Internal medicine Resident Beaumont, Texas, United States
Disclosure(s):
Belal Elsayed, MD: No financial relationships to disclose
Background: Right ventricular (RV) cardiogenic shock is associated with high mortality and complex physiology. In advanced RV failure, prior hemodynamic data or isolated biomarkers such as pulmonary capillary wedge pressure or lactate may not accurately reflect the current shock state, necessitating repeat assessment to guide escalation of care.
Methods: Single-patient case presentation incorporating echocardiography, repeat right heart catheterization, serial perfusion markers, and escalation to mechanical right ventricular support.
Outcome: A 41-year-old man with morbid obesity, atrial fibrillation, chronic kidney disease, and nonischemic cardiomyopathy presented with progressive dyspnea, severe volume overload, hypotension, and multiorgan dysfunction. Transthoracic echocardiography showed preserved left ventricular ejection fraction (50–55%) with severe right ventricular (RV) dilation, moderately reduced RV systolic function, and severe tricuspid regurgitation. A right heart catheterization two months earlier had suggested post-capillary pulmonary hypertension.
Despite vasopressors, inotropes, pulmonary vasodilator therapy, and continuous renal replacement therapy, the patient developed worsening cardiogenic shock with rising lactate levels. Repeat right heart catheterization demonstrated RV-predominant shock with severe right-sided congestion: right atrial pressure 42 mmHg; pulmonary artery pressure 76/52 mmHg (mean 60); cardiac index 1.58 L/min/m²; pulmonary vascular resistance 6.7 Wood units; transpulmonary gradient 29 mmHg; and diastolic pressure gradient 21 mmHg.
Serial venous oximetry–based assumed Fick calculations showed progressive low-flow physiology, with a nadir SvO₂ of 16.2% and estimated cardiac index of approximately 0.85 L/min/m². Subsequent improvement in SvO₂ to 65–68% with cardiac index 2.1–2.38 L/min/m² preceded lactate clearance. Given persistent RV shock physiology, mechanical RV support with an Impella RP device was initiated, resulting in improved cardiac output, reduced vasopressor requirements, and stabilization sufficient for transfer to a quaternary shock center.
Conclusion: In refractory RV cardiogenic shock, reliance on prior hemodynamic data or lactate trends alone may be misleading. Repeat invasive hemodynamic assessment and serial perfusion monitoring can identify ongoing low-flow physiology and guide timely escalation to mechanical RV support as a bridge to advanced shock care.
