Resuscitation of Hypovolemic Shock

191 Resuscitation of Hypovolemic Shock



James Kasiewicz, Juan Carlos Puyana


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.



image 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



image 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.



Neuroendocrine Response


Pressure and stretch receptors in the carotid body and aortic arch play a key role in maintaining perfusion to the heart and brain. The nervous system responds immediately to loss of circulating blood volume with sympathetically mediated arteriolar and venous vasoconstriction. Baroreceptors in the carotid bulb and aortic arch sense decreased stretch in the arterial wall. Afferent vagal fibers carry signals that tonically inhibit central processors. A decrease in the effective circulating blood volume or blood pressure causes release of the chronic inhibition imposed by baroreceptors. This message ascends to the nucleus tractus solitarius in the medulla oblongata, resulting in tonic inhibition of heart rate and up-regulation of the sympathetic system.


Acute hypovolemia initiates multiple endocrine responses. The nucleus tractus solitarius signals the hypothalamus to release corticotropin releasing factor and vasopressin. Consequently, corticotropin (ACTH), cortisol, vasopressin, and glucagon levels increase. Glucagon and cortisol are crucial in providing substrate for energy production. Circulating catecholamines inhibit insulin release to increase glucose level. The renin-aldosterone system is stimulated to minimize loss of fluid or salt. Angiotensin II also promotes vasoconstriction. The summation of the neuroendocrine response is to maximize cardiac function, conserve salt and water for the maintenance of circulating blood volume, and provide nutrients and oxygen to the heart and brain.



Metabolic Response


If hemorrhage is massive, the compensatory mechanisms designed to spare blood flow to the brain and heart may be overwhelmed, as occurs in cases of irreversible shock. However, if the hemorrhage is controlled or fluid replacement therapy is initiated promptly, the patient may enter a phase described as compensatory shock. Recent observations in severely injured patients suggest that continuous monitoring of oxidative metabolism and tissue pH in peripheral organs may be used as indicators of cellular stress and impaired tissue perfusion. Minimally invasive assessment of cellular stress—using interstitial pH, tissue PCO2, and nicotinamide adenine dinucleotide (NADH) autofluorescence (marker of cellular redox state) as read outs—may reflect anaerobic metabolism and dysoxia. These measurements have been obtained from the gut mucosa, skeletal muscle, subcutaneous tissue, and several other organs. Measurements such as tissue PCO2, PO2, and pH in these organs have been correlated with specific measurements of cellular dysfunction specific to those organs.


As a consequence of the stoichiometry of the reactions responsible for the substrate level phosphorylation of adenosine diphosphate (ADP) to form adenosine triphosphate (ATP), anaerobic metabolism is inevitably associated with the net accumulation of protons. Accordingly, determination that tissue pH is not in the acid range should be sufficient to conclude that perfusion (and therefore arterial oxygen content) are sufficient to meet the metabolic demands of the cells, even without knowledge of the actual values for tissue blood flow or oxygen delivery. By the same token, the detection of tissue acidosis should alert the clinician to the possibility that perfusion is inadequate. It seems likely that monitoring tissue PCO2 (tissue capnometry) will play a role in establishing thresholds for and transition points into the metabolic failure associated with circulatory collapse. By eliminating the potentially confounding effects of systemic hypocarbia or hypercarbia, calculating and monitoring the gap between tissue PCO2 and arterial PCO2 may prove to be even more valuable than simply following changes in tissue PCO2.


Weil et al. described a sublingual PCO2 sensor and demonstrated that changes in sublingual PCO2 are more sensitive to changes in cardiac output and blood pressure than any other parameter currently used to quantify hypoperfusion. Shoemaker et al. described the use of transcutaneous oxygen tension (PtcCO2) as an early warning signal of tissue hypoxia and transcutaneous carbon dioxide tension (PtcCO2) as an early signal of tissue hypoperfusion. These authors proposed the use of transcutaneous sensors for the assessment of PtcO2 and PtcCO2 that have been used for years in neonatal medicine as a surrogate measure of arterial blood gases. They showed that compared with survivors, patients who died had significantly lower PtcO2 and higher PtcCO2 values, beginning with the early stage of resuscitation. Periods of PtcCO2 at less than 50 mm Hg for more than 60 minutes or PtcCO2 at greater than 60 mm Hg for more than 30 minutes were associated with 90% mortality and 100% morbidity.


McKinley and colleagues have demonstrated a correlation between skeletal muscle PCO2, PO2, and pH with hemorrhagic shock using fiberoptic sensor technology that allows for continuous monitoring. Both skeletal muscle and gastric mucosa respond similarly to hypotension, and the magnitude of this response is similar for gastric intramucosal pH (pHi) and muscle pH. Skeletal muscle parameters (PO2, PCO2, and pH), however, appear to indicate a greater severity of shock and more prolonged recovery than mixed venous measurements or gastric mucosal parameters. Muscle PO2 may also provide information that is comparable to other more elaborate calculations of O2 delivery and utilization. In one case report, continuous monitoring of skeletal muscle pH, PCO2, and PO2 was able to detect ongoing hemorrhage of a severely injured trauma patient in the setting of “normal” systemic variables. Although preliminary, these findings suggest that continuous monitoring of skeletal muscle pH and related parameters may provide a minimally invasive and more sensitive way of following the resuscitative effort.

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Jul 7, 2016 | Posted by in CRITICAL CARE | Comments Off on Resuscitation of Hypovolemic Shock

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