Manifestations of hypervolemia

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What are the manifestations of hypervolemia?

The ECF compartment is composed of the vascular compartment (one-fourth of ECF volume) and the interstitial compartment (three-fourths of ECF volume). Patients with hypervolemia have expansion of the interstitial compartment; they may or may not have expansion of the vascular compartment.

  • • Patients with primary kidney sodium retention may have elevated jugular venous pressure, pulmonary edema, and peripheral edema.
  • • Patients with CHF may also have elevated jugular venous pressure, pulmonary edema, and peripheral edema.
  • • Patients with cirrhosis may develop portal hypertension and splanchnic vasodilatation. Portal hypertension leads to an increase in hydraulic pressure in the hepatic sinusoids. Fluid in the sinusoids moves across the hepatic capsule into the peritoneum. Ascites formation and splanchnic vasodilatation lead to a state of low effective arterial volume, which in turn leads to avid reabsorption of ingested sodium and water. Kidney retention of sodium and water serves to increase effective arterial volume—but also augments ascites formation. Patients with cirrhosis may also have lower extremity edema. Jugular venous pressure, however, is usually not elevated, and patients with cirrhosis do not develop pulmonary edema.
  • • Patients with the nephrotic syndrome typically have peripheral edema. If primary kidney sodium retention is predominant in an individual patient with the nephrotic syndrome, jugular venous pressure may be elevated. If vascular underfilling from movement of fluid from the intravascular to the interstitial compartment is predominant, the jugular venous pressure will not be elevated.

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