RESUSCITATION FLUIDS

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CHAPTER 18 RESUSCITATION FLUIDS

Martin Schreiber, Brandon Tieu, Laszlo Kiraly, Michael Englehart

The practice of giving intravenous fluids or medication has been used since the 1600s. Slow progress was made after William Harvey provided a modern description of the circulatory system in 1638. William O’Shaughnessy theorized that patients suffering from volume loss secondary to cholera would benefit from restoration of blood to its natural specific gravity. This became the first concept of contemporary intravenous fluid therapy. Thomas Latta was credited with actually applying O’Shaughnessy’s theory and treating victims of cholera in 1832. Later in the century, Sydney Ringer described a physiologic solution with a focus on electrolyte concentrations in his animal models. Despite these early trials, application of these concepts was criticized and largely forgotten until the 20th century. The advent of modern surgery renewed interest in resuscitation as therapy to maintain intravascular volume.

World War I provided tremendous experience with resuscitation of hemorrhagic shock. Cannon’s work eloquently described the natural history and presentation of shock with primary accounts of battlefield victims. His work suggested that a delay in surgical control of bleeding was accompanied by a large increase in mortality. Furthermore, he indicated that aggressive resuscitation without surgical control could worsen hemorrhagic shock. He also indicated that resuscitation with saline could worsen existing acidosis. In subsequent decades, however, much of his work was forgotten or ignored. Then in World War II and the Korean War, practice shifted to resuscitation with plasma and blood. Blalock supported this based on his dog studies, suggesting that crystalloid fluids were rapidly lost from the intravascular space. In 1963, Shires showed that shock is accompanied by a shift of interstitial fluid into the vasculature. This discovery brought renewed interest in salt solution therapy. Subsequent decades have been characterized by further optimization in aggressive resuscitation. Specific gains have been made in the realm of intensive care, monitoring, intravenous access, and endpoints of resuscitation. Despite these advances, many controversies and questions remain. Choice of fluid has been largely unchanged and unexamined. The study of the mechanism of shock at a cellular and molecular level has yet to reveal any applicable treatments. More importantly, the complications of modern resuscitation are commonly seen in trauma intensive care units. Before discussing details on fluids, it is important to understand hemorrhage and the physiologic response.

CLASSES OF SHOCK

Shock is inadequate tissue perfusion. The humoral sympathetic response to shock causes vasoconstriction in the clinical appearance of the patient. These findings were observed by Cannon when he correlated the volume of blood loss with the patient’s clinical signs, symptoms, and blood pressure. His findings have since been validated with repeated observational studies in humans, as well as experimental studies in animals. The classes of shock are now well defined, and provide a quick means of assessing a patient’s blood loss and the level of resuscitation required (Table 1).

Table 1 Classes of Shock

AUTORESUSCITATION

The goal of the body’s compensatory mechanisms during shock is to preserve perfusion to vital organs. Bickell’s 1994 study of delayed fluid resuscitation for hypotensive patients with penetrating torso injuries demonstrated that, in the absence of resuscitation, blood pressure spontaneously increased prior to operative intervention. This finding validates observations made by Cannon, and has further been supported by subsequent data, which demonstrated that during hypotensive resuscitation blood pressure spontaneously rises toward normal in the absence of fluid therapy. Numerous mechanisms exist to account for these findings, specifically vasoconstriction, a reduction in capillary hydrostatic pressure, and hormonal responses. The sum of these responses is reflected in the phases of shock, which in turn help dictate the resuscitation strategy.

Vasoconstriction and Reduction of Capillary Hydrostatic Pressure

Peripheral and splanchnic vasoconstriction help to redirect blood flow away from muscle, skin, bowel, kidneys, and other nonvital organs. This is accomplished through the release of epinephrine, norepinephrine, and vasopressin. By increasing the peripheral vascular resistance, and effectively reducing the circulating volume through which the blood must pass, the mean arterial pressure is increased. Initially, during compensated shock, only the precapillary sphincter is constricted, reducing the capillary hydrostatic pressure and increasing the peripheral resistance. As the shock worsens, both the precapillary and postcapillary sphincters are constricted, leading to anaerobic metabolism, which results in excess lactate and acidosis. As the severity of shock increases, the postcapillary sphincter relaxes secondary to hydrogen ion buildup, releasing the metabolic byproducts into the circulation. The result is reperfusion injury. This is common when the system decompensates, and the patient shows signs of florid shock and global hypoperfusion.

The subsequent decrease in capillary hydrostatic pressure reduces the volume of plasma lost from the vasculature into the interstitial space, and increases return of interstitial fluid into the vascular space. This is an additional method of increasing venous return to the heart. Given the large capacitance of the venous system, larger volumes of circulating blood are stored within the veins compared to the arteries. According to the Frank-Starling laws of cardiac performance, the cardiac output is directly proportional to the venous return to the heart (preload) (Figure 1). As venous return decreases, so does cardiac output, and thereby arterial pressure to perfuse vital organs.

Figure 1 The effect of increased right atrial pressure on cardiac output. Increases in right atrial pressure are accomplished through either an increase in circulating blood volume, or a decrease in venous compliance. Cardiac output increases linearly in response to increased right atrial pressure.

(Adapted from Berne RM, Levy MN: Cardiovascular Physiology, 3rd ed. St. Louis, MO, Mosby, 1977.)

Hormonal Response

In response to hypotension, numerous hormonal pathways are initiated to restore circulating plasma volume. Vasopressin plays a major role in peripheral vasoconstriction. Additionally, it acts to increase free water absorption in the collecting ducts of the kidneys. In response to lower pressures at the afferent arteriole within the kidney, renin is released, triggering the renin/angiotensin/aldosterone cascade. The effect is to increase the absorption of sodium, which in turn increases water absorption. Additionally, angiotensin-II acts as a potent peripheral vasoconstrictor. Finally, cortisol acts to increase extracellular osmolarity and increased lymphatic flow.

The reduction of capillary hydrostatic pressure and the hormonal response increase venous return during the first 1–2 hours following injury, but this may be inconsequential in the setting of severe hemorrhage. Cessation or slowing of ongoing hemorrhage also contributes to a spontaneous rise in blood pressure by limiting ongoing fluid losses. The remainder of the response is carried out through vasoconstriction and the redistribution of blood flow, accounting for the majority of increased venous return. If prolonged, this can have a damaging, and sometimes irreversible effect upon the tissues supplied by the splanchnic circulation. This will result in ischemia and potential reperfusion injury.

Combined, the aforementioned physiologic effects produce the classic signs and symptoms exhibited by patients in hypovolemic shock. The progression from compensated to uncompensated shock gives rise to the physical findings of the systemic insult (Figure 2). Initially, compensated shock affects the periphery, manifesting the symptoms of cool extremities, cyanosis, mottling of the skin, and decreased capillary reperfusion (blanching). As the severity of shock progresses, vasoconstriction affects the torso, producing oliguria as the main clinical sign. Finally, in severe classes of shock, perfusion of the heart and brain are affected, producing cardiac dysrhythmias and a reduced level of consciousness. Over the hours following injury, these mechanisms are in constant flux, in efforts to restore homeostasis to the injured system.