This excellent review article appeared in the New England Journal of Medicine (October 31, 2013):
In trauma, we deal most often with hypovolemic shock owing to exanguination and spinal shock, which is a distributive shock, owing to spinal cord injury.
Of particular interest for the trauma anesthesiologist are the recommendations for vasopressors and inotropic agents and goals for hemodynamic support. The following are excerpts from this NEJM article.
α-adrenergic stimulation will increase vascular tone and blood pressure but can also decrease cardiac output and impair tissue blood flow, especially in the hepatosplanchnic region. For this reason, phenylephrine, an almost pure α-adrenergic agent, is rarely indicated.
Norepinehrine is the vasopressor of first choice; it has predominantly α-adrenergic properties, but its modest β-adrenergic effects help to maintain cardiac output. Administration generally results in a clinically significant increase in mean arterial pressure, with little change in heart rate or cardiac output. The usual dose is 0.1 to 2.0 μg per kilogram of body weight per minute.
Vasopressin deficiency can develop in patients with very hyperkinetic forms of distributive shock, and the administration of low-dose vasopressin may result in substantial increases in arterial pressure. In the Vasopressin and Septic Shock Trial (VASST), investigators found that the addition of low-dose vasopressin to norepinephrine in the treatment of patients with septic shock was safe and may have been associated with a survival benefit for patients with forms of shock that were not severe and for those who also received glucocorticoids. Vasopressin should not be used at doses higher than 0.04 U per minute and should be administered only in patients with a high level of cardiac output.
Dobutamine is the inotropic agent of choice for increasing cardiac output, regardless of whether norepinephrine is also being given. An initial dose of just a few micrograms per kilogram per minute may substantially increase cardiac output. Intravenous doses in excess of 20 μg per kilogram per minute usually provide little additional benefit.
Goals of Hemodynamic Support:
1. Arterial Pressure
The primary goal of resuscitation should be not only to restore blood pressure but also to provide adequate cellular metabolism, for which the correction of arterial hypotension is a prerequisite. Restoring a mean systemic arterial pressure of 65 to 70 mm Hg is a good initial goal, but the level should be adjusted to restore tissue perfusion, assessed on the basis of mental status, skin appearance, and urine output. A mean arterial pressure lower than 65 to 70 mm Hg may be acceptable in a patient with acute bleeding who has no major neurologic problems, with the aim of limiting blood loss and associated coagulopathy, until the bleeding is controlled.
2. Cardiac Output and Oxygen Delivery
Since circulatory shock represents an imbalance between oxygen supply and oxygen requirements, maintaining adequate oxygen delivery to the tissues is essential, but all the strategies to achieve this goal have limitations. After correction of hypoxemia and severe anemia, cardiac output is the principal determinant of oxygen delivery, but the optimal cardiac output is difficult to define.
Mixed Venous Oxygen Saturation:
Measurements of mixed venous oxygen saturation (SvO2) may be helpful in assessing the adequacy of the balance between oxygen demand and supply; SvO2 measurements are also very useful in the interpretation of cardiac output. SvO2 is typically decreased in patients with low-flow states or anemia but is normal or high in those with distributive shock.
Central Venous Oxygen Saturation:
Central venous oxygen saturation (ScvO2) is measured in the superior vena cava by means of a central venous catheter. It reflects the oxygen saturation of the venous blood from the upper half of the body only. Under normal circumstances, ScvO2 is slightly less than SvO2, but in critically ill patients it is often greater.
3. Blood Lactate Level
An increase in the blood lactate level reflects abnormal cellular function. In low-flow states, the primary mechanism of hyperlactatemia is tissue hypoxia with development of anaerobic metabolism, but in distributive shock, the pathophysiology is more complex and may also involve increased glycolysis and inhibition of pyruvate dehydrogenase. In all cases, alterations in clearance can be due to impaired liver function.
The value of serial lactate measurements in the management of shock has been recognized for 30 years. Although changes in lactate take place more slowly than changes in systemic arterial pressure or cardiac output, the blood lactate level should decrease over a period of hours with effective therapy.
In patients with shock and a blood lactate level of more than 3 mmol per liter, one study found that targeting a decrease of at least 20% in the blood lactate level over a 2-hour period seemed to be associated with reduced in-hospital mortality.