308Lu Acute Pulmonary Hypertension Right Ventricular Failure metastatic Prostate Carcinoma
Metastatic Prostate Cancer with Blastic and Lytic Bone Metastases and Acute Right Heart Failure
45-year-old male with metastatic prostate cancer and extensive osseous metastases complicated by pathologic fracture, presents with multiorgan failure, and acute pulmonary hypertension resulting in right ventricular (RV) failure and heart failure.
Acute Right Heart Failure
Echocardiogram Showed
Severely enlarged RV with apex-forming RV and flattening of the ventricular septum in both systole and diastole, consistent with RV pressure and volume overload.
Underfilled left ventricular (LV) cavity, suggestive of reverse Bernheim effect.
RV basal diameter measured at 5.5 cm.
RV function significantly reduced, with preserved function limited to the ape
What is the Reverse Bernheim Effect?
The reverse Bernheim effect occurs when right ventricular (RV) hypertrophy or dilation compresses the left ventricular (LV) cavity, leading to impaired LV filling and reduced LV output. This phenomenon arises due to the abnormal displacement of the interventricular septum into the LV cavity, which compromises LV diastolic filling.
Mechanism:
Right ventricular pressure and volume overload (as seen in pulmonary hypertension and severe RV failure) causes the RV to enlarge.
The interventricular septum bows towards the LV, reducing the LV end-diastolic volume.
This results in decreased LV preload and subsequently reduced cardiac output.
Clinical Context:
Often observed in conditions such as severe pulmonary hypertension, right heart failure, and chronic RV pressure overload.
It is called reverse because the classic Bernheim effect described LV hypertrophy compressing the RV, whereas this involves the opposite situation with RV enlargement compressing the LV.
Pulmonary Tumor Thrombotic Microangiopathy (PTTM) is a rare but severe complication where tumor microemboli (even if not visible on imaging) obstruct pulmonary arterioles.
Mechanism:
Tumor cell emboli trigger fibrocellular intimal proliferation, leading to narrowing and occlusion of small arterioles.
Release of growth factors (e.g., VEGF, PDGF) induces vascular remodeling and vasospasm.
Clinical Clues:
Acute or subacute onset of dyspnea and severe pulmonary hypertension.
Often occurs in adenocarcinomas, including prostate cancer.
No overt large pulmonary emboli on CT-PA.
Diagnosis:
Consider ventilation-perfusion (V/Q) scan or pulmonary angiography.
Confirmed histologically on wedge biopsy (if clinically stable).