Ascites can develop in a variety of disease states (eg, cirrhosis, peritoneal metastasis).  In this case, the presence of jugular venous distension and lower extremity edema shortly after pulmonary embolism (PE) are highly suggestive of right-sided heart failure (RHF) (ie, cor pulmonale) as the cause of this patient's ascites.

Patients with chronic respiratory disorders (eg, emphysema, obstructive sleep apnea) often have baseline pulmonary hypertension due to hypoxia-induced pulmonary vasoconstriction and associated vascular remodelling, which increases the pressure that the right ventricle (RV) must work against to maintain forward flow.  These patients are predisposed to RHF, which can develop subacutely from progressive pulmonary hypertension or acutely in the setting of a PE (due to abrupt obstruction of an already compromised pulmonary capillary bed).

Ascites due to RHF is associated with the following findings:

• Increased hydrostatic pressure: RV dysfunction results in the backup of blood within the venous circulation, leading to increased central venous pressure, which is transmitted to the portal capillaries (ie, hepatic sinusoids).


• Normal oncotic pressure: Although passive congestion from prolonged RHF eventually causes sinusoidal injury, leading to cirrhosis and hepatic synthetic dysfunction (ie hypoalbuminemia), this alteration occurs after a prolonged period (weeks).  Albumin has a half-life of approximately 21 days; therefore, early in the disease process, oncotic pressure remains normal (Choice B).


• Normal capillary permeability: Hepatic congestion is characterized by sinusoidal engorgement, but sinusoidal permeability, which is already high at baseline due to the discontinuous sinusoidal endothelium, remains essentially unchanged.

(Choices A, D, and F)  Portal capillary permeability may be increased in the setting of hepatic malignancies due to disruption of portal capillary integrity; however, it is unaffected by RHF.  Portal oncotic pressure remains normal early in the disease process.

(Choice C)  Both increased portal capillary oncotic pressure and decreased portal capillary hydrostatic pressure would help resolve ascites rather than contribute to its formation.

Educational objective:
Right-sided heart failure promotes the formation of ascites due to increased central venous pressure, which is transmitted to the hepatic sinusoids, leading to increased capillary hydrostatic pressure.  Capillary permeability is unaffected.  Although chronic passive congestion may eventually result in hepatic synthetic dysfunction (hypoalbuminemia) with low oncotic pressures, the oncotic pressure will remain normal for several weeks at least.