidneys.
Figure 3
Figure 3
The proposed mechanism of progression from chronic compensated to acute heart failure is summarized in this figure. Sodium retention and fluid expansion result in an increase of unstressed volume and subsequent splanchnic congestion. This process is slow and takes days to weeks. The fast component often observed in the few days before decompensation is driven by autonomic imbalance with overactivity of the sympathetic nervous system. This results in an intercompartmental fluid shift into the central circulation with a subsequent accelerated increase in central filling pressures. Rapid fluid mobilization also occurs with activity and can explain exercise limitations experienced by heart failure patients. Adapted with permission from Fallick et al.17 Promotional and commercial use of the material in print, digital or mobile device format is prohibited without the permission from the publisher Wolters Kluwer.
Figure 4
Figure 4
This graphic illustrates the hypothesized variation in splanchnic vascular compliance between healthy and disease states. Heart failure is signified by a decrease in total vascular capacitance of the splanchnic compartment. The remaining storage capacity of the splanchnic compartment depends on the body's volume‐loading condition.
Figure 5
Figure 5
In heart failure, the splanchnic vascular compartment has a decreased vascular storage capacitance. Illustrated are different therapeutic approaches to increase the splanchnic vascular capacitance and allow blood redistribution into the splanchnic compartment. ACE indicates angiotensin‐converting enzyme.
See this image and copyright information in PMC

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