Preload-dependent Left Ventricular Collapse During Hemodialysis in a Patient With Cardiorenal Syndrome and Diastolic Dysfunction

Abstract Introduction: Diastolic dysfunction and ventricular interdependence play a significant role in hemodynamic stability, especially in patients with complex cardiovascular and renal comorbidities. We present a compelling case of a 62-year-old male with end-stage renal disease (ESRD) and significant cardiac comorbidities, highlighting the critical interaction between the cardiac preload, ventricular interdependence, and cardiorenal syndrome (CRS), ultimately culminating in the diastolic collapse of the left ventricle (LV) in the setting of preload depletion during hemodialysis. Case Presentation: A 62-year-old male with a past medical history of ESRD on hemodialysis, obesity, dilated cardiomyopathy (EF 30%), chronic atrial fibrillation, and hypertension, presented with altered mental status post-hemodialysis. Despite medical management, he experienced two separate episodes of cardiopulmonary arrest during dialysis. During the third attempt at dialysis, real-time point-of-care ultrasound (POCUS) identified acute LV collapse with hypotension, reversible with volume re-transfusion. Further hemodynamic support with dobutamine allowed the patient to complete dialysis. Ultimately, the patient's surrogate opted to withdraw care in alignment with his preferences, and he passed following palliative extubation. Discussion: Diastolic dysfunction involves abnormal relaxation or filling of the left ventricle (LV), increasing cardiovascular mortality risk. Historically, the focus has been on LV function, but recent studies highlight the importance of the right ventricle (RV) and ventricular interdependence in maintaining hemodynamics. The Frank-Starling mechanism explains how venous return influences cardiac output: increased preload raises end-diastolic pressure, enhancing stroke volume. However, this curve flattens in heart failure, indicating minimal output increase despite higher filling pressures, as seen in this case of preload-dependent LV collapse. This patient's chronic heart failure with reduced ejection fraction (30%) illustrates the impact of decreasing preload from hemodialysis on already compromised cardiac output, leading to cardiopulmonary arrest. The concept of diastolic interdependence—how volume changes in one ventricle affect the other—is crucial, especially in cardiorenal syndrome (CRS), where heart and kidney dysfunction are interlinked. Evidence suggests that diastolic dysfunction itself may exacerbate renal decline. In this case, dialysis-induced preload depletion and chronic CRS compounded the patient's condition, culminating in a fatal outcome despite advanced hemodynamic monitoring and support. This highlights the need for refined management approaches in preload-sensitive patients with complex cardiac and renal comorbidities. Conclusion: Preload optimization and careful management of hemodynamics during dialysis are paramount in patients with diastolic dysfunction and cardiorenal interactions. Understanding the role of ventricular interdependence may better inform clinical strategies to prevent preload-induced cardiac decompensation.