Evaluation of Intravascular Volume

Evaluation of Intravascular Volume

The presence of a volume deficit or over load is best determined by the history and physical examination, including intake & output information, review of medications, underlying medical & surgical conditions, change in weight, & the presence of sign & symptoms compatible with either hypovolemia or hypervolemia. The changes in volume should be assessed at the bed side with little reliance on the clinical laboratory findings.

Most importantly, this assessment must take place before the induction of anesthesia, because most of the available agents and techniques produce myocardial depression and/or vasodilatation. Undertaking such an anesthetic administration in a patient with significant ECF depletion may lead to intractable circulatory collapse.

Hypovolemia

Hypovolemia refers to any condition in which the extracellular fluid volume is reduced (low blood volume), and results in decreased tissue perfusion (supplying an organ or tissue with nutrients and oxygen). It can be produced by either salt or water loss (e.g. vomiting, diarrhea, use of diuretics, trauma and hemorrhage).

In general cardiovascular and central nervous system (CNS) sign predominate during the acute phase of ECF loss. Hypovolemia evokes reflex sympathetic stimulation, resulting in

• Sinus tachycardia: it usually requires a 15%- 30% loss of intravascular volume to elicit such response while the patient is in a supine position.
• A drop in arterial blood pressure usually a loss of intravascular volume of greater than 30% is necessary to elicit a decrease in arterial pressure. The sensitivity of heart rate & blood pressure can be enhanced by evaluating the patient for orthostatic hypotension (tilt test). With the upper body elevated at least 60 degrees, a persistent heart rate increase of > 10 beats per minute& blood pressure decrease of > 15% (compared with supine values) are indicative of moderately sever hypovolemia.
• Symptoms of impaired cerebral perfusion (i.e., sleepiness, apathy, dizziness, light headedness, syncope) may develop. The central nervous system sign may progress with severe ECF deficits, resulting in hyporeflexia, stupor, or coma.
• Dry mucous membranes are usually an early sign, with sunken eyes, longitudinal furrowing of the tongue, and collapsed veins occurring letter, with more deficits.
• Patients exhibit cool, dry, pale skin with diminished capillary refill.
• As the deficit enlarges, skin turgor becomes poor & tenting (lack of skin recoil after elevation) is evident.

Quantification of Fluid Deficit

Exact quantification of the ECF deficit is extremely difficult and probably unnecessary. The clinical finding with hypovolemia can be grouped as to provide as a rough estimate of the size of the deficit. The sign related to a specific degree of volume loss may vary from patient to patient. The categorizations in the following table are not absolute; however, they can be clinically useful when initiating therapy (Table 6.3).

Table 6.3 Categorizing Fluid Deficit

Management of Fluid Deficit and Anesthetic Consideration

Treat the underlining causes Poly ionic balanced salt solution (lactated Ringer's.) is preferable. Because pure ECF volume loss is isotonic loss the replacement fluid should always contain both water and salt. For each percentage of body wt lost as fluid approx. 10ml/kg of balanced salt solution will be needed for replenishment. Reliance on formula or single clinical sign to determine the adequacy of therapy is totally inappropriate. Instead, restoration of normal CNS function and stabilization of homodynamic parameters should be used as a therapeutic guideline. Fluid replacement should be adjusted according to the patient response.

Anesthetic considerations

• Deficit is likely to be accompanied by a decrease in blood pressure; peripheral vasodilatation produced by some anesthetic (thiopentone, halothane) agents can unmask hypovolemia.
• Positive pressure ventilation, blood losses produce exaggerated blood pressure decreases.
• Ketamine is less likely to decrease blood pressure.
• Decreased volume of distribution in hypovolemia produces increased sensitivity of anesthetic drugs and muscle relaxants.

Volume Excess

Hypervolemia is almost always an increase of extracellular volume with peripheral edema, ascites, or other fluid collection. Increased extracellular volume by itself is usually not an emergency, but it depends on how much and where the excess fluid accumulates. If associated with decreased effective intravascular volume (hypovolemia) or increased intravascular volume (e.g., congestive heart failure with pulmonary edema), rapid intervention may be required.

Causes are:

• Iatrogenic, as a result of excessive parenteral fluid administration.
• Specific varieties of cardiac, hepatic & renal dysfunction may either initiate or contribute to the fluid retention.
• Rapid post-op. mobilization of isotonic fluid from third space may result in expansion of the ECF volume despite the appropriate intraoperative fluid management.

Clinical Manifestation

• Edema (peripheral, pulmonary) is frequently noted during physical examination and represents a significant increase in the interstitial compartments of the ECF volume. Usually edema is located in dependent areas (lower extremities, presacral), but on occasions it can also be easily visualized in the scleral conjunctivae.
• Severely increased intravascular volume will be manifested by pulmonary edema, hypoxemia, and respiratory distress.
• Dyspnea, cyanosis, engorgement of neck veins & basal crepitation.
• Excessive lacrimation and salivation, elevated arterial blood pressure, widened pulse pressure, relative bradycardia, distended peripheral veins, and jugular vein distention is highly suggestive of hypervolemia.
• Hematocrit are decreased in water excess
• Hypoalbuminemia is seen in patients with nephrotic syndrome, protein-losing enteropathy, malnutrition, and liver disease. Nephrotic syndrome patients have moderate to severe proteinuria.

Management and Anesthetic Consideration

• Restriction of fluid & salt intake, because the functioning kidneys allow a normalization of ECF volume.
• Consider the likely presence of renal, cardiac or liver disease as an etiology.
• Consider poor inotropic response & increased sensitivity to non depolarizing muscle relaxant; due to low plasma sodium decrease excitability of cells
• Intraoperative management may require the omission of maintenance fluids and the replacement of only that fluid volume which is lost during surgery.
• Diuretic, during or after surgery, to initiate or enhance the desired diuresis.