fluid volume. Clinically it is extremely important to get an accurate body weight of a client with fluid imbalance (Metheny, 2000).
Monitor lung sounds for crackles, monitor respirations for effort, and determine thepresence and severity of orthopnea.
Pulmonary edema results from excessive shifting of fluid from the vascular space into the pulmonary interstitial space and alveoli. Pulmonary edema can interfere with the oxygen-carbon dioxide exchange at the alveolar-capillary membrane (Metheny, 2000), resulting in dyspnea and orthopnea.
With head of bed elevated 30 to 45 degrees, monitor jugular veins for distention in theupright position; assess for positive hepatojugular reflex.
Increased intravascular volumeresults in jugular vein distention, even in a client in the upright position, and also a positivehepatojugular reflex.
Monitor central venous pressure, mean arterial pressure, pulmonary artery pressure,pulmonary capillary wedge pressure, and cardiac output; note and report trends indicatingincreasing pressures over time.
Increased vascular volume with decreased cardiac contractility increases intravascular pressures, which are reflected in hemodynamic parameters. Over time, this increased pressure can result in uncompensated heart failure.
Monitor vital signs; note decreasing blood pressure, tachycardia, and tachypnea.Monitor for gallop rhythms. If signs of heart failure are present, see nursing care plan for
Decreased Cardiac output
Heart failure results in decreased cardiac output and decreased blood pressure. Tissue hypoxia stimulates increased heart and respiratory rates.
Monitor serum osmolality, serum sodium, blood urea nitrogen (BUN)/creatinine ratio,and hematocrit for decreases.
These are all measures of concentration and will decrease(except in the presence of renal failure) with increased intravascular volume. In clients withrenal failure the BUN will increase because of decreased renal excretion.
Monitor intake and output; note trends reflecting decreasing urine output in relation tofluid intake.
Accurately measuring intake and output is very important for the client withfluid volume overload.
Monitor client's behavior for restlessness, anxiety, or confusion; use safety precautionsif symptoms are present.
When excess fluid volume compromises cardiac output, the client will experience tissue hypoxia. Cerebral tissue is extremely sensitive to hypoxia, and theclient may demonstrate restlessness and anxiety before any physiological alterations occur.When the excess fluid volume results in hyponatremia, the cerebral function will also bealtered because of cerebral edema (Fauci et al, 1998).
Monitor for the development of conditions that increase the client's risk for excess fluidvolume.
Common causes are heart failure, renal failure, and liver failure, all of which result in decreased glomerular filtration rate and fluid retention. Other causes are increased intakeof oral or IV fluids in excess of the client's cardiac and renal reserve levels, increased levelsof antidiuretic hormone, or movement of fluid from the interstitial space to the intravascular space (Fauci et al, 1998). Early detection allows the institution of specific treatment measures before the client develops pulmonary edema.
Provide a restricted-sodium diet as appropriate if ordered.
Restricting the sodium in thediet will favor the renal excretion of excess fluid. Take care to avoid hyponatremia.Decreasing sodium can be more important that restricting fluid intake (Fauci et al, 1998).
Monitor serum albumin level and provide protein intake as appropriate.
Serum albuminis the main contributor to serum oncotic pressure, which favors the movement of fluid fromthe interstitial space into the intravascular space. When serum albumin is low, peripheral edema may be severe.
Administer prescribed loop, thiazide, and/or potassium-sparing diuretics as appropriate;these may be given intravenously or orally.
Therapeutic responses to diuretic therapy include natriuresis, diuresis, elimination of edema, vasodilation, reduction of cardiac filling pressures, decreased renal vasculature resistance, and increased renal blood flow (Cody,Kubo, Pickworth, 1994; DePriest, 1997).
Monitor for side effects of diuretic therapy: orthostatic hypotension (especially if client