Evaluation of Intravascular Volume

Evaluation of Intravascular Volume

Clinical estimation of intravascular volume must be relied upon because objective measurements of fluid compartment volumes are not practical in the clini-cal environment. Intravascular volume can be esti-mated using patient history, physical examination,and laboratory analysis, often with the aid of sophisticated hemodynamic monitoring techniques. Regardless of the method employed, serial evalua-tions are necessary to confirm initial impressions and to guide fluid, electrolyte, and blood component therapy. Multiple modalities should complement one another, because all parameters are indirect, nonspecific measures of volume; reliance upon any one parameter may lead to erroneous conclusions.

PATIENT HISTORY

The patient history is an important tool in preop-erative volume status assessment. Important fac-tors include recent oral intake, persistent vomiting or diarrhea, gastric suction, significant blood loss or wound drainage, intravenous fluid and blood administration, and recent hemodialysis if the patient has kidney failure.

PHYSICAL EXAMINATION

Indications of hypovolemia include abnormal skin turgor, dehydration of mucous membranes, thready peripheral pulses, increased resting heart rate and decreased blood pressure, orthostatic heart rate and blood pressure changes from the supine to sitting or standing positions, and decreased urinary flow rate (Table 51–1). Unfortunately, many medica-tions administered during anesthesia, as well as the neuroendocrine stress response to operative proce-dures, alter these signs and render them unreliable in the immediate postoperative period. Intraopera-tively, the fullness of a peripheral pulse, urinary flow rate, and indirect signs such as the response of blood pressure to positive-pressure ventilation and to the vasodilating or negative inotropic effects of anes-thetics, are most often used.

Pitting edema—presacral in the bedridden patient or pretibial in the ambulatory patient—and increased urinary flow are signs of excess extracel-lular water and likely hypervolemia in patients with normal cardiac, hepatic, and renal function. Late signs of hypervolemia in settings such as congestive heart failure may include tachycardia, elevated jugu-lar pulse pressure, pulmonary crackles and rales, wheezing, cyanosis, and pink, frothy pulmonary secretions.

LABORATORY EVALUATION

Several laboratory measurements may be used as surrogates of intravascular volume and adequacy of tissue perfusion, including serial hematocrits, arte-rial blood pH, urinary specific gravity or osmolality, urinary sodium or chloride concentration, serum sodium, and the blood urea nitrogen (BUN) to serum creatinine ratio. However, these measurements are only indirect indices of intravascular volume, and they often cannot be relied upon intraoperatively because they are affected by many perioperative fac-tors and because laboratory results are often delayed. Laboratory signs of dehydration may include rising hematocrit and hemoglobin, progressive metabolic acidosis (including lactic acidosis), urinary specific gravity greater than 1.010, urinary sodium less than 10 mEq/L, urinary osmolality greater than 450 mOsm/L, hypernatremia, and BUN-to-creatinine ratio greater than 10:1. The hemoglobin and hematocrit are usu-ally unchanged in patients with acute hypovolemiasecondary to acute blood loss because there is insuf-ficient time for extravascular fluid to shift into the intravascular space. Radiographic indicators of vol-ume overload include increased pulmonary vascular and interstitial markings (Kerley “B” lines) or diffuse alveolar infiltrates.

HEMODYNAMIC MEASUREMENTS

Central venous pressure (CVP) monitoring has been used in patients with normal cardiac and pulmonary function when volume status is difficult to assess by other means or when rapid or major alterations are expected. However, static CVP readings do not provide an accurate or reliable indication of volume status.

Pulmonary artery pressure monitoring has been used in settings where central venous pressures do not correlate with the clinical assessment or when the patient has primary or secondary right ventricular dysfunction; the latter is usually due to pulmonary or left ventricular disease, respectively. Pulmonary artery occlusion pressure (PAOP) readings of less than 8 mm Hg indicate hypovolemia in the presence of confirmatory clinical signs; however, values less than 15 mm Hg may be associated with relative hypo-volemia in patients with poor ventricular compliance. PAOP measurements greater than 18 mm Hg are elevated and generally imply left ventricular volume overload. The normal relationship between PAOP and left ventricular end-diastolic volume is altered by the presence of mitral valve disease (particularly ste-nosis), severe aortic stenosis, or a left atrial myxoma or thrombus, as well as by increased thoracic and pul-monary airway pressures. All PAOP measurements should be obtained at end expiration and interpreted in the context of the clinical setting. Finally, one should recognize that multiple studies have failed to show that pulmo-nary artery pressure monitoring leads to improved outcomes in critically ill patients, and that echocar-diography provides a much more accurate and less invasive estimate of cardiac filling and function.

Intravascular volume status is often difficult to assess, and goal-directed hemodynamic and fluid therapy utilizing arterial pulse contour analy-sis and estimation of stroke volume variation (eg, LIDCOrapid, Vigileo FloTrak), esophageal Doppler, or transesophageal echocardiography should be considered when accurate determination of hemo-dynamic and fluid status is important. Stroke vol-ume variation (SVV) is calculated as follows:

SVV = SV_max− SV_min/SV_mean

The maximum, minimum and mean SV are calculated for a set period of time by the various measuring devices. During spontaneous ventilation the blood pressure decreases on inspiration. During positive pressure ventilation the opposite occurs. Normal SVV is less than 10–15% for patients on controlled ventilation. Patients with greater degrees of SVV are likely to be responsive to fluid therapy. In addition to providing a better assessment of the patient’s volume and hemodynamic status than that obtained with CVP monitoring, these modali-ties avoid the multiple risks associated with central venous and pulmonary artery catheters.