Abstract A 46-year-old female with a history of hypertension, diabetes, and end stage renal disease (ESRD) on hemodialysis (HD) was admitted for left ankle fracture management. Twenty minutes into post-operative dialysis, she became acutely dyspneic, anxious, and hypotensive (97/34 mmHg) with progression to pulseless electrical activity (PEA) arrest and eventual return of spontaneous circulation. During her hospital course, the patient developed five additional PEA arrests mainly during dialysis sessions. Echocardiogram revealed a preserved left ventricular ejection fraction of 60% and a markedly elevated right ventricular systolic pressure (RVSP) of 86 mmHg. Left and right heart catheterization demonstrated patent epicardial coronary arteries (Figure 1), elevated right atrial pressure of 25 mmHg, pulmonary artery (PA) systolic and diastolic pressures of 71/37 mmHg, and mean PA pressure of 49 mmHg. Findings were consistent with severe PH. Pulmonary embolism was ruled out with a negative CT angiogram. At discharge, the patient was referred to a PH clinic with nitric oxide study. PH affects ∼10% of adults and carries high mortality. In patients with ESRD, PH is typically classified as Group 5 (multifactorial), with underlying etiology attributed to high-flow AV fistula physiology, endothelial dysfunction, impaired nitric oxide signaling, and fluid overload. In this case, acute triggers including HD-related rapid volume shifts likely caused abrupt reductions in cardiac preload and cardiac output, precipitating right ventricular (RV) strain and cardiac arrest.The coexistence of this patient’s ESRD and PH poses substantial challenges in optimizing hemodynamic stability. Conventionally, patients who fall under group 1-4 PH benefit from specific medical therapies. Guidelines for management of PH in patients with ESRD already on HD are limited to aggressive volume removal, AV access management, conversion to peritoneal dialysis, or transfer to a specialized PH clinic. The mainstay goal of volume management is to decrease the risk of intra- or interdialytic hypotension. Notably, volume removal of as little as 350 mL in this patient during dialysis triggered hemodynamic collapse, indicating extremely limited RV preload reserve. Even when dialysis was performed through a tunneled catheter, which typically avoids the high cardiac output associated with AV fistulas, the patient continued to experience episodes of cardiac arrest. Due to the complex interplay between ESRD and severe PH, management requires meticulous volume control, AV access modification, and referral to specialized PH programs for targeted therapy and risk mitigation. Further research is needed to define optimal treatment approaches and improve outcomes in ESRD-associated PH. This abstract is funded by: None
Rajali et al. (Fri,) studied this question.