Right Ventricular Volume Overload Mimicking Pulmonary Embolism: A Case of Intraoperative Fluid Absorption-Induced Ventricular Interdependence

Introduction

The left and right ventricle have profound mechanical interdependence due to their anatomical confinement within a shared pericardial sac, structural continuity through the interventricular septum, and synchronization via mutually encircling myocardial fibers. This functional synergy persists across both physiological conditions and pathological states [1]. Characterized by its thin-walled crescent morphology and peristaltic-like contraction pattern, the right ventricle (RV) has remarkable compliance to acute volume loading while maintaining inherent vulnerability to pressure overload [2]. Acute systemic volume overload precipitates RV chamber dilation, inducing leftward septal displacement that distorts left ventricle (LV) geometry through diastolic constraint. This mechanical interplay reduces LV end-diastolic volume through altered pressure-volume relationships and compromises systolic performance, ultimately increasing LV filling pressures [3]. The resultant pulmonary venous congestion establishes post-capillary pulmonary hypertension, thereby imposing secondary pressure overload on the already compromised RV – a self-perpetuating cycle of biventricular dysfunction [4]. Echocardiographic hallmarks include right ventricular dilation, free wall hypokinesis, tricuspid regurgitation, and abnormal pulmonary artery flow patterns – findings that mimic pulmonary embolism through shared mechanisms of pressure-volume mismatch and ventricular interdependence [5].

Case Report

A 75-year-old woman presented with a 4-day history of intermittent fever (peak axillary temperature 39.2°C) and progressive left periumbilical pain radiating to the ipsilateral lumbar region, accompanied by chills, increased urinary frequency (8–10 episodes daily), urgency, and concentrated urine without hematuria. She denied respiratory, gastrointestinal, or constitutional symptoms and reported partial relief with self-administered ibuprofen (200 mg as needed). Her medical history included poorly controlled stage III hypertension (diagnosed in 2004; blood pressure 140–160/60–90 mmHg on nifedipine sustained-release 10 mg twice daily), type 2 diabetes mellitus (HbA1c 7.1% one month prior to admission; managed with subcutaneous insulin glargine 16 IU daily), and asymptomatic left renal pelvic lithiasis (diagnosed in 2021, conservatively monitored without obstructive complications). She had no history of cardiovascular disease or other systemic comorbidities, and her antihypertensive and antidiabetic regimens had remained stable for over 6 months preceding admission.

On admission, physical examination revealed a temperature of 37.6°C, pulse rate of 98 beats/min, respiratory rate of 20 breaths/min, blood pressure of 140/79 mmHg, and oxygen saturation of 94% on room air. Abdominal examination revealed localized deep palpation tenderness in the left paraumbilical region extending to the ipsilateral costovertebral angle, devoid of peritoneal signs. Multisystem evaluation was unremarkable. Computed tomography (CT) of the urinary tract demonstrated left ureteropelvic junction stones, with the largest measuring 2.0×1.8 cm. An electrocardiogram showed sinus rhythm with complete right bundle branch block. Transthoracic echocardiography revealed mild mitral and tricuspid regurgitation, grade 1 diastolic dysfunction, and preserved left ventricular systolic function. Laboratory investigations showed elevated inflammatory markers (Table 1). She was diagnosed with acute pyelonephritis and obstructive ureteropelvic junction stones. Intravenous ceftazidime was administered based on antimicrobial susceptibility testing results.

On hospital day 10, the patient achieved clinical stability with resolution of fever, marked reduction in abdominal pain, and normalization of inflammatory markers (Table 1). Left ureteroscopic holmium laser lithotripsy with double-J stent placement was performed under total intravenous anesthesia (propofol, remifentanil, and dexmedetomidine), utilizing normal saline irrigation at 150 mL/min via an 80 cmH2O gravity-fed system. At 35 minutes into the procedure (50 minutes after anesthesia induction), she developed acute tachycardia (110 beats/min), tachypnea (35 breaths/min), hypoxia (SpO2 74%), and blood pressure of 112/70 mmHg. Physical examination revealed bilateral diffuse crackles, muffled heart sounds, and persistent sedation status. Fluid balance calculations demonstrated a positive fluid balance of 2430 mL (730 mL lactated Ringer’s solution administered; 1700 mL irrigation fluid absorbed). The procedure was immediately terminated with adjustments to invasive mechanical ventilation parameters for enhanced respiratory support, accompanied by intravenous administration of furosemide 40 mg and dexamethasone 10 mg. Bedside echocardiography revealed findings highly suggestive of pulmonary embolism: right ventricular dilation, reduced free wall motion with apical sparing (McConnell’s sign, Video 1), flattened interventricular septum, D-shaped left ventricle, severe tricuspid regurgitation, and elevated systolic pulmonary artery pressure (58 mmHg), along with characteristic findings including pulmonary ejection acceleration time <60 ms (60/60 sign) and fused elevated mitral E/A waves (Figure 1). Laboratory investigation demonstrated marked elevation of NT-proBNP (3892.0 pg/mL), metabolic acidosis (pH 7.32), hypoxemia (oxygenation index 132 mmHg), hyperlactatemia (2.6 mmol/L), and electrolyte imbalances (Na+ 132 mmol/L, K+ 3.2 mmol/L), while troponin and myocardial enzymes remained within normal ranges (Table 1). Subsequent pulmonary computed tomography angiography (CTPA) excluded thromboembolism, but chest CT confirmed bilateral pulmonary edema (Figure 2). The patient was diagnosed with acute cardiogenic pulmonary edema and type 1 respiratory failure secondary to irrigation fluid absorption syndrome. Following transfer to the ICU for diuresis and escalated respiratory support, successful extubation was achieved on hospital day 11, transitioning to non-invasive ventilation, NT-proBNP decreased to 2235 pg/mL. By day 14, follow-up echocardiography showed residual mild valvular regurgitation with grade 2 diastolic dysfunction (Figure 1), and the proximal diameter of the right ventricular outflow tract decreased from 34 mm to 23 mm. Repeat imaging demonstrated complete resolution of pulmonary edema (Figure 2), corroborated by normalized NT-proBNP levels (136 pg/mL).

