This article explains the pathophysiology well: https://www.ncbi.nlm.nih.gov/books/NBK431048/.

The right ventricle is primarily supplied by the RCA which also supplies the SA node and AV node (90% of hearts because they are right dominant), leading to loss of contractility of the right side, and thus fluid buildup causing elevated central venous pressure. Elevated pressures in the liver and portal system would lead to hepatomegaly and free fluid accumulation in the peritoneum.

The other answers are wrong because: (if I am wrong please correct me)

A) This would be true in a patient with liver or nephrotic syndrome

C) This would be correct if the we increase capillary permeability (example sepsis)

D) This is left heart failure

E) This could be ARDS (not sure though)

F) Malignancy

The right ventricle (RV) receives its arterial blood supply primarily from the right coronary artery (RCA), which arises from the right coronary cusp of the aorta. The division produces the conus artery which supplies blood flow to the right ventricular outflow tract. The sinoatrial node (SA) is also supplied by the RCA from the second division. Coursing in the atrioventricular groove, the RCA then gives off multiple, small branches to supply the anterior RV before dividing terminally into the acute marginal branch (AM) that runs anteriorly along the diaphragm, and the posterior descending artery (PDA) that runs posteriorly. The PDA also supplies the atrioventricular node (AV) in 90% of patients, with a branch of the left circumflex artery providing flow in the remainder of patients. The PDA supplies the inferior wall of both ventricles, and is a terminal branch of the RCA in 85% of patients, but may arise from the left coronary circulation in 15% of the population.

The primary effects of RV ischemia and infarction result from decreased RV contractility. This leads to a reduction in blood flow from the venous system to the lungs, and finally to the left side of the heart. The clinical signs of this are increased right sided heart pressures, increased pulmonary artery (PA) systolic pressures, and decreased left ventricular preload. Symptoms may include peripheral edema especially distention of the jugular vein, hypoxemia, and hypotension.

Additionally, as the RV dilates the motion and function of the interventricular septum is altered. If the RV is dilated secondary to overload or if the septal myocardium is jeopardized by simultaneous left ventricle (LV) ischemia the symptoms of hypotension and cardiac failure may be pronounced. If the septum shifts leftward during diastole it impedes left ventricular filling and as a result cardiac output is decreased. This is termed loss of biventricular interdependence.

This website explains it too:

"A decrease in cardiac output either due to decreased heart rate or stroke volume (e.g., in ventricular failure) results in blood backing up into the venous circulation (increased venous volume) as less blood is pumped into the arterial circulation. The resultant increase in thoracic blood volume increases CVP."