Clinical Assessment Of Volume Status

Volume Loss

Volume loss can often be suspected from the history. Poor oral intake or history of vomiting, diarrhea, poorly controlled diabetes, renal disease, or adrenal disease are suggestive. With moderate volume loss, there may be postural hypotension and possibly a resting tachycardia. There may be narrowing of the pulse pressure. Jugular venous pressure will be difficult to appreciate clinically (assuming no right heart disease). Patients with moderate to severe volume loss may be weak and often have altered sensorium. They may be hypotensive even when recumbent. Mucous membranes will be dry, tissue turgor decreased, and eyes sunken (usually a finding in the pediatric population, along with sunken fontanelles). Oliguria is frequently in accompaniment. Volume loss may be sufficient to induce shock.

Laboratory findings include hemoconcentration (interpretable only if baseline values are known) and, usually, increased creatinine and urea nitrogen levels. In an acute setting, the ratio of urea nitrogen to creatinine will be 20:1 or even greater. Serum [Na +], as explained, in and of itself, reveals nothing about volume status. If the volume loss is extrarenal, then urine [Na+] will be less than 10 meq/L.

Treatment depends on the underlying disorder, but the cornerstone is volume repletion. Treatment is detailed elsewhere in this chapter and, for shock states, in the relevant chapters in this volume.

Volume Overload

Volume overload is most often encountered in disease states where excretion of free water is impaired. Most of these conditions are related to renal disease, diseases that impair blood flow to the kidneys (resulting in Na + retention), diseases that diminish intravascular osmolality (liver failure and low-protein states), or diseases that cause undesirable Na+ retention by various mechanisms. Decreased intravascular osmolality results in a functional intravascular contraction, with expanded interstitial and cellular volume. These are discussed elsewhere in this chapter.

Volume overload clinically manifests as edema, whether peripheral or central (e.g., pulmonary). Early findings are weight gain, resting tachycardia, and peripheral edema. Jugular venous pressure is elevated. If severe, volume overload eventually results in severe right heart failure with resultant anasarca and ascites, and ultimately severe left heart failure, with pulmonary edema and pump failure manifesting as hypotension. Unfortunately, the contracted intervascular volume from hypotension causes the kidney to conserve Na+, exacerbating the problem.

Specific treatments are discussed in this chapter and elsewhere in this volume. ELECTROLYTES

Electrolyte abnormalities are often challenging to diagnose and treat. Overall, each disorder can be assessed with the same general approach. Increased concentration (hyper-) is a result of (1) excess total body amount, (2) shift among compartments, and (3) a relative fluid loss. Decreased concentrations (hypo-) are a result of (1) depleted total body amount, (2) shift among compartments, and (3) relative fluid gain.

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