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Compensatory Intravascular Volume Expansion

Intravascular volume usually must be supplemented to compensate for the venodilation and cardiac depression caused by anesthesia. Sustaining adequate oxygen delivery in relation to oxygen consumption is an important goal of fluid therapy. Tissue oxygen delivery depends on hemoglobin concentration, oxygen tension, organ perfusion pressures, and organ vascular resistance. Organ perfusion pressures depend on systemic arterial pressure and
TABLE 46-22 -- Volume and composition of gastrointestinal fluids
Fluid Source 24-Hour Volume (mL) Na+ (mEq/L) K+ (mEq/L) Cl- (mEq/L) HCO3 - (mEq/L)
Saliva  500–2000   2–10 20–30   8–18 30
Stomach 1000–2000  60–100 10–20 100–130  0
Pancreas  300–800 135–145  5–10  70–90 95–120
Bile  300–600 135–145  5–10  90–130 30–40
Jejunum 2000–4000 120–140  5–10  90–140 30–40
Ileum 1000–2000  80–150  2–8  45–140 30
Colon  60 30  40


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the higher of organ venous pressure or tissue pressure. Arterial pressure depends on cardiac output and systemic vascular resistance. Cardiac output is related to stroke volume and heart rate, and stroke volume depends on preload, contractility, and afterload. Most general and regional anesthetics cause arteriolar and venous dilation, expanding the vascular capacity. The latter reduces peripheral venous pressure and therefore venous return and cardiac output. Fluid must be administered to expand the blood volume to compensate for venodilation. General anesthetics produce myocardial depression (see Chapter 7 ). Increasing cardiac preload by infusing fluid intravascularly to take advantage of the Starling mechanism often returns stroke volume to an acceptable range. Postoperatively, venodilation and myocardial depression rapidly subside when administration of the anesthetic is stopped. Patients with impaired cardiac or renal responses may then become acutely hypervolemic. CVE with 5 to 7 mL/kg of balanced salt solution must occur before or simultaneous with the onset of anesthesia.

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