Resuscitation of Hypovolemic Shock

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191 Resuscitation of Hypovolemic Shock

Fluids have been given intravenously (IV) for the management of fluid deficits for more than 100 years. In 1883, the English physiologist Sidney Ringer discovered that calcium-containing tap water was better than distilled water for maintaining the viability of tissues from animals in vitro. The understanding of the circulatory system and the importance of maintaining adequate circulatory volume were realized long ago. Furthermore, the desired elements and their approximate concentrations in IV fluids for plasma substitution have been known for many years.

The first reported IV transfusion occurred in 1492. In a desperate attempt to save a dying pope, blood was transfused from three youngsters, using a vein-to-vein anastomosis. The pope and all three youngsters died. The first known successful animal-to-animal transfusion was carried out in 1667. In 1818, Dr. James Blundell performed the first successful transfusion on a patient suffering from hemorrhage during childbirth. In 1830, the gold-plated steel needle for IV use was invented. In 1831, a paper published by O’Shaughnessy described the need for administering salts and water to cholera victims, an idea that was put into practice by Thomas Latta soon thereafter. During the 1930s, Baxter and Abbott produced the first commercial saline solutions. In the 1950s, plastic IV tubing replaced rubber tubing, and soon thereafter, the central venous approach for venous access was described by a French military surgeon. This approach represented a breakthrough for estimations of the state of hydration (central venous pressure [CVP] measurements) and the need for volume support.

Blalock’s fundamental work on shock showed that injury precipitated obligatory local and regional fluid losses, the effects of which could be ameliorated by vigorous restoration of intravascular volume. This concept became a cornerstone to the understanding of the pathophysiology of shock and provided the fundamental rationale for IV therapy for hemorrhage and hypovolemia.

The introduction of blood transfusions as the result of contributions by surgeons during World War I and World War II dramatically changed outcomes in cases of severe hemorrhage. During the Korean War, fluid overload became a common and lethal side effect of resuscitation, owing to a lack of knowledge about how infusates disperse and are eliminated during trauma. Between the Korean War and the Vietnam War, Shires and colleagues described the shifts of fluid and electrolytes into cells after severe hemorrhagic shock. As a consequence, treatment of patients with shock was altered during the Vietnam War, leading to better outcomes and a lower incidence of acute renal failure.

Epidemiology of Severe Hemorrhagic Shock

Traumatic injury is the leading cause of death for individuals younger than 44 years of age in the United States. Overall, trauma results in approximately 150,000 deaths per year, and severe hypovolemia due to hemorrhage is a major factor in nearly half of those deaths. Approximately one-third of trauma deaths occur out of hospital, and exsanguination is a major cause of death occurring within 4 hours of injury. The distribution of battlefield injuries in the Vietnam War showed that 25% of deaths occurred as a result of massive exsanguinations and that the victims were not salvageable. An additional 19% of deaths occurred in cases that were deemed salvageable, and these were the result of torso exsanguinations (10%) and peripheral exsanguinations (19%). As evidenced recently in the Iraq campaign, the fighting of the future is likely to involve terrorists and guerrilla interdictions and will be fought by small groups of combatants over shorter time periods with smaller numbers of casualties at any point in time. However, because of the likely locations of these conflicts, evacuation by air may be difficult or impossible, as was the case in Somalia in 1993. As a result, immediate and even ongoing treatment of casualties may be significantly extended. Shock and ensuing circulatory failure, therefore, may result from a variety of different trauma scenarios. Therapies used in the field may vary depending on the time frame from injury to medical evacuation, the skills and resources of first responders, and the field site of combatant injury.

Mechanisms of injury and severity of blood loss as well as prehospital interventions vary widely among trauma centers. Preferred fluid resuscitation strategies and optimal blood pressures are still being studied.^1,² The number of preventable deaths due to hemorrhage are still significant. Definitive control of hemorrhage and resuscitative strategies are the cornerstone of treatment.³

Current State of Knowledge About Inadequate or Incomplete Resuscitation in Hemorrhagic and Hypovolemic Shock

Early studies by Wiggers showed that bleeding animals to a shock state followed by reinfusion of blood would not save the animal’s life. This phenomenon was termed irreversible shock. Clinically, circulatory collapse is the common endpoint of irreversible shock whether it is precipitated by trauma, hemorrhage, or severe hypovolemia.

Hemodynamic Phases of Irreversible Shock

There are four distinct phases of irreversible shock. Phase I is a nonhypotensive period of hemorrhage persisting through a 20% blood volume loss. It is associated with a reduction in cardiac output in the resting individual. In phase II at roughly 20% of blood volume loss, mean arterial pressure decreases due to an inappropriate reduction in sympathetic tone known as Bezold-Jarisch or empty ventricle reflex. There are variations in the blood volume loss required for this reflex, and in animal models it is modulated by the degree of external stress or pain. Arterial blood pressure stabilizes in phase III as the brain triggers an intense vasoconstriction of all nonessential organs. Blood is diverted to the heart and brain. If hypovolemia is not corrected, an irreversible state of shock in phase IV is entered. During hemorrhage there is also increased adhesion of polymorphonuclear neutrophils leading to leukosequestration in the microcirculation. These processes (decreased cardiac output, vasoconstriction, and leukosequestration) lead to impaired tissue perfusion and eventual death.

Cardiovascular and Hemodynamic Response

Shock is defined as inadequate delivery of O₂ to metabolically active tissues. Failure of O₂ delivery can lead to eventual organ dysfunction and ultimate complete circulatory collapse. Guyton described three major stages describing the mechanisms.⁴ First is compensated shock, in which the individual will achieve full recovery with minimal interventions. Regional tissues and organs have different mechanisms to prevent damage. The next stage is decompensated shock. Aggressive resuscitation is required in this stage, or a substantial fraction of individuals will die. There is a poor correlation between changes in cardiac output and systemic blood pressure. Irreversible shock is the last stage. Shock has progressed to the point that all known therapies are inadequate.