How to assess volume status

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How to assess volume status?

Assessment of volume status can be challenging. The wise clinician gathers evidence from the history, physical examination, and laboratory investigations. Each type of evidence has its limitations, and, in many cases, the evidence is conflicting. The following can be helpful in the assessment of volume status:

• History. When assessing a patient with dyspnea, paroxysmal nocturnal dyspnea and orthopnea suggest that heart failure is the culprit.

• Blood pressure. Patients with severe volume contraction may, of course, be hypotensive. However, if there is severe vasoconstriction, blood pressure may be normal even in patients with shock.

• Postural vital signs. In patients with suspected blood loss, an increase in the pulse of at least 30 beats per minute or severe postural dizziness (preventing measurement of standing pulse and blood pressure) suggests a blood loss of at least 1 L.

• Venous pressure. The external jugular vein may be examined. The normal venous pressure is 1 to 8 cm H O. Examination of the external jugular vein can be helpful both in the assessment of volume status and in the assessment of the response to volume replacement or diuresis. Venous pressure may also be measured by insertion of a catheter into the right atrium.

• Peripheral edema. Pitting edema occurs when the interstitial fluid is diluted with fluid with a low concentration of protein. Pitting edema indicates that there is an excess of interstitial fluid but not necessarily an excess of intravascular fluid.

• Skin turgor. The loss of interstitial fluid that occurs with ECF volume contraction causes the skin to recoil more slowly after pinching. Because elasticity of skin decreases with age, however, reduced skin turgor may not be a reliable sign of volume contraction in elderly patients.

• Dry axillae suggest the presence of volume depletion in the elderly. Moist mucous membranes suggest that volume depletion is not present.

• BUN: creatinine ratio. Proximal tubular reabsorption of filtered urea is passively linked to reabsorption of sodium and water. In hypovolemia and in states of low effective arterial volume , proximal tubular reabsorption of sodium, water, and urea will be enhanced. This may cause the BUN:creatinine ratio to exceed 20:1.

• Urine sodium concentration. The urine sodium concentration is typically less than 25 mmol/L in hypovolemia and in states of low effective arterial volume .

• Hematocrit and plasma albumin concentration. Acute loss of fluid from the vascular space can cause hemoconcentration.

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