Shock Review: Goals of Therapy

Shock Review (Part 2 of 2)

(See also Shock Review Part 1: Mechanisms and Therapies)

Shock results from serious illness compromising either vascular muscle tone (most commonly septic shock), the heart's function, or the volume of plasma inside blood vessels. The true goal of treatment for shock is to correct the underlying cause, but except for some causes of shock (STEMI, hypovolemia) that's not usually immediately possible. Interim goals for treatment for shock are to augment perfusion and oxygen delivery and minimize organ damage until the body's natural homeostatic mechanisms return. While simple in theory, the complexity of the body's response to shock and its therapies can make realtime goal-directed management of shock surprisingly challenging.

Systemic Arterial Pressure Goals in Shock

Restoring systemic blood pressure to a mean arterial pressure between 65 - 70 mm Hg is "a good initial goal," but this threshold pressure should not be considered an absolute. Some patients with uncontrolled hypertension at baseline may require a higher MAP goal, for example. On the other hand, healthy people with normotension at baseline and pure hypovolemia from a GI bleed may tolerate MAPs lower than 65 mm Hg while awaiting rapid blood transfusion. Once an acceptable MAP value is achieved with fluid resuscitation and vasopressors, proper management of shock necessitates continued close attention to mental status, urine output, and skin appearance and temperature, along with laboratory values. Upward titration or addition of vasopressors (and/or inotropes for low cardiac output states) is appropriate in patients believed to require higher MAP goals. Urine output particularly should be followed closely with such interventions (goal 0.5 mL/kg/hr), both for feedback on success and to assess need for renal replacement therapy.

Cardiac Output as a Goal of Therapy for Shock

Although cardiac output is a major driver for oxygen delivery to tissues, "the optimal cardiac output is difficult to define." Absent a pulmonary artery catheter, cardiac output is even harder to measure accurately, as described in part 1 of this topic. Further, the "optimal" cardiac output can change in the same patient over time, and can vary widely between patients. Therefore, using a prespecified target for cardiac output is not recommended; rather, a trends in response to treatment should be used (if cardiac output is used at all). As a goal of therapy for shock, cardiac output should take a back seat to other methods of assessing response to therapy, authors suggest.

Oxygen Delivery, SvO2 and ScvO2 in Shock

Mixed venous oxygen saturation (SvO2) is measured in the pulmonary artery; because it requires a Swan-Ganz catheter, it is uncommonly used. Central venous oxygen saturation (ScvO2) is a useful surrogate for SvO2 and is measured in the superior vena cava through an ordinary central venous catheter. ScvO2 only measures venous blood returning from the upper half of the body, while SvO2 samples the true mixed venous blood leaving the right heart. Central (ScvO2) is normally slightly lower than mixed (SvO2), but is often higher than SvO2 in patients in shock. Reported normal ranges for SvO2 vary from 60-80%; a normal SvO2 of 70% is frequently cited. ScvO2 and SvO2 are usually below normal in patients with hypovolemia (including GI hemorrhage) and cardiogenic shock, or low-flow states; they are usually high in people with distributive shock (e.g., septic shock). The use of continuous ScvO2 monitoring as part of the seminal "sepsis bundle" was famously shown to markedly reduce mortality from septic shock; this central tenet of the care of severe sepsis has been questioned and challenged, and is being tested further in three randomized trials.

Using Lactate to Guide Treatment of Shock

Lactate is produced during tissue hypoxemia and hypoperfusion, and is useful but flawed as a goal for the treatment of shock. Lactate production and clearance are complex and inconsistent between shock states and patients. In cardiogenic and hypovolemic shock, lactate rises as tissue hypoxemia results in increased anaerobic metabolism. In distributive (usually septic) shock, mechanisms other than pure tissue ischemia (anaerobic metabolism) may contribute to elevated lactate levels. Impaired liver function (either pre-existing or due to shock) may reduce lactate clearance in any patient with shock, resulting in persistently high lactate values even after perfusion is restored and lactate production normalizes. With the above recognized limitations, serial lactate measurements can undoubtedly be useful for assessing the response to therapies for shock. Lactate clearance has shown promise as a surrogate for central venous oxygenation in randomized trials, and the utility of lactate clearance as a goal of sepsis therapy is periodically debated.

(See also Shock Review Part 1: Mechanisms and Therapies)

With gratitude to: Jean-Louis Vincent and Daniel De Backer. Circulatory shock. N Engl J Med 2013; 369:1726-1734.