Discussion

Establishing a diagnosis in acute hypoxemia can present clinical challenges, as diverse underlying pathologies contribute to a broad differential diagnosis. Essential components of the initial diagnostic workup are comprehensive history collection, physical assessment, laboratory blood tests, electrocardiography, and chest imaging [6]. Our patient developed severe acute hypoxemia during the procedure. Notably, the absence of ventilator high-pressure alarms and preserved bilateral breath sounds on auscultation further ruled out mechanical airway obstruction or significant atelectasis. The conflicting signs posed a diagnostic challenge: diffuse bilateral crackles favored acute heart failure (AHF) over PE, whereas the pronounced D-dimer elevation strongly indicated PE but is atypical for AHF. Two separate meta-analyses demonstrated that point-of-care ultrasound (POCUS) achieved high diagnostic accuracy for both acute heart failure (AHF, sensitivity 71–100%, specificity 72–95%) and PE (sensitivity 89–100%, specificity 95–100%) [6,7]. Despite robust supporting evidence, technical constraints limited POCUS to cardiac assessment, with pulmonary ultrasound omitted. For patients presenting with signs and symptoms of AHF and suspected PE, Arrigo et al advocate the use of clinical gestalt to estimate the pretest probability of PE. Patients deemed to have a high probability of PE (>35%) should undergo CTPA [8]. Although initial bedside echocardiography revealed findings suggestive of PE and D-dimer levels were elevated, CTPA definitively excluded this diagnosis. The temporal correlation between massive irrigation fluid absorption and acute cardiopulmonary decompensation, coupled with markedly elevated NT-proBNP and radiographic evidence of bilateral pulmonary edema, established the diagnosis of acute cardiogenic pulmonary edema. This pathophysiological mechanism was further supported by the rapid clinical improvement following aggressive diuresis and respiratory support, consistent with volume overload-induced cardiac dysfunction rather than primary respiratory pathology.

The initial suspicion for PE in our case arose from characteristic echocardiographic findings. A meta-analysis of 22 studies demonstrated high specificity of several echocardiographic markers in suspected acute PE: pulmonary artery thrombus (specificity 0.99; 95% CI 0.96–1.0), McConnell’s sign (0.97; 95% CI 0.95–0.99), paradoxical septal motion (0.95; 95% CI 0.93–0.97), reduced RV free wall motion (0.91; 95% CI 0.88–0.94), and RV diastolic dilation (0.80; 95% CI 0.61–0.92) [9]. Aligning with these findings, the ESC guidelines endorse the 60/60 sign and reduced tricuspid annular plane systolic excursion as diagnostic criteria for PE [5]. However, except for direct visualization of pulmonary thrombi, most echocardiographic markers reflect secondary RV pressure/volume overload rather than PE-specific pathology. Notably, cases of RV infarction [10] have been reported to mimic PE-related echocardiographic patterns, including McConnell’s sign and RV dysfunction. In our patient, the observed RV dilation, septal flattening, and elevated pulmonary artery pressure likely resulted from acute volume overload secondary to rapid systemic absorption of irrigation fluid. Ventricular interdependence – mediated by shared pericardial constraints and myocardial fiber continuity – explains the hemodynamic cascade: RV volume overload induces septal shift toward the LV, reducing LV end-diastolic volume and ejection fraction [3]. This condition elevates LV filling pressures, transmitted retrograde to the pulmonary circulation, culminating in increased pulmonary capillary wedge pressure and hydrostatic pulmonary edema. Concurrent hypoxia driven pulmonary vasoconstriction further exacerbated post-capillary pulmonary hypertension, creating a self-perpetuating cycle of RV dilation and dysfunction [11]. The risk factors for severe RV dysfunction in this patient remain unclear; however, potential contributors may include uncontrolled hypertension, diastolic dysfunction (albeit mild), undiagnosed underlying pulmonary hypertension, or preexisting right bundle branch block. Future studies should prioritize closer monitoring of right ventricular overload in patients receiving high intraoperative fluid volumes.

The routine use of irrigation fluid in endoscopic procedures, while essential for optimizing visual field and removing surgical debris, carries inherent risks of systemic fluid absorption – a complication that can manifest as dilutional hyponatremia, cerebral edema, or acute cardiopulmonary compromise depending on absorption rate, volume, and fluid composition [12]. A randomized controlled trial demonstrated that intraoperative monitoring of renal pelvic pressure during flexible ureteroscopy significantly reduces irrigation absorption, with operative duration and ureteral injury identified as additional critical determinants [13]. Building upon these findings and corroborated by our case, 3 evidence-based strategies emerge to mitigate fluid overload complications: (1) strict control of surgery duration combined with real-time renal pelvic pressure monitoring [13]; (2) preferential use of bipolar resection devices to minimize fluid extravasation [14]; and (3) preoperative gonadotropin-releasing hormone agonist or danazol administration [15].

Conclusions

Acute RV volume overload from intraoperative fluid absorption can precipitate biventricular dysfunction via ventricular interdependence, with echocardiographic features mimicking pulmonary embolism. Multimodal imaging is critical to exclude thromboembolism and confirm fluid overload etiology. Preventive strategies, including real-time fluid monitoring, are essential to mitigate such complications during endoscopic procedures.