Figure 1.

Dual hemodynamic pathways for acute cardiorenal syndrome. In this schematic, impaired forward flow and decreased effective circulating volume, as would be seen in severe systolic heart failure or cardiogenic shock, leads to arterial underfilling and activation of neurohormonal and inflammatory pathways. Autoregulation of GFR fails and kidney function declines, leading to worsening fluid retention, preload, and afterload. In a separate process, venous congestion and high right-sided pressure predominate, as would be seen in heart failure with preserved ejection fraction or isolated right heart failure. This also leads to decreased kidney function, worsening of fluid retention, and increased preload and afterload. These pathways are not mutually exclusive and often coexist in the same patient to varying degrees. AV, arteriovenous; IAP, intra-abdominal pressure; RAAS, renin-angiotensin-aldosterone system; RBF, renal blood flow; RPF, renal plasma flow; SNS, sympathetic nervous system.