SURGICAL FLUID BALANCE AND SHOCK

Physiologic changes during surgery and anesthesia lead to shifts in fluid balance. For example, epidural, spinal, or caudal anesthesia may all cause variable amounts of sympathetic blockade (see Chapter 61 and Chapter 71 ). Although younger and healthier patients may tolerate sympathectomy, patients who are severely dehydrated or on antihypertensive drugs or diuretics may not be able to respond to the effects of sympathectomy. It is common to administer

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Although inhaled anesthetics do not directly alter fluid losses, all anesthetics may blunt the normal physiologic responses to hypovolemia and the stress response. The stress response to surgery involves an increase in ADH production, which can be blocked with anesthetics. Superimposed are the variable effects of intravenous and inhalational agents on the myocardium, venous return, blood pressure, and the vasculature. Mechanical ventilation can decrease the release of atrial natriuretic hormone and increase the release of ADH, resulting in retention of sodium and fluids.

In addition to blood loss, significant third space loss may occur, which essentially involves fluid that is still in the body but not contributing to intravascular volume, oxygen delivery, or waste removal; this is difficult to measure. Simple restoration of blood volume can be inadequate to ensure survival.^[104] Patients undergoing major surgical procedures require fluid replacement beyond simple blood loss, and the anesthesiologist plays a vital role in assessing and ultimately administering appropriate fluid therapy in intraoperative and postoperative clinical settings.

Shock

Shock can be defined as dysfunction of intracellular processes due to lack of energy. This lack of energy is caused by deficient delivery of oxygen to tissue, resulting in an inability to maintain normal cellular respiration. Although shock is a cellular problem, therapy is directed at the systemic delivery of oxygen to the tissue.

In normal patients, the body maintains a balance between delivery of oxygen (DO₂ ) and global oxygen consumption (VO₂ ). Global oxygen consumption is a measure of the total amount of oxygen consumed by all tissues per minute. The amount of oxygen consumed as a fraction of the amount delivered defines the oxygen extraction ratio (OER):

OER = VO₂ /DO₂

VO₂ in a normal adult undertaking routine activities is approximately 250 mL/min with an extraction ratio of 25%. The OER can be increased to 75% during extreme exercise in a healthy adult. Oxygen not extracted from the blood returns to the lungs and can be measured as the mixed venous saturation (SVO₂ ), which is a measure of global tissue oxygenation. SVO₂ below 60% to 70% is usually indicative of insufficient DO₂ . A mixed venous blood sample is needed because the saturation of venous blood varies depending on the organ being measured. Venous blood returning from the liver has a saturation of 40% to 50%, and blood from the kidneys may have a saturation exceeding 80%.

Oxygen consumption is directly related to cellular metabolic rate. Sympathetic activity, shivering, and physical activity all increase the cellular metabolic rate. As the delivery of oxygen decreases or the consumption increases,

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Tissue hypoxia and shock can result from inappropriate delivery of oxygen or inappropriate use of oxygen. There are two distinct types of shock. Type I involves patients who suffer from decreased delivery of oxygen such as in hypovolemic or cardiogenic shock. Type II involves problems with inappropriate distribution of oxygen delivery such as in septic or neurogenic shock. Regardless of the underlying cause, appropriate fluid management is an absolute necessity.

Proper fluid management of shock can have significant impact on the delivery of oxygen to tissues and prevention of anaerobic metabolism. Until recently, vigorous fluid loading and ionotropes were commonly used in what was called goal-directed therapy during the care of critically ill patients. Goal-directed therapy was based on the principle that critically ill patients had supranormal VO₂ values. It was thought that by increasing DO₂ to supraphysiologic levels, cellular metabolism could be maintained in an aerobic state, and multisystem organ dysfunction could be avoided.^[105] However, in the 1990s, two large, randomized trials showed this therapy to be ineffective and potentially dangerous.^{[106] [107]} Continuing research has demonstrated that identifying and treating volume depletion and poor cardiac function early in shock is beneficial.^{[108] [109] [110]} The key to the different results between the early study by Shoemaker and colleagues ^[105] and later trials is the key of recognizing the difference between early and late shock. Early shock involves acute tissue hypoxemia with end organs not yet sustaining irreversible damage. In type I shock (hypovolemic or cardiogenic), prompt treatment of the underlying cause of tissue hypoperfusion may prevent patients from progressing to late shock and multisystem organ failure. If tissue oxygenation is not restored soon enough, end-organ failure and endothelial cell dysfunction occur, signaling the onset of late shock. With end-organ failure and endothelial cell dysfunction, the body's normal control of regional blood flow is impaired, and further oxygen delivery to tissue is compromised. At this point, further increasing the blood flow with use of overly aggressive volume loading and ionotropes does not improve tissue oxygenation because blood is not being delivered to the tissue that needs it. During early shock, aggressive fluid resuscitation is appropriate to minimize end-organ hypoxemia as quickly as possible. After the patient has progressed to late shock, it is still important to maintain normal intravascular volumes, but overly aggressive therapy with fluids and pressors has been shown to be detrimental.