critical care medicine
Intravenous Fluid Resuscitation
End Point and Monitoring of Fluid Resuscitation
The actual end point of fluid therapy in shock is to optimize tissue perfusion. However, this parameter is not measured directly. Surrogate end points include clinical indicators of end-organ perfusion and measurements of preload. Adequate end-organ perfusion is best indicated by urine output of>0.5 to 1 mL/kg/hour. Heart rate, mental status, and capillary refill may be affected by the underlying disease process and are less reliable markers. Because of compensatory vasoconstriction, mean arterial pressure (MAP) is only a rough guideline; organ hypoperfusion may be present despite apparently normal values. An elevated arterial blood lactate level may reflect hypoperfusion and/or continued sympathetic drive from endogenous catecholamine production; however, lactate levels do not decline for several hours after successful resuscitation. The trend of the base deficit can help indicate whether resuscitation is adequate. Other investigational methods such as measurement of sublingual tissue carbon dioxide or near-infrared spectroscopy to measure tissue oxygenation through the skin may also be considered. Because urine output does not provide a minute-to-minute indication, measures of preload may be helpful in guiding fluid resuscitation for critically ill patients. Central venous pressure (CVP) is the mean pressure in the superior vena cava, reflecting right ventricular end-diastolic pressure or preload. Normal CVP ranges from 2 to 7 mm Hg (3 to 9 cm water). A sick or injured patient with a CVP<3 mm Hg is presumed to be volume depleted and may be given fluids with relative safety. When the CVP is within the normal range, volume depletion cannot be excluded, and the response to 100- to 200-mL fluid boluses should be assessed; a modest increase in CVP in response to fluid generally indicates hypovolemia. An increase of>3 to 5 mm Hg in response to a 100-mL fluid bolus suggests limited cardiac reserve. A CVP>12 to 15 mm Hg casts doubt on hypovolemia as the sole etiology of hypoperfusion, and fluid administration risks fluid overload. Because CVP may be unreliable in assessing volume status or left ventricular function, Pulmonary Artery Catheter (PAC) Monitoring may be considered for diagnosis or for more precise titration of fluid therapy if there is no cardiovascular improvement after initial therapy. Care must be taken when interpreting filling pressures in patients during mechanical ventilation, particularly when positive end-expiratory pressure (PEEP) levels exceeding 10 cm water are being used or during respiratory distress when pleural pressures fluctuate widely. Measurements are made at the end of expiration, and the transducer is referenced to atrial zero levels (mid chest) and carefully calibrated. Ultrasonography of the inferior vena cava and right ventricle can provide information on circulating volume status and overall cardiac function. However, interpretation of the images is highly user dependent and can be complicated by the presence of valvular dysfunction and the use of positive pressure ventilation. Widespread use of ultrasonography to guide volume resuscitation requires more study. Patients with traumatic hemorrhage shock may require a slightly different approach. Experimental and clinical evidence indicates that internal hemorrhage (eg, due to visceral or vascular laceration or crush) may be worsened by resuscitation to normal or supranormal MAP. Thus, some physicians advocate a systolic blood pressure of 80 to 90 mm Hg as the resuscitation end point in such patients pending surgical control of bleeding, unless higher pressure is needed to provide adequate brain perfusion. After blood loss is controlled, hemoglobin is used to guide the need for further transfusion. A target hemoglobin of 9 g/dL (90 g/L) is suggested to minimize the use of blood products. Patients who may have difficulty tolerating moderate anemia (eg, those with coronary or cerebral artery disease) are kept above 30% hematocrit. A higher hematocrit does not improve outcome and, by causing increased blood viscosity, may impair perfusion of capillary beds. 