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Updated: Jan 12, 2026

Induction and Phenotyping of Acute Right Heart Failure in a Large Animal Model of Chronic Thromboembolic Pulmonary Hypertension
Published on: March 17, 2022
Right Ventricular Volume Overload Mimicking Pulmonary Embolism: A Case of Intraoperative Fluid Absorption-Induced
Chunliang Wang1, Yuzhu Fan2, Juan Wang1
1Department of Cardiology, Shijiazhuang Traditional Chinese Medicine Hospital, Shijiazhuang, Hebei, China.
Abstract:
BACKGROUND Ventricular interdependence - mediated by shared pericardial and septal mechanics - can precipitate biventricular dysfunction during acute right ventricular (RV) volume overload. RV dilation impairs left ventricular (LV) compliance through diastolic constraint, elevating pulmonary pressures and triggering a self-perpetuating cycle of cardiopulmonary compromise. This hemodynamic cascade generates echocardiographic signs indistinguishable from pulmonary embolism (PE). CASE REPORT A 75-year-old woman with hypertension and diabetes developed acute hypoxia, tachycardia (110/min), and tachypnea (35/min) during ureteroscopic lithotripsy, accompanied by a positive fluid balance of 2430 mL from irrigation absorption. Bedside echocardiography revealed RV dilation, McConnell's sign, D-shaped LV, severe tricuspid regurgitation, elevated systolic pulmonary artery pressure (58 mmHg), 60/60 sign, and fused mitral E/A waves - findings highly suggestive of PE. Laboratory tests showed metabolic acidosis (pH 7.32), hypoxemia (PaO₂/FiO₂ 132 mmHg), and markedly elevated NT-proBNP (3892 pg/mL). Pulmonary CT angiography excluded thromboembolism but confirmed bilateral pulmonary edema. The diagnosis of fluid absorption-induced cardiogenic pulmonary edema was established. Aggressive diuresis and respiratory support led to symptom resolution, with normalized RV/LV ratio (34 mm → 23 mm) and NT-proBNP (136 pg/mL) on follow-up. CONCLUSIONS Acute volume overload from intraoperative fluid absorption exacerbates RV failure through ventricular interdependence, producing PE-mimicking echocardiographic signs. This case demonstrates that RV dilation, septal flattening, and pulmonary hypertension - classically associated with PE - can originate from non-thromboembolic etiologies. Clinicians must utilize multimodal imaging (echocardiography + CTPA) to discriminate fluid overload syndrome from PE. Preventive strategies, including real-time intraoperative fluid balance monitoring and renal pelvic pressure control, are critical to mitigate hemodynamic decompensation during endoscopic procedures, thereby avoiding misdiagnosis and optimizing critical care outcomes.
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