Principles of Fluid Therapy

Objectives

This chapter will:

1.
Describe the physiologic rationale for fluid resuscitation in the intensive care unit.
2.
Discuss choice of fluid, volume, and end points for intravenous fluid resuscitation.

Administering intravenous (IV) fluid is one of the most common interventions in the intensive care unit (ICU). Although IV fluid can be used to replace free water, electrolytes, glucose, and plasma constituents (e.g., albumin), most IV fluid in the ICU is given to increase intravascular volume. Critically ill adults frequently experience either absolute hypovolemia (resulting from blood loss, diarrhea, decreased oral intake) or effective hypovolemia (increased venous capacitance resulting from sepsis, medications, adrenal insufficiency). IV fluid resuscitation can increase ventricular preload, cardiac output, and oxygen delivery, restoring hemodynamic stability and tissue perfusion. This chapter discusses the physiologic rationale for fluid therapy in the ICU; the volume, rate, and end points of fluid resuscitation; choice of fluid; and areas of ongoing controversy.

Physiologic Rationale for Fluid Administration

Hypovolemia reduces effective circulating blood volume. With mild hypovolemia, compensatory increases in heart rate, cardiac contractility, and peripheral vasoconstriction maintain systemic blood pressure and tissue perfusion. Healthy organs autoregulate their blood flow, redistributing perfusion toward the brain, heart, and kidneys and away from the skin and splanchnic bed. With more severe hypovolemia, activation of the sympathetic, renin-angiotensin, and antidiuretic hormone systems is inadequate to maintain blood pressure. Overt hypotension may be accompanied by signs of end-organ dysfunction (skin mottling, decreased urine output, altered mental status), and decreased oxygen delivery may precipitate anaerobic metabolism and lactic acidosis. Rapid administration of IV fluid to patients with hypovolemia is intended to increase intravascular volume, improve venous return and ventricular filling, and ultimately restore cardiac output, perfusion pressure, and oxygen delivery.

Resuscitation volume, end points, and fluid choice have been predicated largely on this classic physiologic model. However, evolving understanding suggests that the hemodynamic response to fluid administration depends on an intricate interaction of mean systemic filling pressure, right atrial pressure, venous resistance, and ventricular compliance, many of which are deranged during critical illness. Moreover, the traditional Starling model, in which fluid movement across the capillary membrane is governed by the balance of hydrostatic and oncotic pressure, has been challenged by increasing insight into the function of the endothelial glycocalyx. This dynamic network of glycoproteins and proteoglycans bound to the luminal side of endothelial cells regulates the movement of colloids from the intravascular to interstitial space, governing oncotic pressure and endothelial permeability. Damage to the glycocalyx during critical illness disrupts these functions, allowing outflow of protein and fluid into the interstitial space and altering the expected response to colloid and crystalloid administration. Simplistic approaches to fluid resuscitation end points (“central venous pressure > 8 mm Hg”) and fluid choice (“colloids stay in the vascular space”) are evolving to recognize that effects of fluid therapy may vary widely among patients with different pathophysiologic conditions in different phases of critical illness.

Volume, Rate, and End Point of Fluid Administration

Initial Assessment and Management

Determining intravascular volume in critically ill patients is challenging. Physical exam findings such as tachycardia and hypotension are nonspecific and, because of aberrant vascular permeability and oncotic pressure, some critically ill patients with marked peripheral edema may be intravascularly deplete. For patients with a clinical history, physical examination, and laboratory evaluation suggestive of volume depletion, current clinical practice guidelines suggest the initial administration of 20 mL/kg of IV crystalloid, given as boluses of at least 250 to 500 mL over 10 to 30 minutes, with careful monitoring of the patient's hemodynamic response.

The optimal approach to fluid management after an initial empiric fluid bolus is an area of current controversy. Patients with ongoing fluid losses (e.g., severe pancreatitis, burns) may benefit from repeated fluid boluses, sometimes receiving upwards of 10 to 20 L of IV fluid in the days after ICU admission. However, increasing recognition of the detrimental effects of fluid overload on organ function and the potential toxicities of the IV fluids has generated intense interest in objective measures to guide the volume of fluid administered.

Fluid Resuscitation Targets

End point–targeted fluid resuscitation became routine practice for many ICU providers after a 2001 trial of early goal-directed therapy (EGDT) for sepsis. Among 263 patients with sepsis and hypoperfusion, the protocolized administration of 500 mL IV crystalloid boluses every 30 minutes to achieve a central venous pressure (CVP) of 8 to 12 mm Hg, vasopressors to maintain a mean arterial pressure (MAP) of 65 mm Hg, and dobutamine and blood transfusion to attain a mixed venous oxygen saturation of at least 70% resulted in a 16% absolute reduction in mortality. Based on this study, and on related trials of goal-directed fluid therapy in the operating room, protocolized fluid resuscitation targeting CVP, MAP, and venous oxygen saturation or lactate was incorporated into international guidelines and widely adopted as standard-of-care for fluid management in ICU patients with tissue hypoperfusion.

Recently, however, three multicenter trials compared EGDT with care in which invasive resuscitation end points were optional (CVP) or forbidden (venous oxygen saturation) and did not find a benefit for EGDT. Because patients in the recent trials were less severely ill and the volume of fluid was more similar between study arms than in the original EGDT trial, the implications for the volume of fluid that should be administered during early sepsis resuscitation are unclear. Provocative studies from regions in which EGDT is not standard-of-care have shown worse outcomes with early fluid resuscitation among children with severe infection and septic adults. In these trials, administration of IV fluid appeared to precipitate respiratory failure and cardiovascular decompensation, but limited access to hemodynamic monitoring and mechanical ventilation in these studies makes extrapolation challenging. Ongoing trials comparing liberal to conservative fluid management in early septic shock may help determine the optimal volume of early fluid resuscitation (NCT02079402, NCT01663701).

These studies highlight the difficulty of assessing the risks and benefits of IV fluid administration for a given patient, and the limitations of static predictors of a patient's response to fluid (e.g., venous oxygen, lactate, or CVP). Venous oxygen and lactate levels are not sensitive or specific enough to predict whether a patient will experience hemodynamic improvement with an IV fluid bolus. Use of CVP or pulmonary artery occlusion pressure (PAOP) as surrogates for ventricular end-diastolic volume may be confounded by right ventricular compliance, valve regurgitation, and changing intrathoracic pressures. Although a very low or a very high intravascular pressure may provide some information, CVP and PAOP do not accurately or reliably predict patients' hemodynamic response to fluid challenges. In view of the numerous trials demonstrating no outcome benefit from invasive intravascular pressure measurement, focus has shifted to alternative, dynamic measures of “fluid responsiveness.”

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